Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019163 (hepatitis B)
 38,309 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Hepatitis B virus (HBV) is the most meaningful risk factor in chronic hepatitis, cirrhosis and primary hepatocellular carcinoma (PHC). The hepatitis B virus X protein (HBxAg) is a multifunctional protein with many important functions in hepatocellular carcinogenesis. A monoclonal anti-HBxAg antibody was developed in our laboratory and characterized by different methods. Using this antibody HBxAg was detected in formaldehyde fixed paraffin embedded tissue sections of 72 liver biopsies from patients with acute hepatitis, chronic hepatitis, cirrhosis and primary hepatocellular carcinoma. The co-expression of hepatitis B surface antigen (HBsAg), hepatitis B core antigen (HBcAg) and HBxAg was compared. The histological and cytological localization of the detected HBxAg showed a characteristic distribution in different stages of HBV infection. Strong and diffuse nuclear reaction was detected in PHC cases in contrast to the focal, cytoplasmic and nuclear labeling in the acute and chronic B hepatitis cases. Our antibody seems to be a suitable prognostic marker for routine pathohistological diagnosis and for comparative pathological and epidemiological research on the development of PHC.
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PMID:Immunohistochemical assessment and prognostic value of hepatitis B virus X protein in chronic hepatitis and primary hepatocellular carcinomas using anti-HBxAg monoclonal antibody. 1169 43

A novel method was developed for the precise quantitation of viruses using infrared fluorescent detection of foci of infection in conventional cell culture plates. In this assay, termed the infrared fluorescent immunofocus assay (IR-FIFA), appropriate cell cultures were infected with serial dilutions of hepatitis A virus (HAV) or measles virus (MV) and maintained with a semi-solid overlay for 1-5 days. Cell monolayers were fixed with formaldehyde, and then stained in succession with a primary monoclonal antibody and an Alexa Fluor 680 conjugate. Foci of infection (analogous to plaques) were detected by scanning culture plates using the Odyssey infrared imaging system and counted to determine the virus titre, expressed as focus forming units (FFU) per mL, as is done for conventional plaque assays. HAV and MV were used as models of minimally cytopathic viruses, and showed a linear dose-response between focus formation and virus dilution. Viral titres calculated using this method were comparable to conventionally used methods. The IR-FIFA was also successfully adapted to quantify duck hepatitis B virus (DHBV) as a model for a non-cytopathic virus. This simple and sensitive assay will have wide use for the quantitation of non-cytopathic and minimally cytopathic viruses.
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PMID:Infrared fluorescent immunofocus assay (IR-FIFA) for the quantitation of non-cytopathic and minimally cytopathic viruses. 1630 Aug 33

The use of a surrogate virus, namely duck hepatitis B virus (DHBV), has been recommended for testing the virucidal activity of chemical biocides against hepatitis B virus. To date, however, this model has not been recognized as a standard test in European countries, as its laboratory use is associated with considerable difficulties. As previous studies have demonstrated, several alternative procedures may improve the validation of DHBV infection in a cell culture system. Using indirect immunofluorescent antigen staining and the light cycler real-time polymerase chain reaction (PCR) technique, the virucidal activity of peracetic acid (PAA), povidone-iodine (PVP-I) and formaldehyde was tested against DHBV obtained from congenitally infected ducks or prepared from the transfected hepatoma D2 cell line. The results demonstrated that inactivation of DHBV from the D2 cell line was achieved with lower concentrations of the biocides and within shorter exposure time intervals. These lower concentration-exposure time values for DHBV from D2 cells in comparison with DHBV from infected ducks indicated a higher sensitivity of the virus derived from D2 cells. In addition, concentrations of PAA and PVP-I that significantly inactivated DHBV in suspension tests were not able to destroy the viral genome. In conclusion, DHBV from congenitally infected ducks should be used for virucidal testing of chemical biocides against DHBV; DHBV prepared from D2 cells is unsuitable due to its higher sensitivity to biocides. Indirect immunofluorescent staining allows reliable detection of DHBV infectivity, whereas the hepadnavirucidal effect can be evaluated by quantitative PCR.
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PMID:Validation of biocides against duck hepatitis B virus as a surrogate virus for human hepatitis B virus. 1701 65

Efficient hemodialysis requires establishing a permanent stable vascular access. Our study was designed to evaluate formaldehyde-fixed arterial allografts as hemodialysis access for end-stage renal disease. Various parameters were determined for 68 formaldehyde-fixed, cadaver-derived allografts transplanted into 43 hemodialysis patients. The sources of the allografts were determined to be free of cytomegalovirus, hepatitis B and hepatitis C, and HIV infections. These allografts were monitored for rejection, blood flow, patency rates, and complications. Overall, antigenicity of the allografts was reduced after formaldehyde fixation with no acute rejection. The mean access blood flow was 696+/-282 ml with reasonable primary and secondary patency rates even after 3 years. Allograft intimal hyperplasia, determined by immunohistochemistry, was evident as the proliferation of smooth muscle-like cells expressing actin but cells not expressing the endothelial markers von Willebrand factor or CD34. The incidence of thrombus formation was about 37% after allograft transplant with other limited complications of pseudoaneurysms and local infection. Our results support the clinical use of formaldehyde-fixed arterial allografts for hemodialysis access.
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PMID:Clinical studies of hemodialysis access through formaldehyde-fixed arterial allografts. 1797 6

In the early 60s the first specialists for hospital hygiene came on the scene in Scandinavia too. From the outset this new discipline was based on cooperation between doctors and nurses, with the support of hospital-based microbiology laboratories and of sterilization departments. Teaching programs were soon devised, with training being underpinned by manuals featuring working instructions. Automated washing facilities for bedpans, etc. or washing machines for medical instruments became widespread practice very quickly; these initially used hot water, and later steam, for disinfection. For many years now, this equipment is found not only in hospitals but in virtually all healthcare establishments too. This has considerably helped to reduce chemical disinfection of medical instruments. As regards disinfection of heat-sensitive instruments the Scandinavian countries adopted different approaches: Finland gave preference to ethylene oxide sterilization, while Sweden opted for lower temperatures and for formaldehyde (low-temperature, steam formaldehyde (LTSF) sterilization), a technique imported from England and further developed in Sweden. During the 70s there were several cases of hepatitis B infections contracted in hospitals, particularly in dialysis units and by hospital personnel. The requirement that gloves be worn when carrying out working procedures has resulted in a major decrease in the infection rate and has helped to prevent HIV (AIDS) infections. However, to date it has not been possible to offset the risk of bloodborne infection against latex intolerance. Infection statistics were introduced in the 80s and since the late 90s we, too, are waging battle (later than other countries) against resistant bacteria (MRSA, VRE, multi-resistant Gram-negative bacteria). For some years now we no longer use the term "hospital hygiene" either, using instead "infection in healthcare settings" in view of the extended fields of application. Whether our strategy has proved successful for prevention of infection? Who could give a clear answer to such a question? Cost pressures in the healthcare sector will have a negative effect on the infection rate despite the fact that the progress made by science should really bring about a reduction in this rate. This conjures up a situation analogous to that of a downward escalator that one is trying to ascend: it is as if one were not moving, not making any progress.
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PMID:Forty years of control of healthcare-associated infections in Scandinavia. 2020 Jun 70


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