Objective To observe the effect of carvedilol on cardiac function and heart rate variability(HRV) in patients with congestive heart failure(CHF) . Methods Sixty-three patients with CHF were randomly divided into two groups. 33 cases (carvedilol group) were given Carvedilol titrated from low dose to target dose in addition to standard therapy for CHF. The cardiac fuction and HRV of all patients were examined before and after 6 months therapy. Results After 6-month therapy, LV end-diastolic dimension (LVEDD) and LV end-systolic dimension (LVESD) in carvedilol group were significantly lower than those in control group (P

Objective To investigate the effects of breviscapine injection on intestinal mucosal barrier damage induced by intestine ischemia-reperfusion (IIR). Methods 44 old SD rats were randomly divided into four groups:sham,intestine ischemia-reperfusion(IIR),EB+IIR,LN+IIR. Breviscapine injection 20 mg/(kg·d) was given intraperitoneally in EB+IIR group. L-NAME(100 mg/kg)was given intravenously 30 min before surgery in LN+IIR group. Rats were subjected to superior mesenteric artery occlusion consisting of 45 min of ischemia and 4 h of reperfusion;sham laparotomy served as controls. Intestine pathology was assayed by H&E staining. Concen-trations of SIgA,iNOS,eNOS and NO in intestinal mucosa,also endotoxine in plasma,were determined by ELI-SA. Results IIR induced serious intestinal mechanical and immune barrier damage ,evidenced as poor intestine pathology,depression of intestinal SIgA and eNOS levels,elevation of intestinal iNOS/NO levels. However,brevis-capine injection pretreatment could promote eNOS/NO production ,down-regulated iNOS expression ,leading to ele-vating SIgA concentration in intestine ,attenuate endotoxemia induced by IIR. The protection was canceled when application of L-NAME. Conclusion Breviscapine pretreatment attenuates ischemia-reperfusion-induced intestinal mucosal barrier damage via promoting eNOS/NO production.

AIM: To analyze the polymorphic expression of UDP-glucuronosyltransferase UGT1A gene locus in human colorectal epithelium. METHODS: Colorectal tissue samples were obtained from 40 patients with colorectal cancer and 20 normal controls. The levels of UGT1A transcriptions were detected by RT-PCR, exon-1 specific RT-PCR. UGT1A proteins were measured by Western blotting analysis. RESULTS: (1) UGT1A mRNA expression was found to be significantly down-regulated in colorectal cancer tissue as compared with the surrounding healthy tissues (P

Objective To investigate the effects of breviscapine injection on intestinal injury induced by intestine ischemia-reperfusion(IIR). Methods 48 males SD rats with 8-week old were randomly divided into 4 groups:Sham,intestine ischemia-reperfusion(IIR),EB+IIR,TP+IIR. Breviscapine injection 20 mg/(kg·d) was given intraperitoneally in EB + IIR group. TPCA-1(12 mg/kg)was given intravenously 30 min before surgery in TP+IIR group. Rats were subjected to superior mesenteric artery occlusion consisting of 45 min of ischemia and 6 h of reperfusion;sham laparotomy served as controls. Intestine pathology was assayed by H&E staining. Con-centrations of TNF-α,IL-1β,and IL-6 in intestinal mucosa were determined by ELISA. The protein expressions of IκB-α,NF-κB ,ICAM-1of intestine tissue were assayed by western blot. Results IIR induced serious intesti-nal injury ,evidenced as poor intestine pathology ,elevation of TNF-α,IL-1β,and IL-6 levels in intestinal mu- cosa,accompanied with IκB-α/NF-κB/ICAM-1 pathway activation. However,breviscapine injection pretreatment could inhibit IκB-α/NF-κB/ICAM-1 pathway activation,leading to reduction of TNF-α,IL-1β,and IL-6 concen-trations in lung,finally attenuate ALI induced by IIR. Conclusion Breviscapine injection pretreatment could atten-uate inflammation in intestine after IIR injury via inhibiting IκB-α/NF-κB/ICAM-1signaling pathway.