No abstract available.
Anoxia* ; Cochlea* ; Diuretics* ; Guinea*

No abstract available.
Bleomycin* ; Lymphangioma, Cystic*

No abstract available.
Guinea*

BACKGROUND: As a result of exposure to human leukocyte antigen(HLA) by pregnancy, blood transfusion and previous organ transplantation, many patients awaiting renal transplantation can develop HLA antibodies. The level of HLA sensitization is determined by PRA(panel reactive antibody) test using a lymphocyte panel from HLA phenotyped selected donors. In Korea, PRA tests have not been performed routinely for organ transplantations. and there is no available data about HLA sensitization in renal transplantation. METHODS: PRA test was done in 136 sera of chronic renal failure(CRF) patients receiving dialysis (hemodialysis 108, peritoneal dialysis 28) by NIH standard microlymphocytotoxicity method with a frozen lymphocytes panel from 36 HLA-typed donors. PRA positive sera were re-tested after dithiothreitol(DTT) treatment and analyzed for HLA antibody specificities. RESULTS: Thirty five out of 136 sera(25.7%) showed positive PRA values in HLA antibody screening test. The PRA(%) values of the 35 positive sera were distributed into 1-10%(n=8), 10-20%(n=7), 20-50%(n=12) and 50%-100%(n=8). respectively. After DTT treatment, the change of PRA reactivity was divided into three groups. The PRA values of Group A(22 sera: 63%) showed no change, Group B(7 sera: 20%) declined, and Group C(6 sera. 17%) completely disappeared after DTT treatment. The specificities of HLA antibodies were identified in 19 out of 35 sera(54%). The success rate in defining antibody specificities was 0 at PRA values of 1-10% and 70-100%, and high at PRA values of 20-70%. CONCLUSION: We observed that about a quarter of CRF patients have developed HLA antibodies of immunoglobulin class-IgG, mixed IgG and IgM, and IgM HLA antibody in decreasing order of frequency.
Antibodies ; Antibody Specificity ; Blood Transfusion ; Dialysis ; Humans ; Immunoglobulin G ; Immunoglobulin M ; Immunoglobulins ; Isoantibodies* ; Kidney Failure, Chronic* ; Kidney Transplantation ; Korea ; Leukocytes ; Lymphocytes ; Mass Screening ; Organ Transplantation ; Peritoneal Dialysis ; Pregnancy ; Tissue Donors ; Transplants

No abstract available.
Child* ; Humans ; Nephrotic Syndrome*

No abstract available.
Hemolytic-Uremic Syndrome*

No abstract available.
Liver* ; Neoplasm Metastasis*

Annexin-1 (ANX1) is a 37 kDa protein that is induced and secreted by glucocorticosteroid hormone. The secreted ANX1 has been believed to exert its function by binding to its putative rnembrane receptor. In this report we demonstrate that ANXl receptor (ANX1R) signal blocks the interleukin-1B (IL-1B) receptor signal pathway in human peripheral blood mononuclear cells (PBMCs). When PBMCs were treated with both IL-1B (100 ng/ml) and PMA (10 ng/ml) in the absence or presence of dexamethasone for 5 days, dexamethasone (100 nM) suppressed lymphocyte proliferation to 24% of the control. However addition of anti-ANX1 polyclonal antibody of 1:200 and 1:1,000 dilution to this system induced recovery of proliferation to 80% and 40%, respectively, when compared to the control. In the mixed lymphocyte reaction, dexamethasone suppressed lymphocyte proliferation to 9% of that of control when stimulated with IL-1B (100 ng/ml) and phorbol myristate acetate (10 ng/ml). Addition of anti-ANX1 polyclonal antibody (1:1,000) to this system also recovered the proliferation to 20% of that of the control system. In the ANX1 receptor induction experiment using flow cytometry, ANX1 receptor expression on lymphocytes, CD4+ T cells, CD8+ T cells and monocytes increased depending on the externally added IL-1B ranging from 10 to 1,000 ng/ml. From these results, it is evident that dexamethasone induces ANX1 secretion into the culture medium and anti-ANX1 polyclonal antibody abolishes the effects of dexamethasone. Furthermore these results imply that extracellular ANX1 exerts its effects by binding to the receptor on the cell membrane and the activated signal(s) of ANX1R block IL-1B receptor signal in the lymphocytes.
Cell Membrane ; Dexamethasone ; Flow Cytometry ; Humans ; Interleukin-1* ; Lymphocyte Culture Test, Mixed ; Lymphocytes* ; Monocytes ; Signal Transduction ; T-Lymphocytes ; Tetradecanoylphorbol Acetate*

BACKGROUND: Previous reports have suggested that alleles at the plasminogen activator inhibitor-1 (PAI-1) gene are associated with increased risk of developing coronary artery disease, including myocardial infarction and stroke through their effect on PAI-1 levels. Method: We attempted to search English literatures for all reports of possible effects of PAI-1 gene on cardiovascular disease in human published prior to November 1998. We used a Mantel-Haenszel method (fixed effect model) and random effect model, respectively, to perform a meta-analysis of 7 case-control studies that provided information related to the effects of PAI-1 gene on risk of cardiovascular disease. RESULTS: From 7 studies for diagnosed cardiovascular disease, the relative frequencies of the three genotypes among controls was (5G/5G) (homozygous normal), 24.5%; (4G/5G) (heterozygous), 48.2%, and (4G/4G) (homozygous for the mutant, 675 GGGG), 27.3%. These relative frequencies in cases were 21.7% for 5G/5G, 48.0% for 4G/5G, and 30.3% for 4G/4G. In fixed effect model, compared with those with genotype (5G/5G), the overall odds ratio (OR) for cardiovascular disease among those with (4G/5G) was 1.12 (95% CI, 0.93 to 1.34), and it was 1.20 (1.01 to 1.44) for the (4G/4G) genotype. For five studies with myocardial infarction as the outcome, the overall OR of myocardial infarction was 1.20 (0.99 to 1.47) for those with (4G/5G) and 1.24 (1.00, 1.54) for those with (4G/4G) genotypes, respectively. CONCLUSION: Our findings provide support for the weak association between PAI-1 gene and cardiovascular disease, in particular, myocardial infarction.
Alleles ; Cardiovascular Diseases* ; Case-Control Studies* ; Coronary Artery Disease ; Genotype ; Humans ; Myocardial Infarction ; Odds Ratio ; Plasminogen Activator Inhibitor 1* ; Plasminogen Activators ; Polymorphism, Genetic* ; Stroke

No abstract available.
Lymphomatoid Papulosis* ; Mycobacterium* ; Tuberculosis*