AIM： To investigate the clinical characteristics of fulminant hepatitis in pregnancy. METHODS： We compared and analyzed the etiology, clinical characteristics, and laboratory examinations of 25 cases of fulminant he...AIM： To investigate the clinical characteristics of fulminant hepatitis in pregnancy. METHODS： We compared and analyzed the etiology, clinical characteristics, and laboratory examinations of 25 cases of fulminant hepatitis in pregnancy and 30 cases of fulminant hepatitis not in pregnancy. RESULTS： HBV infection and chronic fulminant hepatitis were most common both in the pregnant and in the non-pregnant groups. Jaundice, digestive tract symptoms, increase of bilirubin and thrombinogen activity were the main manifestations. The incidence of hepatic encephalopathy （HE） and hepato-renal syndrome （HRS） was significantly different between the two groups. The incidence of preterm labor, dead fetus and neonatal asphyxia was high. CONCLUSION： Fulminant hepatitis is likely to occur in late pregnancy wibh more severe complications, which significantly influences maternity, perinatal fetus, and newborn.展开更多
AIM: To report the experience in successfully treating pregnant women with severe hepatitis.METHODS: Comprehensive medical treatments were performed under strict monitoring.RESULTS: Pregnant woman with severe hepatiti...AIM: To report the experience in successfully treating pregnant women with severe hepatitis.METHODS: Comprehensive medical treatments were performed under strict monitoring.RESULTS: Pregnant woman with severe hepatitis was successfully rescued.CONCLUSION: Vital measures taken in the treatment of pregnant women with severe hepatitis include termination of the pregnancy at a proper time and control of various complications, such as disseminated intravascular coagulation (DIC), hepatorenal syndrome, hepatic encephalopathy and infection.展开更多
This study was designed to explore the RNA interference technique in inhibition of the expression of the mouse fibrinogen like protein 2(mfgl2),which has been reported to be involved in the development a variety of di...This study was designed to explore the RNA interference technique in inhibition of the expression of the mouse fibrinogen like protein 2(mfgl2),which has been reported to be involved in the development a variety of diseases including fulminant viral hepatitis.A plasmid named p-mfgl2shRNA,complementary to the sequence of mfgl2 was constructed,while another short hairpin RNA(shRNA) which was a mutated form of the mfgl2shRNA sequences was used as a control.A plasmid named pEGFP-mfgl2 expressing the mfgl2-EGFP fusion protein was also constructed for the screening of the effect of p-mfgl2shRNA on mfgl2 expression.By cotransfection of p-mfgl2shRNA and pEGFP-mfgl2 or pcDNA3.1-mfgl2 expression construct into CHO cells or HeLa cells,the inhibition of mfgl2 expression by mfgl2shRNA was analyzed by direct observation through fluorescent microscopy,FACS,RT-PCR and immunohistochemistry staining.The experiments showed the significant inhibitory effect of p-mfgl2shRNA on mfgl2 expression at 48h post-transfection in both CHO and Hela cell lines with the inhibitory efficiency as high as 80.1%.The study demonstrated that the construct of p-mfgl2shRNA successfully interfered with the mfgl2 expression in vitro.展开更多
Male microchimerismis frequent in the adult female liver and is attributed to fetal cells originating frompreviousmale offspring. It has never been studied in pregnant women, female children, or fetuses. We examined i...Male microchimerismis frequent in the adult female liver and is attributed to fetal cells originating frompreviousmale offspring. It has never been studied in pregnant women, female children, or fetuses. We examined its frequency and cellular nature in normal and diseased female livers from fetal life to adulthood. Forty-six liver samples from 29 women, 6 female children, and 11 female fetuses were screened for the Y chromosome via polymerase chain reaction (PCR) assay and fluorescent in situ hybridization (FISH). The X chromosome was used as an internal control. A third PCR assay was used for Y genotyping. The Y chromosome was detected in 5 of 6 children, 7 of 11 fetuses, 3 of 9 women with normal liver, 7 of 10 women with chronic hepatitis C, 5 of 6 women with acute liver disease during pregnancy with male offspring, and 2 of 4 nonpregnant women with fulminant hepatitis. In positive samples, the mean XY/XX ratio was 0.012 (±0.004). In women, male microchimerism was correlated with previous male offspring. Male hepatocytes, detected via FISH combined with anti-hepatocyte immunohistochemistry,were observed only in fetuses (4/9) and in postpartem women (4/6). Y genotypes were different from each other in 4 of 5 female livers. In conclusion, male liver microchimerism is frequent in normal and diseased female livers. The presence of male cells in the liver of female children and fetuses is probably due to the transplacental transmission of fetal cells preexisting in the mother and acquired either from previous pregnancy with male offspring or during the mother’s own fetal life.展开更多
文摘AIM： To investigate the clinical characteristics of fulminant hepatitis in pregnancy. METHODS： We compared and analyzed the etiology, clinical characteristics, and laboratory examinations of 25 cases of fulminant hepatitis in pregnancy and 30 cases of fulminant hepatitis not in pregnancy. RESULTS： HBV infection and chronic fulminant hepatitis were most common both in the pregnant and in the non-pregnant groups. Jaundice, digestive tract symptoms, increase of bilirubin and thrombinogen activity were the main manifestations. The incidence of hepatic encephalopathy （HE） and hepato-renal syndrome （HRS） was significantly different between the two groups. The incidence of preterm labor, dead fetus and neonatal asphyxia was high. CONCLUSION： Fulminant hepatitis is likely to occur in late pregnancy wibh more severe complications, which significantly influences maternity, perinatal fetus, and newborn.
文摘AIM: To report the experience in successfully treating pregnant women with severe hepatitis.METHODS: Comprehensive medical treatments were performed under strict monitoring.RESULTS: Pregnant woman with severe hepatitis was successfully rescued.CONCLUSION: Vital measures taken in the treatment of pregnant women with severe hepatitis include termination of the pregnancy at a proper time and control of various complications, such as disseminated intravascular coagulation (DIC), hepatorenal syndrome, hepatic encephalopathy and infection.
基金supported by the National Natural Science Foundation of China(No.81370179)the Science and Technology Research Project from Chongqing Municipal Education Commission,China(No.KJ1400235)
文摘腺苷酸活化蛋白激酶(AMP activated protein kinase,AMPK)是重要的代谢调节酶及炎症调控新靶点。以往研究显示,AMPK激活剂5-氨基咪唑-4-甲酰胺核苷酸转甲酰酶(5-amino-4-imidazolecarboxamide riboside,AICAR)可通过抑制炎症反应减轻脂多糖/右旋半乳糖胺(lipopolysaccharide/D-galactosamine,LPS/D-gal)诱导的爆发性肝炎。由于炎症可通过激活凝血反应加重组织损伤,本研究旨在以炎症诱导凝血反应为切入点探讨AICAR保肝效应的机制。腹腔注射LPS/D-gal建立爆发性肝炎小鼠模型,用Western blot检测肝内组织因子(tissue factor,TF)、缺氧诱导因子1-α(hypoxia-inducible factor 1α,HIF-1α)以及细胞核内核因子kappa B(nuclear factor kappa B,NF-κB)p65蛋白表达,用实时定量PCR检测肝细胞促红细胞生成素(erythropoietin,EPO)m RNA表达,用试剂盒检测肝组织乳酸(lactic acid,LA)水平。结果显示,LPS/D-gal可促进小鼠肝细胞内TF蛋白表达,提高细胞核内NF-κB p65水平,上调HIF-1α蛋白及EPO m RNA表达,并提高肝组织LA水平;而AICAR干预后,以上指标均明显下调。以上结果提示,AICAR可通过抑制NF-κB活性下调TF表达及凝血活性,从而减轻肝组织缺氧及代谢紊乱,这可能是AICAR减轻LPS/D-gal诱导的爆发性肝炎的新机制。
基金National Natural Science Foundation of China (No.30571643, No.30672380)National Key Basic Research Program of China (No. 2005CB2401,2007CB512904)
文摘This study was designed to explore the RNA interference technique in inhibition of the expression of the mouse fibrinogen like protein 2(mfgl2),which has been reported to be involved in the development a variety of diseases including fulminant viral hepatitis.A plasmid named p-mfgl2shRNA,complementary to the sequence of mfgl2 was constructed,while another short hairpin RNA(shRNA) which was a mutated form of the mfgl2shRNA sequences was used as a control.A plasmid named pEGFP-mfgl2 expressing the mfgl2-EGFP fusion protein was also constructed for the screening of the effect of p-mfgl2shRNA on mfgl2 expression.By cotransfection of p-mfgl2shRNA and pEGFP-mfgl2 or pcDNA3.1-mfgl2 expression construct into CHO cells or HeLa cells,the inhibition of mfgl2 expression by mfgl2shRNA was analyzed by direct observation through fluorescent microscopy,FACS,RT-PCR and immunohistochemistry staining.The experiments showed the significant inhibitory effect of p-mfgl2shRNA on mfgl2 expression at 48h post-transfection in both CHO and Hela cell lines with the inhibitory efficiency as high as 80.1%.The study demonstrated that the construct of p-mfgl2shRNA successfully interfered with the mfgl2 expression in vitro.
文摘Male microchimerismis frequent in the adult female liver and is attributed to fetal cells originating frompreviousmale offspring. It has never been studied in pregnant women, female children, or fetuses. We examined its frequency and cellular nature in normal and diseased female livers from fetal life to adulthood. Forty-six liver samples from 29 women, 6 female children, and 11 female fetuses were screened for the Y chromosome via polymerase chain reaction (PCR) assay and fluorescent in situ hybridization (FISH). The X chromosome was used as an internal control. A third PCR assay was used for Y genotyping. The Y chromosome was detected in 5 of 6 children, 7 of 11 fetuses, 3 of 9 women with normal liver, 7 of 10 women with chronic hepatitis C, 5 of 6 women with acute liver disease during pregnancy with male offspring, and 2 of 4 nonpregnant women with fulminant hepatitis. In positive samples, the mean XY/XX ratio was 0.012 (±0.004). In women, male microchimerism was correlated with previous male offspring. Male hepatocytes, detected via FISH combined with anti-hepatocyte immunohistochemistry,were observed only in fetuses (4/9) and in postpartem women (4/6). Y genotypes were different from each other in 4 of 5 female livers. In conclusion, male liver microchimerism is frequent in normal and diseased female livers. The presence of male cells in the liver of female children and fetuses is probably due to the transplacental transmission of fetal cells preexisting in the mother and acquired either from previous pregnancy with male offspring or during the mother’s own fetal life.
