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41.
湖南省9县市人群钩端螺旋体抗体水平分析 总被引:1,自引:0,他引:1
目的试图从9县市人群钩端螺旋体抗体水平探析钩体主要流行群和隐性与显性感染比例。方法选择以前钩体病发病率较高的9县市中无钩体疫苗接种史的10~65岁常住村民1240人作为对象,于流行高峰前采取外周静脉血,按国家标准方法做显微镜凝集试验(MAT)测15群15型钩体抗体;用SPSS统计软件进行统计学分析。结果9县13群钩体抗体的阳性率和隐性感染率差异有统计学意义的分别有9群(黄疸出血、拜伦、澳洲、流感伤寒、波摩那、秋季、犬群、七日热和曼耗)和3群(黄疸出血、澳洲和波摩那)。交叉阳性率差异亦有统计学意义,最高为湘潭(80.39%)、最低为南县(36.17%)。黄疸出血群隐感率最高为湘潭(38.24%)、最低系岳阳(1.60%)。以黄疸出血群抗体滴度1:≥80为标准推测隐性感染与显性感染比例为53700:1;以≥320为标准,则为11500:1。结论不同县市钩体主要流行群不同,但以黄疸出血群为主;推荐黄疸出血群钩体隐性感染抗体滴度以1:≥200为宜,隐性与显性感染比例约为3万分之一;本地区钩体将以散发为主,流行的概率较小。 相似文献
42.
Magang Shou Wei Lu Prasad H Kari Cathie Xiang Yuexia Liang Ping Lu Dan Cui W Bart Emary Kimberly B Michel Jennifer K Adelsberger Janice E Brunner A David Rodrigues 《European journal of pharmaceutical sciences》2005,26(2):151-161
Enterohepatic recirculation (EHR) occurs via biliary excretion and intestinal reabsorption of a drug. Drug recycling through EHR can lead to a change in pharmacokinetic (PK) properties, such as reduced clearance (CL), extended half-life (T(1/2)) and increased plasma exposure (AUC). As a result, EHR may prolong the pharmacological effect of drugs. In the present study, the compound (Cpd A) was found to exhibit EHR in Rhesus monkeys associated with a reduction in CL (from 3.8 to 0.33 Lh(-1), IV; from 2.3 to 0.4 Lh(-1), PO), and an increase in T(1/2) (from 0.9 to 18 h, IV) and in AUC (from 1.5 to 17.4 microg h/mL, IV; from 2.8 to 16.3 microg h/mL, PO), by comparing the PK in the monkeys via the interruption of EHR (bile-duct cannulation) with that in the intact monkeys. A population four-compartment model was constructed based on recirculation loops incorporating all possible inputs (bile secretion, a lag-time model for gall bladder emptying, routes and amounts of a single dose administration) to fully evaluate the EHR of Cpd A. The plasma concentrations versus time profiles predicted from the model had a good fit to the values observed in the subjects and were further simulated with 90% confidence interval to demonstrate its utility. Thus, the model could be applied as a useful tool to evaluate the drugs or compounds that undergo EHR in different species. 相似文献
43.
Caspase抑制剂的若干药理学研究进展 总被引:2,自引:0,他引:2
细胞凋亡 (apoptosis)失衡与许多疾病密切相关 ,而半胱天冬氨酸蛋白酶 (caspase)是执行细胞凋亡的蛋白酶家族 ,在凋亡过程中发挥关键作用 ,它可通过多种途径发生级联激活。一些天然和合成的caspase抑制剂能够抑制caspase家族中的一种或几种成员而发挥抗凋亡作用 ,有望成为治疗细胞过度凋亡而引起的相关疾病的有效手段。 相似文献
44.
Donghui Cui Raju Subramanian Magang Shou Xiao Yu Michael A Wallace Matthew P Braun Byron H Arison James A Yergey Thomayant Prueksaritanont 《Drug metabolism and disposition》2004,32(8):848-861
Compound A (3-[2-oxo-3-[3-(5,6,7,8-tetrahydro-[1,8]naphthyrindin-2-yl)propyl]-imidazolidin-1-yl]-3(S)-(6-methoxy-pyridin-3-yl)-propionic acid), a potent and selective antagonist of integrin alpha(v)beta(3) receptor, is under development for treatment of osteoporosis. This study describes metabolism and excretion of A in vivo in rats, dogs, and monkeys, and metabolism of A in vitro in primary hepatocytes from rats, dogs, monkeys, and humans. In all three animal species studied, A was primarily excreted as unchanged drug and, to a lesser degree, as phase I and phase II metabolites. Major biotransformation pathways of A included glucuronidation/glucosylation on the carboxylic group to form acyl-linked glucuronides/glucosides; and oxidation on the tetrahydronaphthyridine moiety to generate a carbinolamine and its further metabolized products. Minor pathways involved O-demethylation and hydroxylations on the alkyl chain. Only in rats, a glutathione adduct of A was also observed, and its formation is proposed to be via an iminium intermediate on the tetrahydronaphthyridine ring. Similar metabolic pathways were observed in the incubates of hepatocytes from the corresponding animals as well as from humans. CYP 3A and 2D subfamilies were capable of metabolizing A to its oxidative products. Overall, these in vitro and in vivo findings should provide useful insight on possible biotransformation pathways of A in humans. 相似文献
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47.
目的:观察外周及延脑内侧网状结构注射大黄素、胃电起搏对新西兰白兔胃电的影响,探讨大黄素对胃肠运动的作用机制.方法:采用外周注射及延脑内侧网状结构(P7、P8.5、P9.5、P11)脑立体定位微量注射大黄素、电刺激胃起步点,胃浆膜双极四导联同步记录的方法,分析胃体及胃窦部胃电的平均频率、相位差、负相位比率、波形对应率、幅度等指标.结果:外周注射大黄素胃体1(P=0.031)、胃体2(P=0.047)频率减慢,胃体4(P=0.035)波形对应率降低.胃起搏可有效驱动胃电频率:胃体1(P=0.001)、胃体2(P=0.021)频率明显加快,胃体3相位差减小(P=0.037),胃体2负相位比率升高(P=0.007),胃体3(P=0.001)、胃窦(P=0.046)波形对应率降低.大黄素对于胃起搏引起的效应并无作用,但胃起搏可部分抑制大黄素引起的频率减慢.中枢不同部位微量注射大黄素的作用:P7:胃体2(P=0.026)频率明显减慢;P8.5:胃体1(P=0.045)频率明显减慢,阿托品可"翻转"大黄素引起的频率变慢效应;P9.5:胃窦(P=0.029)频率减慢;而P11:胃体1(P=0.011)频率明显加快.对照组中枢注射生理盐水,P7:胃体2的频率加快(pH8.5),其余部位胃电没有变化.结论:胃起步点起搏对胃电的驱动效应明显.外周注射大黄素对兔胃电主要起抑制作用,而中枢注射大黄素在不同的部位表现出不同的效应. 相似文献
48.
Shou Soeda Kaori Yamada Miho Ohsugi 《Genes to cells : devoted to molecular & cellular mechanisms》2013,18(10):850-858
Mammalian oocytes are arrested at metaphase II due to high MAP kinase activity. After fertilization, oocytes resume meiosis, leading to female chromosome segregation, polar body emission and pronuclear (PN) formation. Previous biochemical studies showed that MAP kinase activity remained high for several hours after fertilization and began to decrease in parallel with PN formation. It has been thought that MAP kinase activity is incompatible with PN formation, and its inactivation is required for the initiation of PN formation in mammalian oocytes. In this study, we revisited this hypothesis by examining MAP kinase activity and PN formation in individual mouse oocytes using cytological analysis. We showed that MAP kinase activity in oocytes could be evaluated using phospho‐ERK1/2 immunofluorescent staining. Co‐immunofluorescent staining of phospho‐ERK1/2 and nuclear pore components showed that PN formation preceded MAP kinase inactivation and could be initiated while MAP kinase activity was still high. Moreover, artificial inactivation of MAP kinase or its downstream target, ribosomal S6 kinase, accelerated but did not rapidly induce PN formation. Our results show that although the MAP kinase pathway negatively regulates PN formation, its inactivation is neither necessary nor sufficient for PN formation. These results suggest the involvement of other essential factor(s) in this process. 相似文献
49.
Liver cancer-related gene CYP2E1 expression in HBV transgenic mice with acute liver injury 总被引:1,自引:0,他引:1
The objective of this research was to study the CYP2E1 gene expression in carbon tetrachloride (CCl4)-induced acute liver injury in hepatitis B virus (HBV) transgenic mice. Twenty-four HBV (?) and 24 HBV (+) transgenic mice aged 8 to 10 weeks were selected for the present study. Intraperitoneal injection of 1.0 μL/g of CCl4 (1:4 dissolved in olive oil) to mice was performed to induce acute liver injury model. Eight normal clean-grade C57BL/6 mice were taken as the control group. The control group received saline intraperitoneally. The mice in each group were killed 3, 6, 12, 24, 48, and 72 h after injection. The liver tissue samples of mice were collected. The liver histological changes at different time points in each group were observed under light microscope. The quantitative PCR methods were utilized to measure the relative mRNA levels of CYP2E1 gene in liver tissues. Immunohistochemistry and Western blot techniques were used to observe tissue expression levels of CYP2E1 in each group. Compared with that of the control group, mRNA and protein expression levels of CYP2E1 significantly increased both in the HBV (?) group and in the HBV (+) group after the CCl4 induced the acute liver injury, and it reached the peak at 72 h after the CCl4 injection. Compared with the HBV (?) group, the mice in the HBV (+) group had severe liver damage and significantly increased CYP2E1 gene and protein expression levels. In the CCl4-induced acute liver injury of HBV transgenic mice, the CYP2E1 gene expression significantly increased. The results provided evidence for the HBV-induced liver damage and liver cancer pathogenesis. 相似文献
50.