Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood from endangered San Joaquin kit foxes (Vulpes macrotis mutica) inhabiting the Elk Hills Naval Petroleum Reserve, Kern County, and the Elkhorn Plain, San Luis Obispo County, California, was collected in 1981, 1982 and 1984 and sera were tested for antibodies against 10 selected pathogens. Proportions of kit fox sera containing antibodies against pathogens were: canine parvovirus, 100% in 1981-1982 and 67% in 1984; infectious canine hepatitis virus, 6% in 1981-1982 and 21% in 1984; canine distemper virus, none in 1981-1982 and 14% in 1984; Francisella tularensis, 8% in 1981-1982 and 31% in 1984; Brucella abortus, 8% in 1981-1982 and 3% in 1984; Brucella canis, 14% in 1981-1982 and none in 1984; Toxoplasma gondii, 6% in 1981-1982; Coccidioides immitis, 3% in 1981-1982; and Yersinia pestis and Leptospira interrogans serotypes canicola, grippotyphosa, hardjo, icterohaemorrhagiae, and pomona, none in 1981-1982. Although antibodies against selected pathogens were present, no clinical indications of disease were observed in these fox populations.
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PMID:Serological survey for selected diseases in the endangered San Joaquin kit fox (Vulpes macrotis mutica). 283 36

A new cell line derived from a woodchuck hepatitis surface antigen-positive woodchuck hepatocellular carcinoma has been established and named T3-HEP-W1. This new cell line was established directly from a primary woodchuck hepatocellular carcinoma. Adaptation of the cells to the in vitro culture condition was completed after 3 months, with the doubling time of 24 hr. The morphologic features of the cell by light microscopy were of an epithelial type. The modal chromosome number was 100. Ornithine and tyrosine aminotransferase activities were detected. Production of albumin was negative. Integration of woodchuck hepatitis virus DNA was demonstrated by Southern blot analysis, although the secretion of woodchuck hepatitis surface antigen was not detected. T3-HEP-W1 is quite different from the previously reported WH257GE10 cell line and provides another in vitro model for the study of human hepatocellular carcinoma related to hepatitis B virus.
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PMID:Establishment of a new cell line from a woodchuck hepatocellular carcinoma. 333 96

The possible immunological mechanisms involved in the progression from acute type B hepatitis to chronic hepatitis can be summarised as follows: following replication of the virus in the hepatocyte nucleus, the surface coat is added and the virus released from the hepatocyte. T cells recognise the foreign viral antigen on the surface of the liver cells and mount a T cell mediated reaction against infected hepatocytes. They also stimulate B cells to produce antibody to LSP, the ensuing antibody-dependent cell-mediated K cell reaction against normal liver membrane antigens contributing to the hepatocyte necrosis. Released virus stimulates anti-viral antibody production which complexes with the virus, the complex being removed by the reticuloendothelial system. With the removal of virus there is no longer any T cell reaction against the virus or helper effect for anti-LSP production and this, together with a normally functioning suppressor T cell system, leads to cessation of liver cell necrosis and recovery from the episode of acute hepatitis. In HBsAg-positive ACH as a result of a quantitative or qualitative defect in the production of antibody to Dane particles there is a failure to clear the virus, with reinfection of further hepatocytes and continuation of both mechanisms of immunological liver cell damage. In patients progressing to HBsAg-negative ACH, however, anti-viral antibody production is adequate and the virus is cleared. In this group of patients the defect probably lies in suppressor T cell function, which is unable to switch off the autoimmune reaction against LSP. The increased frequency of histocompatibility antigens HLA A1 and B8 and the associated high levels of autoantibodies and anti-viral antibodies suggests that this defect may be genetically inherited.
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PMID:Pathogenesis of active chronic hepatitis. 644 63

Determination of serum bile acids has long been regarded as the most sensitive indicator of liver function. An assessment was made of the clinical applicability of RIA evaluation of two of these acids, cholylglycine (CG) and sulpholithochocholyglycine (SLGG), on an empty stomach and 2hr after a cholecystokinetic meal in 109 liver patients ans 20 controls. After the meal test, both acids proved more sensitive than the usual liver function indices. Different mean values were observed for different diseases. They were in good correlation with the extent of histological damage. Values were highest in obstructive icterus, cirrhosis and neoplasia of the liver, fairly highly high in steatofibrosis, ACH and PCH, and normal in viral hepatitis in the course of resolution, aspecific reactive hepatitis, and steatosis. The meal test thus proved a good indicator of liver disease. Its wider use is to be hoped for in order that its limits and applications may be better understood.
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PMID:[Determination of serum bile acids in hepatobiliary diseases. Clinical applicability]. 670 Aug 30

The intrahepatic accumulation of the c-myc protooncogene product was observed on immunofluorescence in each of six patients with chronic hepatitis delta virus infection who exhibited the hepatitis D antigen in their livers. The c-myc product was stained in the same nuclei that contained the hepatitis D antigen. C-myc was not observed in acute hepatitis D or in cases of chronic hepatitis delta virus infection without expression of the hepatitis D antigen. The protooncogene product was detected in only 1 of 32 viral and nonviral liver disorders unrelated to hepatitis delta virus. To confirm these observations, we transfected HBsAg-positive (PCL/PRF/5) and HBsAg-negative (HepG2) transformed liver cell lines with a plasmid containing a hepatitis delta virus cDNA trimer under the control of the SV40 early enhancer/promoter sequences. Whereas baseline c-myc expression was barely detectable in mock-transfected PLC/PRF/5 or HepG2 cells, strong c-myc nuclear fluorescence was observed when these same cells were transfected with the hepatitis D antigen expression vector. Similar results were obtained after infection of HeLa cells with a recombinant vaccinia virus expressing the hepatitis D antigen. Detection of c-myc mRNA sequences by means of in situ hybridization suggested that the c-myc product accumulation was not due to increased amounts of its mRNA. The c-myc protein accumulates selectively in the livers of patients with chronic hepatitis delta virus infection and in the same nuclei that contain the hepatitis D antigen. The expression of c-myc in hepatitis D antigen-containing cells does not require the presence of hepatitis B virus infection.
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PMID:Expression of the c-myc protooncogene product in cells infected with the hepatitis delta virus. 752 69

Surgical resection has been the standard approach for primary and metastatic liver tumors. Long-term survival, however, is limited because of recurrence or hepatic decompensation. Failure of chemotherapeutic regimens or liver transplantation (OLT) to prevent recurrence has resulted in the need for multimodality therapies. We report our experience with preoperative hepatic arterial chemoembolization (CET) followed by OLT in highly select patients. Over a 33-month period, 23 of 41 patients (56%) referred with primary (n = 16) or metastatic neuroendocrine (n = 7) liver tumors met eligibility requirements. Despite mild, self-limited chemical hepatitis, CET was well tolerated in all but three elderly patients who succumbed to liver failure. Four of five patients ultimately received OLT. Three are alive and free of disease at a mean followup of 17 months, one died of recurrent hepatocellular carcinoma, and one (NET) remains well at 33 months with elevated glucagon levels but no measurable disease. All NET patients are alive with resolution of hormonal symptoms. Four of five noncirrhotic patients died of disease, and one has progressive tumor growth. Although OLT following CET achieves superior survival, its application is limited to a minority of patients with such tumors. Careful pretreatment staging and patient selection combined with caution in the use of CET in elderly cirrhotic patients is critical to the success of such therapies.
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PMID:Intrahepatic arterial chemoembolization for hepatocellular carcinoma and metastatic neuroendocrine tumors in the era of liver transplantation. 875 63

To identify environmental, viral, and genetic factors that may influence the risk of developing hepatocellular carcinoma (HCC), large prospective studies are being conducted in Haimen City, China and Senegal, and a case-control study of genetic variation in the detoxification of aflatoxin-B1 was carried out in Shanghai, China. Analysis of 78 HCCs that have occurred among 51,020 men enrolled in a large prospective study in Haimen City, China showed a strong association of HCC with chronic hepatitis B virus (HBV) infection. There were also significant associations of HCC risk with occupation (farming), history of a clinical episode of hepatitis in adulthood, and a family history of HCC. Study of 52 HCC cases and 116 controls for genetic polymorphisms and HCC risk showed a significant association with epoxide hydrolase (EPHX) mutant alleles (1/2, 2/2) and a borderline association with homozygous deletion of the glutathione-S-transferase mu (GSTM1) gene. There was a multiplicative interaction of these polymorphisms with chronic HBV infection such that HBsAg-positive persons who were GSTM1 null and were EPHX 1/2 or 2/2 had 135 times the risk of HCC as HBsAg-negative persons with the wild type genotypes for GSTM1 and EPHX. The risk of HCC is not uniform among persons with chronic HBV or HCV infections. Studies of genetic, viral, and environmental interactions may permit identification of those individuals at highest risk within groups at increased risk of HCC. Prevention strategies could then be targeted at those individuals.
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PMID:Molecular and genetic epidemiology of hepatocellular carcinoma: studies in China and Senegal. 887 9

We compared virus-specific antibody and T-cell responses to influenza virus vaccination in 32 caregivers of Alzheimer's disease (AD) patients and matched control subjects. Caregivers showed a poorer antibody response and virus-specific T-cell response following vaccination compared to the control subjects as measured by fourfold increases in antibody titers to the vaccine and lower levels of virus-induced IL-2 levels in vitro. We performed a second study in which forty-eight medical students were inoculated with a series of three injections of the hepatitis-B (HEP-B) vaccine to coincide with the third day of three, three-day examination blocks. Twelve of the 48 medical students seroconverted after the first injection; these students were characterized by falling into the lower stressed/lower anxiety group of students. Students who reported greater social support and lower anxiety and stress demonstrated a higher antibody response to the vaccine and a more vigorous T-cell response to HEP-B surface antigen at the end of the third examination experience. The differences in antibody and T-cell responses to HEP-B and influenza virus vaccinations provide a demonstration of how stress may be able to alter both the cellular and humoral immune responses to vaccines and novel pathogens in both younger and older adults.
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PMID:The influence of psychological stress on the immune response to vaccines. 962 91

Fibroblast growth factor 2 (FGF2) is an excellent candidate to regulate remyelination based on its proposed actions in oligodendrocyte lineage cell development in conjunction with its involvement in CNS regeneration. To assess the potential for FGF2 to play a role in remyelination, we examined the expression pattern of FGF2 and FGF receptors (FGFRs) in an experimental demyelinating disease with extensive remyelination. Adult mice were intracranially injected with murine hepatitis virus strain A-59 (MHV-A59) to induce focally demyelinated spinal cord lesions that spontaneously remyelinate, with corresponding recovery of motor function. Using kinetic RT-PCR analysis of spinal cord RNA, we found significantly increased levels of FGF2 mRNA transcripts, which peaked during the initial stage of remyelination. Analysis of tissue sections demonstrated that increased levels of FGF2 mRNA and protein were localized within demyelinated regions of white matter, including high FGF2 expression associated with astrocytes. The expression of corresponding FGF receptors was significantly increased in lesion areas during the initial stage of remyelination. In normal and lesioned white matter, oligodendrocyte lineage cells, including progenitors and mature cells, were found to express multiple FGFR types (FGFR1, FGFR2, and/or FGFR3). In addition, in lesion areas, astrocytes expressed FGFR1, FGFR2, and FGFR3. These findings indicate that, during remyelination, FGF2 may play a role in directly regulating oligodendrocyte lineage cell responses and may also act through paracrine or autocrine effects on astrocytes, which are known to synthesize other growth factors and immunoregulatory molecules that influence oligodendrocyte lineage cells.
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PMID:Fibroblast growth factor 2 (FGF2) and FGF receptor expression in an experimental demyelinating disease with extensive remyelination. 1102 Feb 17

The biannual HEP DART conference in Hawaii provided an intimate setting for members of the viral hepatitis community to exchange ideas and information. The leaders in clinical research and drug development gathered with scientists to discuss the recent advances in a field dedicated to understanding and treating hepatitis. The topics ranged from the basic science of pathogenesis and therapeutic models, to the next generation of hepatitis B and hepatitis C virus inhibitors, to the important therapeutic information gleaned from the latest clinical trials. The therapeutic considerations for special populations, such as those co-infected with HIV, those with decompensated liver diseases or difficult-to-treat genotypes, as well as those patients who have failed treatment, emerged as critical clinical topics under discussion.
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PMID:HEP DART 2003: Frontiers in drug development for viral hepatitis. 1501 47


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