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)

A new virus within the family Flaviviridae. 'hepatitis' G/GBV-C, has been incriminated by several authors as a causative factor of idiopathic or cryptogenic fulminant hepatitis, a syndrome of presumed viral aetiology. Review of worldwide data from 22 studies on 364 cases indicates that G/GBV-C infection is present in approximately 20% of idiopathic cases but a similar or even higher prevalence is detected in fulminant hepatitis of viral B, D or C aetiology, reflecting a high rate of parenteral viral exposure rather than a specific aetiology of fulminant hepatic failure. An aetiopathogenic role of G/GBV-C in fulminant hepatitis seems to be further refuted by the analysis of other data in the literature. The presence of G/GBV-C infection in fulminant hepatic failure is largely a result of secondary infection or coinfection. The aetiopathogenetic mystery of cryptogenic or idiopathic fulminant hepatitis remains unsolved.
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PMID:Fulminant hepatitis and the new G/GBV-C flavivirus. 949 12

A focal outbreak of hepatitis was detected in a day-care centre for children centrally located in Pune. The source of infection was suspected to be an 11-year-old child who probably got the infection from his school. Seven out of 15 children from day-care centre developed clinical hepatitis. Two cases of secondary infection were identified among the family contacts of infected children. Sera from all the nine sick children were positive for anti-hepatitis A virus-IgM antibodies. A stool sample from a case of secondary infection showed presence of HAV-RNA by RT-nested PCR. These findings proved that the outbreak was caused by hepatitis A virus.
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PMID:Hepatitis A in day care centre. 1083 60

The strong similarity between GB virus B (GBV-B) and hepatitis C virus (HCV) makes tamarins infected by GBV-B an acceptable surrogate animal model for HCV infection. Even more attractive, for drug discovery purposes, is the idea of constructing chimeric viruses by inserting HCV genes of interest into a GBV-B genome frame. To accomplish this, infectious cDNA clones of both viruses must be available. The characterization of several HCV molecular clones capable of infecting chimpanzees has been published, whereas only one infectious GBV-B clone inducing hepatitis in tamarins has been reported so far. Here we describe the infection of tamarins by intrahepatic injection of RNA transcribed from a genomic GBV-B clone (FL-3) and transmission of the disease from infected to naive tamarins via serum inoculation. The disease resulting from both direct and secondary infection was characterized for viral RNA titre and hepatitis parameters as well as for viral RNA distribution in the hepatic tissue. Host humoral immune response to GBV-B antigens was also monitored. The progression of the disease was compared to that induced by intravenous injection of different amounts of the non-recombinant virus.
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PMID:Generation of infectious and transmissible virions from a GB virus B full-length consensus clone in tamarins. 1156 37

Biological assay of human liver material shows various concentrations of hemoglobin producing material in various diseased states. Cardiac congestion with red atrophy of the liver shows values (Table 21) somewhat below the human normal-94 per cent compared to 162 per cent. It is probable that this is due to atrophy and destruction of the liver cells in the centers of the liver lobules. We believe the remaining liver cells have a normal content of hemoglobin producing factors. Amyloid (tuberculosis) and fatty (alcoholic) degeneration show (Table 22) subnormal values-111 per cent compared to 162 per cent. If we allow for the "dilution" of liver cell weight by the amyloid and fat we observe normal values for the concentration of hemoglobin producing factors. Carcinoma growth in the liver whether primary or secondary shows net figures (Table 23) which are low-75 per cent compared to normal 162 per cent. It appears that cancer tissue, even tumor cells originating from hepatic epithelium, contains no hemoglobin producing factors. If we allow for the "dilution" of the remaining liver cells by the cancer tissue the figures are within normal limits. Cirrhosis and hepatitis (Table 24) with no signs of true hepatic insufficiency or severe hepatic injury but death supervening from secondary infection or hemorrhage will give average normal values -164 per cent compared to normal human of 162 per cent. Icterus is not a factor. Cirrhosis or hepatitis with severe parenchyma injury and signs of hepatic insufficiency give low values (Table 25) in biological assay -48 per cent compared to normal human 162 per cent. It may be surprising that the liver cells hold so tenaciously to these unknown factors influencing hemoglobin production but obviously only in severe liver injury is this concentration seriously reduced.
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PMID:HEMOGLOBIN PRODUCTION FACTORS IN THE HUMAN LIVER : II. LIVER DEGENERATION, CANCER, CIRRHOSIS AND HEPATIC INSUFFICIENCY. 1987 Jan 53

The common pathogens and cases of secondary infection by acupuncture were classified and described, including staphylococcus aureus, mycobacteria, hepatitis virus and some sporadic infections. The above; cases were summed up according to the common pathogens of the secondary infection by acupuncture. Thus it illustrates the features of the secondary infection cases by acupuncture comprehensively and aims to enhance the infection knowledge of the medical staff in the hospital, so that the infection is effectively prevented in medical work.
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PMID:[Research progress of secondary infection cases by acupuncture]. 2696 93

Dengue is the most common mosquito-borne flaviviral infection in the world today. Several factors contribute and act synergistically to cause severe infection. One of these is dysregulated host immunological mediators that cause transient pathophysiology during infection. These mediators act on the endothelium to increase vascular permeability, which leads to plasma leakage compromising hemodynamics and coagulopathy. We conducted a prospective study to explore the expression of pro- and anti-inflammatory cytokines and how they relate to clinical dengue manifestations, by assessing their dynamics through acute dengue infection in adults admitted to the Hospital for Tropical Diseases, Bangkok, Thailand. We performed cytokine analysis at three phases of infection for 96 hospitalized adults together with serotyping of confirmed dengue infection during the outbreaks of 2015 and 2016. The serum concentrations of seven cytokines (interleukin [IL]-2, IL-4, IL-6, IL-8, IL-10, tumor necrosis factor alpha, and interferon gamma) were measured in duplicate using a commercial kit (Bio-Plex Human Cytokine Assay). In this study, the cytokine profile was suggestive of a T-helper 2 response. Most patients had secondary infection, and the levels of viremia were higher in patients with plasma leakage than those without plasma leakage. In addition, we observed that bleeding and hepatitis were associated with significantly higher levels of IL-8 during the early phases of infection. Furthermore, IL-6 levels in the early phase of infection were also elevated in bleeding patients with plasma leakage. These results suggest that IL-6 and IL-8 may act in synergy to cause bleeding in patients with plasma leakage.
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PMID:Cytokine Expression in Dengue Fever and Dengue Hemorrhagic Fever Patients with Bleeding and Severe Hepatitis. 3212 29


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