Germinal centre and plasma cell reaction of the thymus in rheumatic heart disease.
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Biomedical subjects
Publications and source records attributed to U N Bhuyan.
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In view of the depressed immunity in protein malnutrition, an assessment of the lymphoproliferative activity of the constantly stimulated mesenteric lymph node of the guinea pig was undertaken. A significant reduction of this activity was observed in protein deficiency. a) The germinal centers were reduced in number and size; new formation in the medulla was rarely seen. Lymphoid cells showed lowering of mitotic index and mitotic rate and prolongation of mitotic duration and turnover time. Nuclear labeling with (3)H-thymidine was focal and localized to the peripheral zone. b) Mitotic activity and nuclear labeling were less pronounced in the outer cortex and medulla and least in the paracortical area. Specific uptake of (3)H-thymidine paralleled the low labeling index. c) No appreciable reduction in the number of plasma cells in the medulla was observed. Serum gamma-globulin levels were not significantly altered, but albumin levels were consistently reduced. This was suggestive of preferential preservation of plasma cell activity in the malnourished host. d) There were significant lymphopenia and neutropenia with relative increase of neutrophils in the peripheral blood. This might indicate more severe involvement of lymphopoiesis than myelopoiesis in protein malnutrition.
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In view of increased susceptibility to tuberculosis in protein malnutrition, the phenomenon of accelerated granulomatous response by the macrophage was studied in rabbits immunized and subsequently challenged with BCG. Dietary protein depletion resulted in marked retardation of macrophage mobilization and granuloma formation in various organs. The granulomatous index was low in most organs. The granulomas were few, small, abortive and ill-formed by loosely knit epithelioid cells and giant cells. This deficiency of macrophage function might limit the effectiveness of BCG vaccination in the malnourished host.
Two groups of guinea pigs were maintained on high-protein and low-protein diets and immunized with intradermal BCG. Protein deficiency was accompanied by marked inhibition of local and systemic immune responses: a) The BCG nodule was poorly formed. There was marked delay and deficiency in the mobilization of macrophages. b) The draining lymph node was atrophic and showed little or no proliferation of lymphoid cells in the paracortical area. Macrophage accumulation occurred late but became diffuse and marked, in contrast to its consistent scarcity in the BCG nodule. c) In either location epithelioid cell transformation was retarded. Well-formed mature epithelioid cell granulomas were not seen. d) Bacilli persisted for a long time in the skin and lymph node lesions, e) Tuberculin sensitivity was greatly impaired in one-fifth of animals and absent in others. These findings were suggestive of macrophage dysfunction and depression of cell-mediated immunity to BCG in the protein-deficient guinea pig.
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Staphylococcal bacteremia was induced in two groups of rabbits that were pairfed high protein and protein deficient diets. Marked deviations in response were observed as a result of protein deficiency: a) blood clearance of S aureus was delayed; b) persistence and multiplication of bacteria in blood and tissues were pronounced; c) neutrophilic response was poor and transitory; d) mortality was very high and occurred very early and e) focal necrotizing lesions, rather than well-formed abscesses, were found in organs.
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In a large series of patients with insulin-dependent diabetes mellitus who were screened for autoantibodies, two patients were positive for antinuclear antibodies. Both of these patients developed severe renal disease with the renal biopsy findings of membranoproliferative glomerulonephritis. Multiple autoantibodies and circulating immune complexes were demonstrated in their sera. There was evidence suggesting complement consumption. This article illustrates that immune complex glomerulonephritis can occur in some patients with IDDM, particularly in those with antinuclear antibody and polyendocrine involvement, and that renal biopsy in such cases may have prognostic and therapeutic importance.
An 8-week therapy with cyclophosphamide (CP) and alternate-day prednisone was given to 65 patients having steroid-sensitive, frequently relapsing nephrotic syndrome, including 17 with steroid dependence. It induced remissions of less than 6 months in 18 patients, 6 to 36 months in 21 and over 3 years in 26. Considering a remission of 6 months as significant, certain clinical variables were compared in patients without such a response with those getting longer remissions. In the group with frequent relapses a higher proportion of patients aged above 8 years had remissions of over 6 months as well as over 3 years, than those who were younger at CP therapy. Among patients with frequent relapses as well as those with steroid dependence, a post-CP remission of more than 6 months was associated with a better long-term course. The response to CP in both groups was similar regarding the duration of remissions, but a greater proportion of steroid-dependent patients subsequently again showed steroid dependence or frequent relapses. Our findings suggest that a higher age at CP therapy and an ensuing remission of over 6 months are predictors of a better response, and steroid dependence of a less favorable outcome.
Twenty four patients who were HBsAg positive prior to renal transplantation were studied with respect to their hepatic and renal outcome. The kidneys in all patients were obtained from living related donors. The standard immunosuppressive therapy consisted of azathioprine and prednisolone. Post-renal transplant follow-up varied from 32-86 months (mean 55 +/- 9). Renal functions, liver functions, HBsAg and HBsAb status was closely monitored during follow-up. One patient developed acute hepatitis four months after transplantation; this resolved in 10 weeks. Four patients showed transient elevations of liver enzymes. The results of liver biopsy in 16 cases revealed, normal histology (8), virus in hepatocytes (5), and acute hepatitis (3). None of the patients had evidence of chronic liver disease. Two patients died due to chronic rejection/chronic renal failure and two patients died due to septicaemia. Five living patients have mild to moderate chronic rejection. It was concluded that pre-existing HBsAg carrier state in transplant patients had no deteriorating effect on the liver. The mortality was related to chronic rejection and septicaemia.
Thus I would like to conclude by saying that an idiopathic form of obliterative renal arteriopathy account for the rare presentation of severe hypertension and progressive renal failure with or without overt hemolytic anemia and thrombocytopenia in children. It can be labelled as primary malignant nephrosclerosis (NScl) or atypical HUS, based on primary thrombotic angiopathy. This, essentially intimal changes, is seen in diverse conditions and appears to result from primary endothelial injury followed by intimal exudation, thrombosis, and repair by fibrosis. Persistent or recurrence of this process form the basis of progressive obliterative arteriopathy. The result is renal ischemia and renin-angiotensin mediated hypertension. Establishment of a vicious circle would further accelerate HT and lead to end stage renal failure. Early recognition and prompt therapeutic intervention might prove beneficial.