Progress in liver diseases最新文献

{"title":"Regulation of liver-specific gene expression.","authors":"M Chojkier","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76373,"journal":{"name":"Progress in liver diseases","volume":"13 ","pages":"37-61"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20168396","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Active cell death (apoptosis) in liver biology and disease.","authors":"R Schulte-Hermann, W Bursch, B Grasl-Kraupp","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76373,"journal":{"name":"Progress in liver diseases","volume":"13 ","pages":"1-35"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20168395","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Use of novel beta-L(-)-nucleoside analogues for treatment and prevention of chronic hepatitis B virus infection and hepatocellular carcinoma.","authors":"E G Bridges, Y C Cheng","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76373,"journal":{"name":"Progress in liver diseases","volume":"13 ","pages":"231-45"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20168403","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Immunosuppressive therapy in liver transplantation: principles and practice.","authors":"N L Ascher","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76373,"journal":{"name":"Progress in liver diseases","volume":"13 ","pages":"381-95"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20168994","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Molecular biology of bilirubin metabolism.","authors":"P L Jansen,&nbsp;P J Bosma,&nbsp;J R Chowdhury","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>As the genes encoding the glucuronidating enzymes are discovered, it is evident that glucuronidation is a magnificent example of how in evolution, man became adapted to his \"intoxicating\" environment. A superfamily of genes is necessary to dispose of the toxins and carcinogens that are encountered by inhalation and ingestion. The enzymes that glucuronidate endogenous compounds are members of this large family. For the clinician, it is important to remember that jaundice may sometimes be the result of interactions at the level of bilirubin glucuronidation. When jaundice results from inactivation of members of the UGT1 family, conjugation of certain phenols, such as the anesthetic propofol, or synthetic estrogens, such as ethinylestradiol, can also be impaired. In the case of severe bilirubin glucuronidation deficiencies, such as the Crigler Najjar syndrome type I, there are exciting prospects for a possible cure by gene therapy.</p>","PeriodicalId":76373,"journal":{"name":"Progress in liver diseases","volume":"13 ","pages":"125-50"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20168399","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Artificial hepatic support systems.","authors":"A A Demetriou,&nbsp;F Watanabe,&nbsp;J Rozga","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>Severe acute liver failure is associated with high mortality. Improved respiratory and hemodynamic management together with intracranial pressure monitoring and aggressive treatment of cerebral edema have greatly improved patient care. However, many patients die despite optimal medical treatment, because of failure to arrest the progression of cerebral edema. This in turn result in brain stem herniation with rapid neurologic deterioration and death. Liver transplantation has emerged as the definitive treatment for patients with severe acute liver failure. Unfortunately approximately up to one half of the patients with this severe form of liver failure will die while awaiting liver transplantation. There is thus a clear need for a liver support system to provide a \"bridge\" to transplantation. Over the years, many \"bridge\" systems were introduced which promised effective support but had no wide clinical success. Because of our incomplete understanding of the pathophysiology of liver failure and development of cerebral edema, it was felt that use of isolated hepatocytes or ex vivo whole liver perfusion would provide both detoxifying and synthetic functions. Whole liver perfusion appears to be effective but cumbersome and costly because it would require each center, where patients are being treated, to maintain animal colonies for patient treatment. Therefore, cryopreserved isolated xenogeneic hepatocytes appear to be the best candidates for building a \"bridge\" system. In a preliminary clinical study, we have used a porcine hepatocyte-based liver support system (Bioartificial Liver: BAL) to treat patients with acute liver failure as well as patients with acute exacerbation of chronic liver disease. Patients in the first group, who were candidates for transplantation, were successfully bridged to a transplant with excellent survival. No obvious benefit from BAL treatments was seen in the second group. In this group patients where cerebral edema is not a major component of the clinical presentation, it is possible that long-term support will be needed with repeated treatments over several weeks to provide adequate synthetic and detoxifying liver function until the patients' livers recover. For such liver recovery to take place, these chronic patients will need to be treated earlier in the course of their disease when they still have some residual liver mass as well as regenerative capacity. Prospective controlled trials will be initiated as soon as the current phase I study is concluded in order to determine the efficacy of this system in both patient populations.</p>","PeriodicalId":76373,"journal":{"name":"Progress in liver diseases","volume":"13 ","pages":"331-48"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20168408","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Control of vesicle traffic in hepatocytes.","authors":"G Ihrke,&nbsp;A L Hubbard","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76373,"journal":{"name":"Progress in liver diseases","volume":"13 ","pages":"63-99"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20168397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Regulation and function of the multidrug resistance genes in liver.","authors":"J A Silverman,&nbsp;S S Thorgeirsson","doi":"","DOIUrl":"","url":null,"abstract":"<p><p>The P-glycoproteins are integral membrane proteins that function as ATP-dependent transporters. The multidrug resistance genes which encode P-gp comprise a small gene family, with 2 members in humans and 3 in rodents. The P-gp encoded by the mdr1 gene functions as a drug efflux pump to remove drugs from cells and may serve as a barrier to protect cells from cytotoxic agents. In normal tissues, P-gp is localized on the luminal surface of transporting epithelia in the liver, kidney, small intestine, testes, and blood-brain barrier. Transient exposure to drugs transcriptionally increases the level of expression of the mdr1 genes, however, the cellular pathways critical to this regulation are yet unknown. This observation may have some implications on the level of expression in tumors and response to chemotherapy. Examination of the basal level of MDR expression in tumors may not be a reliable predictor of the effect of P-gp on chemotherapy. Induction of MDR transcription by drugs may further impede the effectiveness of anti-cancer agents. This is most obvious for drugs which are substrates for P-gp transport, however, it also applies significantly to compounds which are not themselves substrates but affect the response to other drugs simultaneously or subsequently administered. A clear understanding of the mechanisms that regulate basal and drug-induced mdr transcription will facilitate development of novel agents which circumvent this obstacle or permit targeted modification of mdr expression. Expressed on the bile canalicular surface of the liver, P-gps represent the first ATP-dependent biliary transporters to be characterized. The P-gp encoded by mdr2 is the major form of P-gp expressed in normal liver and transports phospholipids into bile. A defect in this protein leads to severe liver disease caused by chronic inflammation of the biliary system that results from high concentrations of free bile salts. The cellular origin and molecular basis of the ensuing liver tumors in these mice are unclear. It is possible that the chronic damage to the biliary ductules causes an increased growth rate of the surrounding cells, including putative stem cells in the liver. Thus, these mice may serve as a model for carcinogenesis in which the liver is under constant promotion placing the proliferating cells at increased risk to further genetic alterations or expansion of preexisting, but normally quiescent, mutations. Mdr2-deficient animals may also provide a model for human chronic inflammatory liver disease. Clearly, these exciting results indicate that further characterization of the P-gps as normal physiologic canalicular membrane transporters is necessary.</p>","PeriodicalId":76373,"journal":{"name":"Progress in liver diseases","volume":"13 ","pages":"101-23"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20168398","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autoimmune disorders associated with hepatitis C.","authors":"P Marcellin,&nbsp;J P Benhamou","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76373,"journal":{"name":"Progress in liver diseases","volume":"13 ","pages":"247-67"},"PeriodicalIF":0.0,"publicationDate":"1995-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"20168404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Autoantibodies in chronic hepatitis: diagnostic reagents and scientific tools to study etiology, pathogenesis, and cell biology.","authors":"M P Manns","doi":"","DOIUrl":"","url":null,"abstract":"","PeriodicalId":76373,"journal":{"name":"Progress in liver diseases","volume":"12 ","pages":"137-56"},"PeriodicalIF":0.0,"publicationDate":"1994-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18750637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}