学报发展之我见

国家最新的统计数据显示,在我国5000种科技期刊中,高等院校所办的期刊已经达到1347种,其中绝大多数为学报;在我国1124种医学期刊中,学报也占有较大的比例．尽管学报的数量不少,但从期刊的综合评价体系来看,其中高质量者寥寥无几;而获得过“首届国家期刊奖,第二届国家期刊奖提名奖”的第四军医大学学报无疑是其中的佼佼者、尽管我们取得过辉煌的成绩,但依旧无法回避今日严峻的现实．要使学报能够健康地发展,我认为以下几点不容忽视．     

Hypocomplementemic urticarial vasculitis syndrome in identical twins

Hypocomplementemic urticarial vasculitis syndrome (HUVS) is a syndrome of recurrent urticarial vasculitis, arthralgia/arthritis, and hypocomplementemia. Angioedema, ocular inflammation, glomerulonephritis, and obstructive lung disease are other clinical findings. Although the etiology of HUVS is unknown, its resemblance to systemic lupus erythematosus (SLE) suggests a similar pathogenesis. SLE is known to occur in identical twins. This is the first report of a pair of identical twins with HUVS. Concordance for HUVS in identical twins suggests that the pathogenesis of the disease involves abnormal genetic immunoregulation.     

Decay-accelerating factor confers protection against complement-mediated podocyte injury in acute nephrotoxic nephritis

SUMMARY: Decay-accelerating factor (DAF or CD55) is one of a set of regulators that function to protect self cells from deposition of autologous C3b on their surfaces. Its relative importance in vivo, however, is incompletely understood. As one approach to address this issue, we induced nephrotoxic serum (NTS) nephritis in wild-type mice and Daf1 gene-floxed mice devoid of renal DAF expression. For these experiments NTS IgG was administered at a dose (0.5 mg iv) that requires complement for glomerular injury. After 18 hours, renal injury was assessed by proteinuria and by histologic, immunohistochemical, and electron microscopic analyses of kidneys. Fifteen normal and 15 DAF-deficient mice were studied. Baseline albuminuria in the Daf1(-/-) mice was 115.9 +/- 41.4 microg/mg creatinine as compared with 85.7 +/- 32.3 microg/mg creatinine in their Daf1(+/+) littermates (p = 0.075). After administration of NTS IgG, albuminuria increased to 2001.7 +/- 688.7 microg/mg creatinine as compared with 799.7 +/- 340.5 microg/mg creatinine in the controls (p = 0.0003). Glomerular histology was similar in Daf1(-/-) and Daf1(+/+) mice, with essentially no infiltrating leukocytes. In contrast, electron microscopy revealed severe podocyte fusion in the Daf1(-/-) mice but only mild focal changes in the controls. Immunohistochemical staining showed equivalent deposition of the administered (sheep) NTS IgG in the Daf1(-/-) and Daf1(+/+) animals. This contrasted with marked deposition of autologous murine C3 in the former and minimal deposition in the latter. The results show that DAF is essential physiologically for protecting glomeruli against autologous complement attack initiated by the classical pathway.