In order to investigate the levels of stem cell factor (SCF) and its receptor c-kit protein and mRNA in pediatric aplastic anemia (AA) and their relevance to the pathogenesis, immunocytochemical andin situ hybridization were utilized to detect the expression of SCF and its receptor c-kit gene protein and mRNA, respectively in 59 children with AA and 51 normal controls. The relationship between SCF and c-kit and the pathogenesis of AA was analyzed subsequently. The results showed that the positive rate of SCF protein and mRNA expression in children with AA was significantly lower than that in healthy controls (P<0.05). However, there was no significant difference in the positive rate of c-kit protein and mRNA expression between children with AA and control group (P>0.05). It was concluded that the expression of SCF is significantly decreased in children with AA, which may be closely associated with the pathogenesis of the AA. c-kit may be unrelated to the development of pediatric AA. Therefore, AA in children may have abnormalities at SCF/c-kit signal transduction levels.

To examine the relationship between host survival and the type of immune response in different organs during disseminated candidiasis, the murine model of disseminated candidiasis was established by injection withCandida albicans via tail vein. The survival time was observed for up to 60 days. And the expression levels of cytokines in the spleen and kidney, including IFN-γ and IL-4, were determined with RT-PCR. Our results showed that in the spleen, both non-fatal and fatal inoculum caused a type II immune response with steady expression levels of IFN-γ and the obviously increased levels of IL-4. While in the kidney, non-fatal inoculum induced a type I immune response with the obviously increased levels of IFN-γ and the steady expression levels of IL-4. However, fatal inoculum induced a type II immune response with a constant expression of IFN-γ and the evidently increased levels of IL-4. It is concluded that in disseminated candidiasis, host survival is associated with the type of immune responses in the kidney, but not in the spleen.

The effects of diazoxide treatments on electrophysiologic properties in guinea pig papillary muscles undergoing ischemia/reperfusion was studied using intracellular microelectrode technique. Twenty-four guinea pigs were randomly divided into three groups (n=8 in each group). In control group, St. Thomas solution was given. In experimental group, St Thomas solution with diazoxide (100 mol/L) was given. In pretreatment group, the muscle was treated with diazoxide 20 min before arrested with St. Thomas cardioplegia. The results showed that the APD₅₀ and APD₉₀ in experimental and pretreatment groups were significantly shorter after 5 and 10 min reperfusion (P<0.01,P<0.05), but longer after 30 min reperfusion (P<0.01),P<0.05) than in control grou. In experimental and pretreatment groups, APA, OS, Vmax recovered more quickly than those in control group. The time to re-systole after reperfusion in control group was longer than that in experimental and pretreatment groups. There was no significant difference in RP among three groups. The time of arrest in pretreatment group was longer than that in exprimental and pretreatment group (P<0.05). This study indicates that protective effects of St. Thomas solution with diazoxide is better than that of pretreatment with diazoxide or St. Thomas solution alone.

To study the effect of of lidocaine and amiodarone on the transmural heterogeneity of ventricular repolarization in isolated rabbit hearts model of sustained global ischemia and to explore the mechanisms underlying the antiarrhythmic activity of lidocaine and amiodarone, rabbits were randomly divided into 4 groups: control group, ischemia group, lidocaine group and amiodarone group. By the monophasic action potential (MAP) recording technique, MAPs of epicardium, midmyocardium and endocardium were simultaneously recorded across the left ventricular free wall in rabbit hearts perfused by low-flow ischemia (2.5 mL/min) in Langendorff method to study the transmural dispersion of repolarization (TDR) and arrhythmic induced by ischemia. Our results showed that TDR of three myocardial layers in ischemia group were significantly lengthened after ischemia. TDR was increased from 17.5±3.9 ms to 31.2±4.6 ms at the time that concided with the onset of sustained ventricle arrhythmic. Amiodarone could decrease TDR, but lidocaine could increase TDR at initial ischemia, and no significant difference was found at other ischemia time points. 5 cases had ventriclar arrhythmia in ischemia group (62.5%), but no case in lidocaine group (P<0.01) and only 1 case in amiodarone group had ventrilar arrhythmia (P<0.01). No significant difference was found between amiodarone group and lidocaine group. It is concluded that TDR of of three myocardial layers increases significantly at ischemia and it is closely associated with development of ventricular arrhythmia, and amiodarone could decrease TDR, but lidocaine could increase TDR at initial ischemia and has no effects at other ischemia time points.