清肝泄浊法治疗脂肪肝30例临床研究

目的:观察清肝泄浊法治疗脂肪肝的临床疗效.方法:治疗组30例口服自拟清肝泄浊汤,对照组24例口服复方益肝灵,观察肝功能及血脂变化.结果:治疗组30例,有效率90.0%,对照组30例,有效率36.6%.结论:清肝泄浊法治疗脂肪肝的疗效明显,适宜临床推广运用.     

Needle biopsy of the liver for the diagnosis of nonneoplastic liver diseases

The results of 209 liver biopsy needle washings were compared with the corresponding histologic findings. An effort was made to distinguish major categories of liver disease on the basis of cytologic findings. Pigment identification and fat quantitation were also evaluated. It was found that it was often possible to determine whether a liver needle washing was normal or abnormal; however, it was rarely possible to provide specific diagnoses. Pure fatty change and primary cholestasis could be reliably differentiated from the steatosis and bile plugging seen in other liver disorders. Cirrhosis could be suggested in a limited number of cases, although in most cases the findings were nonspecific. Cytology was found to be less reliable than biopsy in the discrimination between the major pigments. Finally, cytology was an acceptable method for detecting and quantitating fatty change.     

Inducing the liver: Understanding the signals that promote murine liver budding

The endoderm emerges as an epithelial sheet that covers the surface of the developing murine embryo. This tissue will produce the entire gut tube as well as associated digestive and respiratory organs including the thyroid, thymus, lung, liver, and pancreas. The emergence of each endodermal organ occurs in a temporally distinct manner that is dependant upon reciprocal inductive interactions between the endoderm and the underlying mesoderm. The emergence of the hepatic endoderm, which occurs using a morphological process termed liver budding, initiates during early somitogenesis in the mouse at approximately 8.25 days post‐coitum (dpc). Explant and transplant studies performed in chicken and mouse have demonstrated that secreted signals from adjacent mesodermal tissues initiate the hepatic gene program from ventral‐fated endoderm. Here, we review the data in support of the roles of members of the fibroblast growth factor (FGF), bone morphogenetic protein (BMP), and Wnt signaling pathways in liver budding and discover that little is known about the precise endogenous signals involved in the molecular and morphological induction of liver budding in the mouse. J. Cell. Physiol. 226: 1727–1731, 2011. © 2010 Wiley‐Liss, Inc.     

Cysteinyl-leukotrienes and the liver

Leukotrienes are potent biological mediators implicated in an increasing number of disease processes. This review outlines the basic biology of leukotrienes and discusses recent developments in our understanding of the specific role of cysteinyl-leukotrienes (cLTs) in cholestasis, hepatic inflammation, portal hypertension, and the pathogenesis of the hepatorenal syndrome (HRS).     

Isoprostanes and the liver

The liver has been central to our understanding of the physiology and biology of the F2-isoprostanes. The discovery of F2-IsoPs and the initial demonstration that they could be used to localize oxidative stress was first demonstrated in a rat model of oxidative liver injury (carbon tetrachloride), and the first demonstration that plasma concentrations are increased in a human disease was in patients with liver failure and the hepatorenal syndrome [J. Clin. Invest. 90 (6) (1992b) 2502; J. Lipid Mediat. 6 (1/3) (1993) 417]. This article will cover the measurement of F2-IsoPs as markers of lipid peroxidation in vivo in liver disease, and review their biological activity as mediators of disease.     

Therapeutic liver repopulation for the treatment of metabolic liver diseases

Orthotopic liver transplantation is the treatment of choice for many inherited and acquired liver diseases. Unfortunately, the supply of donor organs is limiting and therefore many patients cannot benefit from this therapy. In contrast, hepatocyte suspensions can be isolated from a single donor liver can be transplanted into several hosts, and this procedure may help overcome the shortage in donor livers. In classic hepatocyte transplantation, however, only 1% of the liver mass or less can be replaced by donor cells. Recently though, we have used a mouse model of hereditary tyrosinemia to show that > 90% of host hepatocytes can be replaced by a small number of transplanted donor cells in a process we term "therapeutic liver repopulation". This phenomenon is analogous to repopulation of the hematopoietic system after bone marrow transplantation. Liver repopulation occurs when transplanted cells have a growth advantage in the setting of damage to recipient liver cells. Here we will review the current knowledge of this process and discuss the hopeful implications for treatment of liver diseases.     

Portal vein network around the liver lobules demonstrates the lobular structure of the liver

The regularity of a basketlike surrounding of parenchymatous parts of the liver by portal branches proves the lobular organization of the liver. The wall formation of the portal basket (corbicula portalis) is demonstrated by several figures.