Objective:To investigat the treatment effects of reattachment of skin combined with vacuum sealing drainage(VSD)on large avulsion injury of skin of lower limb.Metbods:44 cases of treated by reattachment of with sieve-pore full-thickness skingrafts,the wound surface was filled with polyvinyl alcohol foams(vacuscal)continuous negative pressure drainage was taken for 24h.Result:The average tim of VSD was 7 days.39 cases recovered completely.The flap survival rate in 5 cases was reattaching sieve-pore full-thickness skin grafts combined with VSD,which is a crediable treatment of limbs skin-tear wound。Conclusion:The large avulsion injury of skin of lower limbs could be closed by reattaching sieve-pore full-thickness skin grafts combined with VSD,which is a crediable treatment of limbs skin-ter wond.

Objective To study outcomes of the family doctor contact system and outpatient coordination system in Qingdao.Methods Random selection of 400 community residents and 576 outpatients for a questionnaire survey,using t tests and time series analysis.The purpose is to analyze the number of insured workers,community referrals,costs of hospitalization and the proportion of out-of-pocket payment,and impacts on community healthcare services.Results Number of insured works increased year by year,up to 1,739,931 in 2010.The proportion of community referred hospitalization was raised to 56.97％ in 2010 and increased 54.26％ compared to 2007.Hospitalization costs and the proportion of out-of-pocket payment were reduced.Conclusion The family doctor contact system and outpatient coordination system in Qingdao proved a success,as the practices were highly popular among the employees,and benefited community health centers as well,making it worthwhile to promote.

AIM: To study the effects of prearuptorin C (Pra-C) on myocardial sarcolemma Na~+, K~+-ATPase activity, myocardial mitochondria Na~+, K~+-ATPase, Ca~ 2+ -ATPase, Mg~ 2+ -ATPase activities and apperent Km and Vmax in spontaneously hypertensive (SHR) and renovascular hypertensive rats (RHR). METHODS: ATPase activity was measured with colourmetric method. Apparent Km and Vmax of both Na~+, K~+-ATPase in myocardial sarcolemma and Ca~ 2+ -ATPase in myocardial mitochondria were calculated according to Lineweaven-Burk double-reciprocal plot method with liner regression. RESULTS: The Vmax of both Na~+, K~+-ATPase in myocardial sarcolemma and Ca~ 2+ -ATPase in myocardial mitochondria were lower in SHR untreated group than that in SD control rats, while Km was higher than that in SD control rats. In RHRs untreated group, only Vmax was decreased, while the Km had no statistically change. Pra-C prevented the reduction of ATPase in amount, but not affected their intrinsic characteristics. CONCLUSIONS: The results suggest that both amounts and affinities to ATP of Na~+, K~+-ATPase and Ca~ 2+ -ATPase were decreased in SHRs, but in RHRs, only amounts of ATPase was decreased, while their affinities to ATP were unchanged. Treatment with Pra-C prevents the decrease in amount of ATPase.

[ABSTRACT]AIM:ToinvestigatethedifferenteffectsofERK1/2/PPARα/SCAD(short-chainacyl-CoAdehy-drogenase) signal pathways on the cardiac hypertrophy induced by insulin-like growth factors 1 ( IGF-1) or phenylephrine ( PE) .METHODS:The neonatal rat cardiomyocytes induced by IGF-1 were used as the model of physiological cardiac hypertrophy , and those induced by PE were used as the model of pathological cardiac hypertrophy .The surface area of the cardiomyocytes, the expression of p-ERK1/2, PPARαand SCAD, the activity of SCAD and the content of free fatty acid in the cardiomyocytes were measured .RESULTS:Compared with the control cells , the surface area of the cardiomyocytes in-duced by IGF-1 and PE were both increased .Compared with the controls , the expression of SCAD and PPARα, and the activity of SCAD in the cardiomyocytes induced by IGF-1 were increased , while the expression of p-ERK1/2 was de-creased.However, the cardiomyocytes treated with PE showed decreased expression of SCAD and PPARα, decreased activ-ity of SCAD and increased expression of p-ERK1/2.Meanwhile, the decrease in free fatty acid in IGF-1-induced cardio-myocytes and the increase in PE-induced cardiomyocytes indicated that the fatty acid utilization was increased in the cardio -myocytes induced by IGF-1, but decreased in the cardiomyocytes induced by PE .CONCLUSION: The changes of p-ERK1/2, PPARαand SCAD in the cardiac hypertrophy induced by IGF-1 or PE indicate that the effects of ERK 1/2/PPARα/SCAD signal pathways are different between physiological cardiac hypertrophy and pathological cardiac hypertro -phy , and that SCAD may be a molecular marker of these 2 different cardiac hypertrophies and a potential therapeutic target for pathological cardiac hypertrophy .

AIM:To investigate the change of short-chain acyl-CoA dehydrogenase (SCAD) expression during cardiomyocyte apoptosis and to explore the relationship between SCAD and cardiomyocyte apoptosis .METHODS: The neonatal rat cardiomyocytes treated by tert-butyl hydroperoxide (tBHP) were used as the model of cardiomyocyte apoptosis . The cell viability , the expression of SCAD at mRNA and protein levels , the activity of SCAD and the content of free fatty acids were determined .RESULTS:The mRNA and protein expression of SCAD decreased in the cardiomyocyte apoptosis model.Compared with negative control group , SCAD expression and activity were both significantly decreased in siRNA-1186 group, but the content of free fatty acids were obviously increased in the cardiomyocytes .Meanwhile, SCAD siRNA treatment triggered the same apoptosis as cardiomyocytes treated with tBHP .CONCLUSION: Down-regulation of SCAD may play an important role in primary cardiomyocyte apoptosis .Increase in the expression of SCAD may become an impor-tant part in intervening cardiomyocyte apoptosis .

AIM:To investigate the effect of short-chain acyl-CoA dehydrogenase ( SCAD) on collagen expres-sion and proliferation of rat cardiac fibroblasts and to explore the relationship between SCAD and cardiac fibrosis . METHODS:The model of proliferation and collagen expression of rat cardiac fibroblasts induced by angiotensin II was es -tablished.After treatment with siRNA-1186, the expression of SCAD at mRNA and protein levels , fatty acids beta oxida-tion rate, ATP, the enzyme activity of SCAD and free fatty acids in the rat cardiac fibroblasts were determined . RESULTS:The mRNA and protein expression of SCAD was decreased in the rat cardiac fibroblasts induced by angiotensin II compared with the control cells , and the expression of collagen I and collagen III was significantly upregulated .Com-pared with negative control group , SCAD expression and activity , fatty acid beta-oxidation rate and ATP significantly de-creased in siRNA-1186 group, but the content of free fatty acids were obviously increased in the rat cardiac fibroblasts , and the expression of collagen I and collagen III was significantly up-regulated.CONCLUSION:The expression and synthesis disorder of collagen may be triggered by down-regulation of SCAD .SCAD may be a promising therapeutic target for myocar-dial fibrosis .