To clarify the characteristics of HBV-associated renal lesions, renal biopsies obtained from 22 HBsAg seropositive patients(M:F=32:1) were studied. Other than two(age 4 and 12), all were adults(17-77 y.o.). Twelve of the patients had nephrotic syndrome(NS), 5 NS and hematuria(H), 10 proteinuria and H, one gross H, one microscopic H, and 4 normal urinalysis at the time of biopsy. Light microscopy showed minimal change lesion(MCL) in 9 cases, mesangial proliferative glomerulonephritis(MSPGN) in 6, MPGN type I in 7, MPGN type III in 6, and mebranous nephropathy(MGN) in 5 cases. There were variable immunofluorescent(IF) findings of 25 cases studied; IF staining were predominant with IgG in 10 cases, with IgA in 5 and with IgM in 2 cases. Complements tended to be more strong for C1 &/or C4 than C3. In electron microscopic(EM) studies of MCL group, rare mesangial deposits were noted(3/5). In MSPGN, aside from mesangial deposits, there were occasional subendothelia(2/4) or subepithelial(1/4) deposits. In MPGN type I, in addition to the usual EM features of MPGN, some subepithelial deposits were also observed in 5 cases. In MGN, 3 out of 4 showed subendothelial deposits. Among 7 cases stained for HBsAg all were negative with IF and 2 were positive with PAP method. It is concluded that clinico-pathological findings of HBV-associated nephropathy are variable and partly show lupus-like features, different from primary glomerulopathy.
Adult ; Male ; Female ; Humans ; Biopsy

No abstract available.
Child* ; Humans

This experiment was performed to elucidate the cytologic origin of chemically induced MFH in Wistar rats. The tumor was produced by injections of DMBA(9,10-dimethyl-1,2-benzanthracene). With the produced MFH, cell culture and cloning were performed, followed by establishment of a cell strain, which was investigated by immunohistochemical and electron microscopic studies. The results were as follows. A) By immunohistochemistry of the tumor tissue, fibroblastic cells were positive for MEP-1(specific antibody for fibroblastlike cell of MFH, Takeya, 1993) and Anti-hPH(beta)(Anti-prolyl 4-hydroxylase beta), but negative for TRPM-3 and F4/80. Histiocytelike cells were positive for TRPM-3 and F4/80, but negative for MEP-1 and Anti-hPH(beta). In immunoelectron microscopy, normal spleen macrophage showed linear reactivity in cell membrane for TRPM-3, whereas histiocytelike cells of the tumor disclosed negative reaction. B) At 5 weeks of the primary tumor cell culture, the cells exhibited typical storiform pattern of MFH. C) The established cell strain revealed immunoreactivity for MEP-1 and Anti-hPH(beta), but negative for TRPM-3. The cloned tumor cells showed morphologic characteristics of undifferentiated fibroblastic cell. Latex particle (0.80 micrometer size) phagocytosis was negative in the cloned cell strain. The results of the current study support the concept that principal component cells of MFH is of fibroblastic cell origin.
9,10-Dimethyl-1,2-benzanthracene* ; Animals ; Cell Culture Techniques* ; Cell Membrane ; Clone Cells* ; Cloning, Organism* ; Fibroblasts ; Histiocytoma, Malignant Fibrous* ; Immunohistochemistry ; Macrophages ; Microscopy, Immunoelectron ; Microspheres ; Phagocytosis ; Rats* ; Rats, Wistar ; Spleen

No abstract available.
Asthma*

No abstract available.
Primary Myelofibrosis*

Heat disorders are not uncommon in the military society due to supposedly hard training to overcome the environmental conditions. Twenty-two soldiers with heat disorders were admitted to Chin Hae Naval Hospital June 1969 through July 1970. Hoping that our clinical studies on them contribute to a renewed understanding, the results are reported in summary as follows: 1) Heat disorders occurred with an overall incidence of 3.1 per cent during running in early summer. 2) Of the twenty-two patients, eight (37 per cent) had heat cramps, six (27 per cent) heat exhaustion, five(23 per cent) heat stroke, and three(13 per cent) had undetermined disorder. 3) Ten patients(45 per cent) were comatous, and this occurred most frequently(80 per cent) among those with heat stroke. 4) All patients were grouped into four according to their physical status on admission. Those with heat exhaustion mostly belonged to group I (good) or group II (fair). Those with heat stroke and heat cramps eomprised most of group III (poor) and group IV (grave). 5) Group I and II patients recovered within 12 hours; group III, within 12~24 hours; and group IV, required more than 24 hours of care. 6) One patient with heat stroke, graded V, expired with sudden hypothermia 15 hours following admission. Overall mortality of heat disorders was 4.5 per cent, and that of heat stroke 20 per cent. 7) The rest recovered uneventfully within 19 hours of average.
Chin ; Emergencies* ; Heat Exhaustion ; Heat Stress Disorders ; Heat Stroke ; Hope ; Hot Temperature* ; Humans ; Hypothermia ; Incidence ; Military Personnel ; Mortality ; Running

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*

No abstract available.
Child* ; Humans

No abstract available.

No abstract available.
Infection Control*