Journal of investigative medicine : the official publication of the American Federation for Clinical Research
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Genetic regulation of immunoglobulin G(IgG) responses to pneumococcal capsular polysaccharides (PPS), has been demonstrated in mice but not in humans. Earlier studies from this laboratory showed that healthy adults have a varying capacity to generate IgG antibody to PPS; this study sought to determine whether this capacity is genetically controlled. ⋯ Thus, humans exhibit a variable capacity to respond to PPS. This response is hereditable in a mixed, codominant fashion. The absence of IgG to a PPS, even after antigen is presented in a protein-conjugate form, may reflect a genetically mediated failure to recognize polysaccharide antigens. Since persons who respond to fewer PPS also have lower levels of IgG to PPS to which they do respond, genetically determined deficiencies in events that involve proliferation of committed B lymphocytes may also play a role.
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The encouraging results of the Diabetes Control and Complications Trial emphasize the need for improved methods of glycemic control to prevent the potentially devastating complications of Type I diabetes mellitus. However, current conventional approaches have failed to consistently achieve normal HbAlc levels and increase the risk of hypoglycemia. Pancreas transplantation is a consistently reliable method of achieving postoperative normal glucose levels, but no extensive assessment has been made of the long-term stability of its metabolic benefits. ⋯ Successful pancreas transplantation provides pancreatic islet function that results in normal or near normal glycemic control for up to five years postoperatively in Type I diabetic recipients receiving no exogenous insulin or oral hypoglycemic agent therapy.
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We assessed the effect of a cytokine inhibitor, compound SKF 86002 (a bicyclic imidazole), on changes in renal hemodynamics (renal blood flow and glomerular filtration rate) that occur acutely following immune injury of glomerular mesangial cells. ⋯ The observations indicate that in mesangial cell immune injury, cytokines mediate renal hemodynamic impairment.