To investigate the significance and age characteristics of CVB infections among common diseases of children.CVB Ag and CVB IgM were detected from the sera in 967 children in hospital. Positive rates of CVB Ag and CVB IgM in the upper respiratory tract infection group, the lower respiratory tract infection group, the myocarditis group, the asthma group, the ITP group and the anaphylactoid purpura group were higher than the control group.Most of the children with positive CVB were in the 0～1 year age group and 1～3 years age group had respiratory tract infection. With increasing age,the number of the children with respiratory tract infection gradually decreased,while number of the children with myocarditis,asthma,ITP and anaphylactoid purpura increased in those children with positive CVB. It suggests that, beside respiratory tract infection,CVB plays an important role in pathogenesis of myocarditis,asthma,ITP and allergic purpura in children.

AIM:To investigate the impact of excessive endoplasmic reticulum stress on apoptotic cell death in a rat model of chronic cyclosporine A ( CsA ) nephrotoxicity .METHODS: Male Sprague-Dawley rats on a low-salt diet were subcutaneously injected with vehicle (olive oil, 1 mL· kg-1· d-1) or CsA (15 mg/kg) daily for 1 or 4 weeks.Tu-bulointerstitial fibrosis and apoptotic cell death were estimated by trichrome staining and TUNEL staining .In addition , im-munohistochemistry and immunoblotting were used to evaluate the expression of immunoglobulin -binding protein ( BiP) , eu-karyotic initiation factor 2α(eIF2α), growth arrest and DNA damage-inducible protein 153 (GADD153), caspase-12 and caspase-3.RESULTS:The rats treated with CsA for 1 week did not develop tubulointerstitial fibrosis and TUNEL-positive cells, whereas 4-week treatment with CsA induced typical tubulointerstitial fibrosis and increased TUNEL-positive cells. CsA induced a significant increase in BiP and caspase-12 expression peaked at 1 week, and then returned to normal levels at 4 weeks.In contrast, the expression of eIF2α, GADD153 and caspase-3 in CsA-treated rat kidneys were significantly in-creased in a time-dependent manner .CONCLUSION:Excessive endoplasmic reticulum stress causes apoptotic cell death by depleting molecular chaperones and stimulating the proapoptotic pathway in chronic CsA nephrotoxicity .