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Beginning with an introduction to overseas practices of privilege management, this paper analyzed the current privilege management of medical qualifications in China. On such basis, the authors introduced their insights and specific recommendations for the design and implementation of such management in China. These include: a platform for privilege management, a classified catalogue for medical qualifications, a procedure for the application, approval, examination and dynamic management of the qualifications, and an informatization platform for privilege management.
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Beginning with an introduction to overseas practices of privilege management, this paper analyzed the current privilege management of medical qualifications in China. On such basis, the authors introduced their insights and specific recommendations for the design and implementation of such management in China. These include: a platform for privilege management, a classified catalogue for medical qualifications, a procedure for the application, approval, examination and dynamic management of the qualifications, and an informatization platform for privilege management.
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10.3969/j.issn.1000-3606.2013.06.020
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Objective To analyze the clinical and pathological characteristics of Alport syndrome in children. Methods Clinical and pathological information gathered from 62 patients during March 1989 to August 2012 was retrospectively analyzed. Results Four autosomal recessive Alport syndromes (AR-AS) and 58 X-linked Alport syndromes (XL-AS) were analyzed. Of the XL-AS, 47 were boys and 11 were girls. Most of patients induced by upper respiratory tract infections, and onset with hematuria and proteinuria. There was no signiifcant gender difference in family history, impaired renal tubular proteins, hypertension, im-paired renal function, hearing loss, ocular abnormalities or renal pathological changes under light microscopy. However, extensive lamination and split of glomerular basement membrane (GBM) dense layers were found in 83.0%male and 18.2%female patients (P=0.000) and the rest patients were presented with limited distribution of typical GBM changes. Proteinuria progressed signiif-cantly with age in XL-AS males (r=0.501, P=0.000). Five XL-AS patients developed to end stage renal disease (ESRD) between 11 to 16 years old. Conclusions XL-AS is the main inherited type and severe changes of GBM are common in XL-AS males. Proteinuria increases remarkably with age. The detection of type IV collagen in renal tissue or skin is helpful to diagnose Alport syndrome and conifrm inheritance modes.
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BACKGROUND: One of important mechanisms underlying myocardial fibrosis is that transforming growth factor β1(TGF-β1) stimulates the proliferation and differentiation of cardiac fibroblasts via Smads signaling pathway.Previous studies have confirmed that tanshinone ⅡA can effectively inhibit myocardial fibrosis.But whether blockage of TGF-β1/Smads signaling pathway is involved in this process remains unclear. OBJECTIVE: To investigate the effects of tanshinone ⅡA on TGF-β1 signal transduction in rat cardiac fibroblasts. METHODS: Neonatal rat cardiac fibroblasts were harvested by trypsin digestion and differential attachment and treated with 5 μg/L TGF-βI and different concentrations of tanshinone Ⅱ A(106,10-5 and 10-4 mol/L).At 6,12,and 24 hours after TGF-β1 application,fibronectin expression was detected by reverse transcription-polymerase chain reaction and Western blot analysis.At 15,30,60,and 120 minutes after TGF-β1 application,Smads protein expression was determined by Western blot analysis. RESULTS AND CONCLUSION: Fibronectin mRNA and protein expression began to increase at 6 hours after TGF-β1 application and was 1.3 and 1.8 times higher than initial level,respectively(P < 0.01),at 24 hours after TGF-β1 application.Phosphorylated Smad2/3 protein expression began to increase at 15 minutes after TGF-β1 application,peaked at 1 hour,decreased at 2 hours,but it was still 3.9 times higher than initial level(P < 0.01).Tanshinone ⅡA(10-5 and 10-4 mol/L)pretreatment downregulated fibronectin and phosphorylated Smad2/3 expression(P < 0.05 or P < 0.01)in a dose-dependent manner.These findings demonstrate that TGF-β1 induced fibronectin protein and mRNA expression and Smad2/3 protein expression in a time-dependent manner.Tanshinone ⅡA against myocardial fibrosis was likely related to its inhibition of TGF-β1-induced Smad2/3 phosphorylation and blockage of TGF-β1/Smads signaling pathways within cardiac fibroblasts.