用混合粘合剂碳糊电极测定丁螺环酮

用混合粘合剂碳糊电极测定丁螺环酮张正奇，曾鸽鸣，刘传桂，黎艳飞（湖南大学化学化工系，长沙４１００８２）碳糊电极无毒，制作方便，表面更新容易，应用电位范围广，在药物分析中已有应用［１～５］。我们在液体石腊中加入添加剂，组成混合粘合剂，可显著改善电极的检...     

Unexpected severe reversible cyclosporine A-induced nephrotoxicity in a patient with systemic lupus erythematosus and tubulointerstitial renal disease

We describe a patient with systemic lupus erythematosus and impaired renal function probably mainly due to tubulointerstitial disease. After a six-week course of low-dose cyclosporine A, she developed a severe but reversible loss of glomerular filtration rate and effective renal plasma flow despite of low cyclosporine A plasma levels. Based upon the observed fall of the filtration fraction, the rise in the relative clearance of 99Tc-dimercaptosuccinic acid and the increase in proteinuria, we suggest that in this case the tubules and/or interstitium are the main targets for cyclosporine A nephrotoxicity. Neither our patient's clinical symptoms nor her serologic parameters improved possibly because of the low dosage and/or short duration of cyclosporine A treatment. We conclude that one should be cautious when treating patients with systemic lupus erythematosus and pre-existing renal disease with cyclosporine A especially when tubulointerstitial abnormalities are present and/or other nephrotoxic drugs are used.     

Viral infections in the mouth

Oral hairy leukoplakia (OHL) and Kaposi's sarcoma (KS) are commonly encountered in the HIV-infected patient. A unique feature of OHL is non-cytolytic high level of replication of Epstein–Barr virus (EBV) in the glossal epithelium. The expression of viral-encoded anti-apoptotic proteins concomitant to replicative proteins probably underlies this phenomenon. The question of whether OHL arises from activation of EBV latent in the tongue, or from superinfection by endogenous EBV shed via non-glossal sites or by exogenous EBV remains unresolved. Human herpesvirus 8 (HHV8) is now seen as necessary but not sufficient cause of KS. Expression of HHV8-encoded oncogenic proteins in endothelial cells probably explains the aberrant proliferation of these cells in KS lesions. Studies into why KS is so commonly observed at the palate in HIV-infected patients may provide important clues to its pathogenesis.     

Systemic injection of products of activated neutrophils and H2O2 in myeloperoxidase-immunized rats leads to necrotizing vasculitis in the lungs and gut.

The strong association of anti-neutrophil cytoplasmic antibodies with various forms of systemic vasculitis suggests a role for these autoantibodies in the pathophysiology of systemic vasculitis. In the present study, we tested the hypothesis that release of neutrophil lysosomal enzymes in the presence of an anti-myeloperoxidase (anti-MPO) immune response may underlie the development of systemic vasculitis. Brown Norway rats were immunized with MPO in complete Freund's adjuvant or complete Freund's adjuvant alone. Two weeks after immunization, rats bad developed antibodies to human and rat MPO as measured by enzyme-linked immunosorbent assay. Next, rats were intravenously infused with 400 micrograms of a human neutrophil lysosomal extract containing 200 micrograms of MPO followed by 0.5 ml of a 1 mmol/L solution of H2O2 through a cannula inserted into the right jugular vein. Rats were sacrificed at 4 hours, 24 hours, 7 days, or 14 days, and several organs (lungs, heart, liver, spleen, gut, and kidneys) were examined for vasculitic lesions and inflammatory cell infiltrates. Macroscopically, patchy hemorrhagic spots were observed in the lungs and gut of MPO-immunized rats at days 7 and 14 after systemic infection of the neutrophil lysosomal extract and H2O2. Such changes were not observed at earlier time points or in control immunized rats. Histologically, the lungs of MPO-immunized rats sacrificed at days 7 and 14 showed patchy inflammatory cell infiltrates associated with vasculitis, granuloma formation, giant cells, and foci of hemorrhage. At 14 days, early signs of fibrosis were found with deposition of collagen and proliferation of fibroblasts. Furthermore, a prominent leukocytoclastic vasculitis was found in the small intestine of these rats characterized by fibrinoid necrosis and an extensive neutrophilic infiltrate. No inflammatory changes were found in the other organs studied (heart, liver, spleen, and kidneys). Control immunized rats, sacrificed at days 7 and 14 showed only some small foci of inflammatory infiltrates in the lungs whereas no inflammatory changes were found in the gastrointestinal tract. These studies show that release of products from activated neutrophils in the presence of anti-MPO autoantibodies may be relevant to the pathogenesis of anti-MPO-associated vasculitides.     

Reticuloendothelial Fc receptor function in SLE patients. I. Primary HLA linked defect or acquired dysfunction secondary to disease activity?

Reticuloendothelial system (RES) Fc receptor-mediated immune clearance was measured in 18 patients with systemic lupus erythematosus (SLE). Only two patients, with major disease activity, had a prolonged T 1/2 of the blood disappearance curve of injected IgG coated red cells in comparison to 22 healthy controls. Circulating immune complexes (CIC) were studied with three methods: PEG precipitation, C1q-ELISA and the indirect granulocyte phagocytosis test (IGFT). The T 1/2 of the blood disappearance curve related significantly to the IGFT (r = 0.55, P less than 0.05) and not to the PEG and C1q-ELISA test. Although HLA-DR3 phenotype frequency was significantly increased in our SLE population (P less than 0.05), it was not related to Fc receptor function. Similarly, HLA-DR2 phenotype was not related to RES Fc receptor function. These data do not support the concept that a genetic HLA linked defect in reticuloendothelial Fc receptor function is a primary cause of SLE, predisposing the inflicted individual to immune complex deposition. However, Fc receptor-mediated immune clearance seems to be related to disease activity itself and to levels of CIC.     

"Advising Oliver Mann"--a case-based, small-group orientation to medical school.

In 1998, the authors implemented a new academic orientation built around a problem-based clinical exercise for entering medical students, to prepare them for a curriculum emphasizing active learning in small groups. The exercise enables students to begin their professional studies with a "hands on" understanding of two major emphases of the curriculum: (1) the process of small-group learning that will guide their medical education and (2) the principles of patient care that will guide their future practice of medicine. Called "Advising Oliver Mann," this orientation presents students with a clinical problem that they must work in small groups to solve. By collaborating in teams of ten, they become acquainted with the small-group learning methods at the heart of the school's curriculum. Through solving a clinical problem, they discover vital principles of patient care, such as the need in clinical decision making to integrate the scientific perspective with the perspective of patient and family. In developing "Oliver Mann," the authors came to realize that orientations can be much more than introductions. They can be reflective moments in a busy curriculum, a time for students and faculty to step back and take stock of important issues in education and doctoring. The authors are currently experimenting with exercises linking their freshman orientation with orientations in the second and third years so participants can reflect on the challenges of each new year and carry forward the small-group methods and practice of medicine themes of the new curriculum.