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)

We have studied the localization of Australia antigen, a particulate substance associated with hepatitis, by means of the fluorescent antibody technique. Preparations were made from 61 liver biopsy specimens taken from patients with infectious hepatitis, serum hepatitis, and a variety of other diseases. When tested with fluorescein-conjugated rabbit anti-Au(1) antisera all 26 patients who had Au(1) in their serum had specific fluorescence in their liver cells. The fluorescence appeared in three forms: as discrete particles within the nucleus, diffuse fluorescence of the entire nucleus, and fluorescence of the nuclear rim. Occasionally there were also fluorescent particles in the cytoplasm. Other specimens were tested with the fluorescent antibody including a variety of human tissues, buffy coat smears, peripheral lymphocyte cultures, and cells obtained from bile and duodenal drainage. Among these specimens, fluorescence was found in the cytoplasm of a few cells in the bone marrow of two patients with hepatitis and Au(1) in their serum, and in the liver, spleen, mesentery, and testis of one patient with leukemia, chronic hepatitis, and Au(1) in his serum. We have shown that the presence of fluorescent particles in the liver cells is strongly associated with the presence of Au(1) in the serum and the diagnosis of viral hepatitis. We believe that this study adds support to the hypothesis that Australia antigen is an antigenic determinant of a virus capable of causing hepatitis.
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PMID:The localization of Australia antigen by immunofluorescence. 491 97

An attempt is made to improve the methodology for the detection of lymphocytic Fc receptors, using 125I-labelled protein A from Staphylococcus Aureus (125ISpA) and different immunoglobulins G such as human monomer IgG, Fc antiserum and swine Fc+F'c antiserum. The working conditions and sources of error that might affect the results were established. This methodology was applied to the study of leukemia, chronic hepatitis, allergic diseases and normal cases. In the chronic lymphoid leukemia cases the determinations were repeated at different clinico-biological stages. The values obtained in these cases have always been higher than normal. This method may be used for rapid determination of the presence of Fc receptors; its application in the clinic would furnish useful data. It still remains to be established whether determination of these lymphocytic receptors might contribute data that can be corroborated by the response to the immunodepressor treatment applied in some cases.
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PMID:Detection of lymphocytic Fc receptors with 125I-labelled protein A. 712 14

GM-CSF has been used successfully in autologous BMTs, and more recently in patients undergoing allogeneic BMT, for acute or chronic leukemia. We report two patients with hepatitis-related aplastic anemia who received recombinant human GM-CSF following HLA-identical sibling allogeneic BMTs. Both patients were conditioned with CY 200 mg/kg given over 4 days and received GM-CSF at 250 micrograms/m2 beginning 6 h after marrow infusion and continuing daily until the absolute neutrophil count was > 1.0 x 10(9)/l for 2 days. Both patients had prompt engraftment, achieving an absolute neutrophil count of > 0.5 x 10(9)/l on day 13. Neither patient had side-effects attributable to the GM-CSF although one patient developed severe acute GVHD after the cessation of GM-CSF therapy. Our experience suggests that GM-CSF can be safely used in aplastic anemia patients undergoing BMT and that GM-CSF may be useful to decrease the incidence of graft failure associated with less intensive conditioning regimens.
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PMID:Use of recombinant GM-CSF following allogeneic BMTs for aplastic anemia. 840 68

The objective was designed to assess the clinical efficiency of preventing febrile nonhemolytic transfusion reactions (FNHTR) with transfusion of leukocyte-depleted RBC and platelet concentrates. One hundred patients with cirrhosis of liver, gastric ulcer and cancer were selected to receive RBC concentrates with leukocyte filtration. Another group of 50 patients with liver necrosis, gastric ulcer and cancer were selected to receive non-filtered RBC concentrates. Two hundred and forty patients with acute or chronic leukemia, aplastic anemia, multiple myeloma, thrombocytopenia purpura, diabetes mellitus, cirrhosis of liver, upper gastrointestinal hemorrhage, severe hepatitis, burn and cancer post radioactive or chemical treatment were divided into two group with 120 patients in each one and selected randomly to receive platelet concentrates. The incidence rates of FNHTR in all patients were investigated. Results showed that there was no FNHTR in 100 transfusions with leukocyte-depleted RBC concentrates. Eight out of 50 patients with non-filtrated RBC concentrates showed FNHTR. The incidence of FNHTR was sixteen (16%) in non-filtrated transfusion. Twenty-five and 7 patients manifested FNHTR respectively in non-filtrated or filtrated platelets transfusions. The incidence of FNHTR was 20.83% and 5.83% respectively in non-filtrated or filtrated platelet transfusion. It is concluded that leukocyte-depleted RBC and platelet concentrates reduces FNH TR in blood transfusion.
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PMID:Clinical assessment of preventing febrile nonhemolytic transfusion reaction by leukocyte-depleted blood transfusion. 1251 24