9648621 1 rate 3-6 and 22-24 months old . In the soleus muscle, the be 3-6 and 22-24 months old. In the soleus muscle, t 263 9648621 1 nimals, irrespective of gender . In the EDL, fibres expressin s, irrespective of gender. In the EDL, fibres expr 389 9648621 1 ng individuals of both genders . The V0 of soleus fibres expr dividuals of both genders. The V0 of soleus fibres 594 9648621 0 MyHC isoform decreased (P < 0 . 001) by 40% with age in spite isoform decreased (P < 0.001) by 40% with age in 671 9648621 1 an unchanged MyLC composition . In the EDL, the V0 of fibres nchanged MyLC composition. In the EDL, the V0 of f 734 9648621 1 ffer between males and females . In conclusion, similar age-r between males and females. In conclusion, similar 868 9648621 1 from both male and female rats . The present results demonstr both male and female rats. The present results dem 1007 9648621 1 during ageing in both genders . ng ageing in both genders. 1242 8445982 1 lpain and cathepsin D activity . Chronic exposure to ozone in and cathepsin D activity. Chronic exposure to ozo 124 8445982 0 enates of animals exposed to 1 . 0 ppm ozone than in those of s of animals exposed to 1.0 ppm ozone than in thos 250 8445982 0 those of animals exposed to 0 . 5 ppm ozone or of controls. A e of animals exposed to 0.5 ppm ozone or of contro 300 8445982 1 o 0.5 ppm ozone or of controls . An increase in activity of 2 ppm ozone or of controls. An increase in activity 327 8445982 1 ved in the soluble supernatant . The increase in activity did n the soluble supernatant. The increase in activit 404 8445982 1 y ozone effects on calpastatin . Addition of 32 mM carnitine ne effects on calpastatin. Addition of 32 mM carni 488 8445982 1 tivity proportionately smaller . Cathepsin D activity was lit y proportionately smaller. Cathepsin D activity wa 637 8445982 1 D activity was little altered . Changes in calpain activity tivity was little altered. Changes in calpain acti 678 8445982 1 e to ozone may magnify changes . Ozone exposure may cause cha ozone may magnify changes. Ozone exposure may caus 844 8445982 1 es in brain protein metabolism . brain protein metabolism. 906 10422565 1 ibody specificity was analyzed . The IgA was successfully elu specificity was analyzed. The IgA was successfull 137 10422565 1 citrate buffer and collagenase . The elution procedure did no te buffer and collagenase. The elution procedure d 222 10422565 1 ine of antigen-binding ability . Because of the limited amoun f antigen-binding ability. Because of the limited 446 10422565 1 from which the IgA had derived . Moreover, kidney tissues fro which the IgA had derived. Moreover, kidney tissue 611 10422565 1 ith the kidney lysates, either . The eluted IgA, however, did he kidney lysates, either. The eluted IgA, however 798 10422565 0 emophilus influenzae (34-kDa H . influenzae) was most clearly ilus influenzae (34-kDa H. influenzae) was most cl 936 10422565 1 rming by Western blot analysis . The reactivity of the eluted by Western blot analysis. The reactivity of the e 1085 10422565 0 e eluted IgA with the 34-kDa H . influenzae antigen was seen ted IgA with the 34-kDa H. influenzae antigen was 1137 10422565 1 lar IgA deposits, respectively . The reactivity of serum IgA gA deposits, respectively. The reactivity of serum 1271 10422565 1 trol individuals, respectively . The surerum IgA from the IgA individuals, respectively. The surerum IgA from th 1529 10422565 1 than did healthy control IgAs . These results suggest that t did healthy control IgAs. These results suggest t 1663 10422565 0 ults suggest that the 34-kDa H . influenzae plays an importan suggest that the 34-kDa H. influenzae plays an imp 1704 10422565 1 st certain IgA nephritis cases . rtain IgA nephritis cases. 1800 12192544 1 nd malignant, for many decades . However, surgery has not bee lignant, for many decades. However, surgery has no 125 12192544 1 cordance with research results . In benign cases, surgery has nce with research results. In benign cases, surger 231 12192544 1 s organ preserving as possible . In several instances, howeve an preserving as possible. In several instances, h 317 12192544 1 currence is as low as possible . For instance, total thyroide nce is as low as possible. For instance, total thy 469 12192544 1 high levels of autoantibodies . Several tools, e.g. magnifyi levels of autoantibodies. Several tools, e.g. mag 669 12192544 0 toantibodies. Several tools, e . g. magnifying glasses, bipola ibodies. Several tools, e.g. magnifying glasses, b 687 12192544 0 antibodies. Several tools, e.g . magnifying glasses, bipolar odies. Several tools, e.g. magnifying glasses, bip 689 12192544 1 g the morbidity at a low level . Most recently, minimally inv morbidity at a low level. Most recently, minimall 899 12192544 1 disorders of the thyroid gland . In the case of malignant dis ders of the thyroid gland. In the case of malignan 1038 12192544 0 urgical extent is justified, e . g. in patients with micro-PTC al extent is justified, e.g. in patients with micr 1200 12192544 0 gical extent is justified, e.g . in patients with micro-PTC ( extent is justified, e.g. in patients with micro- 1202 12192544 1 noma, diameter less than 1 cm) . Whether a limited surgical a diameter less than 1 cm). Whether a limited surgi 1285 12192544 0 so justified in other cases, e . g. in any patient with intrat stified in other cases, e.g. in any patient with i 1358 12192544 0 justified in other cases, e.g . in any patient with intrathy ified in other cases, e.g. in any patient with int 1360 12192544 1 ject of ongoing investigations . One of the most intriguing r of ongoing investigations. One of the most intrigu 1524 12192544 1 ry medullary thyroid carcinoma . In these patients, the timin dullary thyroid carcinoma. In these patients, the 1684 12192544 1 ne RET proto-oncogene mutation . Surgery will certainly conti T proto-oncogene mutation. Surgery will certainly 1889 12192544 1 ead of general recommendations . f general recommendations. 2073 7584507 1 re probably cellular in nature . The potentiation of these re obably cellular in nature. The potentiation of the 128 7584507 1 ourse of papilloma progression . Certain strains of the bacte of papilloma progression. Certain strains of the 211 7584507 1 d natural killer cell activity . This study involves the use ural killer cell activity. This study involves the 411 7584507 1 n induced papilloma regression . Papillomas were treated by i uced papilloma regression. Papillomas were treated 559 7584507 0 intralesional injection of a C . parvum suspension. Treated p lesional injection of a C. parvum suspension. Trea 618 7584507 1 tion of a C. parvum suspension . Treated papillomas were biop of a C. parvum suspension. Treated papillomas were 637 7584507 1 t various stages of regression . Tissue samples were subjecte ious stages of regression. Tissue samples were sub 703 7584507 1 fy specific infiltrating cells . Results showed that intrales ecific infiltrating cells. Results showed that int 806 7584507 0 ralesional administration of C . parvum was capable of induci ional administration of C. parvum was capable of i 861 7584507 1 ovine papillomas in 8-15 weeks . Immunological staining revea papillomas in 8-15 weeks. Immunological staining 939 7584507 1 ed infiltration of neutrophils . filtration of neutrophils. 1122 9420350 1 ostic and treatment approaches . Although it could be argued and treatment approaches. Although it could be ar 207 9420350 0 ic options to parents in the E . D. management of febrile chil tions to parents in the E.D. management of febrile 331 9420350 0 options to parents in the E.D . management of febrile childr ons to parents in the E.D. management of febrile c 333 9420350 1 t in a group of these children . METHODS: Convenience sample a group of these children. METHODS: Convenience sa 537 9420350 0 le children presenting to an E . D. at risk for occult bactere ildren presenting to an E.D. at risk for occult ba 605 9420350 0 children presenting to an E.D . at risk for occult bacteremi dren presenting to an E.D. at risk for occult bact 607 9420350 1 at risk for occult bacteremia . A standardized information s isk for occult bacteremia. A standardized informat 638 9420350 1 nformation sheet was presented . A parent survey of preferenc ation sheet was presented. A parent survey of pref 686 9420350 1 survey of preferences followed . RESULTS: In 37 patients, mos y of preferences followed. RESULTS: In 37 patients 727 9420350 1 making process for their child . CONCLUSIONS: While preferred g process for their child. CONCLUSIONS: While pref 872 9420350 0 often not possible when the E . D. is busy. Physicians may fi n not possible when the E.D. is busy. Physicians m 1072 9420350 0 ften not possible when the E.D . is busy. Physicians may find not possible when the E.D. is busy. Physicians may 1074 9420350 1 possible when the E.D. is busy . Physicians may find it desir ble when the E.D. is busy. Physicians may find it 1083 9420350 1 l personal practice preference . sonal practice preference. 1299 9878681 1 YT) and diabetes mellitus (DM) . In contrast to mendelian dis nd diabetes mellitus (DM). In contrast to mendelia 256 9878681 1 factors' are more appropriate . For these diseases, genetic ors' are more appropriate. For these diseases, gen 522 9878681 1 usceptibility is heterogeneous . The well-studied diseases su tibility is heterogeneous. The well-studied diseas 583 9878681 1 ultimately to disease outcome . Two types of such allelic va mately to disease outcome. Two types of such allel 974 9878681 1 biological risk factor traits . For all the three diseases c ogical risk factor traits. For all the three disea 1420 9878681 1 istory is a strong risk factor . CHD is one of the major cont y is a strong risk factor. CHD is one of the major 1525 9878681 1 most industrialized countries . Evidence from epidemiologica industrialized countries. Evidence from epidemiol 1609 9878681 0 , genetic hyperlipidaemias etc . , indicate that lipids play a etic hyperlipidaemias etc., indicate that lipids p 1701 9878681 1 ole in the pathogenesis of CHD . The known lipid-related risk n the pathogenesis of CHD. The known lipid-related 1767 9878681 1 ed levels of Lp(a) lipoprotein . Among the risk factors which vels of Lp(a) lipoprotein. Among the risk factors 2046 9878681 1 vated plasma fibrinogen levels . In addition to the above, hy plasma fibrinogen levels. In addition to the abov 2216 9878681 1 important risk factors for CHD . Among the environmental risk tant risk factors for CHD. Among the environmental 2358 9878681 1 , stress, lack of exercise etc . About 60% of the variability ess, lack of exercise etc. About 60% of the variab 2464 9878681 1 olesterol is genetic in origin . While a few genes have been erol is genetic in origin. While a few genes have 2541 9878681 0 large effects on this trait (e . g., LDLR, familial defective effects on this trait (e.g., LDLR, familial defec 2638 9878681 0 rge effects on this trait (e.g . , LDLR, familial defective ap ffects on this trait (e.g., LDLR, familial defecti 2640 9878681 1 ell as environmental exposures . A proportion of this variati s environmental exposures. A proportion of this va 2847 9878681 1 olesterol levels, respectively . A polymorphism at the apoB g erol levels, respectively. A polymorphism at the a 3013 9878681 1 ly not mediated through lipids . High density lipoprotein cho t mediated through lipids. High density lipoprotei 3123 9878681 1 c lipase (LIPC) gene functions . Mutations in the apoA1 gene ase (LIPC) gene functions. Mutations in the apoA1 3261 9878681 1 lipoprotein cholesterol levels . Polymorphism at the apoA1--C rotein cholesterol levels. Polymorphism at the apo 3430 9878681 1 ated with hypertriglyceridemia . The apo(a) gene which codes with hypertriglyceridemia. The apo(a) gene which c 3512 9878681 1 ng sequence known as Kringle 4 . The size of the gene correla quence known as Kringle 4. The size of the gene co 3690 9878681 1 the size of the Lp(a) protein . The smaller the size of the size of the Lp(a) protein. The smaller the size of 3758 9878681 1 he higher are the Lp(a) levels . (ABSTRACT TRUNCATED) gher are the Lp(a) levels. (ABSTRACT TRUNCATED) 3834 11584368 1 r diseases leading to fibrosis . Anti-inflammatory drugs are eases leading to fibrosis. Anti-inflammatory drugs 112 11584368 1 es that may cause side effects . Therefore, dexamethasone cou at may cause side effects. Therefore, dexamethason 216 11584368 1 ti-inflammatory drug to the KC . The effectiveness of Dexa(5) flammatory drug to the KC. The effectiveness of De 376 11584368 1 le duct ligation (BDL) in rats . Dexa(5)-Man(10)-HSA accumula ct ligation (BDL) in rats. Dexa(5)-Man(10)-HSA acc 510 11584368 1 found almost exclusively in KC . Active dexamethasone was lib almost exclusively in KC. Active dexamethasone wa 687 11584368 1 dotoxin-activated liver slices . In vivo, however, this was a in-activated liver slices. In vivo, however, this 901 11584368 1 ase-1 (TIMP-1) mRNA expression . This was accompanied by a de (TIMP-1) mRNA expression. This was accompanied by 1064 11584368 1 mpared with untreated BDL rats . Dexa(5)-Man(10)-HSA treatmen d with untreated BDL rats. Dexa(5)-Man(10)-HSA tre 1255 11584368 1 s in hepatocytes of BDL livers . In conclusion, our studies s hepatocytes of BDL livers. In conclusion, our stud 1361 11584368 1 to KC with Dexa(5)-Man(10)-HSA . This conjugate reduced intra with Dexa(5)-Man(10)-HSA. This conjugate reduced 1463 11584368 1 ective pharmacologic targeting . Dexa(5)-Man(10)-HSA, however e pharmacologic targeting. Dexa(5)-Man(10)-HSA, ho 1633 11584368 1 leled by TIMP-1 mRNA induction . Targeting of dexamethasone t by TIMP-1 mRNA induction. Targeting of dexamethas 1741 11584368 1 pe in fibrogenesis of BDL rats . fibrogenesis of BDL rats. 1855 8870028 0 . (Papaveraceae) has a long hi 19 8870028 1 diseases in European countries . This plant is of great inter ses in European countries. This plant is of great 127 8870028 1 lso in Chinese herbal medicine . The plant contains, as major n Chinese herbal medicine. The plant contains, as 204 8870028 1 hrine, berberine and coptisine . Other compounds structurally , berberine and coptisine. Other compounds structu 355 8870028 1 flavonoids and phenolic acids . C. majus extracts and its pu onoids and phenolic acids. C. majus extracts and i 492 8870028 0 avonoids and phenolic acids. C . majus extracts and its purif ids and phenolic acids. C. majus extracts and its 495 8870028 1 ties both in vitro and in vivo . both in vitro and in vivo. 635 12898504 0 andated community treatment (e . g. outpatient commitment, adv ed community treatment (e.g. outpatient commitment 62 12898504 0 dated community treatment (e.g . outpatient commitment, advan community treatment (e.g. outpatient commitment, 64 12898504 1 specialty mental health court . Results indicate that the ma ialty mental health court. Results indicate that t 352 12898504 1 f mandated community treatment . However, respondents from th dated community treatment. However, respondents fr 473 12898504 1 paratively similar experiences . Additional studies of the pr ively similar experiences. Additional studies of t 602 12898504 1 rding the use of such mandates . In addition, future studies the use of such mandates. In addition, future stu 752 12898504 0 spondents, as certain terms (e . g. "outpatient commitment") m ents, as certain terms (e.g. "outpatient commitmen 923 12898504 0 ondents, as certain terms (e.g . "outpatient commitment") may ts, as certain terms (e.g. "outpatient commitment" 925 12898504 1 hings to different respondents . to different respondents. 1002 6405813 1 reaction (utilization of ADP) . The kinetic studies were per tion (utilization of ADP). The kinetic studies wer 139 6405813 1 e dehydrogenase as an ATP trap . The Km values for Mg ADP1- a ydrogenase as an ATP trap. The Km values for Mg AD 269 6405813 0 glycerate were approximately 0 . 11 and 0.006 mM, respectively rate were approximately 0.11 and 0.006 mM, respect 348 6405813 0 were approximately 0.11 and 0 . 006 mM, respectively. Recipro approximately 0.11 and 0.006 mM, respectively. Re 357 6405813 1 .11 and 0.006 mM, respectively . Reciprocal plots of 1/v vers nd 0.006 mM, respectively. Reciprocal plots of 1/v 378 6405813 1 ADP1- were apparently parallel . However, product inhibition were apparently parallel. However, product inhibi 604 6405813 1 nzyme for the second substrate . Existence of two sites for 3 for the second substrate. Existence of two sites 942 6405813 1 ospho-D-glycerate is suggested . -D-glycerate is suggested. 1005 6810710 1 e mechanical sieving technique . Glomerular microsomal fracti hanical sieving technique. Glomerular microsomal f 91 6810710 1 d by thin-layer chromatography . The three incubation systems thin-layer chromatography. The three incubation sy 304 6810710 0 incubation systems produced 15 . 3, 20.8, and 40.4% 6-keto-PGF ation systems produced 15.3, 20.8, and 40.4% 6-ket 346 6810710 0 tion systems produced 15.3, 20 . 8, and 40.4% 6-keto-PGF1 alph systems produced 15.3, 20.8, and 40.4% 6-keto-PGF1 352 6810710 0 ms produced 15.3, 20.8, and 40 . 4% 6-keto-PGF1 alpha; 19.1, 2 oduced 15.3, 20.8, and 40.4% 6-keto-PGF1 alpha; 19 362 6810710 0 nd 40.4% 6-keto-PGF1 alpha; 19 . 1, 23.5, and 15.3 PGF2 alpha; .4% 6-keto-PGF1 alpha; 19.1, 23.5, and 15.3 PGF2 a 387 6810710 0 4% 6-keto-PGF1 alpha; 19.1, 23 . 5, and 15.3 PGF2 alpha; 5.7, keto-PGF1 alpha; 19.1, 23.5, and 15.3 PGF2 alpha; 393 6810710 0 PGF1 alpha; 19.1, 23.5, and 15 . 3 PGF2 alpha; 5.7, 9.1, and 3 alpha; 19.1, 23.5, and 15.3 PGF2 alpha; 5.7, 9.1, 403 6810710 0 , 23.5, and 15.3 PGF2 alpha; 5 . 7, 9.1, and 3.9% thromboxane 5, and 15.3 PGF2 alpha; 5.7, 9.1, and 3.9% thrombo 419 6810710 0 5, and 15.3 PGF2 alpha; 5.7, 9 . 1, and 3.9% thromboxane (TX) d 15.3 PGF2 alpha; 5.7, 9.1, and 3.9% thromboxane 424 6810710 0 .3 PGF2 alpha; 5.7, 9.1, and 3 . 9% thromboxane (TX) B2; 36.0, F2 alpha; 5.7, 9.1, and 3.9% thromboxane (TX) B2; 433 6810710 0 d 3.9% thromboxane (TX) B2; 36 . 0, 35.1, and 37.0% PGE2; and % thromboxane (TX) B2; 36.0, 35.1, and 37.0% PGE2; 460 6810710 0 thromboxane (TX) B2; 36.0, 35 . 1, and 37.0% PGE2; and 23.9, mboxane (TX) B2; 36.0, 35.1, and 37.0% PGE2; and 2 466 6810710 0 ne (TX) B2; 36.0, 35.1, and 37 . 0% PGE2; and 23.9, 11.3, and X) B2; 36.0, 35.1, and 37.0% PGE2; and 23.9, 11.3, 476 6810710 0 , 35.1, and 37.0% PGE2; and 23 . 9, 11.3, and 3.4% PGD2, respe 1, and 37.0% PGE2; and 23.9, 11.3, and 3.4% PGD2, 492 6810710 0 , and 37.0% PGE2; and 23.9, 11 . 3, and 3.4% PGD2, respectivel 37.0% PGE2; and 23.9, 11.3, and 3.4% PGD2, respec 498 6810710 0 0% PGE2; and 23.9, 11.3, and 3 . 4% PGD2, respectively. Glomer E2; and 23.9, 11.3, and 3.4% PGD2, respectively. G 507 6810710 1 3, and 3.4% PGD2, respectively . Glomeruli were placed in sus d 3.4% PGD2, respectively. Glomeruli were placed i 529 6810710 1 superfused with Krebs solution . Superfusion with 1.6 x 10(-4 fused with Krebs solution. Superfusion with 1.6 x 623 6810710 0 s solution. Superfusion with 1 . 6 x 10(-4) M arachidonic acid ution. Superfusion with 1.6 x 10(-4) M arachidonic 643 6810710 0 enin from glomeruli, whereas 2 . 7 x 10(-6) M PGE1, PGE2, PGF2 from glomeruli, whereas 2.7 x 10(-6) M PGE1, PGE2, 741 6810710 1 of PGH2 had no effect on renin . When the rapid breakdown of H2 had no effect on renin. When the rapid breakdow 840 6810710 0 reasing the concentration to 1 . 7 x 10(-4) M or stabilizing i ng the concentration to 1.7 x 10(-4) M or stabiliz 935 6810710 0 r stabilizing in Krebs at pH 9 . 4, it stimulated a significan bilizing in Krebs at pH 9.4, it stimulated a signi 980 6810710 1 cant increase in renin release . Reducing the arachidonic aci increase in renin release. Reducing the arachidoni 1037 6810710 0 idonic acid concentration to 1 . 6 x 10(-5) M eliminated both c acid concentration to 1.6 x 10(-5) M eliminated 1087 6810710 1 eased PGE2 synthesis persisted . Finally, using an inhibitor PGE2 synthesis persisted. Finally, using an inhib 1191 6810710 0 GI2 synthesis, azo analog 1 (2 . 8 x 10(-6) M), 6-keto-PGF1 al ynthesis, azo analog 1 (2.8 x 10(-6) M), 6-keto-PG 1255 6810710 1 GE2 synthesis was not affected . These results suggest that t ynthesis was not affected. These results suggest t 1421 6810710 1 vely due to the action of PGI2 . due to the action of PGI2. 1575 6364955 1 not yet been fully elucidated . In this study the intracellu yet been fully elucidated. In this study the intra 107 6364955 1 10-day diet with 800 kcal/day . A decrease in intracellular ay diet with 800 kcal/day. A decrease in intracell 263 6364955 0 llular free Na+ (p less than 0 . 05) and Mg2+ (p less than 0.0 r free Na+ (p less than 0.05) and Mg2+ (p less tha 316 6364955 0 0.05) and Mg2+ (p less than 0 . 01) and in total intracellula ) and Mg2+ (p less than 0.01) and in total intrace 344 6364955 0 ntracellular K+ (p less than 0 . 05) was observed. Furthermore ellular K+ (p less than 0.05) was observed. Furthe 393 6364955 1 p less than 0.05) was observed . Furthermore, plasma aldoster s than 0.05) was observed. Furthermore, plasma ald 410 6364955 0 renin activity (p less than 0 . 05) increased, probably due t n activity (p less than 0.05) increased, probably 477 6364955 1 simultaneous salt restriction . There was also an increase i ltaneous salt restriction. There was also an incre 549 6364955 0 2 concentration (p less than 0 . 05). The observed decrease in centration (p less than 0.05). The observed decrea 621 6364955 1 ncentration (p less than 0.05) . The observed decrease in int ration (p less than 0.05). The observed decrease i 625 6364955 1 be caused by salt restriction . The decrease in intracellula aused by salt restriction. The decrease in intrace 708 6364955 0 induced by hormonal factors, e . g. an altered insulin secreti ed by hormonal factors, e.g. an altered insulin se 794 6364955 0 duced by hormonal factors, e.g . an altered insulin secretion by hormonal factors, e.g. an altered insulin secr 796 6364955 1 . an altered insulin secretion . Possible causes for the know altered insulin secretion. Possible causes for the 826 6364955 1 nd the increase in plasma PGI2 . e increase in plasma PGI2. 969 11418484 1 in self-tolerance maintenance . Furthermore, immunosuppressi elf-tolerance maintenance. Furthermore, immunosupp 128 11418484 1 attributed to apoptotic cells . This study evaluated the con ibuted to apoptotic cells. This study evaluated th 205 11418484 1 ne marrow (BM) transplantation . Sublethally irradiated recip rrow (BM) transplantation. Sublethally irradiated 360 11418484 1 eukocytes of different origins . No graft-versus-host disease ytes of different origins. No graft-versus-host di 508 11418484 1 rsus-host disease was observed . Whereas only a low proportio host disease was observed. Whereas only a low prop 551 11418484 1 ificantly enhanced engraftment . Similar results were obtaine ntly enhanced engraftment. Similar results were ob 830 11418484 1 ls in engraftment facilitation . Overall, these results sugge engraftment facilitation. Overall, these results 1048 11418484 1 tate allogeneic BM engraftment . Such a simple approach could allogeneic BM engraftment. Such a simple approach 1163 11418484 1 conditioning regimen intensity . tioning regimen intensity. 1360 9291235 1 spongiform encephalomyelopathy . To determine whether gag and iform encephalomyelopathy. To determine whether ga 169 9291235 1 ic mice harboring only ts1-env . Neuropathological lesions we ce harboring only ts1-env. Neuropathological lesio 362 9291235 1 in the central nervous system . This implies that gag and po he central nervous system. This implies that gag a 466 9291235 1 m of neurodegeneration in mice . neurodegeneration in mice. 613 12368605 1 lertness or response intensity . STUDY DESIGN: Cross-sectiona ess or response intensity. STUDY DESIGN: Cross-sec 323 12368605 1 STUDY DESIGN: Cross-sectional . METHODS: Review of records f Y DESIGN: Cross-sectional. METHODS: Review of reco 354 12368605 1 ts undergoing the caloric test . RESULTS: Dysrhythmia severe dergoing the caloric test. RESULTS: Dysrhythmia se 428 12368605 1 as present in 40% of the cases . Individuals were entered int esent in 40% of the cases. Individuals were entere 552 12368605 0 mic" group (n = 83) and were 5 . 8 times more likely to remain group (n = 83) and were 5.8 times more likely to r 656 12368605 1 nd visit than to change groups . Stronger response scores wer sit than to change groups. Stronger response score 744 12368605 1 sociated with less dysrhythmia . Higher caloric-induced verti ted with less dysrhythmia. Higher caloric-induced 808 12368605 1 s and lower dysrhythmia scores . Cases in the dysrhythmic gro lower dysrhythmia scores. Cases in the dysrhythmi 927 12368605 0 n the dysrhythmic group were 3 . 8 times more likely to have a dysrhythmic group were 3.8 times more likely to h 966 12368605 1 dividuals in the orderly group . CONCLUSIONS: Dysrhythmia fre uals in the orderly group. CONCLUSIONS: Dysrhythmi 1062 12368605 1 rpretation of the caloric test . Current methods of "mental a ation of the caloric test. Current methods of "men 1169 12368605 1 fail to eliminate dysrhythmia . The presence of dysrhythmia to eliminate dysrhythmia. The presence of dysrhyt 1248 12368605 1 hythmia and response intensity . Nevertheless, our results su ia and response intensity. Nevertheless, our resul 1425 12368605 1 lertness or response intensity . ess or response intensity. 1623 10574952 1 n the development of neoplasia . The consistent chromosomal t development of neoplasia. The consistent chromoso 138 10574952 1 transcription factor 1 (ATF1) . Contribution of the chimeric scription factor 1 (ATF1). Contribution of the chi 318 10574952 1 hain antibody fragment (scFv4) . Transfection of scFv4 into a antibody fragment (scFv4). Transfection of scFv4 i 517 10574952 1 ement-driven reporter activity . The delivery of scFv4 into S -driven reporter activity. The delivery of scFv4 i 669 10574952 1 nd labeling and flow cytometry . Conversely, scFv4 had no eff beling and flow cytometry. Conversely, scFv4 had n 928 10574952 1 ect on viability of HeLa cells . The level of EWS/ATF1 expres n viability of HeLa cells. The level of EWS/ATF1 e 988 10574952 1 an EWS/ATF1 expression vector . These studies demonstrate a WS/ATF1 expression vector. These studies demonstra 1179 10574952 1 thod to explore their function . to explore their function. 1462 11309051 1 wer respiratory tract diseases . This study aims to establish espiratory tract diseases. This study aims to esta 127 11309051 1 go-oesophageal pH and pressure . Twenty-five asymptomatic hea sophageal pH and pressure. Twenty-five asymptomati 222 11309051 1 ophageal pressure and pH-metry . Acid exposure times were ver eal pressure and pH-metry. Acid exposure times wer 331 11309051 1 d exposure times were very low . Only one subject showed any osure times were very low. Only one subject showed 366 11309051 1 ngeal reflux during recumbency . Two distinct upper oesophage reflux during recumbency. Two distinct upper oeso 453 11309051 1 complete manometric quiescence . Negative results, i.e. the e ete manometric quiescence. Negative results, i.e. 659 11309051 0 uiescence. Negative results, i . e. the exclusion of abnormal ence. Negative results, i.e. the exclusion of abno 680 11309051 0 escence. Negative results, i.e . the exclusion of abnormal ce ce. Negative results, i.e. the exclusion of abnorm 682 11309051 1 olutely clear from our results . Categorisation of an individ ly clear from our results. Categorisation of an in 841 11309051 1 a synchronous pharyngeal probe . pH-metry is likely to be of chronous pharyngeal probe. pH-metry is likely to b 955 11309051 1 ryngeal or respiratory disease . al or respiratory disease. 1073 9742301 1 on and may be life threatening . Many of the reactions are im d may be life threatening. Many of the reactions a 65 9742301 1 these reactions are discussed . The most common type is IgA e reactions are discussed. The most common type is 163 9742301 1 st common type is IgA mediated . Clinical manifestations are mmon type is IgA mediated. Clinical manifestations 201 9742301 1 al manifestations are multiple . Systematic investigation is nifestations are multiple. Systematic investigatio 239 9742301 1 fective and may be life saving . ve and may be life saving. 324 7955039 1 adducts at very low abundance . The procedures are based on cts at very low abundance. The procedures are base 193 7955039 1 h a range of PAH diol-epoxides . The antibody recognised DNA ange of PAH diol-epoxides. The antibody recognised 564 7955039 1 ibenz[a,h]anthracene or picene . The antibody also cross-reac [a,h]anthracene or picene. The antibody also cross 705 7955039 1 benz[a]anthracene and chrysene . The degree of cross-reactivi a]anthracene and chrysene. The degree of cross-rea 851 7955039 1 oximate to the base attachment . The antibody also recognised te to the base attachment. The antibody also recog 997 7955039 1 ene and chrysene diol-epoxides . This wide range of recogniti nd chrysene diol-epoxides. This wide range of reco 1156 7955039 1 of PAH adducts by the antibody . When immobilized on Sepharos H adducts by the antibody. When immobilized on Sep 1277 7955039 1 rysene from normal nucleotides . Quantitative measurements wi e from normal nucleotides. Quantitative measuremen 1498 7955039 1 duct/10(10) normal nucleotides . In addition, this immunoadso 10(10) normal nucleotides. In addition, this immun 1732 7955039 1 enzo[a]pyrene and [3H]chrysene . Class-specific immunoenrichm a]pyrene and [3H]chrysene. Class-specific immunoen 1935 7955039 1 components in complex mixtures . The performance characterist nents in complex mixtures. The performance charact 2085 7955039 1 xposures to low levels of PAHs . res to low levels of PAHs. 2284 11904298 0 yanobacterium Synechocystis sp . strain PCC 6803 possesses tw acterium Synechocystis sp. strain PCC 6803 possess 35 11904298 1 and two HCO(3)(-) transporters . We transformed a mutant impa wo HCO(3)(-) transporters. We transformed a mutant 118 11904298 0 and grow in low CO(2) at pH 9 . 0. They are all tagged within grow in low CO(2) at pH 9.0. They are all tagged w 337 11904298 1 nd grow in low CO(2) at pH 9.0 . They are all tagged within s ow in low CO(2) at pH 9.0. They are all tagged wit 339 11904298 1 thin slr1512 (designated sbtA) . We show that SbtA-mediated t slr1512 (designated sbtA). We show that SbtA-media 393 11904298 1 (3)(-) uptake in Synechocystis . Inactivation of slr1509 (hom ) uptake in Synechocystis. Inactivation of slr1509 534 11904298 1 A-mediated HCO(3)(-) transport . We propose that the SbtA-med iated HCO(3)(-) transport. We propose that the Sbt 770 11904298 1 disrupted by inactivating ntpJ . Phylogenetic analyses indica pted by inactivating ntpJ. Phylogenetic analyses i 919 11904298 1 ins, all of which possess ntpJ . The sbtA gene is the first o all of which possess ntpJ. The sbtA gene is the fi 1042 11904298 1 -dependent HCO(3)(-) transport . ndent HCO(3)(-) transport. 1353 7783062 1 . This is a pilot study of zil 9 7783062 1 emic lupus erythematosus (SLE) . METHODS. Forty patients with lupus erythematosus (SLE). METHODS. Forty patients 120 7783062 1 s erythematosus (SLE). METHODS . Forty patients with SLE rece thematosus (SLE). METHODS. Forty patients with SLE 129 7783062 1 rospective, double blind trial . Disease activity was manifes ctive, double blind trial. Disease activity was ma 251 7783062 1 iac, or neurologic involvement . Concomitant administration o or neurologic involvement. Concomitant administrat 415 7783062 1 ntimalarials was not permitted . Disease activity was determi larials was not permitted. Disease activity was de 531 7783062 1 nterleukin 2 receptors (IL-2R) . Total body sulfidopeptide le eukin 2 receptors (IL-2R). Total body sulfidopepti 850 7783062 1 riene E4 (LTE4) concentrations . RESULTS. Overall SLAM (the p E4 (LTE4) concentrations. RESULTS. Overall SLAM ( 960 7783062 1 (LTE4) concentrations. RESULTS . Overall SLAM (the primary me ) concentrations. RESULTS. Overall SLAM (the prima 969 7783062 0 uton compared with placebo (-2 . 1 +/- 1.3, compared with an i compared with placebo (-2.1 +/- 1.3, compared with 1098 7783062 0 pared with placebo (-2.1 +/- 1 . 3, compared with an increase with placebo (-2.1 +/- 1.3, compared with an incr 1106 7783062 0 compared with an increase of 2 . 3 +/- 1.3 with placebo by Day red with an increase of 2.3 +/- 1.3 with placebo b 1140 7783062 0 with an increase of 2.3 +/- 1 . 3 with placebo by Day 57, p = an increase of 2.3 +/- 1.3 with placebo by Day 57 1148 7783062 0 with placebo by Day 57, p = 0 . 048). Changes in individual S placebo by Day 57, p = 0.048). Changes in individ 1180 7783062 1 placebo by Day 57, p = 0.048) . Changes in individual SLAM s ebo by Day 57, p = 0.048). Changes in individual S 1185 7783062 1 ds towards clinical worsening) . Urine LTE4 levels at Day 57 wards clinical worsening). Urine LTE4 levels at Da 1527 7783062 1 group (indicating improvement) . CONCLUSION. Selective 5-lipo (indicating improvement). CONCLUSION. Selective 5 1689 7783062 1 ating improvement). CONCLUSION . Selective 5-lipoxygenase inh improvement). CONCLUSION. Selective 5-lipoxygenas 1701 7783062 1 may be beneficial in mild SLE . be beneficial in mild SLE. 1768 10377230 1 uinones have been investigated . The cytotoxicities were dete es have been investigated. The cytotoxicities were 123 10377230 1 cient (H596 and BE) cell lines . It was shown that the cytoto (H596 and BE) cell lines. It was shown that the c 237 10377230 1 the cross-linking efficiencies . The rates of reduction by DT ross-linking efficiencies. The rates of reduction 412 10377230 1 termined by cyclic voltammetry . A computer model was also us ned by cyclic voltammetry. A computer model was al 575 10377230 1 bstituted diaziridinylquinones . uted diaziridinylquinones. 739 10079000 1 class of cardiovascular drugs . In conscious, normotensive r s of cardiovascular drugs. In conscious, normotens 84 10079000 0 administered intravenously (i . v.) at doses of 0.3, 1, 3 and nistered intravenously (i.v.) at doses of 0.3, 1, 421 10079000 0 dministered intravenously (i.v . ) at doses of 0.3, 1, 3 and 1 stered intravenously (i.v.) at doses of 0.3, 1, 3 423 10079000 0 avenously (i.v.) at doses of 0 . 3, 1, 3 and 10 mg/kg body wei usly (i.v.) at doses of 0.3, 1, 3 and 10 mg/kg bod 439 10079000 0 g/kg body weight, or orally (p . o.) at doses of 1, 3, 10 and body weight, or orally (p.o.) at doses of 1, 3, 10 486 10079000 0 kg body weight, or orally (p.o . ) at doses of 1, 3, 10 and 30 dy weight, or orally (p.o.) at doses of 1, 3, 10 a 488 10079000 0 zed the pressor responses to i . v. angiotensin II (50 ng/kg b he pressor responses to i.v. angiotensin II (50 ng 576 10079000 0 d the pressor responses to i.v . angiotensin II (50 ng/kg bod pressor responses to i.v. angiotensin II (50 ng/k 578 10079000 1 anner and with similar potency . In the following sets of exp and with similar potency. In the following sets o 667 10079000 1 eptor stimulation in the brain . Irbesartan and losartan were stimulation in the brain. Irbesartan and losartan 884 10079000 0 d losartan were administered i . v. or p.o. at doses of 3, 10, artan were administered i.v. or p.o. at doses of 3 929 10079000 0 losartan were administered i.v . or p.o. at doses of 3, 10, 3 tan were administered i.v. or p.o. at doses of 3, 931 10079000 0 an were administered i.v. or p . o. at doses of 3, 10, 30 and re administered i.v. or p.o. at doses of 3, 10, 30 937 10079000 0 were administered i.v. or p.o . at doses of 3, 10, 30 and 10 administered i.v. or p.o. at doses of 3, 10, 30 a 939 10079000 1 , 30 and 100 mg/kg body weight . The responses to 100 ng angi and 100 mg/kg body weight. The responses to 100 ng 988 10079000 0 the lateral brain ventricle (i . c.v.), namely blood pressure ateral brain ventricle (i.c.v.), namely blood pres 1073 10079000 0 e lateral brain ventricle (i.c . v.), namely blood pressure in eral brain ventricle (i.c.v.), namely blood pressu 1075 10079000 0 lateral brain ventricle (i.c.v . ), namely blood pressure incr al brain ventricle (i.c.v.), namely blood pressure 1077 10079000 1 g, were recorded for up to 3 h . While both angiotensin AT1 r re recorded for up to 3 h. While both angiotensin 1195 10079000 0 inhibition, irbesartan: 62% i . v., 39% p.o.; losartan: 62% i bition, irbesartan: 62% i.v., 39% p.o.; losartan: 1401 10079000 0 nhibition, irbesartan: 62% i.v . , 39% p.o.; losartan: 62% i.v tion, irbesartan: 62% i.v., 39% p.o.; losartan: 62 1403 10079000 0 n, irbesartan: 62% i.v., 39% p . o.; losartan: 62% i.v., 46% p besartan: 62% i.v., 39% p.o.; losartan: 62% i.v., 1411 10079000 0 irbesartan: 62% i.v., 39% p.o . ; losartan: 62% i.v., 46% p.o sartan: 62% i.v., 39% p.o.; losartan: 62% i.v., 46 1413 10079000 0 .v., 39% p.o.; losartan: 62% i . v., 46% p.o.; respectively), 39% p.o.; losartan: 62% i.v., 46% p.o.; respective 1431 10079000 0 ., 39% p.o.; losartan: 62% i.v . , 46% p.o.; respectively), ir % p.o.; losartan: 62% i.v., 46% p.o.; respectively 1433 10079000 0 .o.; losartan: 62% i.v., 46% p . o.; respectively), irbesartan losartan: 62% i.v., 46% p.o.; respectively), irbes 1441 10079000 0 .; losartan: 62% i.v., 46% p.o . ; respectively), irbesartan w sartan: 62% i.v., 46% p.o.; respectively), irbesar 1443 10079000 0 of vasopressin release (76% i . v., 65% p.o.) and drinking (6 asopressin release (76% i.v., 65% p.o.) and drinki 1551 10079000 0 f vasopressin release (76% i.v . , 65% p.o.) and drinking (63% opressin release (76% i.v., 65% p.o.) and drinking 1553 10079000 0 essin release (76% i.v., 65% p . o.) and drinking (63% i.v., 7 release (76% i.v., 65% p.o.) and drinking (63% i. 1561 10079000 0 sin release (76% i.v., 65% p.o . ) and drinking (63% i.v., 79% elease (76% i.v., 65% p.o.) and drinking (63% i.v. 1563 10079000 0 65% p.o.) and drinking (63% i . v., 79% p.o.) than losartan ( p.o.) and drinking (63% i.v., 79% p.o.) than losar 1585 10079000 0 5% p.o.) and drinking (63% i.v . , 79% p.o.) than losartan (58 o.) and drinking (63% i.v., 79% p.o.) than losarta 1587 10079000 0 and drinking (63% i.v., 79% p . o.) than losartan (58% i.v., drinking (63% i.v., 79% p.o.) than losartan (58% i 1595 10079000 0 nd drinking (63% i.v., 79% p.o . ) than losartan (58% i.v., 33 inking (63% i.v., 79% p.o.) than losartan (58% i.v 1597 10079000 0 79% p.o.) than losartan (58% i . v., 33% p.o and 22% i.v., 56% .o.) than losartan (58% i.v., 33% p.o and 22% i.v. 1620 10079000 0 % p.o.) than losartan (58% i.v . , 33% p.o and 22% i.v., 56% p .) than losartan (58% i.v., 33% p.o and 22% i.v., 1622 10079000 0 than losartan (58% i.v., 33% p . o and 22% i.v., 56% p.o., res losartan (58% i.v., 33% p.o and 22% i.v., 56% p.o. 1630 10079000 0 n (58% i.v., 33% p.o and 22% i . v., 56% p.o., respectively). % i.v., 33% p.o and 22% i.v., 56% p.o., respective 1642 10079000 0 (58% i.v., 33% p.o and 22% i.v . , 56% p.o., respectively). We i.v., 33% p.o and 22% i.v., 56% p.o., respectively 1644 10079000 0 ., 33% p.o and 22% i.v., 56% p . o., respectively). We conclud % p.o and 22% i.v., 56% p.o., respectively). We co 1652 10079000 0 33% p.o and 22% i.v., 56% p.o . , respectively). We conclude p.o and 22% i.v., 56% p.o., respectively). We conc 1654 10079000 1 i.v., 56% p.o., respectively) . We conclude that systemicall , 56% p.o., respectively). We conclude that system 1670 10079000 1 central angiotensin receptors . The degree of central angiot ral angiotensin receptors. The degree of central a 1796 10079000 1 tatives of this class of drugs . es of this class of drugs. 1952 10644489 1 ts experience T cell depletion . A subset of these patients a perience T cell depletion. A subset of these patie 72 10644489 1 us through the T cell receptor . We hypothesized that T cell rough the T cell receptor. We hypothesized that T 300 10644489 1 an activated T cell population . We found that moderately inc tivated T cell population. We found that moderatel 466 10644489 1 of the remaining naive T cells . METHODS: A total of 30 blunt e remaining naive T cells. METHODS: A total of 30 746 10644489 1 enge or Fas (CD95) stimulation . RESULTS: A wide range of apo or Fas (CD95) stimulation. RESULTS: A wide range o 1290 10644489 1 seen in the patients' T cells . Apoptosis is increased when in the patients' T cells. Apoptosis is increased 1367 10644489 1 o T cells of normal volunteers . However, at the time a patie ells of normal volunteers. However, at the time a 1470 10644489 1 o increased level of apoptosis . In fact, the point of maximu reased level of apoptosis. In fact, the point of m 1566 10644489 1 diminished apoptotic response . Increased T cell apoptosis c nished apoptotic response. Increased T cell apopto 1680 10644489 1 t in maximally anergic T cells . These data suggest that pati maximally anergic T cells. These data suggest that 1823 10644489 1 ell depletion upon stimulation . However, patients who later epletion upon stimulation. However, patients who l 1946 10644489 1 never experience T cell anergy . CONCLUSIONS: Increased level experience T cell anergy. CONCLUSIONS: Increased 2111 10644489 1 mediate cause of T cell anergy . However, unusually high leve te cause of T cell anergy. However, unusually high 2261 10644489 1 y and subsequent organ failure . subsequent organ failure. 2482 11714325 0 value of Lupinus splendens, L . rotundiflorus, L. elegans, L e of Lupinus splendens, L. rotundiflorus, L. elega 112 11714325 0 splendens, L. rotundiflorus, L . elegans, L. simulans, L. exa dens, L. rotundiflorus, L. elegans, L. simulans, L 130 11714325 0 . rotundiflorus, L. elegans, L . simulans, L. exaltatus, L. r undiflorus, L. elegans, L. simulans, L. exaltatus, 142 11714325 0 us, L. elegans, L. simulans, L . exaltatus, L. reflexus, and . elegans, L. simulans, L. exaltatus, L. reflexus, 155 11714325 0 , L. simulans, L. exaltatus, L . reflexus, and L. madrensis s simulans, L. exaltatus, L. reflexus, and L. madren 169 11714325 0 exaltatus, L. reflexus, and L . madrensis species from Mexic tatus, L. reflexus, and L. madrensis species from 186 11714325 1 cies from Mexico were analyzed . The seeds of these species w from Mexico were analyzed. The seeds of these spec 231 11714325 1 were a good source of protein . All the species showed a hig a good source of protein. All the species showed 289 11714325 1 lfur amino acids were limiting . Cyanogenic glycosides were a amino acids were limiting. Cyanogenic glycosides w 391 11714325 1 present in low concentrations . Lupanine was the major alkal ent in low concentrations. Lupanine was the major 507 11714325 0 kaloid in Lupinus reflexus (26 . 63 mg/g of sample). Cytisine d in Lupinus reflexus (26.63 mg/g of sample). Cyti 633 11714325 1 eflexus (26.63 mg/g of sample) . Cytisine was not found in an us (26.63 mg/g of sample). Cytisine was not found 652 11714325 1 d in any of the studied lupins . L. reflexus showed the highe any of the studied lupins. L. reflexus showed the 705 11714325 0 n any of the studied lupins. L . reflexus showed the highest of the studied lupins. L. reflexus showed the hig 708 11714325 0 highest acute toxicity, and L . elegans exhibited no toxicit est acute toxicity, and L. elegans exhibited no to 759 11714325 1 s evaluated using a mice model . The alkaloid was reduced by luated using a mice model. The alkaloid was reduce 822 11714325 1 educed by hot-water extraction . The protein efficiency ratio d by hot-water extraction. The protein efficiency 872 11714325 0 d seeds was relatively poor (1 . 1-1.5). These results suggest ds was relatively poor (1.1-1.5). These results su 951 11714325 0 eds was relatively poor (1.1-1 . 5). These results suggest tha as relatively poor (1.1-1.5). These results sugges 955 11714325 1 was relatively poor (1.1-1.5) . These results suggest that t relatively poor (1.1-1.5). These results suggest t 958 11714325 1 e used in mixture with cereals . d in mixture with cereals. 1238 15365399 0 fect of Helicobacter pylori (H . pylori) eradication on gastr of Helicobacter pylori (H. pylori) eradication on 48 15365399 1 eflux disease is controversial . We aimed to investigate the disease is controversial. We aimed to investigate 121 15365399 0 to investigate the effect of H . pylori eradication in this g vestigate the effect of H. pylori eradication in t 162 15365399 1 tion in this group of patients . MATERIALS AND METHODS: Thirt in this group of patients. MATERIALS AND METHODS: 208 15365399 0 ur consecutive patients with H . pylori infection and reflux nsecutive patients with H. pylori infection and re 272 15365399 1 ) were enrolled into the study . Twenty-four hour intra-esoph e enrolled into the study. Twenty-four hour intra- 357 15365399 0 months after eradication of H . pylori, which was achieved u hs after eradication of H. pylori, which was achie 488 15365399 0 ved using lansoprazole 30 mg b . i.d., amoxycillin 1 g b.i.d., sing lansoprazole 30 mg b.i.d., amoxycillin 1 g b. 543 15365399 0 d using lansoprazole 30 mg b.i . d., amoxycillin 1 g b.i.d., a ng lansoprazole 30 mg b.i.d., amoxycillin 1 g b.i. 545 15365399 0 using lansoprazole 30 mg b.i.d . , amoxycillin 1 g b.i.d., and lansoprazole 30 mg b.i.d., amoxycillin 1 g b.i.d. 547 15365399 0 0 mg b.i.d., amoxycillin 1 g b . i.d., and clarithromycin 500 b.i.d., amoxycillin 1 g b.i.d., and clarithromycin 567 15365399 0 mg b.i.d., amoxycillin 1 g b.i . d., and clarithromycin 500 mg i.d., amoxycillin 1 g b.i.d., and clarithromycin 5 569 15365399 0 b.i.d., amoxycillin 1 g b.i.d . , and clarithromycin 500 mg b d., amoxycillin 1 g b.i.d., and clarithromycin 500 571 15365399 0 ., and clarithromycin 500 mg b . i.d. for 14 days. H. pylori w d clarithromycin 500 mg b.i.d. for 14 days. H. pyl 601 15365399 0 and clarithromycin 500 mg b.i . d. for 14 days. H. pylori was clarithromycin 500 mg b.i.d. for 14 days. H. pylor 603 15365399 0 nd clarithromycin 500 mg b.i.d . for 14 days. H. pylori was e arithromycin 500 mg b.i.d. for 14 days. H. pylori 605 15365399 1 ycin 500 mg b.i.d. for 14 days . H. pylori was evaluated in b 500 mg b.i.d. for 14 days. H. pylori was evaluated 618 15365399 0 n 500 mg b.i.d. for 14 days. H . pylori was evaluated in biop mg b.i.d. for 14 days. H. pylori was evaluated in 621 15365399 1 and 3 months after eradication . RESULTS: Eighteen patients ( months after eradication. RESULTS: Eighteen patie 790 15365399 1 42 years) completed the study . Three months after the treat ears) completed the study. Three months after the 880 15365399 0 incter resting pressure (P > 0 . 05). The percentage of total r resting pressure (P > 0.05). The percentage of t 1064 15365399 1 er resting pressure (P > 0.05) . The percentage of total time sting pressure (P > 0.05). The percentage of total 1068 15365399 1 s, and decreased in 8 patients . There was a significant decr d decreased in 8 patients. There was a significant 1169 15365399 0 tburn and regurgitation (P < 0 . 01). Esophagitis persisted in and regurgitation (P < 0.01). Esophagitis persist 1255 15365399 1 n and regurgitation (P < 0.01) . Esophagitis persisted in 16 regurgitation (P < 0.01). Esophagitis persisted i 1259 15365399 1 and disappeared in 2 patients . Esophagitis score decreased disappeared in 2 patients. Esophagitis score decre 1327 15365399 0 t change in 12 patients (P < 0 . 05). CONCLUSION: H. pylori er nge in 12 patients (P < 0.05). CONCLUSION: H. pylo 1412 15365399 1 ange in 12 patients (P < 0.05) . CONCLUSION: H. pylori eradic in 12 patients (P < 0.05). CONCLUSION: H. pylori e 1416 15365399 0 ents (P < 0.05). CONCLUSION: H . pylori eradication does not (P < 0.05). CONCLUSION: H. pylori eradication does 1431 15365399 1 ome reflux associated symptoms . eflux associated symptoms. 1647 9776811 0 zed in the ear and caused by R . aquaspersa is presented. The n the ear and caused by R. aquaspersa is presented 75 9776811 1 by R. aquaspersa is presented . The patient was a 60-year-ol . aquaspersa is presented. The patient was a 60-ye 100 9776811 1 ad had the disease for 5 years . The lesion was darkly pigmen d the disease for 5 years. The lesion was darkly p 188 9776811 1 ented, infiltrative and crusty . Sclerotic cells were seen on , infiltrative and crusty. Sclerotic cells were se 246 9776811 1 the characteristic sporulation . Itraconazole therapy at a do haracteristic sporulation. Itraconazole therapy at 398 9776811 1 nths produced complete healing . produced complete healing. 485 10064071 1 o activation of lymphoid cells . A possible explanation how t ivation of lymphoid cells. A possible explanation 176 10064071 1 microdomains in cell membranes . Cross-linking of GPI-anchore domains in cell membranes. Cross-linking of GPI-an 349 10064071 1 the Src-tyrosine kinase family . We have studied cellular res rc-tyrosine kinase family. We have studied cellula 560 10064071 1 nges in the actin cytoskeleton . We found that raft patches f in the actin cytoskeleton. We found that raft patc 698 10064071 1 1 accumulate filamentous actin . Most interestingly, we obser umulate filamentous actin. Most interestingly, we 815 10064071 1 centers of signal transduction . Using a Lck kinase-deficient rs of signal transduction. Using a Lck kinase-defi 1009 10064071 1 ne accumulation in the patches . These observations show a li cumulation in the patches. These observations show 1226 10064071 1 ton with raft membrane domains . ith raft membrane domains. 1359 6795893 1 hLH and hFSH in pregnant women . The immunological affinity o nd hFSH in pregnant women. The immunological affin 241 6795893 0 ty of hLH-beta antiserum was 7 . 9% with hCG-beta, 3.4% with h hLH-beta antiserum was 7.9% with hCG-beta, 3.4% w 297 6795893 0 erum was 7.9% with hCG-beta, 3 . 4% with hLH-alpha and 0.41% w was 7.9% with hCG-beta, 3.4% with hLH-alpha and 0. 317 6795893 0 eta, 3.4% with hLH-alpha and 0 . 41% with LER 907 as compared 3.4% with hLH-alpha and 0.41% with LER 907 as comp 341 6795893 1 compared to 100% with hLH-beta . Serum mean levels of hLH in red to 100% with hLH-beta. Serum mean levels of hL 392 6795893 0 in non pregnant women were 248 . 5 ng/ml serum before the firs n pregnant women were 248.5 ng/ml serum before the 449 6795893 1 e the first injection of LH-RF . The first injection caused a first injection of LH-RF. The first injection cau 499 6795893 0 in the serum hLH level to 2185 . 0 ng/ml serum. After the seco e serum hLH level to 2185.0 ng/ml serum. After the 570 6795893 1 LH level to 2185.0 ng/ml serum . After the second injection o vel to 2185.0 ng/ml serum. After the second inject 584 6795893 1 first LH-RF on the second peak . Serum mean values of hLH-bet LH-RF on the second peak. Serum mean values of hL 776 6795893 0 normal menstrual women were 2 . 60 ng/ml before the first inj al menstrual women were 2.60 ng/ml before the firs 840 6795893 1 /ml before the first injection . The hLH-beta response to the efore the first injection. The hLH-beta response t 876 6795893 1 ntly greater than to the first . The first peak of hLH-beta w greater than to the first. The first peak of hLH-b 967 6795893 0 e first peak of hLH-beta was 4 . 30 ng/ml serum and the second st peak of hLH-beta was 4.30 ng/ml serum and the s 1001 6795893 0 erum and the second peak was 5 . 07 ng/ml serum. The FSH respo and the second peak was 5.07 ng/ml serum. The FSH 1042 6795893 1 cond peak was 5.07 ng/ml serum . The FSH response to the seco peak was 5.07 ng/ml serum. The FSH response to the 1057 6795893 1 that after the first injection . The value of the serum mean after the first injection. The value of the serum 1173 6795893 0 uring pregnancy were between 0 . 57 and 0.81 ng/ml and showed pregnancy were between 0.57 and 0.81 ng/ml and sh 1253 6795893 0 gnancy were between 0.57 and 0 . 81 ng/ml and showed no signif y were between 0.57 and 0.81 ng/ml and showed no s 1262 6795893 1 ere depressed during gestation . Thus LH-RF two step stimulat epressed during gestation. Thus LH-RF two step sti 1432 6795893 1 is and release of gonadotropin . d release of gonadotropin. 1561 10421819 1 ss, and by airway inflammation . Inhaled allergens are the mo nd by airway inflammation. Inhaled allergens are t 113 10421819 1 stimuli known to cause asthma . Methods for studying inhaled uli known to cause asthma. Methods for studying in 192 10421819 1 ergen-induced airway responses . Allergen inhalation by a sen -induced airway responses. Allergen inhalation by 415 10421819 1 and airway hyperresponsiveness . The late response and airway irway hyperresponsiveness. The late response and a 591 10421819 1 ophils and metachromatic cells . Allergen-induced airway infl s and metachromatic cells. Allergen-induced airway 717 10421819 1 or stimulating the bone marrow . The newly formed cells traff imulating the bone marrow. The newly formed cells 964 10421819 1 d cells traffic to the airways . These increases in granulocy ls traffic to the airways. These increases in gran 1011 10421819 1 ked by inhaled corticosteroids . In human subjects, allergen- y inhaled corticosteroids. In human subjects, alle 1105 10421819 1 creases responsiveness to IL-5 . Inhaled corticosteroids also es responsiveness to IL-5. Inhaled corticosteroids 1322 10421819 1 r release from the bone marrow . ease from the bone marrow. 1559 8735698 1 . Potassium currents were meas 1 8735698 0 e pipette, 160 mM in the bath) . 2. In cell-attached patches, ette, 160 mM in the bath). 2. In cell-attached pat 289 8735698 1 ipette, 160 mM in the bath). 2 . In cell-attached patches, th e, 160 mM in the bath). 2. In cell-attached patche 292 8735698 1 f roughly 8 channels microns-2 . Outward macroscopic currents ghly 8 channels microns-2. Outward macroscopic cur 435 8735698 1 potentials positive to -60 mV . The probability of opening r ntials positive to -60 mV. The probability of open 541 8735698 1 1 mV for patches from mdx mice . 3. Tail currents were linear for patches from mdx mice. 3. Tail currents were l 668 8735698 0 V for patches from mdx mice. 3 . Tail currents were linear in patches from mdx mice. 3. Tail currents were line 671 8735698 1 mV, reversing close to -100 mV . The single channel current a eversing close to -100 mV. The single channel curr 762 8735698 0 ielding a value of 19 +/- 1 pS . 4. At 0 mV, the delayed rect ng a value of 19 +/- 1 pS. 4. At 0 mV, the delayed 1006 8735698 1 ding a value of 19 +/- 1 pS. 4 . At 0 mV, the delayed rectifi a value of 19 +/- 1 pS. 4. At 0 mV, the delayed re 1009 8735698 1 0 +/- 20 ms and 600 +/- 200 ms . Prepulses of 500 ms duration 20 ms and 600 +/- 200 ms. Prepulses of 500 ms dur 1113 8735698 1 g 50% of its maximum at -50 mV . 5. Single channel activity w of its maximum at -50 mV. 5. Single channel activ 1256 8735698 0 0% of its maximum at -50 mV. 5 . Single channel activity was its maximum at -50 mV. 5. Single channel activity 1259 8735698 1 recorded using small pipettes . Both single channel conducta rded using small pipettes. Both single channel con 1318 8735698 1 h the macroscopic current data . 6. In excised patches, the d macroscopic current data. 6. In excised patches, 1425 8735698 0 he macroscopic current data. 6 . In excised patches, the dela croscopic current data. 6. In excised patches, the 1428 8735698 1 n, unmasking other K+ channels . A Ca(2+)-dependent K+ channe masking other K+ channels. A Ca(2+)-dependent K+ c 1517 8735698 1 ly at stronger depolarizations . A K+ channel of 63 pS was un stronger depolarizations. A K+ channel of 63 pS w 1717 8735698 1 hed in solutions devoid of ATP . This channel was not observe n solutions devoid of ATP. This channel was not ob 1814 8735698 1 atches excised from mdx fibers . s excised from mdx fibers. 1880 10995772 1 ypical macula densa morphology . Transgenic mice carrying a 1 l macula densa morphology. Transgenic mice carryin 142 10995772 1 kcrossed with Ren-1(d-/-) mice . Homozygous Ren-1(d)-null mic sed with Ren-1(d-/-) mice. Homozygous Ren-1(d)-nul 303 10995772 1 tion of normal renal structure . Homologous recombination in of normal renal structure. Homologous recombinatio 416 10995772 1 fically into the Ren-1(d) gene . When introduced into the ger ly into the Ren-1(d) gene. When introduced into th 603 10995772 1 r cells throughout development . Parallel backcross experimen ls throughout development. Parallel backcross expe 806 10995772 1 n the absence of regranulation . These data demonstrate that absence of regranulation. These data demonstrate 986 10995772 1 the differences in granulation . The use of BAC modification ifferences in granulation. The use of BAC modifica 1309 10995772 1 f key physiological mechanisms . physiological mechanisms. 1475 10404712 1 orticotropin releasing factors . This study examines whether otropin releasing factors. This study examines whe 167 10404712 1 iated with reduced opioid tone . METHODS: We measured the adr with reduced opioid tone. METHODS: We measured th 290 10404712 0 ntravenous bolus of naloxone 0 . 125 microg/kg in 13 depressed enous bolus of naloxone 0.125 microg/kg in 13 depr 404 10404712 1 ents and 13 healthy volunteers . RESULTS: The mean cortisol r and 13 healthy volunteers. RESULTS: The mean corti 472 10404712 0 was significantly reduced (P<0 . 05), and the ACTH response wa ignificantly reduced (P<0.05), and the ACTH respon 540 10404712 1 uced in the depressed subjects . CONCLUSIONS: These findings in the depressed subjects. CONCLUSIONS: These find 628 10404712 1 tone is reduced in depression . Various mechanisms for the f is reduced in depression. Various mechanisms for 741 10404712 1 n of alpha-adrenergic pathways . CLINICAL IMPLICATIONS: Reduc alpha-adrenergic pathways. CLINICAL IMPLICATIONS: 867 10404712 1 ociated with opiate withdrawal . Opioid pathways may have a r ed with opiate withdrawal. Opioid pathways may hav 1045 10404712 1 pment of novel antidepressants . LIMITATIONS OF THE STUDY: Th of novel antidepressants. LIMITATIONS OF THE STUD 1198 10404712 1 reach statistical significance . statistical significance. 1397 6316563 1 oscopic cranial calcifications . Before death, the infant sho ic cranial calcifications. Before death, the infan 278 6316563 1 ures, and respiratory distress . Serum IgM and complement fix and respiratory distress. Serum IgM and complemen 374 6316563 1 to HSV were elevated at birth . Light and electron microscop SV were elevated at birth. Light and electron micr 448 6316563 1 rmed the presence of the virus . the presence of the virus. 546 9715834 1 affects 75 million US citizens . A number of pharmacologic tr ts 75 million US citizens. A number of pharmacolog 43 9715834 1 ly to nonpharmacologic methods . Long the mainstay of chronic nonpharmacologic methods. Long the mainstay of ch 173 9715834 1 iated with osteoarthritis (OA) . Several non-NSAID, non-narco with osteoarthritis (OA). Several non-NSAID, non- 481 9715834 1 lable for noninflammatory pain . Acetaminophen is as effectiv for noninflammatory pain. Acetaminophen is as eff 563 9715834 1 College of Rheumatology (ACR) . Propoxyphene, widely believe ege of Rheumatology (ACR). Propoxyphene, widely be 739 9715834 1 han acetaminophen or ibuprofen . A relatively new analgesic, cetaminophen or ibuprofen. A relatively new analge 890 9715834 1 for NSAID-related side effects . For localized chronic pain a SAID-related side effects. For localized chronic p 1079 9715834 1 is also an effective analgesic . so an effective analgesic. 1176 12951467 0 acrophage-like cell line, J774 . 1; preincubation of macrophag hage-like cell line, J774.1; preincubation of macr 168 12951467 1 nd incubation with LPS and CHX . The first challenge of LPS a cubation with LPS and CHX. The first challenge of 329 12951467 1 ing nor the expression of CD14 . Instead, phosphorylation of or the expression of CD14. Instead, phosphorylatio 428 12951467 1 ading to MAP kinase activation . On the other hand, LPS-induc to MAP kinase activation. On the other hand, LPS- 794 12951467 1 Erk1/Erk2 or JNK was observed . These results suggest that d /Erk2 or JNK was observed. These results suggest t 1214 12951467 1 th higher doses of LPS and CHX . gher doses of LPS and CHX. 1420 14599560 1 conditions of oxidative stress . A novel therapeutic approach tions of oxidative stress. A novel therapeutic app 60 14599560 1 entation with a redox catalyst . This provides a means to tar ion with a redox catalyst. This provides a means t 233 14599560 1 dox balance largely unaffected . We have previously reported alance largely unaffected. We have previously repo 445 14599560 1 that enhance cancer cell death . This paper presents a detail enhance cancer cell death. This paper presents a d 571 14599560 1 1 transcription factor peptide . The structure and redox pote nscription factor peptide. The structure and redox 742 14599560 1 2)O(2)-induced PC12 cell death . )-induced PC12 cell death. 983 8160886 0 e in rat peripheral tissues [A . L. Vallerand, F. Perusse, an rat peripheral tissues [A. L. Vallerand, F. Peruss 122 8160886 0 n rat peripheral tissues [A. L . Vallerand, F. Perusse, and L peripheral tissues [A. L. Vallerand, F. Perusse, 125 8160886 0 al tissues [A. L. Vallerand, F . Perusse, and L. J. Bukowieck ssues [A. L. Vallerand, F. Perusse, and L. J. Buko 139 8160886 0 . Vallerand, F. Perusse, and L . J. Bukowiecki. Am. J. Physio lerand, F. Perusse, and L. J. Bukowiecki. Am. J. P 155 8160886 0 allerand, F. Perusse, and L. J . Bukowiecki. Am. J. Physiol 2 and, F. Perusse, and L. J. Bukowiecki. Am. J. Phys 158 8160886 0 Perusse, and L. J. Bukowiecki . Am. J. Physiol 259 (Regulato sse, and L. J. Bukowiecki. Am. J. Physiol 259 (Reg 170 8160886 0 usse, and L. J. Bukowiecki. Am . J. Physiol 259 (Regulatory I and L. J. Bukowiecki. Am. J. Physiol 259 (Regulat 174 8160886 0 e, and L. J. Bukowiecki. Am. J . Physiol 259 (Regulatory Inte d L. J. Bukowiecki. Am. J. Physiol 259 (Regulatory 177 8160886 0 9 (Regulatory Integrative Comp . Physiol. 28): R1043-R1049, 1 gulatory Integrative Comp. Physiol. 28): R1043-R10 219 8160886 0 tory Integrative Comp. Physiol . 28): R1043-R1049, 1990]. To Integrative Comp. Physiol. 28): R1043-R1049, 1990] 228 8160886 1 ysiol. 28): R1043-R1049, 1990] . To test whether norepinephri . 28): R1043-R1049, 1990]. To test whether norepin 253 8160886 1 2-3H(N)]deoxy-D-glucose method . NE was administered in consc N)]deoxy-D-glucose method. NE was administered in 490 8160886 0 various doses (ranging from 1 . 9 to 25.1 nmol.kg-1.min-1) du ous doses (ranging from 1.9 to 25.1 nmol.kg-1.min- 562 8160886 0 doses (ranging from 1.9 to 25 . 1 nmol.kg-1.min-1) during 4 d s (ranging from 1.9 to 25.1 nmol.kg-1.min-1) durin 570 8160886 0 (ranging from 1.9 to 25.1 nmol . kg-1.min-1) during 4 days via ing from 1.9 to 25.1 nmol.kg-1.min-1) during 4 day 577 8160886 0 ing from 1.9 to 25.1 nmol.kg-1 . min-1) during 4 days via mini rom 1.9 to 25.1 nmol.kg-1.min-1) during 4 days via 582 8160886 1 pumps implanted subcutaneously . At doses > 10 nmol.kg-1.min- implanted subcutaneously. At doses > 10 nmol.kg-1 642 8160886 0 utaneously. At doses > 10 nmol . kg-1.min-1, NE maximally stim ously. At doses > 10 nmol.kg-1.min-1, NE maximally 662 8160886 0 ously. At doses > 10 nmol.kg-1 . min-1, NE maximally stimulate . At doses > 10 nmol.kg-1.min-1, NE maximally stim 667 8160886 1 mately 3 times above controls) . NE infusion (18.8 nmol.kg-1. y 3 times above controls). NE infusion (18.8 nmol. 866 8160886 0 ove controls). NE infusion (18 . 8 nmol.kg-1.min-1) increased ontrols). NE infusion (18.8 nmol.kg-1.min-1) incre 883 8160886 0 trols). NE infusion (18.8 nmol . kg-1.min-1) increased the cir ). NE infusion (18.8 nmol.kg-1.min-1) increased th 890 8160886 0 ). NE infusion (18.8 nmol.kg-1 . min-1) increased the circulat infusion (18.8 nmol.kg-1.min-1) increased the cir 895 8160886 0 irculating levels of NE from 1 . 1 +/- 0.1 to 19.2 +/- 0.4 nM ating levels of NE from 1.1 +/- 0.1 to 19.2 +/- 0. 948 8160886 0 ng levels of NE from 1.1 +/- 0 . 1 to 19.2 +/- 0.4 nM (P < 0.0 vels of NE from 1.1 +/- 0.1 to 19.2 +/- 0.4 nM (P 956 8160886 0 s of NE from 1.1 +/- 0.1 to 19 . 2 +/- 0.4 nM (P < 0.001), whi NE from 1.1 +/- 0.1 to 19.2 +/- 0.4 nM (P < 0.001) 964 8160886 0 from 1.1 +/- 0.1 to 19.2 +/- 0 . 4 nM (P < 0.001), which is in 1.1 +/- 0.1 to 19.2 +/- 0.4 nM (P < 0.001), which 972 8160886 0 0.1 to 19.2 +/- 0.4 nM (P < 0 . 001), which is in the range o to 19.2 +/- 0.4 nM (P < 0.001), which is in the ra 984 8160886 1 e in isolated brown adipocytes . At all concentrations tested isolated brown adipocytes. At all concentrations t 1111 8160886 1 the heart and skeletal muscles . NE treatment did not signifi eart and skeletal muscles. NE treatment did not si 1221 8160886 1 f circulating free fatty acids . The capacity of brown adipos culating free fatty acids. The capacity of brown a 1360 8160886 1 mes), or the heart (3-4 times) . (ABSTRACT TRUNCATED AT 250 WO or the heart (3-4 times).(ABSTRACT TRUNCATED AT 2 1613 10543393 1 lasma of heterozygous carriers . We compared the abilities of of heterozygous carriers. We compared the abiliti 270 10543393 1 d mouse peritoneal macrophages . Recombinant apoA-I(R151C)Par se peritoneal macrophages. Recombinant apoA-I(R151 693 10543393 1 eric forms at a ratio of 60:40 . Normal apoA-I and apoA-I(R15 forms at a ratio of 60:40. Normal apoA-I and apoA- 785 10543393 1 DMPC emulsions at equal rates . Both isoforms associated com emulsions at equal rates. Both isoforms associate 861 10543393 1 h DPPC during cholate dialysis . Normal apoA-I formed one sin C during cholate dialysis. Normal apoA-I formed on 932 10543393 0 icle with a mean diameter of 9 . 3 nm, whereas apoA-I(R151)Par with a mean diameter of 9.3 nm, whereas apoA-I(R15 1000 10543393 0 icles with mean diameters of 9 . 3 nm (containing 74% of apoA- with mean diameters of 9.3 nm (containing 74% of 1086 10543393 0 (containing 74% of apoA-I), 10 . 6 nm, and 12.1 nm, respective aining 74% of apoA-I), 10.6 nm, and 12.1 nm, respe 1122 10543393 0 4% of apoA-I), 10.6 nm, and 12 . 1 nm, respectively. Compared apoA-I), 10.6 nm, and 12.1 nm, respectively. Comp 1135 10543393 1 nm, and 12.1 nm, respectively . Compared to normal apoA-I, a and 12.1 nm, respectively. Compared to normal apoA 1154 10543393 1 % higher affinity constant, Km . During incubations for 10 mi her affinity constant, Km. During incubations for 1311 10543393 1 ynthetic cholesterol from SMCs . In the lipid-free form, apoA tic cholesterol from SMCs. In the lipid-free form, 1493 10543393 1 d mouse-peritoneal macrophages . In conclusion, in addition t se-peritoneal macrophages. In conclusion, in addit 1662 10543393 1 rol-efflux-promoting abilities . fflux-promoting abilities. 1880 12054068 1 sformed non-Hodgkin's lymphoma . It has shown high response r ed non-Hodgkin's lymphoma. It has shown high respo 178 12054068 1 Genentech/F Hoffmann La Roche) . Complications include myelos tech/F Hoffmann La Roche). Complications include m 391 12054068 1 lodysplasia and hypothyroidism . The role of this promising n plasia and hypothyroidism. The role of this promis 492 12054068 1 ned in phase II and III trials . In February 2001, ABN Amro P n phase II and III trials. In February 2001, ABN A 574 12054068 1 S $70 million in 2003 [422363] . Corixa and GlaxoSmithKline a million in 2003 [422363]. Corixa and GlaxoSmithKl 697 12054068 1 nch in the US in 2002 [424619] . n the US in 2002 [424619]. 772 7135920 1 ng phenol extraction procedure . The poly (A)-containing mRNA enol extraction procedure. The poly (A)-containing 144 7135920 1 on oligo(dT)-cellulose columns . The resulting mRNA preparati igo(dT)-cellulose columns. The resulting mRNA prep 227 7135920 1 --60% of SA7-derived sequences . SA7 late mRNA was efficientl of SA7-derived sequences. SA7 late mRNA was effic 339 7135920 1 authentic SA7 virion proteins . The main translation product entic SA7 virion proteins. The main translation pr 536 7135920 1 ed as intact SA7 hexon protein . intact SA7 hexon protein. 654 15235872 1 IFN) therapy on HCC recurrence . METHODS: Of 187 patients wit therapy on HCC recurrence. METHODS: Of 187 patient 261 15235872 1 age (10, 22, 23, and 26 years) . RESULTS: At the time of diag 10, 22, 23, and 26 years). RESULTS: At the time of 420 15235872 0 tumorous liver was F0 or F1, i . e., low-grade hepatitis. The ous liver was F0 or F1, i.e., low-grade hepatitis. 584 15235872 0 morous liver was F0 or F1, i.e . , low-grade hepatitis. The mo s liver was F0 or F1, i.e., low-grade hepatitis. T 586 15235872 1 F1, i.e., low-grade hepatitis . The mothers of all 4 young a i.e., low-grade hepatitis. The mothers of all 4 yo 608 15235872 1 had HBV-related liver disease . Three cases developed recurr HBV-related liver disease. Three cases developed r 690 15235872 1 es developed recurrence of HCC . In these patients, long-term veloped recurrence of HCC. In these patients, long 731 15235872 1 more than 3 years of follow-up . CONCLUSIONS: (1) Young adult than 3 years of follow-up. CONCLUSIONS: (1) Young 896 15235872 1 mother-to-infant transmission . Transplacental transmission er-to-infant transmission. Transplacental transmis 1056 15235872 1 operation for HBV-related HCC . ation for HBV-related HCC. 1371 9580254 1 from donors of different ages . The arterial segments were d donors of different ages. The arterial segments w 128 9580254 1 evident cardiovascular disease . Total glycosaminoglycan cont nt cardiovascular disease. Total glycosaminoglycan 274 9580254 1 ing the first 40 years of life . Changes in the content of hy he first 40 years of life. Changes in the content 351 9580254 1 an sulfate are less noticeable . The content of chondroitin s lfate are less noticeable. The content of chondroi 434 9580254 1 matan sulfate remains constant . Plasma LDL-affinity chromato sulfate remains constant. Plasma LDL-affinity chr 545 9580254 1 nity glycosaminoglycan species . Remarkably, only glycosamino glycosaminoglycan species. Remarkably, only glycos 714 9580254 1 human thoracic aortas studied . These results suggest that a n thoracic aortas studied. These results suggest t 868 9580254 1 eased deposition of plasma LDL . However, the alternative exp deposition of plasma LDL. However, the alternativ 1026 9580254 1 r analysis cannot be ruled out . lysis cannot be ruled out. 1254 12970354 1 l surface is poorly understood . This issue was addressed by face is poorly understood. This issue was addresse 156 12970354 1 nd alpha2B-AR in HEK293T cells . Inhibition of endogenous Rab pha2B-AR in HEK293T cells. Inhibition of endogenou 475 12970354 1 xpression of AT1R and beta2-AR . The accumulated receptors we sion of AT1R and beta2-AR. The accumulated recepto 729 12970354 1 sport from the ER to the Golgi . In contrast, dominant-negati from the ER to the Golgi. In contrast, dominant-n 919 12970354 1 lar distribution of alpha2B-AR . Similarly, expression of dom istribution of alpha2B-AR. Similarly, expression o 1034 12970354 1 R-stimulated ERK1/2 activation . These data indicate that Rab mulated ERK1/2 activation. These data indicate tha 1301 12970354 1 rom the ER to the cell surface . he ER to the cell surface. 1554 11207669 1 . The role of nitric oxide (NO 1 11207669 1 nduced mechanisms is not clear . Microinjection of glutamate d mechanisms is not clear. Microinjection of gluta 146 11207669 1 vertebral nerve activity (VNA) . Thus, in the present study, bral nerve activity (VNA). Thus, in the present st 347 11207669 1 ses in the DM and RVLM of cats . 2. Histochemical methods usi n the DM and RVLM of cats. 2. Histochemical method 475 11207669 0 in the DM and RVLM of cats. 2 . Histochemical methods using he DM and RVLM of cats. 2. Histochemical methods u 478 11207669 1 of NOS in both the DM and RVLM . 3. Microinjection of N(G)-ni S in both the DM and RVLM. 3. Microinjection of N( 686 11207669 0 NOS in both the DM and RVLM. 3 . Microinjection of N(G)-nitro n both the DM and RVLM. 3. Microinjection of N(G)- 689 11207669 1 mate-induced pressor responses . Interestingly, the increase induced pressor responses. Interestingly, the incr 909 11207669 1 VLM in a dose-dependent manner . 4. We also examined whether n a dose-dependent manner. 4. We also examined whe 1173 11207669 0 in a dose-dependent manner. 4 . We also examined whether NO dose-dependent manner. 4. We also examined whethe 1176 11207669 1 xcitatory amino acid receptors . N-Methyl-D-aspartate (NMDA) tory amino acid receptors. N-Methyl-D-aspartate (N 1304 11207669 1 oprionic acid (AMPA) were used . Consistent with the results nic acid (AMPA) were used. Consistent with the res 1413 11207669 1 onses induced by NMDA and AMPA . No difference was found betw induced by NMDA and AMPA. No difference was found 1589 11207669 1 AMPA-induced pressor responses . 5. To investigate the possib induced pressor responses. 5. To investigate the p 1684 11207669 0 A-induced pressor responses. 5 . To investigate the possibili uced pressor responses. 5. To investigate the poss 1687 11207669 1 ponses in the DM were examined . The results showed that CNQX s in the DM were examined. The results showed that 1905 11207669 1 o alter AMPA-induced responses . 6. Our results suggest that er AMPA-induced responses. 6. Our results suggest 2032 11207669 0 lter AMPA-induced responses. 6 . Our results suggest that act AMPA-induced responses. 6. Our results suggest tha 2035 11207669 1 n NO levels in the DM and RVLM . This implies that NO may pla levels in the DM and RVLM. This implies that NO ma 2171 11207669 1 glutamate-activation mechanism . mate-activation mechanism. 2277 7973749 0 lism syndrome occurs in only 0 . 9-4% of patients with long bo syndrome occurs in only 0.9-4% of patients with lo 38 7973749 1 ly with intramedullary nailing . Earlier publications have sh th intramedullary nailing. Earlier publications ha 123 7973749 0 intramedullary manipulation, e . g. reaming and nailing, can p medullary manipulation, e.g. reaming and nailing, 192 7973749 0 tramedullary manipulation, e.g . reaming and nailing, can pro dullary manipulation, e.g. reaming and nailing, ca 194 7973749 1 high pressures of up to 1 bar . The design of the new non-sl pressures of up to 1 bar. The design of the new n 258 7973749 1 pressure in the femoral cavity . We measured the intramedulla ure in the femoral cavity. We measured the intrame 378 7973749 1 nd a piezo pressure transducer . We simulated a proximal frac piezo pressure transducer. We simulated a proximal 552 7973749 1 ling and 20 nailing procedures . On average we detected a max and 20 nailing procedures. On average we detected 638 7973749 0 tected a maximum pressure of 0 . 26 bar during drilling and 0. d a maximum pressure of 0.26 bar during drilling a 686 7973749 0 0.26 bar during drilling and 0 . 63 bar during nailing. During bar during drilling and 0.63 bar during nailing. D 715 7973749 1 ng and 0.63 bar during nailing . During reaming the pressure d 0.63 bar during nailing. During reaming the pres 737 7973749 1 sis and reached the metaphysis . When the tried to enlarge th nd reached the metaphysis. When the tried to enlar 851 7973749 1 e measured high pressure peaks . During nailing we detected s sured high pressure peaks. During nailing we detec 973 7973749 1 ses lasting a few milliseconds . The results show that the ne asting a few milliseconds. The results show that t 1043 7973749 1 ry pressure than slotted nails . It is possible to avoid a da essure than slotted nails. It is possible to avoid 1156 7973749 1 a careful operative technique . reful operative technique. 1247 12766201 1 gical systems to be integrated . Heterotypic complexes occur systems to be integrated. Heterotypic complexes o 119 12766201 1 clearance from the oral cavity . In this study, we used a pep ance from the oral cavity. In this study, we used 265 12766201 1 volving MG2 and other proteins . The library was panned with ng MG2 and other proteins. The library was panned 409 12766201 1 occurs in salivary lactoferrin . Blotting experiments confirm s in salivary lactoferrin. Blotting experiments co 554 12766201 1 c complex in vitro and in vivo . Periodate treatment of MG2 d plex in vitro and in vivo. Periodate treatment of 659 12766201 1 did not affect the interaction . A synthetic lactoferrin pept ot affect the interaction. A synthetic lactoferrin 718 12766201 1 eraction identified by panning . This complex may enhance the ion identified by panning. This complex may enhanc 909 12766201 1 onents in the oral environment . s in the oral environment. 1003 15705296 1 tis-specific genes or isoforms . The regulatory processes gov pecific genes or isoforms. The regulatory processe 219 15705296 1 eculiar chromatin organization . The signalling cascades and ar chromatin organization. The signalling cascades 420 15705296 1 germ cell regulatory circuits . This paper reports on the un cell regulatory circuits. This paper reports on t 618 15705296 1 M exerts as a master regulator . Targeted inactivation of the rts as a master regulator. Targeted inactivation o 696 15705296 1 CREM and ACT has been achieved . ACT selectively associates w and ACT has been achieved. ACT selectively associa 772 15705296 1 highly expressed in germ cells . It has been found that KIF17 y expressed in germ cells. It has been found that 868 15705296 1 racellular localization of ACT . Thus, the activity of a tran lular localization of ACT. Thus, the activity of a 957 15705296 1 its intracellular localization . The conservation of these el ntracellular localization. The conservation of the 1117 15705296 1 echanisms of human infertility . isms of human infertility. 1338 12213253 1 rase levels are slightly lower . Unlike the overproduced este levels are slightly lower. Unlike the overproduced 231 12213253 0 s for only a small fraction (0 . 033-0.045%) of the total extr only a small fraction (0.033-0.045%) of the total 366 12213253 0 only a small fraction (0.033-0 . 045%) of the total extractabl a small fraction (0.033-0.045%) of the total extra 372 12213253 1 istant and susceptible strains . The enzyme was purified to a t and susceptible strains. The enzyme was purified 461 12213253 1 lar molecular weight of 62,000 . However, preparative isoelec olecular weight of 62,000. However, preparative is 578 12213253 0 s possess one MCE with pI of 7 . 3, while susceptible insects sess one MCE with pI of 7.3, while susceptible ins 682 12213253 0 s possess a MCE with a pI of 6 . 6. Purified MCE from both pop sess a MCE with a pI of 6.6. Purified MCE from bot 740 12213253 1 possess a MCE with a pI of 6.6 . Purified MCE from both popul ss a MCE with a pI of 6.6. Purified MCE from both 742 12213253 1 as for alpha-naphthyl acetate . The kinetic analysis suggest or alpha-naphthyl acetate. The kinetic analysis su 879 12213253 1 thion than for naphthyl esters . Malathion-specific resistanc than for naphthyl esters. Malathion-specific resi 1109 12213253 1 terase in the resistant strain . e in the resistant strain. 1225 8603006 1 ction of programmed cell death . We have analysed the presenc of programmed cell death. We have analysed the pr 189 8603006 1 lls from 35 patients by RT-PCR . Transcripts for IL-10 were d rom 35 patients by RT-PCR. Transcripts for IL-10 w 301 8603006 1 s with non-progressive disease . In cell preparations from pa h non-progressive disease. In cell preparations fr 385 8603006 0 only 2/15 samples (P < or = 0 . 01). The Epstein-Barr virus s 2/15 samples (P < or = 0.01). The Epstein-Barr vi 502 8603006 1 y 2/15 samples (P < or = 0.01) . The Epstein-Barr virus statu 5 samples (P < or = 0.01). The Epstein-Barr virus 506 8603006 1 een the two groups of patients . Thus, IL-10 mRNA expression he two groups of patients. Thus, IL-10 mRNA expres 654 8603006 1 d with non-progressive disease . This finding may support oth h non-progressive disease. This finding may suppor 780 8603006 1 e therapy of progressive B-CLL . rapy of progressive B-CLL. 908 10793093 1 ere infected with the parasite . GKO and p55KO, but not wild- nfected with the parasite. GKO and p55KO, but not 287 10793093 1 after infection, respectively . Typical inflammatory granulo r infection, respectively. Typical inflammatory gr 465 10793093 1 mas were found only in WT mice . In contrast, knockout mice p ere found only in WT mice. In contrast, knockout m 525 10793093 1 nuloma formation in p55KO mice . Besides, both groups of knoc a formation in p55KO mice. Besides, both groups of 763 10793093 1 -forming unit counts in organs . Compared with WT, splenocyte ing unit counts in organs. Compared with WT, splen 899 10793093 1 but higher levels of IFN-gamma . Moreover, splenocytes from i igher levels of IFN-gamma. Moreover, splenocytes f 1132 10793093 1 or infected p55KO and GKO mice . On the contrary, the additio fected p55KO and GKO mice. On the contrary, the ad 1332 10793093 1 and lower T cell proliferation . Taken together, these findin ower T cell proliferation. Taken together, these f 1478 10793093 1 marked T cell unresponsiveness . d T cell unresponsiveness. 1700 8209377 1 following chronic Cd exposure . However, nephrotoxicity foll owing chronic Cd exposure. However, nephrotoxicity 153 8209377 1 following chronic Cd exposure . In the present study, the se owing chronic Cd exposure. In the present study, t 295 8209377 1 d doses of Cd-MT was evaluated . The Cd-MT was administered v es of Cd-MT was evaluated. The Cd-MT was administe 399 8209377 1 , five times/week, for 9 weeks . Renal toxicity was evaluated e times/week, for 9 weeks. Renal toxicity was eval 628 8209377 1 ase, protein, and MT excretion . In naive rats, a bolus dose protein, and MT excretion. In naive rats, a bolus 718 8209377 0 naive rats, a bolus dose of 0 . 15 mg Cd/kg as Cd-MT was neph e rats, a bolus dose of 0.15 mg Cd/kg as Cd-MT was 752 8209377 1 Cd/kg as Cd-MT was nephrotoxic . In comparison, a two-fold hi as Cd-MT was nephrotoxic. In comparison, a two-fo 789 8209377 1 quired to cause nephrotoxicity . In Cd-pretreated rats, a bol d to cause nephrotoxicity. In Cd-pretreated rats, 873 8209377 0 reated rats, a bolus dose of 0 . 45 mg Cd/kg as Cd-MT was nece d rats, a bolus dose of 0.45 mg Cd/kg as Cd-MT was 915 8209377 1 an the levels in naive animals . Although a bolus dose of 3 m e levels in naive animals. Although a bolus dose o 1101 8209377 0 renal Cd concentration about 1 . 5 times that found after admi Cd concentration about 1.5 times that found after 1192 8209377 0 ound after administration of 0 . 15 mg Cd/kg as Cd-MT, it did after administration of 0.15 mg Cd/kg as Cd-MT, it 1237 8209377 1 ot produce any nephro-toxicity . The results of this study su oduce any nephro-toxicity. The results of this stu 1298 8209377 1 ined level over a 24-hr period . Furthermore, the preexisting level over a 24-hr period. Furthermore, the preexi 1516 8209377 1 r sequestration of incoming Cd . We conclude that mere accumu uestration of incoming Cd. We conclude that mere a 1694 8209377 1 determinants of nephrotoxicity . minants of nephrotoxicity. 1945 9302809 1 t for insect sting anaphylaxis . The design was a cross-secti insect sting anaphylaxis. The design was a cross- 194 9302809 1 n 13 allergy clinics in Israel . A self-administered question allergy clinics in Israel. A self-administered que 374 9302809 1 cts on occupational activities . Of the 204 respondents who w n occupational activities. Of the 204 respondents 562 9302809 0 e part of the labour force, 48 . 5% reported adverse effects o t of the labour force, 48.5% reported adverse effe 624 9302809 1 outine occupational activities . The factors with a significa e occupational activities. The factors with a sign 687 9302809 0 s type of work (blue collar vs . white collar: OR = 3.22, p < e of work (blue collar vs. white collar: OR = 3.22 829 9302809 0 ollar vs. white collar: OR = 3 . 22, p < 0.001: army vs. white vs. white collar: OR = 3.22, p < 0.001: army vs. 851 9302809 0 white collar: OR = 3.22, p < 0 . 001: army vs. white collar: O collar: OR = 3.22, p < 0.001: army vs. white coll 861 9302809 0 OR = 3.22, p < 0.001: army vs . white collar: OR = 5.28, p = 3.22, p < 0.001: army vs. white collar: OR = 5.28 874 9302809 0 army vs. white collar: OR = 5 . 28, p = 0.001); (2) severity vs. white collar: OR = 5.28, p = 0.001); (2) seve 896 9302809 0 white collar: OR = 5.28, p = 0 . 001); (2) severity of the all collar: OR = 5.28, p = 0.001); (2) severity of th 906 9302809 0 c reaction (severe reaction vs . mild/moderate reaction: OR = ction (severe reaction vs. mild/moderate reaction: 970 9302809 0 mild/moderate reaction: OR = 2 . 34, p = 0.007). Our findings moderate reaction: OR = 2.34, p = 0.007). Our find 1002 9302809 0 ate reaction: OR = 2.34, p = 0 . 007). Our findings suggest th eaction: OR = 2.34, p = 0.007). Our findings sugge 1012 9302809 1 eaction: OR = 2.34, p = 0.007) . Our findings suggest that se on: OR = 2.34, p = 0.007). Our findings suggest th 1017 9302809 1 ients' occupational activities . This factor requires special ' occupational activities. This factor requires sp 1131 9302809 1 ntion by the medical community . Social workers and occupatio by the medical community. Social workers and occu 1196 9302809 1 d management of these patients . agement of these patients. 1310 11443739 1 trict physiological regulation . The current study sought to physiological regulation. The current study sough 124 11443739 1 tured thyroid epithelial cells . Porcine thyroid cells cultur thyroid epithelial cells. Porcine thyroid cells c 245 11443739 1 t stimulate cAMP/PKA signaling . This morphogenetic event is mulate cAMP/PKA signaling. This morphogenetic even 398 11443739 1 e the initiation of locomotion . In this system, the extracel initiation of locomotion. In this system, the ext 570 11443739 1 nd nuclear accumulation of ERK . Inhibition of ERK activation clear accumulation of ERK. Inhibition of ERK activ 803 11443739 1 ells from beginning to migrate . PD98059 inhibited cell sprea from beginning to migrate. PD98059 inhibited cell 910 11443739 1 n of thyroid cell locomotility . Akt (PKB) signaling was also thyroid cell locomotility. Akt (PKB) signaling was 1085 11443739 1 he initiation of cell movement . Wortmannin did not, however, itiation of cell movement. Wortmannin did not, how 1280 11443739 1 ck activation of ERK signaling . These findings, therefore, i tivation of ERK signaling. These findings, therefo 1344 11443739 1 s of thyroid cell locomotility . These findings are incorpora thyroid cell locomotility. These findings are inco 1477 11443739 1 (cAMP/PKA) signaling pathways . P/PKA) signaling pathways. 1725 11588465 1 ase may injure various tissues . The release of polymorphonuc ay injure various tissues. The release of polymorp 74 11588465 1 rotease inhibitor, ulinastatin . In stored blood preparations se inhibitor, ulinastatin. In stored blood prepara 220 11588465 1 ge days as hemolysis increases . We hypothesized that polymor ys as hemolysis increases. We hypothesized that po 351 11588465 1 cing hemolysis in stored blood . Haptoglobin binds to free he hemolysis in stored blood. Haptoglobin binds to fr 473 11588465 1 hemoglobin to reduce hemolysis . The purpose of the study was lobin to reduce hemolysis. The purpose of the stud 531 11588465 1 in comparison with haptoglobin . DESIGN: In vitro study. SETT mparison with haptoglobin. DESIGN: In vitro study. 669 11588465 1 globin. DESIGN: In vitro study . SETTING: Laboratory in a uni n. DESIGN: In vitro study. SETTING: Laboratory in 693 11588465 1 atory in a university hospital . SUBJECTS: Nine 2-day-old pac in a university hospital. SUBJECTS: Nine 2-day-ol 739 11588465 1 om the Japan Red Cross Society . INTERVENTIONS: Each MAP-CRC e Japan Red Cross Society. INTERVENTIONS: Each MAP 926 11588465 1 or 50,000 units of ulinastatin . They were stored at 4 degree ,000 units of ulinastatin. They were stored at 4 d 1121 11588465 1 hey were stored at 4 degrees C . MEASUREMENTS AND MAIN RESULT ere stored at 4 degrees C. MEASUREMENTS AND MAIN R 1154 11588465 1 sium were measured for 25 days . Free haptoglobin concentrati were measured for 25 days. Free haptoglobin concen 1340 11588465 1 n concentration was calculated . Total and free hemoglobin co centration was calculated. Total and free hemoglob 1387 11588465 1 atin groups showed no increase . Total and free haptoglobin c groups showed no increase. Total and free haptoglo 1567 11588465 1 p than in the other two groups . Free haptoglobin concentrati n in the other two groups. Free haptoglobin concen 1690 11588465 1 control and ulinastatin groups . Polymorphonuclear leukocyte ol and ulinastatin groups. Polymorphonuclear leuko 1792 11588465 1 erences among the three groups . Potassium concentration incr es among the three groups. Potassium concentration 1936 11588465 1 est value in the control group . CONCLUSIONS: Adding haptoglo alue in the control group. CONCLUSIONS: Adding hap 2046 11588465 1 ing storage of the preparation . The polymorphonuclear leukoc torage of the preparation. The polymorphonuclear l 2172 11588465 1 in MAP-CRC stored for 25 days . AP-CRC stored for 25 days. 2297 11670440 1 = CH(2)C(6)H(5), are presented . Results from pyrolysis of (B 2)C(6)H(5), are presented. Results from pyrolysis 174 11670440 0 er mild thermal conditions (ca . 275 degrees C). Flow-tube py ld thermal conditions (ca. 275 degrees C). Flow-tu 387 11670440 1 conditions (ca. 275 degrees C) . Flow-tube pyrolysis produces tions (ca. 275 degrees C). Flow-tube pyrolysis pro 403 11670440 1 adiating acicular crystallites . Bi(2)S(3) was characterized ing acicular crystallites. Bi(2)S(3) was character 607 11670440 1 d scanning electron microscopy . nning electron microscopy. 697 11903574 1 ility and possibly cell growth . It has been reported that th and possibly cell growth. It has been reported th 145 11903574 1 al breast tissue are available . This investigation was aimed east tissue are available. This investigation was 358 11903574 1 nostic marker in breast cancer . METHODS AND RESULTS: Section c marker in breast cancer. METHODS AND RESULTS: Se 577 11903574 1 malignant cases were examined . The monoclonal antibody CD9 gnant cases were examined. The monoclonal antibody 730 11903574 1 lex immunoperoxidase technique . The results were assessed se mmunoperoxidase technique. The results were assess 868 11903574 1 tem of 3+, 2+, 1+ and negative . All normal and benign epithe f 3+, 2+, 1+ and negative. All normal and benign e 967 11903574 1 lls were strongly stained (3+) . In female breast carcinomas, ere strongly stained (3+). In female breast carcin 1034 11903574 1 , 49% were 2+, and 11% were 1+ . Both cases of male breast ca were 2+, and 11% were 1+. Both cases of male brea 1106 11903574 1 le breast carcinomas scored 3+ . For female breast cancers, t east carcinomas scored 3+. For female breast cance 1154 11903574 1 d progesterone receptor status . No significant statistical c gesterone receptor status. No significant statisti 1329 11903574 1 d with any of these parameters . We then examined 11 axillary h any of these parameters. We then examined 11 axi 1408 11903574 1 s from some of the above cases . Three of these cases had a C m some of the above cases. Three of these cases ha 1495 11903574 1 seven were 2+, and one was 1+ . The metastatic tumours in al n were 2+, and one was 1+. The metastatic tumours 1570 11903574 1 ses were strongly stained (3+) . CONCLUSIONS: Immunostaining ere strongly stained (3+). CONCLUSIONS: Immunostai 1637 11903574 1 ormation for clinical purposes . ion for clinical purposes. 1764 10072716 1 ction of vasodilator mediators . In some cases, this function of vasodilator mediators. In some cases, this fun 129 10072716 1 ease of constrictor substances . The endothelial mediators ar of constrictor substances. The endothelial mediato 212 10072716 1 ell-vascular wall interactions . The endothelium-derived fact ascular wall interactions. The endothelium-derived 365 10072716 1 perpolarizing factor(s) (EDHF) . In most vascular diseases, t larizing factor(s) (EDHF). In most vascular diseas 513 10072716 1 the endothelium is attenuated . In advanced atherosclerotic endothelium is attenuated. In advanced atheroscler 599 10072716 1 latation may even be abolished . Various degrees and forms of ion may even be abolished. Various degrees and for 696 10072716 1 o NO, prostacyclin and/or EDHF . The levels of bradykinin and prostacyclin and/or EDHF. The levels of bradykini 1084 10072716 1 tensin-converting enzyme (ACE) . ACE degrades bradykinin and n-converting enzyme (ACE). ACE degrades bradykinin 1208 10072716 1 n and generates angiotensin II . Bradykinin stimulates endoth generates angiotensin II. Bradykinin stimulates e 1262 10072716 1 cells to release vasodilators . The actions of the kinin are s to release vasodilators. The actions of the kini 1327 10072716 1 n very severe arterial lesions . Angiotensin II may be in par y severe arterial lesions. Angiotensin II may be i 1440 10072716 1 o the vasodilator action of NO . Thus, impairment of the gene vasodilator action of NO. Thus, impairment of the 1573 10072716 1 strictor effect of the peptide . By potentiating bradykinin, tor effect of the peptide. By potentiating bradyki 1696 10072716 1 eukocytes to the vascular wall . ytes to the vascular wall. 1925 14741404 1 dels are difficult to generate . We are applying this approac are difficult to generate. We are applying this ap 239 14741404 1 spinal muscular atrophy (SMA) . SMA is caused by mutations i al muscular atrophy (SMA). SMA is caused by mutati 335 14741404 1 val of motor neuron gene (SMN) . The SMN protein is ubiquitou f motor neuron gene (SMN). The SMN protein is ubiq 406 14741404 1 egeneration in the spinal cord . The reasons for this motor n ration in the spinal cord. The reasons for this mo 574 14741404 1 ty, however, are still unclear . SMN is essential for the via owever, are still unclear. SMN is essential for th 649 14741404 1 els of SMA extremely difficult . Here we describe a different f SMA extremely difficult. Here we describe a diff 791 14741404 1 ilence SMN expression in cells . We designed double-stranded e SMN expression in cells. We designed double-stra 898 14741404 1 terato-carcinoma cell line P19 . The siRNAs reduced both Smn o-carcinoma cell line P19. The siRNAs reduced both 1053 14741404 1 P19 cells compared to controls . These results illustrate tha ells compared to controls. These results illustrat 1143 14741404 1 ble tool to study SMN function . ool to study SMN function. 1373 11160439 1 bility has not been determined . It has become increasingly c y has not been determined. It has become increasin 206 11160439 1 en several interacting systems . Targeting neuropeptide neuro veral interacting systems. Targeting neuropeptide 398 11160439 1 tic approach for schizophrenia . A considerable database is c pproach for schizophrenia. A considerable database 575 11160439 1 neuropeptide neurotensin (NT) . In this report, we demonstra opeptide neurotensin (NT). In this report, we demo 759 11160439 1 atent inhibition (LI) paradigm . Blockade of NT neurotransmis inhibition (LI) paradigm. Blockade of NT neurotra 1044 11160439 1 idol-induced enhancement of LI . In addition, SR 142948A bloc induced enhancement of LI. In addition, SR 142948A 1380 11160439 1 eared animals deficient in PPI . We also provide evidence of animals deficient in PPI. We also provide evidenc 1546 11160439 1 curve in isolation-reared rats . These novel findings, togeth in isolation-reared rats. These novel findings, t 1696 11160439 1 l class of antipsychotic drugs . ss of antipsychotic drugs. 1850 14645096 1 ream transcriptional processes . The translocation of cargo t transcriptional processes. The translocation of ca 255 14645096 1 to support efficient transport . In this report we have exami pport efficient transport. In this report we have 467 14645096 1 sing scanning force microscopy . We show that the initial doc scanning force microscopy. We show that the initia 572 14645096 1 rs at nanomolar concentrations . Later stages of transport in nanomolar concentrations. Later stages of transpo 678 14645096 1 ransport receptors and the NPC . Using calcium-depleted nucle ort receptors and the NPC. Using calcium-depleted 856 14645096 1 d for other regions of the NPC . other regions of the NPC. 1026 11523942 1 entification of these proteins . As part of an ongoing study ication of these proteins. As part of an ongoing s 187 11523942 1 pe reference strain NCTC 11637 . Proteins were separated by t ference strain NCTC 11637. Proteins were separated 440 11523942 1 nd stained with Coomassie G250 . Intensely-stained spots were ained with Coomassie G250. Intensely-stained spots 536 11523942 1 acterised by mass spectrometry . Proteins were then identifie ised by mass spectrometry. Proteins were then iden 668 11523942 1 published nucleotide sequences . Ninety-three of the most int shed nucleotide sequences. Ninety-three of the mos 810 11523942 0 35 genes, giving a ratio of 2 . 7 protein gene-products per g enes, giving a ratio of 2.7 protein gene-products 933 11523942 1 protein gene-products per gene . The products of the tsaA, pf in gene-products per gene. The products of the tsa 966 11523942 1 s present in multiple isoforms . Peptide mass fingerprinting sent in multiple isoforms. Peptide mass fingerprin 1077 11523942 1 lational protein modifications . These results suggest that H nal protein modifications. These results suggest t 1183 11523942 0 . These results suggest that H . pylori proteins are subject se results suggest that H. pylori proteins are sub 1213 11523942 1 ost-translational modification . Comparative proteomics of H. ranslational modification. Comparative proteomics 1294 11523942 0 n. Comparative proteomics of H . pylori strains should greatl mparative proteomics of H. pylori strains should g 1323 11523942 1 c properties of this bacterium . perties of this bacterium. 1422 11052958 1 al muscle of obese individuals . Muscle was obtained from obe scle of obese individuals. Muscle was obtained fro 158 11052958 0 ese [body mass index (BMI), 38 . 3 +/- 3.1 kg/m(2)] and lean ( body mass index (BMI), 38.3 +/- 3.1 kg/m(2)] and l 217 11052958 0 y mass index (BMI), 38.3 +/- 3 . 1 kg/m(2)] and lean (BMI, 23. s index (BMI), 38.3 +/- 3.1 kg/m(2)] and lean (BMI 225 11052958 0 3.1 kg/m(2)] and lean (BMI, 23 . 8 +/- 0.9 kg/m(2)) women, and g/m(2)] and lean (BMI, 23.8 +/- 0.9 kg/m(2)) women 254 11052958 0 (2)] and lean (BMI, 23.8 +/- 0 . 9 kg/m(2)) women, and fatty a and lean (BMI, 23.8 +/- 0.9 kg/m(2)) women, and fa 262 11052958 1 from (14)C-labeled fatty acids . Palmitate oxidation, which i (14)C-labeled fatty acids. Palmitate oxidation, wh 382 11052958 0 activity, was depressed (P < 0 . 05) by approximately 50% with ity, was depressed (P < 0.05) by approximately 50% 517 11052958 0 roximately 50% with obesity (6 . 8 +/- 2.2 vs. 13.7 +/- 1.4 nm ately 50% with obesity (6.8 +/- 2.2 vs. 13.7 +/- 1 558 11052958 0 ly 50% with obesity (6.8 +/- 2 . 2 vs. 13.7 +/- 1.4 nmole CO(2 % with obesity (6.8 +/- 2.2 vs. 13.7 +/- 1.4 nmole 566 11052958 0 % with obesity (6.8 +/- 2.2 vs . 13.7 +/- 1.4 nmole CO(2).g(- h obesity (6.8 +/- 2.2 vs. 13.7 +/- 1.4 nmole CO(2 571 11052958 0 th obesity (6.8 +/- 2.2 vs. 13 . 7 +/- 1.4 nmole CO(2).g(-1).h esity (6.8 +/- 2.2 vs. 13.7 +/- 1.4 nmole CO(2).g( 575 11052958 0 ty (6.8 +/- 2.2 vs. 13.7 +/- 1 . 4 nmole CO(2).g(-1).h(-1)). T .8 +/- 2.2 vs. 13.7 +/- 1.4 nmole CO(2).g(-1).h(-1 583 11052958 0 2 vs. 13.7 +/- 1.4 nmole CO(2) . g(-1).h(-1)). The CPT-1-indep 13.7 +/- 1.4 nmole CO(2).g(-1).h(-1)). The CPT-1- 597 11052958 0 13.7 +/- 1.4 nmole CO(2).g(-1) . h(-1)). The CPT-1-independent +/- 1.4 nmole CO(2).g(-1).h(-1)). The CPT-1-indepe 603 11052958 1 - 1.4 nmole CO(2).g(-1).h(-1)) . The CPT-1-independent event nmole CO(2).g(-1).h(-1)). The CPT-1-independent e 610 11052958 0 tion was also depressed (P < 0 . 01) by approximately 45%. The was also depressed (P < 0.01) by approximately 45% 698 11052958 1 P < 0.01) by approximately 45% . There were significant negat .01) by approximately 45%. There were significant 723 11052958 0 negative relationships (P < 0 . 05) for adiposity with palmit tive relationships (P < 0.05) for adiposity with p 777 11052958 0 iposity with palmitate (r = -0 . 76) and palmitoyl carnitine ( ty with palmitate (r = -0.76) and palmitoyl carnit 818 11052958 0 nd palmitoyl carnitine (r = -0 . 82) oxidation. Muscle CPT-1 a lmitoyl carnitine (r = -0.82) oxidation. Muscle CP 854 11052958 1 arnitine (r = -0.82) oxidation . Muscle CPT-1 and citrate syn ine (r = -0.82) oxidation. Muscle CPT-1 and citrat 868 11052958 0 were also significantly (P < 0 . 05) reduced ( approximately 3 also significantly (P < 0.05) reduced ( approximat 979 11052958 1 pproximately 35%) with obesity . CPT-1 (r = -0.48) and citrat imately 35%) with obesity. CPT-1 (r = -0.48) and c 1025 11052958 0 %) with obesity. CPT-1 (r = -0 . 48) and citrate synthase (r = th obesity. CPT-1 (r = -0.48) and citrate synthase 1040 11052958 0 ) and citrate synthase (r = -0 . 65) activities were significa citrate synthase (r = -0.65) activities were sign 1073 11052958 0 ties were significantly (P < 0 . 05) related to adiposity. The were significantly (P < 0.05) related to adiposity 1114 11052958 1 P < 0.05) related to adiposity . These data suggest that lesi .05) related to adiposity. These data suggest that 1139 11052958 1 n skeletal muscle with obesity . letal muscle with obesity. 1333 7901997 1 ated during fasting of the ewe . Euglycemic hyperinsulinemia during fasting of the ewe. Euglycemic hyperinsulin 66 7901997 1 cine oxidation rate to decline . However, it is unclear wheth oxidation rate to decline. However, it is unclear 140 7901997 1 n-mediated glucose utilization . To better delineate the mech iated glucose utilization. To better delineate the 273 7901997 1 etion by somatostatin infusion . Glucose was infused at a var by somatostatin infusion. Glucose was infused at 395 7901997 1 trations 125 and 150% of basal . Leucine rate of appearance ( ons 125 and 150% of basal. Leucine rate of appeara 491 7901997 1 nfusion of [15N, 1-13C]leucine . Fraction of leucine appearan on of [15N, 1-13C]leucine. Fraction of leucine app 574 7901997 1 ation of fetal 14CO2 excretion . Each fetus was studied durin of fetal 14CO2 excretion. Each fetus was studied 700 7901997 1 a 5-day complete maternal fast . Changes were noted in fetal ay complete maternal fast. Changes were noted in f 800 7901997 0 idation, which declined from 8 . 4 +/- 1.2 to 5.0 +/- 0.8 mumo on, which declined from 8.4 +/- 1.2 to 5.0 +/- 0.8 870 7901997 0 which declined from 8.4 +/- 1 . 2 to 5.0 +/- 0.8 mumol/min in h declined from 8.4 +/- 1.2 to 5.0 +/- 0.8 mumol/m 878 7901997 0 declined from 8.4 +/- 1.2 to 5 . 0 +/- 0.8 mumol/min in the fe ned from 8.4 +/- 1.2 to 5.0 +/- 0.8 mumol/min in t 885 7901997 0 from 8.4 +/- 1.2 to 5.0 +/- 0 . 8 mumol/min in the fed state 8.4 +/- 1.2 to 5.0 +/- 0.8 mumol/min in the fed s 893 7901997 1 state during glucose infusion . Basal leucine oxidation was e during glucose infusion. Basal leucine oxidation 946 7901997 0 vated during fasting (11 +/- 1 . 5 mumol/min, P < 0.05) and de during fasting (11 +/- 1.5 mumol/min, P < 0.05) a 1009 7901997 0 g (11 +/- 1.5 mumol/min, P < 0 . 05) and declined to 8.0 +/- 1 +/- 1.5 mumol/min, P < 0.05) and declined to 8.0 1028 7901997 0 n, P < 0.05) and declined to 8 . 0 +/- 1.4 mumol/min during gl < 0.05) and declined to 8.0 +/- 1.4 mumol/min duri 1050 7901997 0 .05) and declined to 8.0 +/- 1 . 4 mumol/min during glucose in and declined to 8.0 +/- 1.4 mumol/min during gluco 1058 7901997 0 during glucose infusion (P = 0 . 056). Leucine carbon Ra was u g glucose infusion (P = 0.056). Leucine carbon Ra 1101 7901997 1 g glucose infusion (P = 0.056) . Leucine carbon Ra was unchan cose infusion (P = 0.056). Leucine carbon Ra was u 1106 7901997 1 declined in the fed state only . Leucine oxidation was invers ned in the fed state only. Leucine oxidation was i 1226 7901997 0 oncentration (oxidation = 12-0 . 26 x glucose concentration, r tration (oxidation = 12-0.26 x glucose concentrati 1315 7901997 0 x glucose concentration, r = 0 . 42, P = 0.004). Leucine oxida cose concentration, r = 0.42, P = 0.004). Leucine 1349 7901997 0 concentration, r = 0.42, P = 0 . 004). Leucine oxidation was n ntration, r = 0.42, P = 0.004). Leucine oxidation 1359 7901997 1 ntration, r = 0.42, P = 0.004) . Leucine oxidation was not co ion, r = 0.42, P = 0.004). Leucine oxidation was n 1364 7901997 0 h insulin concentration (r = 0 . 2). Changes in fetal glucose ulin concentration (r = 0.2). Changes in fetal glu 1436 7901997 1 nsulin concentration (r = 0.2) . Changes in fetal glucose con n concentration (r = 0.2). Changes in fetal glucos 1439 7901997 1 iated glucose utilization rate . glucose utilization rate. 1622 11217967 0 ca Caturra (Coffea arabica var . Caturra) and Robusta ROM (Co turra (Coffea arabica var. Caturra) and Robusta RO 130 11217967 0 usta ROM (Coffea canephora var . ROM) green coffee beans show ROM (Coffea canephora var. ROM) green coffee beans 178 11217967 1 ical amounts of polysaccharide . Cell wall material (CWM) was amounts of polysaccharide. Cell wall material (CWM 271 11217967 0 raction with water, 1 M KOH, 0 . 3% NaClO2, 4 M KOH and 8 M KO on with water, 1 M KOH, 0.3% NaClO2, 4 M KOH and 8 442 11217967 1 3% NaClO2, 4 M KOH and 8 M KOH . The monosaccharide compositi ClO2, 4 M KOH and 8 M KOH. The monosaccharide comp 473 11217967 1 htly more mannose than Robusta . In the latter, more arabinog more mannose than Robusta. In the latter, more ara 600 11217967 1 galactomannan than in Arabica . Linkage analysis indicated t ctomannan than in Arabica. Linkage analysis indica 783 11217967 1 igher than previously reported . No major difference in the s than previously reported. No major difference in 946 11217967 1 nans between species was found . The arabinogalactans were he between species was found. The arabinogalactans we 1042 11217967 1 of their arabinan side-chains . Compared to Arabica, Robusta heir arabinan side-chains. Compared to Arabica, Ro 1190 11217967 1 actans with longer side chains . It is concluded that there w s with longer side chains. It is concluded that th 1300 11217967 1 atures of their galactomannans . Differences were apparent bo s of their galactomannans. Differences were appare 1514 11217967 1 r consistently between species . sistently between species. 1781 11446768 1 in normal and diseased corneas . Total RNA was isolated from rmal and diseased corneas. Total RNA was isolated 113 11446768 1 om normal and diseased corneas . cDNA was synthesized from in rmal and diseased corneas. cDNA was synthesized fr 170 11446768 1 -I, TGF-beta2, FGF-2, and VEGF . After normalization to beta2 GF-beta2, FGF-2, and VEGF. After normalization to 398 11446768 1 ficantly different from normal . Antibodies to IGF-I, BMP-2, tly different from normal. Antibodies to IGF-I, BM 521 11446768 1 used for immunohistochemistry . A total of 93 corneas were u for immunohistochemistry. A total of 93 corneas w 604 11446768 1 /ABK), and 23 diabetic corneas . The VEGF RNA levels were sig , and 23 diabetic corneas. The VEGF RNA levels wer 773 11446768 1 reased in the diabetic corneas . BMP-2 gene expression was lo d in the diabetic corneas. BMP-2 gene expression w 900 11446768 1 e PBK/ABK and diabetic corneas . IGF-I and BMP-4 RNA levels w /ABK and diabetic corneas. IGF-I and BMP-4 RNA lev 981 11446768 1 vels were increased in PBK/ABK . In the immunohistochemical s were increased in PBK/ABK. In the immunohistochemi 1035 11446768 1 those found at the mRNA level . The only exception was IGF-I e found at the mRNA level. The only exception was 1134 11446768 1 ficant increase in mRNA levels . TGF-beta2 mRNA and protein l t increase in mRNA levels. TGF-beta2 mRNA and prot 1305 11446768 1 normal in all diseased corneas . Thus, no alterations in the l in all diseased corneas. Thus, no alterations in 1387 11446768 1 unique to keratoconus corneas . In contrast, PBK/ABK corneas ue to keratoconus corneas. In contrast, PBK/ABK co 1483 11446768 1 elevations of BMP-4 and IGF-I . Diabetic corneas were unique ations of BMP-4 and IGF-I. Diabetic corneas were u 1568 11446768 1 eir increased VEGF mRNA levels . These data suggest that whil ncreased VEGF mRNA levels. These data suggest that 1634 11446768 1 hat are unique to that disease . re unique to that disease. 1818 11701729 0 eral fat area (LVFA; n = 8) vs . small visceral fat area (SVF fat area (LVFA; n = 8) vs. small visceral fat area 273 11701729 1 by magnetic resonance imaging . The subjects were matched fo agnetic resonance imaging. The subjects were match 356 11701729 1 , body fat percentage, and age . The impact of the loss of 50 y fat percentage, and age. The impact of the loss 433 11701729 1 striction was assessed as well . The results were compared wi tion was assessed as well. The results were compar 542 11701729 1 l weight control women (n = 8) . LVFA subjects manifested mar ght control women (n = 8). LVFA subjects manifeste 628 11701729 1 sal and pulsatile GH secretion . Moreover, visceral obesity w nd pulsatile GH secretion. Moreover, visceral obes 782 11701729 1 approximate entropy statistic . In contrast, SVFA subjects p oximate entropy statistic. In contrast, SVFA subje 916 11701729 1 hose in normal weight controls . GH half-life and distributio in normal weight controls. GH half-life and distri 1082 11701729 1 fferent among the study groups . Importantly, weight loss did nt among the study groups. Importantly, weight los 1162 11701729 1 oximately 40% of visceral fat) . Normal GH kinetics in SVFA w tely 40% of visceral fat). Normal GH kinetics in S 1418 11701729 1 influenced by weight reduction . Thus, GH neuroregulation app enced by weight reduction. Thus, GH neuroregulatio 1506 11701729 1 n their visceral adipose depot . Because weight loss did not ir visceral adipose depot. Because weight loss did 1643 11701729 1 fat in visceral adipose tissue . n visceral adipose tissue. 1911 7045520 1 ith minimal growth stimulation . The pathogenic yeast Candida inimal growth stimulation. The pathogenic yeast Ca 179 7045520 1 unts of hen egg-white lysozyme . This susceptibility was evid of hen egg-white lysozyme. This susceptibility was 291 7045520 1 dose-dependent killing process . Transmitted and scanning ele dependent killing process. Transmitted and scannin 382 7045520 0 rvations on lysozyme-treated C . albicans yeast cells reveale ons on lysozyme-treated C. albicans yeast cells re 464 7045520 1 n the organization of the wall . Ongoing structural modificat organization of the wall. Ongoing structural modi 759 7045520 1 heavy metal dye ruthenium red . A disruption in the permeabi y metal dye ruthenium red. A disruption in the per 874 7045520 1 cteristics in light microscopy . The superimposed osmotic imb stics in light microscopy. The superimposed osmoti 1033 7045520 1 ied as the cause of cell death . It is proposed that lysozyme s the cause of cell death. It is proposed that lys 1111 7045520 0 oposed that lysozyme acts on C . albicans by two distinct com d that lysozyme acts on C. albicans by two distinc 1151 7045520 1 ic protein kind of interaction . otein kind of interaction. 1398 15782248 1 nphosphate and fluoride anions . K+ cations can only be detec phate and fluoride anions. K+ cations can only be 153 15782248 1 resence of dihydrogenphosphate . ce of dihydrogenphosphate. 225 10547541 1 d metastasis of various tumors . The authors examined CD44 st astasis of various tumors. The authors examined CD 221 10547541 1 uct (EHBD)/ampullary carcinoma . METHODS: In 36 EHBD/ampullar EHBD)/ampullary carcinoma. METHODS: In 36 EHBD/amp 358 10547541 1 biotin immunoperoxidase method . The relation between express n immunoperoxidase method. The relation between ex 574 10547541 1 tient outcome was investigated . To verify the lack of CD44v6 outcome was investigated. To verify the lack of C 685 10547541 1 t hybridization were performed . RESULTS: Immunohistochemical ridization were performed. RESULTS: Immunohistoche 875 10547541 0 d that 13 of 36 carcinomas (36 . 1%) expressed the CD44v6 prot t 13 of 36 carcinomas (36.1%) expressed the CD44v6 952 10547541 1 ) expressed the CD44v6 protein . Only 2 of 13 CD44v6-expressi ressed the CD44v6 protein. Only 2 of 13 CD44v6-exp 985 10547541 0 -expressing primary tumors (15 . 4%) had regional lymph node m essing primary tumors (15.4%) had regional lymph n 1036 10547541 0 owing no CD44v6 expression (60 . 9%) had lymph node metastases no CD44v6 expression (60.9%) had lymph node metas 1133 10547541 0 stases (Fisher exact test, P<0 . 01). Moreover, a lack of CD44 s (Fisher exact test, P<0.01). Moreover, a lack of 1187 10547541 1 es (Fisher exact test, P<0.01) . Moreover, a lack of CD44v6 e isher exact test, P<0.01). Moreover, a lack of CD4 1191 10547541 0 generalized Wilcoxon test, P<0 . 05). Eleven of 13 CD44v6 posi alized Wilcoxon test, P<0.05). Eleven of 13 CD44v6 1311 10547541 1 ralized Wilcoxon test, P<0.05) . Eleven of 13 CD44v6 positive ed Wilcoxon test, P<0.05). Eleven of 13 CD44v6 pos 1315 10547541 1 was correlated with prognosis . RT-PCR and Southern blot hyb correlated with prognosis. RT-PCR and Southern blo 1419 10547541 1 e negative for CD44v6 staining . CONCLUSIONS: The results of ative for CD44v6 staining. CONCLUSIONS: The result 1554 10547541 1 with EHBD/ampullary carcinoma . EHBD/ampullary carcinoma. 1798 11396942 1 er G protein-coupled receptors . A(3) ARs mutated in transmem protein-coupled receptors. A(3) ARs mutated in tra 202 11396942 1 d adenylyl cyclase (AC) assays . Three mutant receptors, A229 nylyl cyclase (AC) assays. Three mutant receptors, 408 11396942 1 tive in both functional assays . The potency of the A(3) agon in both functional assays. The potency of the A(3) 556 11396942 1 08A and A229E mutant receptors . Cl-IB-MECA was much less pot nd A229E mutant receptors. Cl-IB-MECA was much les 793 11396942 1 uble mutation of the DRY motif . The degree of constitutive a mutation of the DRY motif. The degree of constitut 930 11396942 1 for the PLC signaling pathway . The results indicated that s the PLC signaling pathway. The results indicated t 1053 11396942 1 protein-uncoupled conformation . in-uncoupled conformation. 1233 14667178 1 es fat absorption by about 30% . However, the mean weight los t absorption by about 30%. However, the mean weigh 107 14667178 1 he degree of fat malabsorption . It was hypothesised that lip gree of fat malabsorption. It was hypothesised tha 216 14667178 1 take in normal-weight subjects . Fourteen healthy, lean subje in normal-weight subjects. Fourteen healthy, lean 375 14667178 0 s, five females; aged 25 +/- 1 . 3 years) were studied twice, ve females; aged 25 +/- 1.3 years) were studied tw 449 14667178 1 ice, in a double-blind fashion . The subjects received a high in a double-blind fashion. The subjects received a 504 14667178 1 essed during the following 8 h . Blood samples were taken at during the following 8 h. Blood samples were take 802 14667178 1 f plasma cholecystokinin (CCK) . Each subject performed a 3 d sma cholecystokinin (CCK). Each subject performed 901 14667178 1 ollection following each study . Energy intake during the day tion following each study. Energy intake during th 974 14667178 0 listat (10,220 (SEM 928) kJ) v . control (9405 (SEM 824) kJ) t (10,220 (SEM 928) kJ) v. control (9405 (SEM 824) 1059 14667178 0 ntrol (9405 (SEM 824) kJ) (P=0 . 02). On both days plasma CCK (9405 (SEM 824) kJ) (P=0.02). On both days plasma 1093 14667178 1 l (9405 (SEM 824) kJ) (P=0.02) . On both days plasma CCK incr 05 (SEM 824) kJ) (P=0.02). On both days plasma CCK 1097 14667178 0 days plasma CCK increased (P<0 . 05) after the preload. Plasma plasma CCK increased (P<0.05) after the preload. P 1137 14667178 1 sed (P<0.05) after the preload . Plasma CCK 20 min following P<0.05) after the preload. Plasma CCK 20 min follo 1159 14667178 0 oad was less after orlistat (4 . 1 (SEM 0.9) pmol/l) v. contro as less after orlistat (4.1 (SEM 0.9) pmol/l) v. c 1240 14667178 0 ess after orlistat (4.1 (SEM 0 . 9) pmol/l) v. control (5.3 (S fter orlistat (4.1 (SEM 0.9) pmol/l) v. control (5 1249 14667178 0 istat (4.1 (SEM 0.9) pmol/l) v . control (5.3 (SEM 0.9) pmol/ (4.1 (SEM 0.9) pmol/l) v. control (5.3 (SEM 0.9) 1262 14667178 0 SEM 0.9) pmol/l) v. control (5 . 3 (SEM 0.9) pmol/l (P=0.028); .9) pmol/l) v. control (5.3 (SEM 0.9) pmol/l (P=0. 1274 14667178 0 pmol/l) v. control (5.3 (SEM 0 . 9) pmol/l (P=0.028); however l) v. control (5.3 (SEM 0.9) pmol/l (P=0.028); how 1283 14667178 0 rol (5.3 (SEM 0.9) pmol/l (P=0 . 028); however there was no di 5.3 (SEM 0.9) pmol/l (P=0.028); however there was 1298 14667178 1 min between the two study days . Fat excretion was greater fo etween the two study days. Fat excretion was great 1401 14667178 0 orlistat (1017 (SEM 168) kJ) v . control (484 (SEM 90) kJ) (P tat (1017 (SEM 168) kJ) v. control (484 (SEM 90) k 1469 14667178 0 control (484 (SEM 90) kJ) (P=0 . 004). In conclusion, in healt ol (484 (SEM 90) kJ) (P=0.004). In conclusion, in 1501 14667178 1 ol (484 (SEM 90) kJ) (P=0.004) . In conclusion, in healthy, l 84 (SEM 90) kJ) (P=0.004). In conclusion, in healt 1506 14667178 1 lost due to fat malabsorption . due to fat malabsorption. 1725 10068273 1 . Emil J Freireich is a pionee 2 10068273 1 ral and leukemia in particular . This essay in his honor sugg nd leukemia in particular. This essay in his honor 107 10068273 1 o include two additional ideas . The first concept is that le lude two additional ideas. The first concept is th 259 10068273 1 rarchies, headed by stem cells . In both normal and leukemic ies, headed by stem cells. In both normal and leuk 385 10068273 1 ic cells respond to regulators . It follows that acute myelog lls respond to regulators. It follows that acute m 537 10068273 1 idered as a dependent neoplasm . The second concept is that c d as a dependent neoplasm. The second concept is t 626 10068273 1 ld be considered as two phases . The first, or proximal phase considered as two phases. The first, or proximal 711 10068273 1 ssion to apoptosis or recovery . Distal responses are describ to apoptosis or recovery. Distal responses are de 917 10068273 1 esponses are described briefly . Regulated drug sensitivity i ses are described briefly. Regulated drug sensitiv 957 10068273 1 t be used to improve treatment . used to improve treatment. 1071 7801777 1 d rotating glass sphere method . Procainamide of 136.0, 34.0, ating glass sphere method. Procainamide of 136.0, 110 7801777 0 re method. Procainamide of 136 . 0, 34.0, 8.5 mumol.L-1 in vit thod. Procainamide of 136.0, 34.0, 8.5 mumol.L-1 i 131 7801777 0 hod. Procainamide of 136.0, 34 . 0, 8.5 mumol.L-1 in vitro and Procainamide of 136.0, 34.0, 8.5 mumol.L-1 in vitr 137 7801777 0 Procainamide of 136.0, 34.0, 8 . 5 mumol.L-1 in vitro and 10 m inamide of 136.0, 34.0, 8.5 mumol.L-1 in vitro and 142 7801777 0 mide of 136.0, 34.0, 8.5 mumol . L-1 in vitro and 10 mg.kg-1 i of 136.0, 34.0, 8.5 mumol.L-1 in vitro and 10 mg.k 150 7801777 0 5 mumol.L-1 in vitro and 10 mg . kg-1 in vivo inhibited signif ol.L-1 in vitro and 10 mg.kg-1 in vivo inhibited s 173 7801777 1 28%, 8%, and 24%, respectively . It showed that procainamide 8%, and 24%, respectively. It showed that procaina 297 7801777 1 nhibition on platelet adhesion . tion on platelet adhesion. 396 10961895 1 normal differentiated tissues . A potential expression and p al differentiated tissues. A potential expression 126 10961895 1 astic, 96%; immunoblastic, 4%) . All patients were enrolled b , 96%; immunoblastic, 4%). All patients were enrol 294 10961895 1 -containing regimens (n = 143) . The characteristics of these aining regimens (n = 143). The characteristics of 649 10961895 1 ; bone marrow involvement, 15% . Of the 222 patients studied, e marrow involvement, 15%. Of the 222 patients stu 987 10961895 1 cells by immunohistochemistry . The overall 5-year survival s by immunohistochemistry. The overall 5-year surv 1109 10961895 0 those without (40% vs 54%, P = . 02). Multivariate analysis in without (40% vs 54%, P =.02). Multivariate analys 1243 10961895 1 e without (40% vs 54%, P =.02) . Multivariate analysis incorp hout (40% vs 54%, P =.02). Multivariate analysis i 1247 10961895 0 ive parameter on survival (P = . 03, relative risk [RR] = 1.6) arameter on survival (P =.03, relative risk [RR] = 1436 10961895 0 P =.03, relative risk [RR] = 1 . 6) in addition to LDH (P =.02 3, relative risk [RR] = 1.6) in addition to LDH (P 1463 10961895 0 = 1.6) in addition to LDH (P = . 02, RR = 1.6), stage (P =.03, ) in addition to LDH (P =.02, RR = 1.6), stage (P 1490 10961895 0 ddition to LDH (P =.02, RR = 1 . 6), stage (P =.03, RR = 1.7), on to LDH (P =.02, RR = 1.6), stage (P =.03, RR = 1501 10961895 0 (P =.02, RR = 1.6), stage (P = . 03, RR = 1.7), and ECOG scale 02, RR = 1.6), stage (P =.03, RR = 1.7), and ECOG 1516 10961895 0 = 1.6), stage (P =.03, RR = 1 . 7), and ECOG scale (P =.05, R 6), stage (P =.03, RR = 1.7), and ECOG scale (P =. 1527 10961895 0 RR = 1.7), and ECOG scale (P = . 05, RR = 1.6). A second analy 1.7), and ECOG scale (P =.05, RR = 1.6). A second 1551 10961895 0 and ECOG scale (P =.05, RR = 1 . 6). A second analysis incorpo COG scale (P =.05, RR = 1.6). A second analysis in 1562 10961895 1 ECOG scale (P =.05, RR = 1.6) . A second analysis incorporat scale (P =.05, RR = 1.6). A second analysis incor 1565 10961895 0 that survivin expression (P = . 02, RR = 1.6) remained a prog survivin expression (P =.02, RR = 1.6) remained a 1667 10961895 0 vin expression (P =.02, RR = 1 . 6) remained a prognostic fact xpression (P =.02, RR = 1.6) remained a prognostic 1678 10961895 0 ival independently of IPI (P = . 001, RR = 1.5). Survivin expr independently of IPI (P =.001, RR = 1.5). Survivin 1749 10961895 0 dently of IPI (P =.001, RR = 1 . 5). Survivin expression may b y of IPI (P =.001, RR = 1.5). Survivin expression 1761 10961895 1 tly of IPI (P =.001, RR = 1.5) . Survivin expression may be c f IPI (P =.001, RR = 1.5). Survivin expression may 1764 10961895 1 diffuse large B-cell lymphoma . (Blood. 2000;96:1921-1925) use large B-cell lymphoma. (Blood. 2000;96:1921-19 1872 10961895 0 large B-cell lymphoma. (Blood . 2000;96:1921-1925) e B-cell lymphoma. (Blood. 2000;96:1921-1925) 1880 15527837 0 ith bovine (NSP4[A]) (Wyatt, R . G., Mebus, C.A., Yolken, R.H. ovine (NSP4[A]) (Wyatt, R.G., Mebus, C.A., Yolken, 310 15527837 0 h bovine (NSP4[A]) (Wyatt, R.G . , Mebus, C.A., Yolken, R.H., ine (NSP4[A]) (Wyatt, R.G., Mebus, C.A., Yolken, R 312 15527837 0 SP4[A]) (Wyatt, R.G., Mebus, C . A., Yolken, R.H., Kalica, A.R ]) (Wyatt, R.G., Mebus, C.A., Yolken, R.H., Kalica 323 15527837 0 4[A]) (Wyatt, R.G., Mebus, C.A . , Yolken, R.H., Kalica, A.R., (Wyatt, R.G., Mebus, C.A., Yolken, R.H., Kalica, 325 15527837 0 , R.G., Mebus, C.A., Yolken, R . H., Kalica, A.R., James, H.D. ., Mebus, C.A., Yolken, R.H., Kalica, A.R., James, 337 15527837 0 R.G., Mebus, C.A., Yolken, R.H . , Kalica, A.R., James, H.D., Mebus, C.A., Yolken, R.H., Kalica, A.R., James, H 339 15527837 0 C.A., Yolken, R.H., Kalica, A . R., James, H.D., Jr., Kapikia , Yolken, R.H., Kalica, A.R., James, H.D., Jr., Ka 351 15527837 0 .A., Yolken, R.H., Kalica, A.R . , James, H.D., Jr., Kapikian, Yolken, R.H., Kalica, A.R., James, H.D., Jr., Kapi 353 15527837 0 , R.H., Kalica, A.R., James, H . D., Jr., Kapikian, A.Z., Chan ., Kalica, A.R., James, H.D., Jr., Kapikian, A.Z., 364 15527837 0 R.H., Kalica, A.R., James, H.D . , Jr., Kapikian, A.Z., Chanoc Kalica, A.R., James, H.D., Jr., Kapikian, A.Z., C 366 15527837 0 Kalica, A.R., James, H.D., Jr . , Kapikian, A.Z., Chanock, R. ca, A.R., James, H.D., Jr., Kapikian, A.Z., Chanoc 371 15527837 0 James, H.D., Jr., Kapikian, A . Z., Chanock, R.M., 1979. Rota s, H.D., Jr., Kapikian, A.Z., Chanock, R.M., 1979. 385 15527837 0 ames, H.D., Jr., Kapikian, A.Z . , Chanock, R.M., 1979. Rotavi H.D., Jr., Kapikian, A.Z., Chanock, R.M., 1979. R 387 15527837 0 r., Kapikian, A.Z., Chanock, R . M., 1979. Rotaviral immunity apikian, A.Z., Chanock, R.M., 1979. Rotaviral immu 400 15527837 0 , Kapikian, A.Z., Chanock, R.M . , 1979. Rotaviral immunity in ikian, A.Z., Chanock, R.M., 1979. Rotaviral immuni 402 15527837 0 ian, A.Z., Chanock, R.M., 1979 . Rotaviral immunity in gnotob A.Z., Chanock, R.M., 1979. Rotaviral immunity in g 409 15527837 1 virus induced by bovine virus . Science 203(4380), 548-550) s induced by bovine virus. Science 203(4380), 548- 515 15527837 0 porcine (NSP4[B]) (Hoshino, Y . , Saif, L.J., Sereno, M.M., C ine (NSP4[B]) (Hoshino, Y., Saif, L.J., Sereno, M. 577 15527837 0 NSP4[B]) (Hoshino, Y., Saif, L . J., Sereno, M.M., Chanock, R. B]) (Hoshino, Y., Saif, L.J., Sereno, M.M., Chanoc 587 15527837 0 P4[B]) (Hoshino, Y., Saif, L.J . , Sereno, M.M., Chanock, R.M. ) (Hoshino, Y., Saif, L.J., Sereno, M.M., Chanock, 589 15527837 0 ino, Y., Saif, L.J., Sereno, M . M., Chanock, R.M., Kapikian, Y., Saif, L.J., Sereno, M.M., Chanock, R.M., Kapik 601 15527837 0 o, Y., Saif, L.J., Sereno, M.M . , Chanock, R.M., Kapikian, A. , Saif, L.J., Sereno, M.M., Chanock, R.M., Kapikia 603 15527837 0 L.J., Sereno, M.M., Chanock, R . M., Kapikian, A.Z., 1988. Inf Sereno, M.M., Chanock, R.M., Kapikian, A.Z., 1988 616 15527837 0 J., Sereno, M.M., Chanock, R.M . , Kapikian, A.Z., 1988. Infec ereno, M.M., Chanock, R.M., Kapikian, A.Z., 1988. 618 15527837 0 M., Chanock, R.M., Kapikian, A . Z., 1988. Infection immunity hanock, R.M., Kapikian, A.Z., 1988. Infection immu 632 15527837 0 , Chanock, R.M., Kapikian, A.Z . , 1988. Infection immunity of nock, R.M., Kapikian, A.Z., 1988. Infection immuni 634 15527837 1 ck, R.M., Kapikian, A.Z., 1988 . Infection immunity of piglet .M., Kapikian, A.Z., 1988. Infection immunity of p 641 15527837 1 ring the corresponding antigen . J. Virol. 62(3), 744-748) ro the corresponding antigen. J. Virol. 62(3), 744-74 806 15527837 0 g the corresponding antigen. J . Virol. 62(3), 744-748) rotav corresponding antigen. J. Virol. 62(3), 744-748) 809 15527837 0 orresponding antigen. J. Virol . 62(3), 744-748) rotaviruses. ponding antigen. J. Virol. 62(3), 744-748) rotavir 816 15527837 1 l. 62(3), 744-748) rotaviruses . Following primary infection (3), 744-748) rotaviruses. Following primary infec 845 15527837 1 rather than genotype specific . Antibody responses to NSP4s er than genotype specific. Antibody responses to N 1182 15527837 1 on of amino acids (aa) 131-141 . In contrast, NSP4 genotypes amino acids (aa) 131-141. In contrast, NSP4 genot 1338 15527837 1 icted poorly their "serotypes" . In piglets, antibodies to NS poorly their "serotypes". In piglets, antibodies 1457 15527837 1 rotavirus in primary infection . Thus, in an approach to immu irus in primary infection. Thus, in an approach to 1716 15527837 1 otavirus disease and infection . rus disease and infection. 1903 14670349 1 cellular immune response(CIR) . Different genes have been de ular immune response(CIR). Different genes have be 148 14670349 1 y explain the forms of leprosy . The major histocompatibility lain the forms of leprosy. The major histocompatib 254 14670349 1 x (MHC) play an important role . The aim of the study was to C) play an important role. The aim of the study wa 321 14670349 1 r genes in LL Mexican patients . Six families (26 LL, three T es in LL Mexican patients. Six families (26 LL, th 470 14670349 1 ere compared with 204 controls . Class I typing was done by t ompared with 204 controls. Class I typing was done 597 14670349 1 class II typing using PCR-SSOP . Haplotype segregation correl II typing using PCR-SSOP. Haplotype segregation c 697 14670349 1 vo and in vitro using lepromin . Haplotype sharing was signif d in vitro using lepromin. Haplotype sharing was s 785 14670349 0 ated in the affected sibs (p=0 . 01). Six healthy sibs were no in the affected sibs (p=0.01). Six healthy sibs we 857 14670349 1 in the affected sibs (p=0.01) . Six healthy sibs were non-re he affected sibs (p=0.01). Six healthy sibs were n 861 14670349 1 ur of them were DQ1 homozgotes . DQ1 was significantly associ them were DQ1 homozgotes. DQ1 was significantly a 948 14670349 1 ith LL and with non-responders . We set up macrophage activat L and with non-responders. We set up macrophage ac 1014 14670349 1 occurred in the context or DQ1 . When DQ1 was present on macr red in the context or DQ1. When DQ1 was present on 1169 14670349 0 to eliminate the bacilli (p=0 . 03). DRB1*1501 DQA1*0102-DQB1 liminate the bacilli (p=0.03). DRB1*1501 DQA1*0102 1356 14670349 1 eliminate the bacilli (p=0.03) . DRB1*1501 DQA1*0102-DQB1*060 nate the bacilli (p=0.03). DRB1*1501 DQA1*0102-DQB 1360 14670349 0 articipation in susceptibility . QBP 5.11/5.12 promoter prese ipation in susceptibility. QBP 5.11/5.12 promoter 1497 14670349 0 ation in susceptibility. QBP 5 . 11/5.12 promoter present in t in susceptibility. QBP 5.11/5.12 promoter present 1504 14670349 0 in susceptibility. QBP 5.11/5 . 12 promoter present in the me usceptibility. QBP 5.11/5.12 promoter present in t 1509 14670349 0 mentioned haplotype, and QAP 1 . 4, linked to DRB1*1301/02 hap oned haplotype, and QAP 1.4, linked to DRB1*1301/0 1567 14670349 1 aplotypes were also associated . Two mechanisms are suggested ypes were also associated. Two mechanisms are sugg 1625 14670349 1 g a protective T-cell response . rotective T-cell response. 2047 10620572 1 BPH) and prostate cancer (PCa) . METHODS: Serum samples were and prostate cancer (PCa). METHODS: Serum samples 387 10620572 1 PCa, and 89 patients with BPH . tPSA and cPSA were measured and 89 patients with BPH. tPSA and cPSA were meas 576 10620572 1 with the Roche Elecsys system . RESULTS: The median cPSA/tPS the Roche Elecsys system. RESULTS: The median cPS 711 10620572 0 patients with BPH and PCa (78 . 7% vs 90.7%, 25.5% vs 12.1%, ents with BPH and PCa (78.7% vs 90.7%, 25.5% vs 12 842 10620572 0 with BPH and PCa (78.7% vs 90 . 7%, 25.5% vs 12.1%, and 36.8% BPH and PCa (78.7% vs 90.7%, 25.5% vs 12.1%, and 851 10620572 0 PH and PCa (78.7% vs 90.7%, 25 . 5% vs 12.1%, and 36.8% vs 14. d PCa (78.7% vs 90.7%, 25.5% vs 12.1%, and 36.8% v 858 10620572 0 a (78.7% vs 90.7%, 25.5% vs 12 . 1%, and 36.8% vs 14.3%, respe .7% vs 90.7%, 25.5% vs 12.1%, and 36.8% vs 14.3%, 867 10620572 0 90.7%, 25.5% vs 12.1%, and 36 . 8% vs 14.3%, respectively; P %, 25.5% vs 12.1%, and 36.8% vs 14.3%, respectivel 878 10620572 0 5.5% vs 12.1%, and 36.8% vs 14 . 3%, respectively; P <0.001). vs 12.1%, and 36.8% vs 14.3%, respectively; P <0.0 887 10620572 0 % vs 14.3%, respectively; P <0 . 001). No correlations of cPSA 14.3%, respectively; P <0.001). No correlations of 910 10620572 1 14.3%, respectively; P <0.001) . No correlations of cPSA and , respectively; P <0.001). No correlations of cPSA 915 10620572 1 mor stage and grade were found . ROC analysis showed that cPS tage and grade were found. ROC analysis showed tha 991 10620572 0 tPSA (areas under the curve, 0 . 632 vs 0.568), whereas the cP (areas under the curve, 0.632 vs 0.568), whereas t 1076 10620572 0 as under the curve, 0.632 vs 0 . 568), whereas the cPSA/tPSA r der the curve, 0.632 vs 0.568), whereas the cPSA/t 1085 10620572 0 og/L (areas under the curve, 0 . 851 vs 0.838). CONCLUSIONS: C (areas under the curve, 0.851 vs 0.838). CONCLUSIO 1311 10620572 0 as under the curve, 0.851 vs 0 . 838). CONCLUSIONS: Compared w der the curve, 0.851 vs 0.838). CONCLUSIONS: Compa 1320 10620572 1 der the curve, 0.851 vs 0.838) . CONCLUSIONS: Compared with t he curve, 0.851 vs 0.838). CONCLUSIONS: Compared w 1325 10620572 1 alone does not have any effect . does not have any effect. 1576 10407261 1 an 20 identified mannoproteins . Some of them can be released identified mannoproteins. Some of them can be rel 85 10407261 1 to wall structural components . A number of covalently linke all structural components. A number of covalently 275 10407261 1 released after SDS extraction . They can be divided into the ased after SDS extraction. They can be divided int 359 10407261 1 an be released with 30 mM NaOH . The SDS-extractable proteins released with 30 mM NaOH. The SDS-extractable pro 465 10407261 1 of enzymes, mainly glucanases . Nothing is known, however, a nzymes, mainly glucanases. Nothing is known, howev 579 10407261 1 of covalently linked proteins . In order to investigate the ovalently linked proteins. In order to investigate 656 10407261 1 mutants obtained was examined . They grew somewhat more slow nts obtained was examined. They grew somewhat more 902 10407261 1 Calcofluor white and Congo red . In addition, the triple and fluor white and Congo red. In addition, the triple 1078 10407261 1 had a decreased mating ability . All these properties were mo decreased mating ability. All these properties we 1162 10407261 1 ly equivalent in the cell wall . uivalent in the cell wall. 1356 8077369 1 secretion, and on hair growth . Hair growth was assessed by etion, and on hair growth. Hair growth was assesse 228 8077369 1 by the Ferriman-Gallwey score . All of the above determinati he Ferriman-Gallwey score. All of the above determ 284 8077369 1 onths of finasteride treatment . Basal and GnRH-stimulated go of finasteride treatment. Basal and GnRH-stimulat 392 8077369 1 n secretions were not affected . Indeed, finasteride did not retions were not affected. Indeed, finasteride did 461 8077369 1 he pulsatility of LH secretion . No change was seen in estrad lsatility of LH secretion. No change was seen in e 529 8077369 1 inding globulin concentrations . Serum concentrations of cort g globulin concentrations. Serum concentrations of 684 8077369 1 month of finasteride treatment . The F levels returned to pre of finasteride treatment. The F levels returned t 788 8077369 1 reatment levels after 3 months . Plasma levels of dihydrotest ent levels after 3 months. Plasma levels of dihydr 849 8077369 1 d during finasteride treatment . A significant increase in te ing finasteride treatment. A significant increase 979 8077369 1 ns was observed after 3 months . Finasteride did not modify t s observed after 3 months. Finasteride did not mod 1062 8077369 1 lfate to ACTH-(1-24) injection . Conversely, finasteride blun to ACTH-(1-24) injection. Conversely, finasteride 1198 8077369 1 e to corticotropin stimulation . Three months of finasteride corticotropin stimulation. Three months of finaste 1275 8077369 1 sed the Ferriman-Gallwey score . In conclusion, finasteride s he Ferriman-Gallwey score. In conclusion, finaster 1365 8077369 1 fecting gonadotropin secretion . ng gonadotropin secretion. 1522 15627654 1 onal regulation of lipogenesis . The aim of the present work regulation of lipogenesis. The aim of the present 141 15627654 1 e during fasting and refeeding . The regulation of hexokinase ing fasting and refeeding. The regulation of hexok 341 15627654 1 arker of the lipogenic pathway . The in vivo association of S of the lipogenic pathway. The in vivo association 512 15627654 1 tin immunoprecipitation assays . Fasting decreased, and refee mmunoprecipitation assays. Fasting decreased, and 672 15627654 1 protein levels in each tissue . The concomitant measurement ein levels in each tissue. The concomitant measure 768 15627654 1 ritional regulation in rodents . These data elucidate the imp nal regulation in rodents. These data elucidate th 1070 15627654 1 abolism and energy homeostasis . sm and energy homeostasis. 1223 14731965 1 localization signals by import . Various approaches have now ization signals by import. Various approaches have 162 14731965 1 s expected of import receptors . This article focuses on earl ected of import receptors. This article focuses on 292 14731965 1 ied candidate import receptors . andidate import receptors. 426 12753076 1 ioid receptor agonists in mice . A single s.c. injection of ( receptor agonists in mice. A single s.c. injection 332 12753076 0 r agonists in mice. A single s . c. injection of (-)U-50,488H nists in mice. A single s.c. injection of (-)U-50, 344 12753076 0 agonists in mice. A single s.c . injection of (-)U-50,488H pr sts in mice. A single s.c. injection of (-)U-50,48 346 12753076 1 nor-binaltorphimine (nor-BNI) . Furthermore, a single s.c. p binaltorphimine (nor-BNI). Furthermore, a single s 523 12753076 0 -BNI). Furthermore, a single s . c. pre-treatment with (-)U-50 . Furthermore, a single s.c. pre-treatment with (- 548 12753076 0 NI). Furthermore, a single s.c . pre-treatment with (-)U-50,4 Furthermore, a single s.c. pre-treatment with (-)U 550 12753076 1 gonist-induced antinociception . In contrast, repeated s.c. a t-induced antinociception. In contrast, repeated s 655 12753076 0 ption. In contrast, repeated s . c. administration of (-)U-50, . In contrast, repeated s.c. administration of (-) 680 12753076 0 ion. In contrast, repeated s.c . administration of (-)U-50,48 In contrast, repeated s.c. administration of (-)U- 682 12753076 1 0,488H-induced antinociception . Under these conditions, we d H-induced antinociception. Under these conditions, 795 12753076 0 onstrated here that repeated s . c. injection of (-)U-50,488H ated here that repeated s.c. injection of (-)U-50, 857 12753076 0 strated here that repeated s.c . injection of (-)U-50,488H si ed here that repeated s.c. injection of (-)U-50,48 859 12753076 1 e4,Gly-ol5] enkephalin (DAMGO) . Using the guanosine-5'-o-(3- y-ol5] enkephalin (DAMGO). Using the guanosine-5'- 1055 12753076 1 evel of kappa-opioid receptors . Repeated administration of ( of kappa-opioid receptors. Repeated administration 1332 12753076 1 alamus and periaqueductal gray . These results suggest that r s and periaqueductal gray. These results suggest t 1681 12753076 1 eptor-mediated antinociception . -mediated antinociception. 1974 11075308 1 alternate propellant (MDI-AP) . The pharmacokinetics of sing rnate propellant (MDI-AP). The pharmacokinetics of 211 11075308 0 administered by intravenous (i . v.) and inhalation routes was istered by intravenous (i.v.) and inhalation route 303 11075308 0 ministered by intravenous (i.v . ) and inhalation routes was a tered by intravenous (i.v.) and inhalation routes 305 11075308 1 nvolving 24 healthy volunteers . In a separate study, 6 healt ing 24 healthy volunteers. In a separate study, 6 417 11075308 1 and expired air was determined . Following i.v. administratio xpired air was determined. Following i.v. administ 597 11075308 0 ir was determined. Following i . v. administration, MF was det s determined. Following i.v. administration, MF wa 610 11075308 0 was determined. Following i.v . administration, MF was detec determined. Following i.v. administration, MF was 612 11075308 1 for at least 8 hours postdose . The half-life (t1/2) followi at least 8 hours postdose. The half-life (t1/2) fo 691 11075308 0 e half-life (t1/2) following i . v. administration was 4.5 hou f-life (t1/2) following i.v. administration was 4. 725 11075308 0 half-life (t1/2) following i.v . administration was 4.5 hours life (t1/2) following i.v. administration was 4.5 727 11075308 0 wing i.v. administration was 4 . 5 hours. In contrast, followi i.v. administration was 4.5 hours. In contrast, fo 749 11075308 1 . administration was 4.5 hours . In contrast, following DPI a inistration was 4.5 hours. In contrast, following 757 11075308 1 s estimated to be less than 1% . Only two plasma samples foll imated to be less than 1%. Only two plasma samples 991 11075308 1 ability in 92% of the subjects . A separate study with 6 heal ty in 92% of the subjects. A separate study with 6 1167 11075308 1 ed was extensively metabolized . These results indicate that s extensively metabolized. These results indicate 1430 11075308 1 he chronic treatment of asthma . ronic treatment of asthma. 1615 6664451 1 colloid osmotic pressure (COP) . On the basis of the Starling id osmotic pressure (COP). On the basis of the Sta 96 6664451 1 of cerebral interstitial fluid . To test the hypothesis that rebral interstitial fluid. To test the hypothesis 276 6664451 1 10 patients with increased ICP . In these 10 patients, the de tients with increased ICP. In these 10 patients, t 545 6664451 1 judging from CT scan findings . In addition to ICP, various ing from CT scan findings. In addition to ICP, var 663 6664451 1 ing and after albumin infusion . Hematological studies includ nd after albumin infusion. Hematological studies i 870 6664451 1 fter administration of albumin . The raised ICP (27.4 +/- S.E administration of albumin. The raised ICP (27.4 +/ 1109 6664451 0 of albumin. The raised ICP (27 . 4 +/- S.E. 1.6 mmHg) decrease bumin. The raised ICP (27.4 +/- S.E. 1.6 mmHg) dec 1129 6664451 0 in. The raised ICP (27.4 +/- S . E. 1.6 mmHg) decreased signif he raised ICP (27.4 +/- S.E. 1.6 mmHg) decreased s 1137 6664451 0 . The raised ICP (27.4 +/- S.E . 1.6 mmHg) decreased signific raised ICP (27.4 +/- S.E. 1.6 mmHg) decreased sig 1139 6664451 0 he raised ICP (27.4 +/- S.E. 1 . 6 mmHg) decreased significant ised ICP (27.4 +/- S.E. 1.6 mmHg) decreased signif 1142 6664451 0 eased significantly down to 19 . 1 (+/- 1.9) mmHg and remained significantly down to 19.1 (+/- 1.9) mmHg and rem 1185 6664451 0 nificantly down to 19.1 (+/- 1 . 9) mmHg and remained stable f antly down to 19.1 (+/- 1.9) mmHg and remained sta 1194 6664451 1 of MABP, pulse rate and PaCO2 . CVP elevated significantly a ABP, pulse rate and PaCO2. CVP elevated significan 1297 6664451 1 fter administration of albumin . This results suggested that administration of albumin. This results suggested 1447 6664451 1 culatory volume was maintained . A significant increase of to ory volume was maintained. A significant increase 1522 6664451 1 bumin-globulin ratio was noted . (ABSTRACT TRUNCATED AT 250 WO -globulin ratio was noted.(ABSTRACT TRUNCATED AT 2 1630 10735847 1 of transcriptional regulation . Here we report the character ranscriptional regulation. Here we report the char 155 10735847 1 enome sequence of strain 26695 . We demonstrate that the resp sequence of strain 26695. We demonstrate that the 325 10735847 1 cids of their receiver domains . An analysis of the in vitro of their receiver domains. An analysis of the in v 620 10735847 1 inase-response regulator pairs . Furthermore, we provide evid -response regulator pairs. Furthermore, we provide 806 10735847 1 he transmitter domain of HP165 . ansmitter domain of HP165. 1065 12749235 1 hod employed for its detection . METHODOLOGY: We evaluated th mployed for its detection. METHODOLOGY: We evaluat 229 12749235 1 is and 36 with Crohn's disease . We also correlated the prese d 36 with Crohn's disease. We also correlated the 469 12749235 1 ease and inflammatory activity . Thirty healthy individuals c and inflammatory activity. Thirty healthy individu 592 12749235 1 ls comprised the control group . RESULTS: Anti-neutrophil cyt mprised the control group. RESULTS: Anti-neutrophi 648 12749235 0 ic antibody was detected in 27 . 5% of the patients with ulcer tibody was detected in 27.5% of the patients with 714 12749235 0 ulcerative colitis, and in 14 . 3% of those with Crohn's coli rative colitis, and in 14.3% of those with Crohn's 768 12749235 1 of those with Crohn's colitis . Perinuclear staining pattern hose with Crohn's colitis. Perinuclear staining pa 801 12749235 1 ar patterns were also observed . There was no correlation bet tterns were also observed. There was no correlatio 905 12749235 1 the studied clinical variables . No patient of the control gr tudied clinical variables. No patient of the contr 1011 12749235 1 group presented positive test . CONCLUSIONS: A positive anti p presented positive test. CONCLUSIONS: A positive 1068 12749235 1 or ulcerative colitis patients . cerative colitis patients. 1309 8400711 1 to identify individual animals . DNA profiles of a variety of entify individual animals. DNA profiles of a varie 142 8400711 1 fferent oligonucleotide probes . The probes tested were four nt oligonucleotide probes. The probes tested were 276 8400711 0 ere four multilocus probes [33 . 6, 33.15, JE46, and (TGTC)5] our multilocus probes [33.6, 33.15, JE46, and (TGT 327 8400711 0 ur multilocus probes [33.6, 33 . 15, JE46, and (TGTC)5] and si ltilocus probes [33.6, 33.15, JE46, and (TGTC)5] a 333 8400711 1 Q7 (D10S28), and MS43 (D12S11) . Each of the probes was chemi 10S28), and MS43 (D12S11). Each of the probes was 482 8400711 1 scence catalyzed by the enzyme . Initial screening against zo e catalyzed by the enzyme. Initial screening again 676 8400711 0 at three multilocus probes [33 . 15, 33.6, (TGTC)5] gave infor ree multilocus probes [33.15, 33.6, (TGTC)5] gave 850 8400711 0 e multilocus probes [33.15, 33 . 6, (TGTC)5] gave informative tilocus probes [33.15, 33.6, (TGTC)5] gave informa 857 8400711 1 locus' probes (MS1 and CMM101) . The other five probes appear ' probes (MS1 and CMM101). The other five probes a 1016 8400711 1 example, YNH24 against canids) . Subsequent screenings of pop le, YNH24 against canids). Subsequent screenings o 1117 8400711 1 is of observed bandsharing (S) . Large heterologous populatio observed bandsharing (S). Large heterologous popu 1251 8400711 0 erse band patterns (S < or = 0 . 2). Geographically isolated a band patterns (S < or = 0.2). Geographically isola 1362 8400711 1 e band patterns (S < or = 0.2) . Geographically isolated and/ d patterns (S < or = 0.2). Geographically isolated 1365 8400711 0 frequencies of bandsharing (0 . 6 < or = S < or = 0.95).(ABST uencies of bandsharing (0.6 < or = S < or = 0.95). 1560 8400711 0 sharing (0.6 < or = S < or = 0 . 95).(ABSTRACT TRUNCATED AT 25 ng (0.6 < or = S < or = 0.95).(ABSTRACT TRUNCATED 1580 8400711 1 ing (0.6 < or = S < or = 0.95) . (ABSTRACT TRUNCATED AT 250 WO 0.6 < or = S < or = 0.95).(ABSTRACT TRUNCATED AT 2 1584 10803994 1 nal to the magnitude of injury . Laparoscopic surgery has bee o the magnitude of injury. Laparoscopic surgery ha 109 10803994 1 ponse compared to open surgery . Postoperative immune functio compared to open surgery. Postoperative immune fu 211 10803994 1 rgery compared to open surgery . The aim of this study was to compared to open surgery. The aim of this study w 351 10803994 1 ular immunity in a swine model . Twenty domestic female pigs immunity in a swine model. Twenty domestic female 474 10803994 1 ) or open cholecystectomy (OC) . Cellular immune functions we open cholecystectomy (OC). Cellular immune functio 593 10803994 1 ration of the peripheral blood . There was a significant redu n of the peripheral blood. There was a significant 776 10803994 0 to preoperative values (p < 0 . 05). The reduction of mitogen reoperative values (p < 0.05). The reduction of mi 927 10803994 1 preoperative values (p < 0.05) . The reduction of mitogen-ind erative values (p < 0.05). The reduction of mitoge 931 10803994 0 than after OC on day 1 (p = 0 . 03). The mean DTH reaction wa after OC on day 1 (p = 0.03). The mean DTH reacti 1048 10803994 1 n after OC on day 1 (p = 0.03) . The mean DTH reaction was 29 er OC on day 1 (p = 0.03). The mean DTH reaction w 1052 10803994 0 . The mean DTH reaction was 29 . 7 +/- 3.7 mm2 in the LC group mean DTH reaction was 29.7 +/- 3.7 mm2 in the LC 1082 10803994 0 an DTH reaction was 29.7 +/- 3 . 7 mm2 in the LC group compare H reaction was 29.7 +/- 3.7 mm2 in the LC group co 1090 10803994 0 in the LC group compared to 13 . 9 +/- 1.2 mm2 in the OC group e LC group compared to 13.9 +/- 1.2 mm2 in the OC 1127 10803994 0 C group compared to 13.9 +/- 1 . 2 mm2 in the OC group (p < 0. up compared to 13.9 +/- 1.2 mm2 in the OC group (p 1135 10803994 0 1.2 mm2 in the OC group (p < 0 . 001). There was no difference m2 in the OC group (p < 0.001). There was no diffe 1164 10803994 1 m2 in the OC group (p < 0.001) . There was no difference in p the OC group (p < 0.001). There was no difference 1169 10803994 1 values between the two groups . Suppression of cellular immu es between the two groups. Suppression of cellular 1259 10803994 1 occurred after both LC and OC . The magnitude and duration o rred after both LC and OC. The magnitude and durat 1323 10803994 1 proliferation and DTH response . feration and DTH response. 1494 8119684 1 the intraoperative assessment . Laparotomy revealed severe p intraoperative assessment. Laparotomy revealed sev 383 8119684 1 s in computer tomography films . The sensitivity and specific computer tomography films. The sensitivity and spe 536 8119684 1 ere 80% and 100%, respectively . A second assessment was perf 0% and 100%, respectively. A second assessment was 668 8119684 1 py in the treatment of varices . The patients were divided in the treatment of varices. The patients were divid 892 8119684 1 erotherapy computer tomography . All patients underwent elect erapy computer tomography. All patients underwent 1065 8119684 1 deemed hemodynamically stable . Patients in group A required ed hemodynamically stable. Patients in group A req 1154 8119684 1 tely than did group B patients . Eight patients in group A an than did group B patients. Eight patients in group 1303 8119684 0 p A and six in group B (57% vs . 16%, p < 0.05) had variceal nd six in group B (57% vs. 16%, p < 0.05) had vari 1357 8119684 0 in group B (57% vs. 16%, p < 0 . 05) had variceal recurrence a oup B (57% vs. 16%, p < 0.05) had variceal recurre 1369 8119684 0 n during mean follow-ups of 20 . 8 and 19.9 mo, respectively. ing mean follow-ups of 20.8 and 19.9 mo, respectiv 1445 8119684 0 mean follow-ups of 20.8 and 19 . 9 mo, respectively. The mean follow-ups of 20.8 and 19.9 mo, respectively. The 1454 8119684 1 20.8 and 19.9 mo, respectively . The mean time elapsed before and 19.9 mo, respectively. The mean time elapsed b 1473 8119684 0 or group A than for group B (4 . 1 +/- 3.3 vs. 11.8 +/- 2.7 mo oup A than for group B (4.1 +/- 3.3 vs. 11.8 +/- 2 1569 8119684 0 A than for group B (4.1 +/- 3 . 3 vs. 11.8 +/- 2.7 mo, p < 0. an for group B (4.1 +/- 3.3 vs. 11.8 +/- 2.7 mo, p 1577 8119684 0 an for group B (4.1 +/- 3.3 vs . 11.8 +/- 2.7 mo, p < 0.05). r group B (4.1 +/- 3.3 vs. 11.8 +/- 2.7 mo, p < 0. 1582 8119684 0 or group B (4.1 +/- 3.3 vs. 11 . 8 +/- 2.7 mo, p < 0.05). Amon oup B (4.1 +/- 3.3 vs. 11.8 +/- 2.7 mo, p < 0.05). 1586 8119684 0 B (4.1 +/- 3.3 vs. 11.8 +/- 2 . 7 mo, p < 0.05). Among patien .1 +/- 3.3 vs. 11.8 +/- 2.7 mo, p < 0.05). Among p 1594 8119684 0 3.3 vs. 11.8 +/- 2.7 mo, p < 0 . 05). Among patients who devel s. 11.8 +/- 2.7 mo, p < 0.05). Among patients who 1606 8119684 1 vs. 11.8 +/- 2.7 mo, p < 0.05) . Among patients who developed 1.8 +/- 2.7 mo, p < 0.05). Among patients who deve 1610 8119684 1 B experienced repeat bleeding . (ABSTRACT TRUNCATED AT 250 WO perienced repeat bleeding.(ABSTRACT TRUNCATED AT 2 1725 8533127 1 induce platelet activation (1) . More recently, it has been d e platelet activation (1). More recently, it has b 173 8533127 1 platelet functional responses . It has been suggested that t elet functional responses. It has been suggested t 271 8533127 1 ase of nitric oxide (NO) (2-3) . In contrast, we have previou f nitric oxide (NO) (2-3). In contrast, we have pr 388 8533127 1 that does not involves NO (4) . Considering that an alterati does not involves NO (4). Considering that an alt 615 8533127 1 gation, GPIb-IX and GPIIb-IIIa . n, GPIb-IX and GPIIb-IIIa. 919 14505214 1 A sequences in DRB 1 haplotype . The aim of the study was to uences in DRB 1 haplotype. The aim of the study wa 214 14505214 1 thy controls in our population . Serum samples from 78 consec ontrols in our population. Serum samples from 78 c 362 14505214 1 nd SDS-lysed bacterial extract . There was no significant inc S-lysed bacterial extract. There was no significan 664 14505214 1 bacteria were used as antigen . The APA levels did not corre eria were used as antigen. The APA levels did not 895 14505214 1 orrelate with serum CRP levels . Infection with P. mirabilis ate with serum CRP levels. Infection with P. mirab 951 14505214 0 m CRP levels. Infection with P . mirabilis is found to have n levels. Infection with P. mirabilis is found to h 969 14505214 1 ical or aggravating role in RA . or aggravating role in RA. 1039 11146340 1 sculitis of arteries and veins . Endothelial dysfunction is o tis of arteries and veins. Endothelial dysfunction 155 11146340 1 f the prominent features of BD . Adrenomedullin (AM) is a pep prominent features of BD. Adrenomedullin (AM) is 219 11146340 1 not been previously described . OBJECTIVE: To detect changes been previously described. OBJECTIVE: To detect ch 432 11146340 1 e liquid chromatography (HPCL) . We also investigated if dise uid chromatography (HPCL). We also investigated if 617 11146340 1 f BD correlates with AM levels . METHODS: Forty-two consecuti correlates with AM levels. METHODS: Forty-two cons 707 11146340 0 nsecutive patients with BD (38 . 5 +/- 11.1 years, 19 male and tive patients with BD (38.5 +/- 11.1 years, 19 mal 760 11146340 0 patients with BD (38.5 +/- 11 . 1 years, 19 male and 23 femal ents with BD (38.5 +/- 11.1 years, 19 male and 23 769 11146340 0 x-matched control subjects (39 . 5 +/- 10.9 years, 8 male and ched control subjects (39.5 +/- 10.9 years, 8 male 858 11146340 0 control subjects (39.5 +/- 10 . 9 years, 8 male and 12 female rol subjects (39.5 +/- 10.9 years, 8 male and 12 f 867 11146340 1 e) were included in this study . We measured plasma AM levels re included in this study. We measured plasma AM l 926 11146340 1 erythrocyte sedimentation rate . RESULTS: Mean +/- SD plasma rocyte sedimentation rate. RESULTS: Mean +/- SD pl 1106 11146340 0 levels in patients with BD (73 . 22 +/- 25.55 pmol/l) were sig s in patients with BD (73.22 +/- 25.55 pmol/l) wer 1169 11146340 0 patients with BD (73.22 +/- 25 . 55 pmol/l) were significantly nts with BD (73.22 +/- 25.55 pmol/l) were signific 1179 11146340 0 re significantly higher (p < 0 . 001) than in healthy control gnificantly higher (p < 0.001) than in healthy con 1223 11146340 0 healthy control volunteers (21 . 35 +/- 12.37 pmol/l). Patient hy control volunteers (21.35 +/- 12.37 pmol/l). Pa 1267 11146340 0 ntrol volunteers (21.35 +/- 12 . 37 pmol/l). Patients with act volunteers (21.35 +/- 12.37 pmol/l). Patients wit 1277 11146340 1 teers (21.35 +/- 12.37 pmol/l) . Patients with active BD had (21.35 +/- 12.37 pmol/l). Patients with active BD 1288 11146340 0 r plasma AM concentrations (79 . 32 +/- 21.89 pmol/l) with pat sma AM concentrations (79.32 +/- 21.89 pmol/l) wit 1354 11146340 0 M concentrations (79.32 +/- 21 . 89 pmol/l) with patients with centrations (79.32 +/- 21.89 pmol/l) with patients 1364 11146340 0 ents with inactive disease (67 . 44 +/- 29.92 pmol/l). On the with inactive disease (67.44 +/- 29.92 pmol/l). On 1415 11146340 0 inactive disease (67.44 +/- 29 . 92 pmol/l). On the other hand ive disease (67.44 +/- 29.92 pmol/l). On the other 1425 11146340 1 sease (67.44 +/- 29.92 pmol/l) . On the other hand, patients (67.44 +/- 29.92 pmol/l). On the other hand, pati 1436 11146340 0 the disease (mean duration, 13 . 9 +/- 3.8 years) had signific isease (mean duration, 13.9 +/- 3.8 years) had sig 1520 11146340 0 ase (mean duration, 13.9 +/- 3 . 8 years) had significantly hi mean duration, 13.9 +/- 3.8 years) had significant 1528 11146340 0 ly higher plasma AM levels (83 . 99 +/- 19.71 pmol/l; p = 0.00 gher plasma AM levels (83.99 +/- 19.71 pmol/l; p = 1583 11146340 0 plasma AM levels (83.99 +/- 19 . 71 pmol/l; p = 0.005) than pa a AM levels (83.99 +/- 19.71 pmol/l; p = 0.005) th 1593 11146340 0 (83.99 +/- 19.71 pmol/l; p = 0 . 005) than patients (62.45 +/- 9 +/- 19.71 pmol/l; p = 0.005) than patients (62.4 1610 11146340 0 ; p = 0.005) than patients (62 . 45 +/- 26.57 pmol/l) with sho 0.005) than patients (62.45 +/- 26.57 pmol/l) wit 1633 11146340 0 5) than patients (62.45 +/- 26 . 57 pmol/l) with shorter durat an patients (62.45 +/- 26.57 pmol/l) with shorter 1643 11146340 0 the disease (mean duration, 5 . 5 +/- 2.3 years). All acute- disease (mean duration, 5. 5 +/- 2.3 years). All a 1709 11146340 0 ase (mean duration, 5. 5 +/- 2 . 3 years). All acute-phase rea mean duration, 5. 5 +/- 2.3 years). All acute-phas 1718 11146340 1 duration, 5. 5 +/- 2.3 years) . All acute-phase reaction par tion, 5. 5 +/- 2.3 years). All acute-phase reactio 1727 11146340 1 ncreased in the active disease . CONCLUSION: Considering its sed in the active disease. CONCLUSION: Considering 1827 11146340 1 ecially in the chronic disease . ly in the chronic disease. 1985 11972865 1 es tubulointerstitial injuries . Using the progressive kidney bulointerstitial injuries. Using the progressive k 139 11972865 1 titial injury in ADR nephrosis . At 12 weeks, experimental an l injury in ADR nephrosis. At 12 weeks, experiment 373 11972865 1 ncidence of glomerulosclerosis . Initial pathology of the tub nce of glomerulosclerosis. Initial pathology of th 555 11972865 1 o occur in individual nephrons . Immunohistochemistry demonst ur in individual nephrons. Immunohistochemistry de 671 11972865 1 ell nuclear antigen expression . Protein levels of OPN in the uclear antigen expression. Protein levels of OPN i 848 11972865 1 roteinuria by western blotting . Vimentin- and OPN-expressing nuria by western blotting. Vimentin- and OPN-expre 957 11972865 1 e cells or ED-1-positive cells . In addition, we found thromb ls or ED-1-positive cells. In addition, we found t 1117 11972865 1 nterstitial inflammatory cells . These results suggest that c titial inflammatory cells. These results suggest t 1309 11972865 1 titial injury in ADR nephrosis . l injury in ADR nephrosis. 1504 8034026 1 erentiation of many cell types . To identify receptor tyrosin iation of many cell types. To identify receptor ty 144 8034026 1 mouse yolk sac and fetal liver . Sequence analysis of PCR amp yolk sac and fetal liver. Sequence analysis of PC 386 8034026 1 hreonine kinase related clones . Two of these receptors, tek ine kinase related clones. Two of these receptors, 583 8034026 1 r endothelial cell development . Two other clones, 9B4 and 9A othelial cell development. Two other clones, 9B4 a 750 8034026 1 as ryk and SK2 (rat homologue) . Here we describe the twelve k and SK2 (rat homologue). Here we describe the tw 875 8034026 1 nt of the hematopoietic system . the hematopoietic system. 1065 12372301 1 g (Hh) signaling in Drosophila . Here, we demonstrate that on ) signaling in Drosophila. Here, we demonstrate th 91 12372301 1 ined in the early mouse embryo . Embryonic fibroblasts lackin in the early mouse embryo. Embryonic fibroblasts l 278 12372301 1 ding cells when expressing Shh . We have developed a biochemi cells when expressing Shh. We have developed a bio 464 12372301 1 release of soluble Hh proteins . This activity is disrupted b se of soluble Hh proteins. This activity is disrup 590 12372301 1 tion for all of these proteins . for all of these proteins. 814 14633408 1 inal diseases in animal models . Further evaluation in primat diseases in animal models. Further evaluation in p 127 14633408 1 ate and those of other animals . Prior work has shown that AA nd those of other animals. Prior work has shown th 304 14633408 1 than AAV2 in the rodent retina . In this study, we evaluated AAV2 in the rodent retina. In this study, we evalu 512 14633408 1 rior, nasal, macula, temporal) . rAAV5 led to a rapid onset o nasal, macula, temporal). rAAV5 led to a rapid on 721 14633408 1 ion persisting up to 10 months . Postoperative electrophysiol ersisting up to 10 months. Postoperative electroph 834 14633408 1 served following gene transfer . Quantitative analysis of gen d following gene transfer. Quantitative analysis o 949 14633408 1 y of 22% in the injected areas . Evaluation of cell types usi 22% in the injected areas. Evaluation of cell type 1065 14633408 1 preferentially transduced rods . No significant differences w rentially transduced rods. No significant differen 1273 14633408 1 ariation in retinal topography . Immunohistochemical studies ion in retinal topography. Immunohistochemical stu 1414 14633408 1 basis for the observed tropism . Our results support the util for the observed tropism. Our results support the 1585 14633408 1 eceptor degeneration therapies . or degeneration therapies. 1671 12925912 1 iverse body and fin coloration . More than 40 established col e body and fin coloration. More than 40 establishe 79 12925912 1 ies have been selectively bred . The complementary DNAs for 2 ave been selectively bred. The complementary DNAs 148 12925912 1 ere cloned from the caudal fin . Two cDNA isoforms for 6-pyru loned from the caudal fin. Two cDNA isoforms for 6 346 12925912 1 oned from the Red Tail variety . The deduced amino acid seque from the Red Tail variety. The deduced amino acid 521 12925912 1 o the mammalian PTPS sequences . The cDNA for xanthine dehydr mammalian PTPS sequences. The cDNA for xanthine d 647 12925912 1 ding frame of 1331 amino acids . Although it shows a higher o frame of 1331 amino acids. Although it shows a hig 789 12925912 1 omain that is specific to XDHs . Northern blot analysis indic that is specific to XDHs. Northern blot analysis 951 12925912 1 iver, but absent in the muscle . In the caudal fins, guppy va but absent in the muscle. In the caudal fins, gup 1084 12925912 1 mong the color guppy varieties . The results implied that hig the color guppy varieties. The results implied tha 1325 12925912 1 c chromatophores is less clear . omatophores is less clear. 1560 7992624 1 stepwise solid-phase procedure . The chloromethyl resin and M ise solid-phase procedure. The chloromethyl resin 111 7992624 1 in were used as solid supports . A new reagent of 0.5 mol.L-1 re used as solid supports. A new reagent of 0.5 mo 178 7992624 0 d supports. A new reagent of 0 . 5 mol.L-1 DDSi/1.5 mol.L-1 ph ports. A new reagent of 0.5 mol.L-1 DDSi/1.5 mol.L 198 7992624 0 orts. A new reagent of 0.5 mol . L-1 DDSi/1.5 mol.L-1 phenol/D A new reagent of 0.5 mol.L-1 DDSi/1.5 mol.L-1 phe 204 7992624 0 reagent of 0.5 mol.L-1 DDSi/1 . 5 mol.L-1 phenol/DCM was appl ent of 0.5 mol.L-1 DDSi/1.5 mol.L-1 phenol/DCM was 215 7992624 0 nt of 0.5 mol.L-1 DDSi/1.5 mol . L-1 phenol/DCM was applied fo 0.5 mol.L-1 DDSi/1.5 mol.L-1 phenol/DCM was appli 221 7992624 1 e removal of N alpha-Boc group . TFMSA was the cleaving reage oval of N alpha-Boc group. TFMSA was the cleaving 285 7992624 1 TFMSA was the cleaving reagent . After purification by C-18 c was the cleaving reagent. After purification by C 317 7992624 1 cording to amino acid analysis . The bioactivity of synthetic ng to amino acid analysis. The bioactivity of synt 412 7992624 1 ogesterone production in vitro . Eight peptides, GlyTyrAlaLys erone production in vitro. Eight peptides, GlyTyrA 513 7992624 1 t basal progesterone secretion . However, peptide GlySerTyr e al progesterone secretion. However, peptide GlySer 804 7992624 1 n basal progesterone secretion . So far, no reasonable relati al progesterone secretion. So far, no reasonable r 895 7992624 1 ture and bioactivity was found . and bioactivity was found. 975 6763907 0 r responses to acute insulin i . v. injection (0.12 U.I. per K ponses to acute insulin i.v. injection (0.12 U.I. 69 6763907 0 responses to acute insulin i.v . injection (0.12 U.I. per Kg nses to acute insulin i.v. injection (0.12 U.I. pe 71 6763907 0 cute insulin i.v. injection (0 . 12 U.I. per Kg of body weight insulin i.v. injection (0.12 U.I. per Kg of body w 85 6763907 0 insulin i.v. injection (0.12 U . I. per Kg of body weight) hav in i.v. injection (0.12 U.I. per Kg of body weight 90 6763907 0 sulin i.v. injection (0.12 U.I . per Kg of body weight) have i.v. injection (0.12 U.I. per Kg of body weight) 92 6763907 1 th mild essential hypertension . The hypoglycaemia test was c ld essential hypertension. The hypoglycaemia test 185 6763907 1 r a week of atenolol treatment . In six patients the test was eek of atenolol treatment. In six patients the tes 271 6763907 1 ed after propranolol treatment . Following insulin injection, ter propranolol treatment. Following insulin injec 343 6763907 1 heart rate rose significantly . Atenolol treatment abolished t rate rose significantly. Atenolol treatment abol 519 6763907 1 tely these hemodynamic changes . By contrast, propranolol cau these hemodynamic changes. By contrast, propranolo 593 6763907 1 ving the heart rate unmodified . During hypoglycaemia, plasma the heart rate unmodified. During hypoglycaemia, p 720 6763907 1 during the glycaemic recovery . Plasma noradrenaline rose le ng the glycaemic recovery. Plasma noradrenaline ro 868 6763907 1 significant after 30 and 60 m . Neither atenolol, nor propra ificant after 30 and 60 m. Neither atenolol, nor p 980 6763907 1 ma catecholamine concentration . These data indicate that bet techolamine concentration. These data indicate tha 1090 6763907 1 lary release of catecholamines . We conclude therefore that b release of catecholamines. We conclude therefore t 1211 6763907 1 1 selectivity of the drug used . ectivity of the drug used. 1472 12882229 1 rties and distribution of each . Sodium channels are heteromu and distribution of each. Sodium channels are het 242 12882229 1 and one or more beta subunits . Ten genes encode an alpha su one or more beta subunits. Ten genes encode an alp 386 12882229 0 ressed in the cerebellum: Nav1 . 1, Nav1.2, Nav1.3 and Nav1.6. d in the cerebellum: Nav1.1, Nav1.2, Nav1.3 and Na 490 12882229 0 n the cerebellum: Nav1.1, Nav1 . 2, Nav1.3 and Nav1.6. Three g cerebellum: Nav1.1, Nav1.2, Nav1.3 and Nav1.6. Th 498 12882229 0 rebellum: Nav1.1, Nav1.2, Nav1 . 3 and Nav1.6. Three genes enc lum: Nav1.1, Nav1.2, Nav1.3 and Nav1.6. Three gene 506 12882229 0 av1.1, Nav1.2, Nav1.3 and Nav1 . 6. Three genes encode beta su , Nav1.2, Nav1.3 and Nav1.6. Three genes encode be 517 12882229 1 1.1, Nav1.2, Nav1.3 and Nav1.6 . Three genes encode beta subu Nav1.2, Nav1.3 and Nav1.6. Three genes encode beta 519 12882229 1 re expressed in the cerebellum . However, Nav1.3 and Nabeta3 pressed in the cerebellum. However, Nav1.3 and Nab 612 12882229 0 the cerebellum. However, Nav1 . 3 and Nabeta3 have been found cerebellum. However, Nav1.3 and Nabeta3 have been 627 12882229 1 y in the developing cerebellum . All sodium channels recorded the developing cerebellum. All sodium channels rec 691 12882229 1 tify the isoforms electrically . Thus, most of the expression the isoforms electrically. Thus, most of the expre 838 12882229 1 the level of mRNA and protein . In situ hybridization and im level of mRNA and protein. In situ hybridization a 987 12882229 0 lls predominantly express Nav1 . 2, Nav1.6, Nabeta1, and Nabet redominantly express Nav1.2, Nav1.6, Nabeta1, and 1100 12882229 0 ominantly express Nav1.2, Nav1 . 6, Nabeta1, and Nabeta2. Prot ntly express Nav1.2, Nav1.6, Nabeta1, and Nabeta2. 1108 12882229 1 , Nav1.6, Nabeta1, and Nabeta2 . Protein for Nav1.2 and Nav1. 1.6, Nabeta1, and Nabeta2. Protein for Nav1.2 and 1132 12882229 0 and Nabeta2. Protein for Nav1 . 2 and Nav1.6 is localized pri Nabeta2. Protein for Nav1.2 and Nav1.6 is localize 1150 12882229 0 2. Protein for Nav1.2 and Nav1 . 6 is localized primarily in g otein for Nav1.2 and Nav1.6 is localized primarily 1161 12882229 1 n granule cell parallel fibers . Purkinje cells express Nav1. nule cell parallel fibers. Purkinje cells express 1218 12882229 0 s. Purkinje cells express Nav1 . 1, Nav1.6, Nabeta1 and Nabeta rkinje cells express Nav1.1, Nav1.6, Nabeta1 and N 1247 12882229 0 nje cells express Nav1.1, Nav1 . 6, Nabeta1 and Nabeta2. The s ells express Nav1.1, Nav1.6, Nabeta1 and Nabeta2. 1255 12882229 1 1, Nav1.6, Nabeta1 and Nabeta2 . The somato-dendritic localiz v1.6, Nabeta1 and Nabeta2. The somato-dendritic lo 1278 12882229 0 dendritic localization of Nav1 . 1 and Nav1.6 in Purkinje cell itic localization of Nav1.1 and Nav1.6 in Purkinje 1321 12882229 0 ocalization of Nav1.1 and Nav1 . 6 in Purkinje cells suggests zation of Nav1.1 and Nav1.6 in Purkinje cells sugg 1332 12882229 1 integration of synaptic input . Deep cerebellar nuclei neuro gration of synaptic input. Deep cerebellar nuclei 1431 12882229 0 nuclei neurons expressed Nav1 . 1 and Nav1.6 as well as Nabet ei neurons expressed Nav1.1 and Nav1.6 as well as 1478 12882229 0 rons expressed Nav1.1 and Nav1 . 6 as well as Nabeta1. Bergman expressed Nav1.1 and Nav1.6 as well as Nabeta1. Be 1489 12882229 1 and Nav1.6 as well as Nabeta1 . Bergmann glia expressed Nav1 Nav1.6 as well as Nabeta1. Bergmann glia expressed 1510 12882229 0 . Bergmann glia expressed Nav1 . 6, but not granule cell layer gmann glia expressed Nav1.6, but not granule cell 1540 12882229 1 granule cell layer astrocytes . Some sodium channel isoforms ule cell layer astrocytes. Some sodium channel iso 1581 12882229 1 mals with mutations or disease . Electrophysiological studies with mutations or disease. Electrophysiological st 1718 12882229 0 ical studies suggest that Nav1 . 6 is responsible for spontane studies suggest that Nav1.6 is responsible for spo 1766 12882229 1 the cerebellum remain unknown . cerebellum remain unknown. 1932 12972372 1 sis or continue with pregnancy . The objective of these exper r continue with pregnancy. The objective of these 220 12972372 1 lpha) and E2 (PGE2) production . Epithelial and stromal cells and E2 (PGE2) production. Epithelial and stromal 442 12972372 0 eated with 17beta-estradiol (0 . 1 and 1.0 nM) and/or progeste with 17beta-estradiol (0.1 and 1.0 nM) and/or pro 578 12972372 0 th 17beta-estradiol (0.1 and 1 . 0 nM) and/or progesterone (1. beta-estradiol (0.1 and 1.0 nM) and/or progesteron 586 12972372 0 1.0 nM) and/or progesterone (1 . 0 and 10 nM) in a manner desi M) and/or progesterone (1.0 and 10 nM) in a manner 615 12972372 1 ctuations of the estrous cycle . All cell types expressed est ions of the estrous cycle. All cell types expresse 704 12972372 1 rone receptor mRNA and protein . Intercaruncular stromal cell receptor mRNA and protein. Intercaruncular stromal 791 12972372 1 onsive to steroidal regulation . Estrogen suppressed expressi e to steroidal regulation. Estrogen suppressed exp 871 12972372 0 n ICAR stromal cells (P< or =0 . 05). Progesterone and estroge R stromal cells (P< or =0.05). Progesterone and es 966 12972372 1 AR stromal cells (P< or =0.05) . Progesterone and estrogen + romal cells (P< or =0.05). Progesterone and estrog 970 12972372 0 ession from controls (P> or =0 . 05). Steroid treatment did no n from controls (P> or =0.05). Steroid treatment d 1085 12972372 1 on from controls (P> or =0.05) . Steroid treatment did not af om controls (P> or =0.05). Steroid treatment did n 1089 12972372 0 ion in any cell type (P> or =0 . 05), however, estrogen decrea n any cell type (P> or =0.05), however, estrogen d 1171 12972372 0 ls except CAR stroma (P< or =0 . 05). The results indicate tha cept CAR stroma (P< or =0.05). The results indicat 1261 12972372 1 xcept CAR stroma (P< or =0.05) . The results indicate that in CAR stroma (P< or =0.05). The results indicate th 1265 12972372 1 PGE2 is influenced by estrogen . is influenced by estrogen. 1398 9664047 1 and not the other ARF proteins . Using this antibody, ARF6 wa ot the other ARF proteins. Using this antibody, AR 166 9664047 1 NRK, BHK, COS, and HeLa cells . In NRK cells, by immunofluor BHK, COS, and HeLa cells. In NRK cells, by immuno 324 9664047 1 ion in the juxtanuclear region . This pattern of localization n the juxtanuclear region. This pattern of localiz 538 9664047 1 pressed in NRK, or HeLa, cells . Treatments which perturb cor ed in NRK, or HeLa, cells. Treatments which pertur 676 9664047 1 f cortical actin rearrangement . ARF6 activation and subseque tical actin rearrangement. ARF6 activation and sub 906 9664047 1 nt and spreading in HeLa cells . Furthermore, phorbol ester t d spreading in HeLa cells. Furthermore, phorbol es 1202 9664047 1 erved in cells expressing T27N . Taken together, these observ in cells expressing T27N. Taken together, these o 1358 9664047 1 nd cortical actin cytoskeleton . rtical actin cytoskeleton. 1493 10548126 1 the diagnosis of poliomyelitis . To probe captured IgM we use iagnosis of poliomyelitis. To probe captured IgM w 150 10548126 0 ik M, Rysa T, Akram DS, Hovi T . J Clin Microbiol 1993;31:242 Rysa T, Akram DS, Hovi T. J Clin Microbiol 1993;3 330 10548126 1 lin Microbiol 1993;31:2427-32) . However, this assay is not d icrobiol 1993;31:2427-32). However, this assay is 365 10548126 1 some and potentially hazardous . OBJECTIVES: To develop a non and potentially hazardous. OBJECTIVES: To develop 524 10548126 1 teps and reagents to a minimum . STUDY DESIGN: Replacement of and reagents to a minimum. STUDY DESIGN: Replaceme 648 10548126 1 xidase-conjugated streptavidin . To study sensitivity and pol e-conjugated streptavidin. To study sensitivity an 830 10548126 1 ve tests with the in-house RIA . In addition, sera from 40 he sts with the in-house RIA. In addition, sera from 1012 10548126 1 ere used to assess specificity . RESULTS: While results with sed to assess specificity. RESULTS: While results 1156 10548126 1 irions is difficult to control . Moreover, examination of ser s is difficult to control. Moreover, examination o 1440 10548126 1 d other enterovirus infections . The latter were also seen in er enterovirus infections. The latter were also se 1646 10548126 1 tter were also seen in the RIA . CONCLUSION: Cross-reactive e were also seen in the RIA. CONCLUSION: Cross-react 1684 10548126 1 c IgM for poliovirus diagnosis . Biotinylation of the virions for poliovirus diagnosis. Biotinylation of the vi 1882 10548126 1 ed to aggravate these problems . aggravate these problems. 1947 8816806 1 ctal cancers over 10 years ago . However, the mechanism of th cancers over 10 years ago. However, the mechanism 194 8816806 1 e changes has remained obscure . el-Deiry and coworkers [el-D nges has remained obscure. el-Deiry and coworkers 256 8816806 0 iry and coworkers [el-Deiry, W . S., Nelkin, B. D., Celano, P nd coworkers [el-Deiry, W. S., Nelkin, B. D., Cela 293 8816806 0 and coworkers [el-Deiry, W. S . , Nelkin, B. D., Celano, P., coworkers [el-Deiry, W. S., Nelkin, B. D., Celano, 296 8816806 0 rs [el-Deiry, W. S., Nelkin, B . D., Celano, P., Yen, R. C., l-Deiry, W. S., Nelkin, B. D., Celano, P., Yen, R. 308 8816806 0 [el-Deiry, W. S., Nelkin, B. D . , Celano, P., Yen, R. C., Fal eiry, W. S., Nelkin, B. D., Celano, P., Yen, R. C. 311 8816806 0 . S., Nelkin, B. D., Celano, P . , Yen, R. C., Falco, J. P., H Nelkin, B. D., Celano, P., Yen, R. C., Falco, J. 323 8816806 0 kin, B. D., Celano, P., Yen, R . C., Falco, J. P., Hamilton, B. D., Celano, P., Yen, R. C., Falco, J. P., Hamil 332 8816806 0 , B. D., Celano, P., Yen, R. C . , Falco, J. P., Hamilton, S. D., Celano, P., Yen, R. C., Falco, J. P., Hamilton 335 8816806 0 lano, P., Yen, R. C., Falco, J . P., Hamilton, S. R. & Baylin P., Yen, R. C., Falco, J. P., Hamilton, S. R. & B 346 8816806 0 o, P., Yen, R. C., Falco, J. P . , Hamilton, S. R. & Baylin, S , Yen, R. C., Falco, J. P., Hamilton, S. R. & Bayl 349 8816806 0 C., Falco, J. P., Hamilton, S . R. & Baylin, S. B. (1991) Pr Falco, J. P., Hamilton, S. R. & Baylin, S. B. (199 363 8816806 0 , Falco, J. P., Hamilton, S. R . & Baylin, S. B. (1991) Proc. co, J. P., Hamilton, S. R. & Baylin, S. B. (1991) 366 8816806 0 ., Hamilton, S. R. & Baylin, S . B. (1991) Proc. Natl. Acad. milton, S. R. & Baylin, S. B. (1991) Proc. Natl. A 379 8816806 0 Hamilton, S. R. & Baylin, S. B . (1991) Proc. Natl. Acad. Sci ton, S. R. & Baylin, S. B. (1991) Proc. Natl. Acad 382 8816806 0 R. & Baylin, S. B. (1991) Proc . Natl. Acad. Sci. USA 88, 347 Baylin, S. B. (1991) Proc. Natl. Acad. Sci. USA 88 395 8816806 0 aylin, S. B. (1991) Proc. Natl . Acad. Sci. USA 88, 3470-3474 , S. B. (1991) Proc. Natl. Acad. Sci. USA 88, 3470 401 8816806 0 S. B. (1991) Proc. Natl. Acad . Sci. USA 88, 3470-3474], usi . (1991) Proc. Natl. Acad. Sci. USA 88, 3470-3474] 407 8816806 0 . (1991) Proc. Natl. Acad. Sci . USA 88, 3470-3474], using a 91) Proc. Natl. Acad. Sci. USA 88, 3470-3474], usi 412 8816806 1 mucosa of unaffected patients . These authors suggested that sa of unaffected patients. These authors suggested 707 8816806 1 c role in colon carcinogenesis . To test this hypothesis, we e in colon carcinogenesis. To test this hypothesis 824 8816806 1 over three orders of magnitude . Using this assay on 12 color three orders of magnitude. Using this assay on 12 959 8816806 0 sal specimens, we observed a 1 . 8- to 2.5-fold increase in MT pecimens, we observed a 1.8- to 2.5-fold increase 1059 8816806 0 imens, we observed a 1.8- to 2 . 5-fold increase in MTase mRNA , we observed a 1.8- to 2.5-fold increase in MTase 1067 8816806 1 mucosa from the same patients . There was no significant dif sa from the same patients. There was no significan 1184 8816806 1 fected and unaffected patients . Furthermore, when the assay d and unaffected patients. Furthermore, when the a 1283 8816806 1 levels was no longer observed . These data are in contrast t ls was no longer observed. These data are in contr 1467 8816806 1 markers of cell proliferation . ers of cell proliferation. 1671 8624296 1 lung cancer (SCLC), is unknown . We therefore investigated wh cancer (SCLC), is unknown. We therefore investigat 116 8624296 1 ppressed in patients with SCLC . PATIENTS AND METHODS: We det sed in patients with SCLC. PATIENTS AND METHODS: W 235 8624296 1 e different cytokines measured . RESULTS: Compares to normal ferent cytokines measured. RESULTS: Compares to no 612 8624296 1 gamma upon mitogen stimulation . TNF alpha-secretion was sign upon mitogen stimulation. TNF alpha-secretion was 793 8624296 1 ut not in SCLC limited disease . In contrast, secretion of IL t in SCLC limited disease. In contrast, secretion 898 8624296 1 and IL-1 beta was not reduced . In patients with NSCLC, secr IL-1 beta was not reduced. In patients with NSCLC, 966 8624296 1 lpha was significantly reduced . Reduction of IFN gamma secre was significantly reduced. Reduction of IFN gamma 1049 8624296 1 significant in localized NSCLC . Secretion of TNF alpha, IL-1 ficant in localized NSCLC. Secretion of TNF alpha, 1167 8624296 1 and IL-1 beta was not impaired . In addition, cytokine secret L-1 beta was not impaired. In addition, cytokine s 1234 8624296 1 upon ineffective chemotherapy . Furthermore, TGF beta 1 supp ineffective chemotherapy. Furthermore, TGF beta 1 1401 8624296 1 tures from healthy individuals . CONCLUSIONS: Suppression of from healthy individuals. CONCLUSIONS: Suppressio 1578 8624296 1 d upon reduction of tumor load . These results may suggest in n reduction of tumor load. These results may sugge 1790 8624296 1 or cells and the immune system . TGF beta 1 secreted by SCLC lls and the immune system. TGF beta 1 secreted by 1872 8624296 1 as that found in SCLC patients . However, whether or not tumo at found in SCLC patients. However, whether or not 1991 8624296 1 patients is presently unclear . ents is presently unclear. 2128 12615819 1 (> or =10 IU/l) at a young age . We sought to determine wheth =10 IU/l) at a young age. We sought to determine 207 12615819 1 poor reproductive performance . METHODS: A retrospective coh reproductive performance. METHODS: A retrospectiv 326 12615819 1 reatment between 1987 and 1998 . All women were < 40 years of ent between 1987 and 1998. All women were < 40 yea 571 12615819 1 nd had normal menstrual cycles . Participants were sent a pos d normal menstrual cycles. Participants were sent 662 12615819 1 llowing cessation of treatment . RESULTS: After adjusting for ng cessation of treatment. RESULTS: After adjustin 825 12615819 0 eri-menopause [hazard ratios 2 . 4, 95% confidence interval (C enopause [hazard ratios 2.4, 95% confidence interv 1011 12615819 0 95% confidence interval (CI) 1 . 52-3.78, and 2.76, 95% CI 1.7 onfidence interval (CI) 1.52-3.78, and 2.76, 95% C 1045 12615819 0 onfidence interval (CI) 1.52-3 . 78, and 2.76, 95% CI 1.78-4.2 ence interval (CI) 1.52-3.78, and 2.76, 95% CI 1.7 1050 12615819 0 interval (CI) 1.52-3.78, and 2 . 76, 95% CI 1.78-4.29 respecti val (CI) 1.52-3.78, and 2.76, 95% CI 1.78-4.29 res 1060 12615819 0 1.52-3.78, and 2.76, 95% CI 1 . 78-4.29 respectively, P = 0.0 -3.78, and 2.76, 95% CI 1.78-4.29 respectively, P 1073 12615819 0 -3.78, and 2.76, 95% CI 1.78-4 . 29 respectively, P = 0.0001]. , and 2.76, 95% CI 1.78-4.29 respectively, P = 0.0 1078 12615819 0 1.78-4.29 respectively, P = 0 . 0001]. Poor responders were s -4.29 respectively, P = 0.0001]. Poor responders w 1101 12615819 1 4.29 respectively, P = 0.0001] . Poor responders were six tim respectively, P = 0.0001]. Poor responders were si 1107 12615819 0 s respectively (hazard ratio 5 . 97 and 23.9, P = 0.015 and 0. pectively (hazard ratio 5.97 and 23.9, P = 0.015 a 1303 12615819 0 vely (hazard ratio 5.97 and 23 . 9, P = 0.015 and 0.002 respec (hazard ratio 5.97 and 23.9, P = 0.015 and 0.002 r 1313 12615819 0 ard ratio 5.97 and 23.9, P = 0 . 015 and 0.002 respectively). atio 5.97 and 23.9, P = 0.015 and 0.002 respective 1322 12615819 0 5.97 and 23.9, P = 0.015 and 0 . 002 respectively). Poor respo and 23.9, P = 0.015 and 0.002 respectively). Poor 1332 12615819 1 0.015 and 0.002 respectively) . Poor responders and those wi 5 and 0.002 respectively). Poor responders and tho 1350 12615819 0 compared with controls (P < 0 . 007). CONCLUSIONS: Both poor ared with controls (P < 0.007). CONCLUSIONS: Both 1518 12615819 1 ared with controls (P < 0.007) . CONCLUSIONS: Both poor respo with controls (P < 0.007). CONCLUSIONS: Both poor 1523 12615819 1 reased risk of early menopause . d risk of early menopause. 1688 11781286 1 ancreas remain largely unknown . Here, we characterize ethano as remain largely unknown. Here, we characterize e 155 11781286 1 ules critical for this disease . METHODS: We measured activit critical for this disease. METHODS: We measured ac 474 11781286 1 ulation of ethanol metabolites . We measured the effects of e on of ethanol metabolites. We measured the effects 629 11781286 1 ion by using a gel shift assay . RESULTS: Pancreas metabolize y using a gel shift assay. RESULTS: Pancreas metab 746 11781286 1 tive and nonoxidative pathways . Acinar cells are the main so and nonoxidative pathways. Acinar cells are the ma 830 11781286 1 nol metabolism in the pancreas . Compared with the liver, FAE etabolism in the pancreas. Compared with the liver 902 11781286 1 ereas that of ADH is much less . FAEEs activated NF-kappa B a that of ADH is much less. FAEEs activated NF-kapp 1012 11781286 1 nhibited NF-kappa B activation . Ethanol decreased NF-kappa B ted NF-kappa B activation. Ethanol decreased NF-ka 1103 11781286 1 h was potentiated by cyanamide . CONCLUSION: Oxidative and no potentiated by cyanamide. CONCLUSION: Oxidative a 1202 11781286 1 tly in pancreatic acinar cells . Ethanol may regulate NF-kapp n pancreatic acinar cells. Ethanol may regulate NF 1332 11781286 1 pathway's effect predominates . These regulatory mechanisms way's effect predominates. These regulatory mechan 1459 11781286 1 hanol toxicity to the pancreas . toxicity to the pancreas. 1540 11121406 1 ar responses to IGF-I in vitro . This capacity of IGFBP-1 to sponses to IGF-I in vitro. This capacity of IGFBP- 178 11121406 1 igh molecular weight multimers . Since the ability of some pr olecular weight multimers. Since the ability of so 317 11121406 1 n of IGFBP-1 upon IGF-I action . Following incubation with pu IGFBP-1 upon IGF-I action. Following incubation wi 537 11121406 1 esis using reducing conditions . Dephosphorylated IGFBP-1 pol using reducing conditions. Dephosphorylated IGFBP- 731 11121406 1 ative (phosphorylated) IGFBP-1 . Exposure to IGF-I stimulated (phosphorylated) IGFBP-1. Exposure to IGF-I stimu 852 11121406 1 tamination of IGFBP-1 in vitro . An IGFBP-1 mutant in which G ation of IGFBP-1 in vitro. An IGFBP-1 mutant in wh 921 11121406 1 g compared with native IGFBP-1 . Tg localized in fibroblast m pared with native IGFBP-1. Tg localized in fibrobl 1091 11121406 1 A IGFBP-1 failed to polymerize . Although the mutant IGFBP-1 BP-1 failed to polymerize. Although the mutant IGF 1247 11121406 1 FBP-1 had no inhibitory effect . The addition of higher conce had no inhibitory effect. The addition of higher 1414 11121406 1 meric IGFBP-1 that was present . In conclusion, IGFBP-1 is a IGFBP-1 that was present. In conclusion, IGFBP-1 1610 11121406 1 ht covalently linked multimers . Polymerization is an importa valently linked multimers. Polymerization is an im 1760 11121406 1 es cellular responses to IGF-I . llular responses to IGF-I. 1878 12370101 1 , P815, and sarcoma 180 (S180) . METHODS: Tumor cells (K562, 5, and sarcoma 180 (S180). METHODS: Tumor cells (K 191 12370101 1 ansmission electron microscope . MTT assay was performed to m ssion electron microscope. MTT assay was performed 368 12370101 1 liferation and inhibition rate . DNA content was assayed by f ation and inhibition rate. DNA content was assayed 447 12370101 1 was assayed by flow cytometry . According to protocols of tr assayed by flow cytometry. According to protocols 490 12370101 1 ls L1210, P388, Heps, and S180 . The survival rate and weight 210, P388, Heps, and S180. The survival rate and w 612 12370101 1 er the treatment of test drugs . RESULTS: The antitumor effec e treatment of test drugs. RESULTS: The antitumor 699 12370101 0 ls K562, L1210, and P815 (P <0 . 01). In vivo experiments show 62, L1210, and P815 (P <0.01). In vivo experiments 817 12370101 1 562, L1210, and P815 (P <0.01) . In vivo experiments showed t L1210, and P815 (P <0.01). In vivo experiments sho 821 12370101 0 388 or L1210 tumor cells (P <0 . 01). Tumor growth induced wit r L1210 tumor cells (P <0.01). Tumor growth induce 991 12370101 1 or L1210 tumor cells (P <0.01) . Tumor growth induced with He 210 tumor cells (P <0.01). Tumor growth induced wi 995 12370101 1 also significantly suppressed . Furthermore, significant sup significantly suppressed. Furthermore, significan 1061 12370101 1 ministration of L-asparaginase . CONCLUSION: Recombinant L-as tration of L-asparaginase. CONCLUSION: Recombinant 1202 12370101 1 ical treatment of these tumors . treatment of these tumors. 1413 9276623 1 g prolonged hormonal treatment . Dysplasia, a pre-neoplastic longed hormonal treatment. Dysplasia, a pre-neopla 165 9276623 1 eta (E2) (T + E2-treated rats) . Concurrent with DLP dysplasi E2) (T + E2-treated rats). Concurrent with DLP dys 386 9276623 1 eration in the dysplastic foci . The aim of this study was to on in the dysplastic foci. The aim of this study w 677 9276623 1 E2-induced hyperprolactinemia . Bromocriptine (Br), at a dos nduced hyperprolactinemia. Bromocriptine (Br), at 797 9276623 1 uitary prolactin (PRL) release . Serum PRL levels were lowere y prolactin (PRL) release. Serum PRL levels were l 911 9276623 1 ng/ml in Br co-treated animals . The latter values were compa in Br co-treated animals. The latter values were 1041 9276623 1 hose in untreated control rats . In addition, Br co-treatment in untreated control rats. In addition, Br co-trea 1111 9276623 1 of eight rats) in most animals . In contrast, Br co-treatment ght rats) in most animals. In contrast, Br co-trea 1293 9276623 1 pared with T + E2-treated rats . These data extend the many p with T + E2-treated rats. These data extend the m 1467 9276623 1 PRL on rat prostatic functions . However, the current study i n rat prostatic functions. However, the current st 1583 9276623 1 ic dysplasia induction in vivo . splasia induction in vivo. 1682 15317943 1 ner ear and lateral-line organ . One mutant line, ru920, was ar and lateral-line organ. One mutant line, ru920, 229 15317943 1 tically evoked escape response . Despite apparently normal nu ly evoked escape response. Despite apparently norm 347 15317943 1 raverses transduction channels . This hair-cell-specific phen ses transduction channels. This hair-cell-specific 542 15317943 1 ctrical transduction apparatus . Positional cloning revealed al transduction apparatus. Positional cloning reve 644 15317943 1 gs of the human gene myosin VI . The ru920 line therefore pro the human gene myosin VI. The ru920 line therefor 830 15317943 1 roteins in mechanotransduction . ns in mechanotransduction. 961 15839281 0 ze the room temperature (T= 23 . 5 degrees C) time behavior of e room temperature (T= 23.5 degrees C) time behavi 50 15839281 1 ernally applied electric field . To the authors' knowledge, t ly applied electric field. To the authors' knowled 278 15839281 1 me-resolved optical transients . According to a previous [J. solved optical transients. According to a previous 399 15839281 0 ts. According to a previous [J . Opt. Soc. Am. A 22, 377 (200 ccording to a previous [J. Opt. Soc. Am. A 22, 377 427 15839281 0 ccording to a previous [J. Opt . Soc. Am. A 22, 377 (2005)] o ing to a previous [J. Opt. Soc. Am. A 22, 377 (200 432 15839281 0 ing to a previous [J. Opt. Soc . Am. A 22, 377 (2005)] observ o a previous [J. Opt. Soc. Am. A 22, 377 (2005)] o 437 15839281 0 to a previous [J. Opt. Soc. Am . A 22, 377 (2005)] observatio previous [J. Opt. Soc. Am. A 22, 377 (2005)] obser 441 15839281 1 ) electrooptic effects coexist . Because of its nondestructiv ctrooptic effects coexist. Because of its nondestr 688 15839281 1 ters of crystals are important . of crystals are important. 933 7990489 1 treatment of diabetes mellitus . However, very few scientific ment of diabetes mellitus. However, very few scien 97 7990489 0 the efficacy and toxicity of A . herba alba. In this study fe fficacy and toxicity of A. herba alba. In this stu 205 7990489 1 and toxicity of A. herba alba . In this study feeding diabet toxicity of A. herba alba. In this study feeding d 217 7990489 0 abetic rats and rabbits with 0 . 39 g/kg body weight of the aq c rats and rabbits with 0.39 g/kg body weight of t 273 7990489 1 eight loss of diabetic animals . loss of diabetic animals. 581 9331960 1 horbol myristate acetate (PMA) . In nuclei of vitamin E-defic l myristate acetate (PMA). In nuclei of vitamin E- 184 9331960 1 NA with and without tocopherol . A23187, verapamil, and PMA d th and without tocopherol. A23187, verapamil, and 324 9331960 1 RNA-polymerase activity by 25% . The effect of the combinatio olymerase activity by 25%. The effect of the combi 613 9331960 1 ith tocopherol-binding protein . ocopherol-binding protein. 834 6710589 1 ned IgM anti-H but not anti-A1 . A1 cells were agglutinated w gM anti-H but not anti-A1. A1 cells were agglutina 156 6710589 1 t not in the antiglobulin test . One hour after the survival in the antiglobulin test. One hour after the surv 259 6710589 1 cells remained after 24 hours . This study suggests that Ah s remained after 24 hours. This study suggests tha 419 6710589 1 d only with Ah or Oh red cells . y with Ah or Oh red cells. 510 14741191 1 e in heart and skeletal muscle . In contrast to liver, brain, heart and skeletal muscle. In contrast to liver, b 195 14741191 0 l muscle galactitol reaches 22 . 90+/-1.62 (M+/-SE) and 38.88+ cle galactitol reaches 22.90+/-1.62 (M+/-SE) and 3 377 14741191 0 e galactitol reaches 22.90+/-1 . 62 (M+/-SE) and 38.88+/-2.62 actitol reaches 22.90+/-1.62 (M+/-SE) and 38.88+/- 384 14741191 0 s 22.90+/-1.62 (M+/-SE) and 38 . 88+/-2.62 micromol/g tissue, 90+/-1.62 (M+/-SE) and 38.88+/-2.62 micromol/g tis 403 14741191 0 +/-1.62 (M+/-SE) and 38.88+/-2 . 62 micromol/g tissue, respect 62 (M+/-SE) and 38.88+/-2.62 micromol/g tissue, re 410 14741191 1 alactose-1-phosphate (Gal-1-P) . Sixteen-day-old suckling G/G ose-1-phosphate (Gal-1-P). Sixteen-day-old sucklin 506 14741191 1 ser extent, in skeletal muscle . Heart and skeletal muscle of xtent, in skeletal muscle. Heart and skeletal musc 615 14741191 1 te under conditions of loading . The data suggest that heart der conditions of loading. The data suggest that h 845 14741191 1 itol and galactonate excretion . The ability of heart and mus and galactonate excretion. The ability of heart an 1041 14741191 1 oute for galactose disposition . for galactose disposition. 1263 12510892 1 ing specific molecular markers . No specific differences in t pecific molecular markers. No specific differences 250 12510892 0 between Simulium sanctipauli V . & D., Simulium sirbanum V. & en Simulium sanctipauli V. & D., Simulium sirbanum 341 12510892 0 en Simulium sanctipauli V. & D . , Simulium sirbanum V. & D., mulium sanctipauli V. & D., Simulium sirbanum V. & 346 12510892 0 i V. & D., Simulium sirbanum V . & D., Simulium soubrense V. & D., Simulium sirbanum V. & D., Simulium soubrens 368 12510892 0 & D., Simulium sirbanum V. & D . , Simulium soubrense V. & D., Simulium sirbanum V. & D., Simulium soubrense V. 373 12510892 0 V. & D., Simulium soubrense V . & D., Simulium squamosum End D., Simulium soubrense V. & D., Simulium squamosu 396 12510892 0 D., Simulium soubrense V. & D . , Simulium squamosum Enderlei Simulium soubrense V. & D., Simulium squamosum End 401 12510892 0 derlein and Simulium yahense V . & D., except in the number o in and Simulium yahense V. & D., except in the num 455 12510892 0 in and Simulium yahense V. & D . , except in the number of A s d Simulium yahense V. & D., except in the number o 460 12510892 0 he 5' end of the IGS (two in S . squamosum and four or five i end of the IGS (two in S. squamosum and four or f 534 12510892 0 on 310 of the 3' end (a C in S . squamosum and a G in the oth 0 of the 3' end (a C in S. squamosum and a G in th 621 12510892 1 uamosum and a G in the others) . However, genetic distances w um and a G in the others). However, genetic distan 655 12510892 1 and between species overlapped . These DNA sequences had no s etween species overlapped. These DNA sequences had 721 12510892 1 btained were mostly unresolved . Although most sequences from ed were mostly unresolved. Although most sequences 823 12510892 1 Although most sequences from S . squamosum clustered together ugh most sequences from S. squamosum clustered tog 855 12510892 1 to those in other cytospecies . These results could be expla hose in other cytospecies. These results could be 948 12510892 1 morphism and recent speciation . ism and recent speciation. 1084 9549342 0 ion routes are limited to be i . v. route. To increase the cli outes are limited to be i.v. route. To increase th 117 9549342 0 n routes are limited to be i.v . route. To increase the clini tes are limited to be i.v. route. To increase the 119 9549342 1 s are limited to be i.v. route . To increase the clinical use limited to be i.v. route. To increase the clinica 126 9549342 1 , oral dosage form is required . However, in the case of oral l dosage form is required. However, in the case of 204 9549342 1 aving strong protease activity . To decrease the protease act strong protease activity. To decrease the proteas 323 9549342 1 ed concomitantly with proteins . Aprotinin, soybean trypsin i ncomitantly with proteins. Aprotinin, soybean tryp 424 9549342 1 esentative protease inhibitors . Gel-forming polymers have bo ative protease inhibitors. Gel-forming polymers ha 548 9549342 1 ing effect on protein/peptides . The usefulness of these prot ffect on protein/peptides. The usefulness of these 661 9549342 1 SF and vasopressin derivatives . d vasopressin derivatives. 800 11893721 1 okaryotic and eukaryotic cells . Critical to the development otic and eukaryotic cells. Critical to the develop 156 11893721 1 -activity relationships (SARs) . To this end, a positive-sele vity relationships (SARs). To this end, a positive 415 11893721 1 (RDO)-directed repair activity . We demonstrate that RDO-dire -directed repair activity. We demonstrate that RDO 561 11893721 1 atch recognition protein, MutS . SAR studies demonstrate that recognition protein, MutS. SAR studies demonstrate 739 11893721 1 ule is functionally asymmetric . The RNA-containing strand en s functionally asymmetric. The RNA-containing stra 813 11893721 1 nfers the information transfer . the information transfer. 961 11294962 1 MA) immunofluorescent findings . The study included 116 untre mmunofluorescent findings. The study included 116 242 11294962 1 ples and 29 healthy volunteers . IgA anti-tTG, EMA, and anti- and 29 healthy volunteers. IgA anti-tTG, EMA, and 472 11294962 1 (AGA) antibodies were measured . Serum total IgA was measured antibodies were measured. Serum total IgA was mea 540 11294962 1 as measured in the CD patients . Two IgA-deficient untreated asured in the CD patients. Two IgA-deficient untre 589 11294962 1 ated CD patients were excluded . IgA EMA and IgA AGA were pos CD patients were excluded. IgA EMA and IgA AGA wer 644 11294962 1 the 114 untreated CD patients . Elevated IgA anti-tTG were f 114 untreated CD patients. Elevated IgA anti-tTG w 752 11294962 1 trols and 2/29 (7%) volunteers . Four of the untreated CD pat and 2/29 (7%) volunteers. Four of the untreated C 928 11294962 1 for all the serological tests . IgA anti-tTG concentrations all the serological tests. IgA anti-tTG concentrat 1053 11294962 0 ther groups (Mann-Whitney, p<0 . 00001) and compared well with groups (Mann-Whitney, p<0.00001) and compared well 1194 11294962 0 ll with IgA EMA titres (r(2)=0 . 54; p<0.0001). th IgA EMA titres (r(2)=0.54; p<0.0001). 1247 11294962 0 IgA EMA titres (r(2)=0.54; p<0 . 0001). MA titres (r(2)=0.54; p<0.0001). 1255 11294962 0 A titres (r(2)=0.54; p<0.0001) . res (r(2)=0.54; p<0.0001). 1261 12529537 1 oward herbivores and pathogens . Plant defense is regulated b herbivores and pathogens. Plant defense is regula 102 12529537 1 unction as signaling molecules . Glucosinolate content was an on as signaling molecules. Glucosinolate content w 261 12529537 1 oxyacetic acid, or by wounding . In addition, several signal etic acid, or by wounding. In addition, several si 502 12529537 1 sgenic NahG line were analyzed . In parallel, expression of g c NahG line were analyzed. In parallel, expression 607 12529537 1 cosyltransferase was monitored . After MeJA treatment, the am transferase was monitored. After MeJA treatment, t 756 12529537 1 P79B3 were both highly induced . Specifically, the indole glu were both highly induced. Specifically, the indol 929 12529537 0 hylglucosinolate accumulated 1 . 5-fold in response to 2,6-dic ucosinolate accumulated 1.5-fold in response to 2, 1122 12529537 1 2,6-dichloro-isonicotinic acid . In general, few changes were ichloro-isonicotinic acid. In general, few changes 1175 12529537 1 icularly after MeJA treatments . The findings were supported rly after MeJA treatments. The findings were suppo 1412 12529537 1 roducing mpk4 and cpr1 mutants . The present data indicate th ing mpk4 and cpr1 mutants. The present data indica 1625 12529537 1 not environmentally controlled . Thus, different defense path nvironmentally controlled. Thus, different defense 1887 12529537 1 ion of specific glucosinolates . f specific glucosinolates. 2018 11082049 1 me example of polarized growth . In contrast to yeast species ample of polarized growth. In contrast to yeast sp 91 11082049 1 rized growth of the hyphal tip . In many fungi, including Ash growth of the hyphal tip. In many fungi, includin 272 11082049 1 ocess called hyphal maturation . Hyphal maturation refers to called hyphal maturation. Hyphal maturation refer 384 11082049 1 wing hyphae of mature mycelium . This process is essential fo hyphae of mature mycelium. This process is essenti 523 11082049 1 fficient expansion of mycelium . We report for the first time ent expansion of mycelium. We report for the first 586 11082049 1 mportant for hyphal maturation . This novel A. gossypii gene ant for hyphal maturation. This novel A. gossypii 708 11082049 0 yphal maturation. This novel A . gossypii gene encodes a pres maturation. This novel A. gossypii gene encodes a 722 11082049 1 -activated kinase)-like kinase . Its closest homolog is the S vated kinase)-like kinase. Its closest homolog is 798 11082049 0 . Its closest homolog is the S . cerevisiae Cla4 protein kina closest homolog is the S. cerevisiae Cla4 protein 828 11082049 0 iae Cla4 protein kinase; the A . gossypii protein is therefor la4 protein kinase; the A. gossypii protein is the 867 11082049 1 in is therefore called AgCla4p . Agcla4 deletion strains are therefore called AgCla4p. Agcla4 deletion strains 913 11082049 1 tips than in young hyphal tips . Both results support the imp than in young hyphal tips. Both results support th 1158 11082049 1 f AgCla4p in hyphal maturation . AgCla4p is also required for la4p in hyphal maturation. AgCla4p is also require 1227 11082049 1 m actin rings and chitin rings . Despite the requirement of A in rings and chitin rings. Despite the requirement 1368 11082049 1 een in Agcla4 deletion strains . The possibility that AgCla4p n Agcla4 deletion strains. The possibility that Ag 1643 11082049 1 d/or actin cables is discussed . actin cables is discussed. 1794 8294701 1 . The efficacy of selective sy 10 8294701 1 and myocardial oxygen tension . BACKGROUND. Because incomple myocardial oxygen tension. BACKGROUND. Because inc 251 8294701 1 ial oxygen tension. BACKGROUND . Because incomplete protectio xygen tension. BACKGROUND. Because incomplete prot 263 8294701 1 dded to a retroinfusion system . METHODS. Regional myocardial to a retroinfusion system. METHODS. Regional myoca 495 8294701 1 retroinfusion system. METHODS . Regional myocardial function oinfusion system. METHODS. Regional myocardial fun 504 8294701 1 emia), followed by reperfusion . During ischemia, group A (n , followed by reperfusion. During ischemia, group 745 8294701 1 not supported by retroinfusion . RESULTS. In group A, subendo upported by retroinfusion. RESULTS. In group A, su 982 8294701 1 rted by retroinfusion. RESULTS . In group A, subendocardial s by retroinfusion. RESULTS. In group A, subendocard 991 8294701 1 a to 11 +/- 5% during ischemia . In contrast, systolic dyskin 11 +/- 5% during ischemia. In contrast, systolic d 1122 8294701 0 d in group B (-2 +/- 4%, p < 0 . 001) and group C (-2 +/- 5%, group B (-2 +/- 4%, p < 0.001) and group C (-2 +/- 1198 8294701 0 and group C (-2 +/- 5%, p < 0 . 001). During ischemia, the de group C (-2 +/- 5%, p < 0.001). During ischemia, t 1233 8294701 1 group C (-2 +/- 5%, p < 0.001) . During ischemia, the decreas C (-2 +/- 5%, p < 0.001). During ischemia, the de 1238 8294701 0 unced in group A (41 +/- 15 vs . 27 +/- 12 mm Hg) than in gro in group A (41 +/- 15 vs. 27 +/- 12 mm Hg) than i 1348 8294701 0 than in group B (40 +/- 10 vs . 19 +/- 10 mm Hg, p = 0.1) or in group B (40 +/- 10 vs. 19 +/- 10 mm Hg, p = 0. 1396 8294701 0 10 vs. 19 +/- 10 mm Hg, p = 0 . 1) or group C (33 +/- 11 vs. s. 19 +/- 10 mm Hg, p = 0.1) or group C (33 +/- 11 1420 8294701 0 0.1) or group C (33 +/- 11 vs . 12 +/- 8 mm Hg, p = 0.002). or group C (33 +/- 11 vs. 12 +/- 8 mm Hg, p = 0.0 1448 8294701 0 - 11 vs. 12 +/- 8 mm Hg, p = 0 . 002). During ischemia, myocar vs. 12 +/- 8 mm Hg, p = 0.002). During ischemia, m 1471 8294701 1 vs. 12 +/- 8 mm Hg, p = 0.002) . During ischemia, myocardial 2 +/- 8 mm Hg, p = 0.002). During ischemia, myocar 1476 8294701 1 rved > 0 mm Hg only in group A . CONCLUSIONS. Preservation of > 0 mm Hg only in group A. CONCLUSIONS. Preservati 1568 8294701 1 g only in group A. CONCLUSIONS . Preservation of regional myo y in group A. CONCLUSIONS. Preservation of regiona 1581 8294701 1 venous retroperfusion in pigs . us retroperfusion in pigs. 1812 15050861 1 have been shown to be involved . Neural cell adhesion molecul been shown to be involved. Neural cell adhesion mo 121 15050861 1 dance, and synaptic plasticity . Disturbance of these neurode , and synaptic plasticity. Disturbance of these ne 271 15050861 1 one etiology for mood disorder . We therefore undertook genet tiology for mood disorder. We therefore undertook 368 15050861 1 sis of NCAM1 in mood disorders . METHODS: We determined the c f NCAM1 in mood disorders. METHODS: We determined 436 15050861 1 ning detected 11 polymorphisms . The genotypic, allelic, and detected 11 polymorphisms. The genotypic, allelic, 631 15050861 1 = 78), all from central Japan . RESULTS: Three single nucleo ), all from central Japan. RESULTS: Three single n 859 15050861 0 elic associations, nominal p = . 04, p =.02, and p =.004, resp associations, nominal p =.04, p =.02, and p =.004, 1044 15050861 0 ociations, nominal p =.04, p = . 02, and p =.004, respectively ions, nominal p =.04, p =.02, and p =.004, respect 1052 15050861 0 ominal p =.04, p =.02, and p = . 004, respectively, all p >.05 l p =.04, p =.02, and p =.004, respectively, all p 1064 15050861 0 p =.004, respectively, all p > . 05 after Bonferroni correctio 04, respectively, all p >.05 after Bonferroni corr 1091 15050861 1 after Bonferroni corrections) . Furthermore, the haplotype l r Bonferroni corrections). Furthermore, the haplot 1124 15050861 0 ant three-marker haplotype is . 005). CONCLUSIONS: Our result hree-marker haplotype is .005). CONCLUSIONS: Our r 1304 15050861 1 hree-marker haplotype is .005) . CONCLUSIONS: Our results sug marker haplotype is .005). CONCLUSIONS: Our result 1309 15050861 1 sorder in Japanese individuals . r in Japanese individuals. 1478 6849159 1 d after a 50 km marathon event . Ninety-five per cent of the er a 50 km marathon event. Ninety-five per cent of 124 6849159 0 hologically elevated values, i . e. CK-MB concentrations were ically elevated values, i.e. CK-MB concentrations 214 6849159 0 logically elevated values, i.e . CK-MB concentrations were el ally elevated values, i.e. CK-MB concentrations we 216 6849159 1 icative of myocardial necrosis . Results indicate that a rise ve of myocardial necrosis. Results indicate that a 319 6849159 1 common after marathon running . We therefore believe that ca on after marathon running. We therefore believe th 401 6849159 1 ng strenuous muscular exercise . renuous muscular exercise. 573 10946585 1 able for the control of action . Results from the five percep for the control of action. Results from the five p 167 10946585 1 argue against this assumption . Experiment 1 demonstrates th e against this assumption. Experiment 1 demonstrat 280 10946585 0 emonstrates that subliminal (0 . 8-2%) local changes in interv trates that subliminal (0.8-2%) local changes in i 326 10946585 1 of synchronized finger tapping . If this compensation is base nchronized finger tapping. If this compensation is 486 10946585 1 d the temporal order threshold . However, that hypothesis is temporal order threshold. However, that hypothesi 711 10946585 0 by additional analyses of Exp . 1 and the results of Exp. 2, dditional analyses of Exp. 1 and the results of Ex 780 10946585 0 Exp. 1 and the results of Exp . 2, a combined synchronizatio 1 and the results of Exp. 2, a combined synchroni 806 10946585 1 d temporal order judgment task . Experiments 3-5 further show poral order judgment task. Experiments 3-5 further 870 10946585 1 ations in synchronized tapping . Experiment 5, a combined syn s in synchronized tapping. Experiment 5, a combine 1075 10946585 1 t depend on explicit detection . Overall, the results suggest end on explicit detection. Overall, the results su 1233 10946585 1 of auditory temporal judgment . uditory temporal judgment. 1454 9914487 1 glutathione peroxidases (GPx) . In contrast to the more unif athione peroxidases (GPx). In contrast to the more 157 9914487 1 inst alimentary hydroperoxides . In order to get an idea of i alimentary hydroperoxides. In order to get an idea 425 9914487 1 hy of selenoprotein expression . The selenium-dependent expre selenoprotein expression. The selenium-dependent 551 9914487 1 tein in HepG2 and CaCo-2 cells . Furthermore, the selenocyste in HepG2 and CaCo-2 cells. Furthermore, the seleno 711 9914487 1 and baby hamster kidney cells . GI-GPx mRNA levels increased baby hamster kidney cells. GI-GPx mRNA levels incr 981 9914487 1 els remained almost unaffected . In cells grown in selenium-p emained almost unaffected. In cells grown in selen 1123 9914487 1 and immunochemical reactivity . Upon selenium repletion immu immunochemical reactivity. Upon selenium repletion 1233 9914487 1 ts maximum level before 3 days . SECIS efficiencies decreased ximum level before 3 days. SECIS efficiencies decr 1413 9914487 1 he order PHGPx > cGPx > GI-GPx . The augmentation of SECIS ef der PHGPx > cGPx > GI-GPx. The augmentation of SEC 1478 9914487 1 eas it was marginal for GI-GPx . The high mRNA stability unde t was marginal for GI-GPx. The high mRNA stability 1614 9914487 1 in the gastrointestinal tract . he gastrointestinal tract. 1934 15081931 1 PIs) atazanavir and tipranavir . The sample pre-treatment con atazanavir and tipranavir. The sample pre-treatmen 220 15081931 1 r and 50 microl for tipranavir . Chromatographic separation w 50 microl for tipranavir. Chromatographic separat 394 15081931 0 nertsil ODS3 column (50 mm x 2 . 0 mm i.d., particle size 5 mi il ODS3 column (50 mm x 2.0 mm i.d., particle size 473 15081931 0 ODS3 column (50 mm x 2.0 mm i . d., particle size 5 microm), column (50 mm x 2.0 mm i.d., particle size 5 micr 480 15081931 0 DS3 column (50 mm x 2.0 mm i.d . , particle size 5 microm), wi olumn (50 mm x 2.0 mm i.d., particle size 5 microm 482 15081931 0 methanol, at a flow rate of 0 . 5 ml/min. The analytical run anol, at a flow rate of 0.5 ml/min. The analytical 605 15081931 1 , at a flow rate of 0.5 ml/min . The analytical run time was a flow rate of 0.5 ml/min. The analytical run time 614 15081931 0 The analytical run time was 5 . 5 min. The triple quadrupole analytical run time was 5.5 min. The triple quadru 645 15081931 1 nalytical run time was 5.5 min . The triple quadrupole mass s ical run time was 5.5 min. The triple quadrupole m 651 15081931 1 s used for drug quantification . The assay was linear over a d for drug quantification. The assay was linear ov 798 15081931 0 ver a concentration range of 0 . 05-10 microg/ml for atazanavi concentration range of 0.05-10 microg/ml for ataz 852 15081931 0 microg/ml for atazanavir and 0 . 1-75 microg/ml for tipranavir g/ml for atazanavir and 0.1-75 microg/ml for tipra 889 15081931 1 .1-75 microg/ml for tipranavir . Saquinavir-d5 was used as in microg/ml for tipranavir. Saquinavir-d5 was used 919 15081931 1 was used as internal standard . The intra- and inter-day coe used as internal standard. The intra- and inter-da 964 15081931 0 of variation were less than 3 . 8% for atazanavir and less th ariation were less than 3.8% for atazanavir and le 1033 15081931 0 or atazanavir and less than 10 . 4% for tipranavir. Accuracies azanavir and less than 10.4% for tipranavir. Accur 1068 15081931 1 less than 10.4% for tipranavir . Accuracies were within +/-7. than 10.4% for tipranavir. Accuracies were within 1086 15081931 0 r. Accuracies were within +/-7 . 3 and +/-7.2% for atazanavir curacies were within +/-7.3 and +/-7.2% for atazan 1115 15081931 0 es were within +/-7.3 and +/-7 . 2% for atazanavir and tiprana re within +/-7.3 and +/-7.2% for atazanavir and ti 1126 15081931 1 r and tipranavir, respectively . Both drugs were stable under tipranavir, respectively. Both drugs were stable 1173 15081931 1 us relevant storage conditions . The validated concentration levant storage conditions. The validated concentra 1239 15081931 1 1 (HIV-1)-infected individuals . The developed method could e V-1)-infected individuals. The developed method co 1391 15081931 1 ication of protease inhibitors . on of protease inhibitors. 1527 9370936 1 tal role in viral pathogenesis . We show here that cytomegalo ole in viral pathogenesis. We show here that cytom 216 9370936 1 th the mRNA and protein levels . Increased IL-8 production wa e mRNA and protein levels. Increased IL-8 producti 425 9370936 1 cal CMV isolates Toledo or C1F . The increase in IL-8 product MV isolates Toledo or C1F. The increase in IL-8 pr 613 9370936 1 hil transendothelial migration . The latter was independent o ransendothelial migration. The latter was independ 815 9370936 1 g antibodies specific for IL-8 . Direct infection of endothel ibodies specific for IL-8. Direct infection of end 979 9370936 1 hil transendothelial migration . Neutrophils play an importan ransendothelial migration. Neutrophils play an imp 1126 9370936 1 d to enhance CMV dissemination . Increased production of chem enhance CMV dissemination. Increased production of 1302 9370936 1 ally contributing to pathology . contributing to pathology. 1505 12513828 1 and patients were investigated . To better understand how com atients were investigated. To better understand ho 320 12513828 1 ony formation and self-renewal . Based on granulocyte colony- ormation and self-renewal. Based on granulocyte co 576 12513828 1 ny-stimulating factor (GM-CSF) . The results revealed that: 1 imulating factor (GM-CSF). The results revealed th 847 12513828 0 . The results revealed that: 1 . BFU-E derived from PBPCs pro results revealed that: 1. BFU-E derived from PBPC 877 12513828 1 PO+SCF compared with EPO alone . 2. Compared patients to norm F compared with EPO alone. 2. Compared patients to 1044 12513828 0 SCF compared with EPO alone. 2 . Compared patients to normal ompared with EPO alone. 2. Compared patients to no 1047 12513828 0 ced after EPO plus SCF or IL-3 . 3. There was a significantly fter EPO plus SCF or IL-3. 3. There was a signific 1163 12513828 1 after EPO plus SCF or IL-3. 3 . There was a significantly in r EPO plus SCF or IL-3. 3. There was a significant 1166 12513828 1 used in conjunction with G-CSF . Comparing the frequencies of in conjunction with G-CSF. Comparing the frequenci 1295 12513828 0 lly to G-CSF alone than donors . 4. There was a significant i o G-CSF alone than donors. 4. There was a signific 1477 12513828 1 to G-CSF alone than donors. 4 . There was a significant incr -CSF alone than donors. 4. There was a significant 1480 12513828 1 combined with other cytokines . GMix was identified as the o ined with other cytokines. GMix was identified as 1625 12513828 0 of clonogenic progenitor cells . 5. Donors have a high AUC th onogenic progenitor cells. 5. Donors have a high A 1775 12513828 1 clonogenic progenitor cells. 5 . Donors have a high AUC than genic progenitor cells. 5. Donors have a high AUC 1778 12513828 0 ease AUC in G-CSF alone (P = 0 . 0067). AUC in G-CSF alone (P = 0.0067). 1887 12513828 1 UC in G-CSF alone (P = 0.0067) . G-CSF alone (P = 0.0067). 1893 7881554 1 phalosporin C and cephamycin C . We characterized a wild-type sporin C and cephamycin C. We characterized a wild 128 7881554 1 sopenicillin N synthase (IPNS) . L-Lysine epsilon-aminotransf icillin N synthase (IPNS). L-Lysine epsilon-aminot 437 7881554 1 hat strain NP1 is a lat mutant . NP1 recovered LAT, ACVS and train NP1 is a lat mutant. NP1 recovered LAT, ACVS 561 7881554 1 sformed with the cloned region . DNA sequencing showed that t ed with the cloned region. DNA sequencing showed t 646 7881554 1 half of the ACVS gene (pcbAB) . The activities of ACVS and I of the ACVS gene (pcbAB). The activities of ACVS 882 7881554 1 to depend upon LAT expression . Gene fusions constructed to epend upon LAT expression. Gene fusions constructe 952 7881554 1 for LAT, ACVS and IPNS (pcbC) . LAT, ACVS and IPNS (pcbC). 1130 9553393 1 and bedridden elderly persons . The subjects were 149 person bedridden elderly persons. The subjects were 149 p 139 9553393 1 alth and welfare organizations . All of the subjects had a fa and welfare organizations. All of the subjects had 320 9553393 1 residence or own room at home . A follow-up study of admissi dence or own room at home. A follow-up study of ad 408 9553393 1 as performed from 1991 to 1996 . The main results were as fol rformed from 1991 to 1996. The main results were a 490 9553393 0 ain results were as follows: 1 . During the study (about 5 ye esults were as follows: 1. During the study (about 527 9553393 1 the study (about 5 years), 42 . 9% (N = 64) of subjects were study (about 5 years), 42.9% (N = 64) of subjects 565 9553393 0 jects were staying at home, 38 . 9% (N = 58) died at home, and were staying at home, 38.9% (N = 58) died at home 614 9553393 0 (N = 58) died at home, and 16 . 8% (N = 25) were admitted to 58) died at home, and 16.8% (N = 25) were admitte 647 9553393 0 were admitted to nursing homes . 2. To find factors influenci admitted to nursing homes. 2. To find factors infl 690 9553393 1 e admitted to nursing homes. 2 . To find factors influencing itted to nursing homes. 2. To find factors influen 693 9553393 1 al, hazard model was conducted . Major factors found were hig azard model was conducted. Major factors found wer 813 9553393 1 nd difficulty in communication . The admission rate to nursin fficulty in communication. The admission rate to n 926 9553393 0 nts 90 years of age or greater . 3. The admission rate to nur 0 years of age or greater. 3. The admission rate t 1025 9553393 1 90 years of age or greater. 3 . The admission rate to nursin ears of age or greater. 3. The admission rate to n 1028 9553393 0 pared to the rest of the group . 4. Remarkable differences in to the rest of the group. 4. Remarkable differenc 1151 9553393 1 ed to the rest of the group. 4 . Remarkable differences in ho the rest of the group. 4. Remarkable differences 1154 9553393 1 hose admitted to nursing homes . Among the subjects living al admitted to nursing homes. Among the subjects livi 1297 9553393 1 mes than those staying at home . In the case of two or three- han those staying at home. In the case of two or t 1468 9553393 1 he household lacked caregivers . usehold lacked caregivers. 1602 12150483 1 relies upon T-cell reactivity . Hence, most studies on antim es upon T-cell reactivity. Hence, most studies on 153 12150483 1 r role in disease pathogenesis . OBJECTIVE: To determine the e in disease pathogenesis. OBJECTIVE: To determine 304 12150483 1 h some features of the disease . DESIGN: Study of the profile e features of the disease. DESIGN: Study of the pr 486 12150483 1 hole culture filtrate proteins . Correlation of immunoblot an culture filtrate proteins. Correlation of immunobl 639 12150483 1 ing, and response to treatment . RESULTS: On immunoblot, band and response to treatment. RESULTS: On immunoblot, 796 12150483 0 32 kDa, antigen 85 complex (45 . 8% of serum samples). ELISA w a, antigen 85 complex (45.8% of serum samples). EL 936 12150483 1 mplex (45.8% of serum samples) . ELISA with this antigen show (45.8% of serum samples). ELISA with this antigen 957 12150483 1 72% and a specificity of 100% . Positive antibody titers to and a specificity of 100%. Positive antibody titer 1036 12150483 0 rs to Ag85 were observed in 79 . 4% of patients with non-cavit Ag85 were observed in 79.4% of patients with non- 1090 12150483 0 n-cavitary tuberculosis (P = 0 . 012) and in 95.8% of patients itary tuberculosis (P = 0.012) and in 95.8% of pat 1143 12150483 0 rculosis (P = 0.012) and in 95 . 8% of patients who were cured sis (P = 0.012) and in 95.8% of patients who were 1158 12150483 0 berculosis chemotherapy (P = 0 . 0001). By contrast, an antibo losis chemotherapy (P = 0.0001). By contrast, an a 1231 12150483 1 osis chemotherapy (P = 0.0001) . By contrast, an antibody res chemotherapy (P = 0.0001). By contrast, an antibod 1237 12150483 1 cavitations or with prognosis . CONCLUSIONS: Our data show t tations or with prognosis. CONCLUSIONS: Our data s 1377 12150483 1 of tuberculous Mexican Indians . berculous Mexican Indians. 1602 9486565 0 most common human cytokeratins . i.e., Nos. 8, 18, and 19, in common human cytokeratins. i.e., Nos. 8, 18, and 1 103 9486565 0 t common human cytokeratins. i . e., Nos. 8, 18, and 19, in ep mon human cytokeratins. i.e., Nos. 8, 18, and 19, 106 9486565 0 common human cytokeratins. i.e . , Nos. 8, 18, and 19, in epit n human cytokeratins. i.e., Nos. 8, 18, and 19, in 108 9486565 0 human cytokeratins. i.e., Nos . 8, 18, and 19, in epithelial n cytokeratins. i.e., Nos. 8, 18, and 19, in epith 114 9486565 1 ted in the ISOBM TD-5 Workshop . Seven research groups from u n the ISOBM TD-5 Workshop. Seven research groups f 195 9486565 1 of the antibody specificities . The complex assembly of cyto he antibody specificities. The complex assembly of 324 9486565 1 single cytokeratins necessary . The concordance of the evalu le cytokeratins necessary. The concordance of the 644 9486565 1 ndent of the technologies used . As antigens purified individ of the technologies used. As antigens purified in 734 9486565 1 zed shorter peptides were used . In order to elucidate the ep horter peptides were used. In order to elucidate t 930 9486565 1 of the antigens were performed . Competitive cross-inhibition e antigens were performed. Competitive cross-inhib 1096 9486565 1 BIAcore, and ELISA technology . All 30 antibodies could conv ore, and ELISA technology. All 30 antibodies could 1292 9486565 1 h regard to target cytokeratin . One MAb (192) had to be dele ard to target cytokeratin. One MAb (192) had to be 1378 9486565 1 specificity against its target . Six antibodies bound selecti ficity against its target. Six antibodies bound se 1496 9486565 1 nant, and synthesized antigens . The immunodominant part of t and synthesized antigens. The immunodominant part 1667 9486565 1 ion of amino acid (aa) 270-400 . Out of the six MAbs reactive f amino acid (aa) 270-400. Out of the six MAbs rea 1797 9486565 0 th cytokeratin 8, four MAbs, i . e., 178, 199, 202, and 206, w tokeratin 8, four MAbs, i.e., 178, 199, 202, and 2 1860 9486565 0 cytokeratin 8, four MAbs, i.e . , 178, 199, 202, and 206, wer keratin 8, four MAbs, i.e., 178, 199, 202, and 206 1862 9486565 1 with a closely related epitope . The remaining antibody, 192, a closely related epitope. The remaining antibody, 1997 9486565 1 , presented dual specificities . At least two closely related sented dual specificities. At least two closely re 2056 9486565 1 be identified in cytokeratin 8 . In cytokeratin 18 four disti entified in cytokeratin 8. In cytokeratin 18 four 2150 9486565 1 and 200) out of 14 antibodies . Since MAb 193 is known to re 200) out of 14 antibodies. Since MAb 193 is known 2356 9486565 1 s shown by competitive binding . The remaining four anticytok wn by competitive binding. The remaining four anti 2579 9486565 1 itive binding to this filament . Cytokeratin 19, reactive wit binding to this filament. Cytokeratin 19, reactiv 2712 9486565 1 he large immunodominant region . MAbs 179, 195, 197, and 204 rge immunodominant region. MAbs 179, 195, 197, and 2856 9486565 0 11-335 also known as the KS 19 . 1 epitope, and MAbs 182, 183, 5 also known as the KS 19.1 epitope, and MAbs 182, 2952 9486565 0 aa 346-367, known as the BM 19 . 21 epitope. One antibody, 231 6-367, known as the BM 19.21 epitope. One antibody 3048 9486565 1 known as the BM 19.21 epitope . One antibody, 231, was selec n as the BM 19.21 epitope. One antibody, 231, was 3059 9486565 1 h aa 356-370 in cytokeratin 19 . A complex pattern of binding 356-370 in cytokeratin 19. A complex pattern of bi 3138 9486565 1 ee cytokeratins was documented . Out of the 29 classifiable a tokeratins was documented. Out of the 29 classifia 3376 9486565 0 e in this very short region, i . e., from aa 311 to 370 in all this very short region, i.e., from aa 311 to 370 i 3473 9486565 0 in this very short region, i.e . , from aa 311 to 370 in all c is very short region, i.e., from aa 311 to 370 in 3475 9486565 1 0 in all cytokeratin filaments . The remaining seven antibodi all cytokeratin filaments. The remaining seven ant 3525 9486565 1 ayed unique binding properties . The implications of the find unique binding properties. The implications of the 3593 9486565 1 od for tumor marker evaluation . r tumor marker evaluation. 3797 12408923 1 in a topical cream formulation . Sample preparation involves topical cream formulation. Sample preparation invo 207 12408923 1 xtraction prior to LC analysis . The method uses a Hypersil C tion prior to LC analysis. The method uses a Hyper 282 12408923 0 C(18) BDS, 5 micrometer, 250x4 . 6 mm I.D. column maintained a BDS, 5 micrometer, 250x4.6 mm I.D. column maintai 341 12408923 0 DS, 5 micrometer, 250x4.6 mm I . D. column maintained at 35 de micrometer, 250x4.6 mm I.D. column maintained at 348 12408923 0 , 5 micrometer, 250x4.6 mm I.D . column maintained at 35 degr icrometer, 250x4.6 mm I.D. column maintained at 35 350 12408923 1 umn maintained at 35 degrees C . The mobile phase comprises m aintained at 35 degrees C. The mobile phase compri 385 12408923 0 , v/v/v/v) at a flow rate of 1 . 0 ml/min. Robustness was eval /v/v) at a flow rate of 1.0 ml/min. Robustness was 507 12408923 1 ) at a flow rate of 1.0 ml/min . Robustness was evaluated by a flow rate of 1.0 ml/min. Robustness was evaluate 516 12408923 1 entred design (CCF) experiment . The method shows good select d design (CCF) experiment. The method shows good s 613 12408923 1 sensitivity and repeatability . The conditions allow the sep itivity and repeatability. The conditions allow th 690 12408923 1 stances contained in the cream . es contained in the cream. 829 11342960 0 . oncofetal antigen-immature l PURPOSE: The 32 to 44 kDa. oncofetal antigen-immat 25 11342960 1 carcinoma as well as lymphoma . OFA-iLR has been implicated inoma as well as lymphoma. OFA-iLR has been implic 211 11342960 1 iveness, metastasis and growth . Interferon-gamma producing e ss, metastasis and growth. Interferon-gamma produc 285 11342960 1 or OFA-iLR have been described . MATERIALS AND METHODS: The 4 A-iLR have been described. MATERIALS AND METHODS: 424 11342960 1 w cytometry and immunoblotting . Spontaneous or therapy induc ometry and immunoblotting. Spontaneous or therapy 609 11342960 1 etastatic renal cell carcinoma . Proliferative and cytokine ( atic renal cell carcinoma. Proliferative and cytok 739 11342960 1 ombinant OFA-iLR were assessed . RESULTS: Using flow cytometr ant OFA-iLR were assessed. RESULTS: Using flow cyt 926 11342960 1 tected in all 13 tumors tested . Immunoblotting revealed diff d in all 13 tumors tested. Immunoblotting revealed 1002 11342960 1 inoma and normal kidney tissue . OFA-iLR specific proliferati and normal kidney tissue. OFA-iLR specific prolif 1110 11342960 1 ected in all 6 patients tested . Importantly evidence was als in all 6 patients tested. Importantly evidence wa 1225 11342960 1 ance OFA-iLR specific immunity . CONCLUSIONS: This study demo OFA-iLR specific immunity. CONCLUSIONS: This study 1392 11342960 1 in human renal cell carcinoma . OFA-iLR specific effector T uman renal cell carcinoma. OFA-iLR specific effect 1516 11342960 1 e and, thus, tumor progression . , thus, tumor progression. 1726 12798100 1 moss species as bioindicators . Our research was part of an species as bioindicators. Our research was part o 129 12798100 1 lution by standardized methods . Sampling was performed at 11 n by standardized methods. Sampling was performed 425 12798100 1 Hungary in the autumn of 1997 . Moss species of Hypnum cupre ary in the autumn of 1997. Moss species of Hypnum 509 12798100 0 es of Hypnum cupressiforme (72 . 4%) were preferred. But where Hypnum cupressiforme (72.4%) were preferred. But 551 12798100 1 siforme (72.4%) were preferred . But where it could not be co me (72.4%) were preferred. But where it could not 570 12798100 1 cted, other species were taken . Unwashed, dried samples were other species were taken. Unwashed, dried samples 633 12798100 1 als were determined by ICP-AES . The results reflect local em ere determined by ICP-AES. The results reflect loc 760 12798100 1 reflect local emission points . Background mean levels of Cd ect local emission points. Background mean levels 803 12798100 1 European means [NORD 9 (1994)] . Probably, that was due not o ean means [NORD 9 (1994)]. Probably, that was due 913 12798100 1 tals compared to other species . The results are presented on compared to other species. The results are present 1085 12798100 0 R program (Golden Software Inc . Co). gram (Golden Software Inc. Co). 1190 12798100 1 gram (Golden Software Inc. Co) . (Golden Software Inc. Co). 1195 7751246 1 s a modified-live BRSV vaccine . Ninety mixed-breed, 5- to 6- odified-live BRSV vaccine. Ninety mixed-breed, 5- 193 7751246 1 6 groups with 15 animals/group . Calves in 5 of the groups we ups with 15 animals/group. Calves in 5 of the grou 306 7751246 1 a modified-live virus vaccine . The remaining 15 calves were dified-live virus vaccine. The remaining 15 calves 443 7751246 1 ained as unvaccinated controls . Immune responses were measur as unvaccinated controls. Immune responses were m 509 7751246 1 lymphocyte blastogenesis assay . All vaccines induced product ocyte blastogenesis assay. All vaccines induced pr 705 7751246 1 he modified-live virus vaccine . All of the vaccines induced dified-live virus vaccine. All of the vaccines ind 1045 7751246 1 roliferative responses to BRSV . Results suggest that commerc erative responses to BRSV. Results suggest that co 1117 7751246 1 antibodies in immunized cattle . odies in immunized cattle. 1344 8508764 1 ochondrial intermembrane space . The role of the second sorti drial intermembrane space. The role of the second 251 8508764 1 residues or an acidic residue . With a number of these mutan dues or an acidic residue. With a number of these 498 8508764 1 g to the matrix space occurred . The accumulation in the matr the matrix space occurred. The accumulation in the 675 8508764 1 evel of intramitochondrial ATP . At low levels of matrix ATP, of intramitochondrial ATP. At low levels of matrix 758 8508764 1 like the wild-type precursors . The results: (i) suggest the the wild-type precursors. The results: (i) sugges 879 8508764 1 ic phase of the inner membrane . ase of the inner membrane. 1471 7440272 1 ring a breath-holding interval . DLCO measured during a slow a breath-holding interval. DLCO measured during a 146 7440272 1 C) does not vary as VA changes . Since VA is reached by inhal es not vary as VA changes. Since VA is reached by 283 7440272 1 O and VA was due to hysteresis . To test this hypothesis, bre VA was due to hysteresis. To test this hypothesis 486 7440272 1 s reached by exhaling from TLC . At 72% TLC, DLCO was 22% hig ched by exhaling from TLC. At 72% TLC, DLCO was 22 689 7440272 0 compared to inhalation (P < 0 . 02). At 52% TLC, DLCO was 19% ared to inhalation (P < 0.02). At 52% TLC, DLCO wa 786 7440272 1 pared to inhalation (P < 0.02) . At 52% TLC, DLCO was 19% hig to inhalation (P < 0.02). At 52% TLC, DLCO was 19 790 7440272 0 compared to exhalation (P < 0 . 005). DCLO measured during a ared to exhalation (P < 0.005). DCLO measured duri 887 7440272 1 ared to exhalation (P < 0.005) . DCLO measured during a slow to exhalation (P < 0.005). DCLO measured during a 892 7440272 0 tion limb of the CLCO/VA curve . these data indicate that the limb of the CLCO/VA curve. these data indicate tha 981 7440272 1 CO with respect to lung volume . th respect to lung volume. 1063 9862795 1 cular devices and biomaterials . A limitation of some protein devices and biomaterials. A limitation of some pr 237 9862795 1 guishable recognition surfaces . Here, we have explored metho able recognition surfaces. Here, we have explored 364 9862795 1 seful self-assembly properties . RESULTS: Escherichia coli gl self-assembly properties. RESULTS: Escherichia co 494 9862795 1 two symmetry-related surfaces . These histidines drive a met symmetry-related surfaces. These histidines drive 619 9862795 1 dent self-assembly of GS tubes . Immobilization of GS on the self-assembly of GS tubes. Immobilization of GS on 687 9862795 1 ng and atomic force microscopy . The utility of Ni2+-NTA as a d atomic force microscopy. The utility of Ni2+-NTA 998 9862795 1 cent to the natural histidines . CONCLUSIONS: Current genetic to the natural histidines. CONCLUSIONS: Current ge 1151 9862795 1 iologically assembled proteins . Ni2+-NTA serves as a mask to ically assembled proteins. Ni2+-NTA serves as a ma 1305 9862795 1 containing functional His-tags . This strategy may be extende ining functional His-tags. This strategy may be ex 1460 9862795 1 cids with a myriad of reagents . with a myriad of reagents. 1564 15280361 1 ified as core and mannan types . The former contain 13-14 man as core and mannan types. The former contain 13-1 100 15280361 1 ss known as hyperglycosylation . The selection of substrates own as hyperglycosylation. The selection of substr 285 15280361 1 retical and practical question . To identify hyperglycosylati al and practical question. To identify hyperglycos 380 15280361 1 major exoglucanase as a model . Our results indicate that ne r exoglucanase as a model. Our results indicate th 558 15280361 1 harged counterparts promote it . On the basis of the tridimen d counterparts promote it. On the basis of the tri 695 15280361 1 addition of alpha-1,6-mannoses . The presence of Glu in the X ion of alpha-1,6-mannoses. The presence of Glu in 926 15280361 1 drive evolution of these sites . However, a comparison of inv evolution of these sites. However, a comparison o 1074 15280361 0 on of invertases secreted by S . cerevisiae and Pichia anomal invertases secreted by S. cerevisiae and Pichia a 1125 15280361 1 ubjected to positive selection . ted to positive selection. 1238 10920365 1 ionization (TurboIonSpray(R)) . Chromatographic separation i zation (TurboIonSpray(R)). Chromatographic separat 400 10920365 0 th a mobile phase containing 0 . 25% water only. The total run mobile phase containing 0.25% water only. The tota 505 10920365 1 se containing 0.25% water only . The total run time per sampl ntaining 0.25% water only. The total run time per 520 10920365 0 otal run time per sample is 11 . 0 min giving chromatographic run time per sample is 11.0 min giving chromatogra 557 10920365 1 separation of the enantiomers . Compared with previous metho ration of the enantiomers. Compared with previous 626 10920365 1 gedness and higher sensitivity . The limits of quantification ss and higher sensitivity. The limits of quantific 748 10920365 0 tion for each enantiomer are 5 . 00 microg/L from 0.5 mL whole for each enantiomer are 5.00 microg/L from 0.5 mL 804 10920365 0 iomer are 5.00 microg/L from 0 . 5 mL whole blood and 7.50 ng/ are 5.00 microg/L from 0.5 mL whole blood and 7.5 823 10920365 0 from 0.5 mL whole blood and 7 . 50 ng/g (ppb) using 0.333 g b 0.5 mL whole blood and 7.50 ng/g (ppb) using 0.33 846 10920365 0 od and 7.50 ng/g (ppb) using 0 . 333 g brain tissue, respectiv d 7.50 ng/g (ppb) using 0.333 g brain tissue, resp 868 10920365 1 3 g brain tissue, respectively . Similar assay specifications rain tissue, respectively. Similar assay specifica 901 10920365 1 erived for the two enantiomers . The method has been validate d for the two enantiomers. The method has been val 973 10920365 0 alytical working ranges like e . g. 5.00 to 1000 microg/L and cal working ranges like e.g. 5.00 to 1000 microg/L 1171 10920365 0 ytical working ranges like e.g . 5.00 to 1000 microg/L and 20 l working ranges like e.g. 5.00 to 1000 microg/L a 1173 10920365 0 cal working ranges like e.g. 5 . 00 to 1000 microg/L and 200 t orking ranges like e.g. 5.00 to 1000 microg/L and 1176 10920365 0 L and 200 to 40000 microg/L (0 . 200 to 40.0 mg/L). For rat b 200 to 40000 microg/L (0. 200 to 40.0 mg/L). For 1225 10920365 0 o 40000 microg/L (0. 200 to 40 . 0 mg/L). For rat brain tissue 00 microg/L (0. 200 to 40.0 mg/L). For rat brain t 1236 10920365 1 microg/L (0. 200 to 40.0 mg/L) . For rat brain tissue the val g/L (0. 200 to 40.0 mg/L). For rat brain tissue th 1244 10920365 0 dated concentration range is 7 . 50 to 750 ng/g (ppb). concentration range is 7.50 to 750 ng/g (ppb). 1305 10920365 1 ange is 7.50 to 750 ng/g (ppb) . is 7.50 to 750 ng/g (ppb). 1326 9704450 1 ot be used as blood substitute . Hemoglobin has to be modifie used as blood substitute. Hemoglobin has to be mo 90 9704450 1 er molecularly or encapsulated . First generation molecularly lecularly or encapsulated. First generation molecu 156 9704450 1 nical trial--some in Phase III . There are a number of these. trial--some in Phase III. There are a number of t 262 9704450 1 I. There are a number of these . Polyhemoglobin is formed by ere are a number of these. Polyhemoglobin is forme 291 9704450 1 lecularly and intramolecularly . A crosslinked single hemoglo arly and intramolecularly. A crosslinked single he 392 9704450 1 ng hemoglobin intramolecularly . Recombinant hemoglobin from moglobin intramolecularly. Recombinant hemoglobin 488 9704450 0 Recombinant hemoglobin from E . coli is formed by fusion of t mbinant hemoglobin from E.coli is formed by fusion 519 9704450 1 ts of each hemoglobin molecule . Conjugated hemoglobin is for each hemoglobin molecule. Conjugated hemoglobin i 588 9704450 1 n molecule to soluble polymers . A second generation system f ecule to soluble polymers. A second generation sys 682 9704450 1 se-catalase is being developed . A third generation hemoglobi talase is being developed. A third generation hemo 793 9704450 1 mble a complete red blood cell . a complete red blood cell. 970 11883643 1 id-potential local anesthetics . The relationships between th tential local anesthetics. The relationships betwe 154 11883643 1 nd excised human skin in vitro . METHODS: The extent and mech cised human skin in vitro. METHODS: The extent and 412 11883643 1 ral-to-apical (b-a) directions . The MTT test was performed t o-apical (b-a) directions. The MTT test was perfor 598 11883643 1 d to determine cellular damage . In vitro transdermal permeab determine cellular damage. In vitro transdermal pe 655 11883643 1 by using side-by-side chambers . Passive diffusion and iontop ing side-by-side chambers. Passive diffusion and i 790 11883643 1 ced permeability were measured . RESULTS: In Caco-2 monolayer ermeability were measured. RESULTS: In Caco-2 mono 867 11883643 1 btained for the two directions . In the b-a direction, the va ed for the two directions. In the b-a direction, t 992 11883643 1 ater than in the a-b direction . A plot of drug permeability than in the a-b direction. A plot of drug permeabi 1099 11883643 0 A plot of drug permeability vs . the number of carbons in the t of drug permeability vs. the number of carbons i 1131 11883643 1 sing lipophilicity of the drug . If the log D(oct) of the est lipophilicity of the drug. If the log D(oct) of th 1273 11883643 0 oct) of the ester was > or = 3 . 4 and the MW > 385 Da, no mea of the ester was > or = 3.4 and the MW > 385 Da, n 1318 11883643 1 Caco-2 permeability was found . Cell damage was also higher -2 permeability was found. Cell damage was also hi 1385 11883643 1 the more lipophilic compounds . In excised human skin, the r more lipophilic compounds. In excised human skin, 1447 11883643 0 oxychain was parabolic (r2 = 0 . 95). Introducing low-level el ain was parabolic (r2 = 0.95). Introducing low-lev 1598 11883643 1 hain was parabolic (r2 = 0.95) . Introducing low-level electr was parabolic (r2 = 0.95). Introducing low-level e 1602 11883643 1 acid esters increased clearly . CONCLUSIONS: Lipophilicity a esters increased clearly. CONCLUSIONS: Lipophilic 1755 11883643 1 oles in the permeation process . A very high lipophilicity ha in the permeation process. A very high lipophilici 1857 11883643 1 intestinally and transdermally . Iontophoresis significantly tinally and transdermally. Iontophoresis significa 1976 11883643 1 and less lipophilic compounds . less lipophilic compounds. 2068 9201890 0 ed with Anopheles albitarsis s . l. catches mainly performed t th Anopheles albitarsis s.l. catches mainly perfor 44 9201890 0 with Anopheles albitarsis s.l . catches mainly performed thr Anopheles albitarsis s.l. catches mainly performe 46 9201890 1 ion, SP (Brazil), are reported . Two species of the complex w SP (Brazil), are reported. Two species of the comp 147 9201890 0 lex were recognized, namely An . albitarsis s.s. and species ere recognized, namely An. albitarsis s.s. and spe 202 9201890 0 nized, namely An. albitarsis s . s. and species B. This latter , namely An. albitarsis s.s. and species B. This l 216 9201890 0 zed, namely An. albitarsis s.s . and species B. This latter p namely An. albitarsis s.s. and species B. This lat 218 9201890 1 albitarsis s.s. and species B . This latter predominated bot tarsis s.s. and species B. This latter predominate 233 9201890 1 d in the dwelling environments . The crepuscular rhythms show the dwelling environments. The crepuscular rhythms 316 9201890 1 ing females caught during dusk . The absence of differences b emales caught during dusk. The absence of differen 426 9201890 1 or both species of the complex . th species of the complex. 536 8066445 1 the hosts and their parasites . The overall rate of nucleoti hosts and their parasites. The overall rate of nuc 265 8066445 1 r of magnitude greater in lice . The difference in synonymous magnitude greater in lice. The difference in synon 537 8066445 1 magnitude in generation times . itude in generation times. 680 15172865 1 current early pregnancy losses . We report pregnancy outcome nt early pregnancy losses. We report pregnancy out 202 15172865 1 l controls followed from birth . METHODS: The outcomes of 94 trols followed from birth. METHODS: The outcomes o 387 15172865 1 study from birth are presented . Outcome measures included th from birth are presented. Outcome measures includ 530 15172865 1 cy, and maternal complications . Possible predictors of low b nd maternal complications. Possible predictors of 656 15172865 1 low birth weight are assessed . Outcomes were compared by th birth weight are assessed. Outcomes were compared 710 15172865 1 her exact test, as appropriate . Correction was made for mult xact test, as appropriate. Correction was made for 868 15172865 1 d for analysis of birth weight . RESULTS: Compared with contr analysis of birth weight. RESULTS: Compared with 980 15172865 0 later menarche (median age 15 . 4 versus 13.0 years) and firs r menarche (median age 15.4 versus 13.0 years) and 1060 15172865 0 che (median age 15.4 versus 13 . 0 years) and first pregnancy median age 15.4 versus 13.0 years) and first pregn 1072 15172865 0 first pregnancy (median age 23 . 7 versus 20.1 years), and mor pregnancy (median age 23.7 versus 20.1 years), an 1116 15172865 0 ncy (median age 23.7 versus 20 . 1 years), and more spontaneou median age 23.7 versus 20.1 years), and more spont 1128 15172865 1 ous abortions (36% versus 10%) . Babies of SS subjects had a bortions (36% versus 10%). Babies of SS subjects h 1186 15172865 0 d a lower gestational age (P < . 001) and lower birth weight ( ower gestational age (P <.001) and lower birth wei 1242 15172865 0 1) and lower birth weight (P < . 001), the latter being signif d lower birth weight (P <.001), the latter being s 1275 15172865 1 le-related events in pregnancy . There was no difference in p lated events in pregnancy. There was no difference 1359 15172865 0 bjects (Fisher exact test, P = . 007 after adjustment for mult s (Fisher exact test, P =.007 after adjustment for 1563 15172865 1 justment for multiple testing) . Two SS subjects died, a mort ent for multiple testing). Two SS subjects died, a 1606 15172865 0 ts died, a mortality rate of 2 . 1%. CONCLUSION: The increased ed, a mortality rate of 2.1%. CONCLUSION: The incr 1651 15172865 1 died, a mortality rate of 2.1% . CONCLUSION: The increased fe a mortality rate of 2.1%. CONCLUSION: The increas 1654 15172865 1 ckle cell disease is confirmed . LEVEL OF EVIDENCE: II-2 cell disease is confirmed. LEVEL OF EVIDENCE: II-2 1775