Endothelial progenitor cells have self-replication and multi-differentiation potentials. They participate in the maintenance of vascular dynamics and physiological reconstruction. Though the research of endothelial progenitor cells has become a current hot spot, there are a series of unknown factors from the fields of the basic research to the clinical application. This article reviews the advances in research on endothelial progenitor cells,particularly the roles in ischemic cerebrovascular disease.

Objective To evaluate the effect of celastrol postconditioning on focal cerebral ischemiareperfusion (I/R) injury in rats.Methods Sixty-four Sprague-Dawle rats (32 males,32 females),weighing 250300 g,were randomized into 4 groups using a random number table (n =16 each):sham operation group (group S) ; celastrol control group (group S + C) ; focal cerebral I/R group (group I/R) ; celastrol postconditioning group (group I/R + C).Focal cerebral I/R were produced by middle cerebral artery occlusion (MCAO).Dimethyl sulfoxide (DMSO) 0.3 ml/kg was injected intraperitoneally after shame operation in group S.Celastrol 3 mg/kg was injected intraperitoneally after shame operation in group S + C.DMSO 0.3 ml/kg was injected intraperitoneally at 5 min of reperfusion in group I/R.Celastrol 3 mg/kg was injected intraperitoneally at 5 min of reperfusion in group I/R + C.The neurologic deficit was scored at 5 min before reperfusion and 24 h of reperfusion.The infarct size was detected by TTC staining,and then the percentage of infarct size was calculated.The pathological changes in CA1 region of ischemic hippocampus were detected by HE staining.The activity of nicotinamide adenine dinucleotide phosphate oxidase (NOX),content of reactive oxygen species (ROS) and expression of NOX1 and NOX2 mRNA (by RT-PCR) in ischemic brain tissues were detected.Results Compared with S and S + C groups,the neurologic deficit scores,infarct size,percentage of infarct size,NOX activity and ROS content were significantly increased,and the expression of NOX1 mRNA and NOX2 mRNA was up-regulated in I/R and I/R + C groups (P ＜ 0.01).Compared with group I/R,the neurologic deficit scores,infarct size,percentage of infarct size,NOX activity and ROS content were significantly decreased,and the expression of NOX1 mRNA and NOX2 mRNA was down-regulated in group I/R+ C (P ＜ 0.01).There was no significant difference in the parameters mentioned above between group S and group S + C (P ＞ 0.05).The pathological changes in CAl region of ischemic hippocampus were significantly attenuated in group I/R + C (P ＜ 0.01).Conclusion Postconditioning with celastrol can auenuate focal cerebral [/R injury in rats and inhibiton of oxidative stress response in brain tissues may be involved in the mechanism.

Objective A LC/MS/MS method is developed for determination of paraquat in biological tissue.Methods The samples were pretreated with solid phase extraction using Oasis WCX cartridges and separated with HPLC,paraquat could be identified by LC/MS/MS.Result Calibration curves were linear on injection of amounts ranging from 0.02～20?g/ml and the limit of detection was 10ng/ml(S/N≥3).Conclusion The described menthod was proved to be sensitive,rapid and accurate,it will be applied in identification and determination of paraquat in biological tissues.

Objective To evaluate the role of angiotensin-converting enzyme (ACE) gene polymorphism in the progression of renal diseases. Methods ACE gene polymorphism was analyzed in 77 patients with end stage renal failure (ESRF) and 150 normal control. Results The frequences of DD and DI genotype were significantly higher in ESRF patients than normal control (DD, 15.6% VS 6.0%, P

Objective To investigate the effects of EGB on hepatic fibrosis and expression of Activin A in rats with fibrosis.Methods From Oct.2004 to Apr.2005,the study was conducted in 30 adult male rats in the pepartment of Gastroenterology,the people's Hospital of Wuhan University.The rats were randomized into 3 groups:control group,model group and treatment group.Except the rats in the control group,others were induced to hepatic fibrosis by intraperitoneal injection of CCl_4 twice a week for 8 weeks.Those rats in the treatment group were intragastrically administered with EGB establish model of everyday.At the end of the 8th week,all rats were sacrificed.The samples of liver was staining with HE.The expression of Activin A was determined by immunohistochemistry and RT-PCR.Results The grade of fibrosis in EGB-treated groups were lower than that in the model group(P

[Objective] To explore the counteractive mechanism of Tongmai Injection (IT) for excitotoxicity in rats with cerebral ischemia/reperfusion by observing the glutamic acid (Glu) content and N-methyl-D-aspartate (NMDA) receptor activity in rats cortex. [ Methods ] Rat models with cerebral ischemia/reperfusion were established by four-vessel occlusion. Glu content and NMDA receptor activity were examined by radioimmunoassay and the effects of TI on Glu and NMDA receptor were also observed. [ Results ] Glu content and NMDA receptor activity were both increased in the model group and TI could counteract the above changes. [Conclusion] Cerebral ischemia/reperfusion can induce excitotoxicity and TI can protect the cerebral cortex.

AIM:Activin A,a member of transforming growth factor superfamily,is the negative regulator factor in liver regeneration. In this study,the effects of extract of Ginkgo Biloba on hepatic fibrosis and the expression of Activin A in rats with cirrhosis were investigated. METHODS:The experiment was performed at in the Central Laboratory of Wuhan First Hospital from September 2005 to December 2006. ①Thirty-six male SD rats of(160?20) g were randomized into 3 groups:control group,model group and treatment group. ② Except the rats in the control group,others were intraperitoneally injected with 500 mL/L CCl4 for 8 weeks to establish models of hepatic fibrosis. Meanwhile,the extract treatment group was infused with the extract of Ginkgo Biloba(Chinese drugs preparation laboratory of Wuhan First Hospital,detected by Hubeu Wushi Medicine Industry Co.,Ltd. No. 02-391) daily for 8 weeks. ③After administration,all anesthetized rats were sacrificed. Blood samples were collected for the determination of liver function biochemical indexes. Liver tissue samples were used for histopathological examinations. The expression of Activin A was determined by immunohistochemistry and RT-PCR. RESULTS:All 36 rats were involved in the final analysis. ①The liver function in extract treatment group was significantly improved compared with that in model group. ②The grade of fibrosis in extract treatment group were remarkably lower than that in model group under light microscope. ③The positive staining of Activin A in treatment group was significantly reduced compared with model group. ④The expression of Activin A mRNA in extract treatment group was significantly reduced compared with model group. CONCLUSION:Extract of Ginkgo Biloba can effectively decrease the expression of Activin A in rats with hepatic fibrosis caused by CCl4,and lessen the degree of hepatic fibrosis.

Objective To study the effect of endothelial progenitor cells on the behavior of chronic cerebral ischemic rats. Methods Adult rats were treated using the protocol of chronic cerebral ischemic model. Then translated the endothelial progenitor cells in vein to them, and Morris water maze was carried out to test the learning and merrory ability of the rats. The cell proliferation, vascular distribution and the plasma VEGF levels were day of 2nd to 5th of experimental group ( EPC group ) were significantly shorter than the control group ( PBS group), which were(44.45 ±9.44)s,(38.32±1.51)s,(34.95 ±6.76)s,(24.46 ±5.47)s and (52.79±6.47 ) s, ( 43.15 ± 11.21 ) s, ( 50.29 ± 11.41 ) s, ( 53.75 ± 7.35 ) s, (P ＜ 0.01 ) respectively. The time of EPC group spend in the first quadrant were significantly longer than that of the PBS group, which were (26. 76 ±of the EPC group( 26.8 ± 5.76 ) was higher than that of the conrespondering areas in the control group( 12.17 ±ments of capillaries were (P＜0.05) shorter in the PBS groups( (3.4 ±0.24) μm) than in the EPC groups( (2.8± 0.2 )μm) significantly, EPC group could significantly (P ＜ 0.05 ) increased the number of branch points in the boundary regions of ischemia compared with the number in the PBS group (respectively (210. 1 ± 13.80 ) and (164.2 ± 12.3 )). Three-dimensional cerebral vessel surface area in the ipsilateral hemisphere significantly increased in the EPC group compared with the PBS group (respectively (84365 ± 3897 )μm2/0. 002mm3 and group in the plasma VEGF levels ( ( 63.91 ± 6.71 ) pg/ml; ( 21. 81 ± 4.25 ) pg/ml, respectively (P ＜ 0.05, P ＜0.01 ). Conclusion There are positive behavioral effects of endotbelial progenitor cells in chronic cerebral ischemic rats. The possible mechanisns mavbe involve the nerve protection and regeneration of the vascular associated with the VEGF. The endothelial progenitor cells maybe have a great prospect in the therapy of chronic cerebral ischemic disease.

Objective To investigate the effect and safety of self-made blenderized diet used for nutritional support treatment in the ICU critically ill patients with diabetes. Methods 74 ICU critically ill patients with diabetes were randomly divided into two groups:study group and control group. The self-made blenderized diet were given to the patients in study group and enteral nutrition to the patients in control group for nutritional support treatment for four weeks. Then glucose metabolism, various nutrition indicators and gastrointestinal dysfunction were observed in these two groups. Results The fasting blood glucose and fructosamine levels were decreased significantly,while the nutritional indicators was significantly higher after treatment than at baseline in all patients. There was no significant difference in the levels of fasting blood glucose, postprandial glucose, fructosamine and nutritional indicators between two groups after treatment,so were the incidence of the hypoglycemia and gastrointestinal complications. Conclusion The self-made blenderized diet was a good enteral nutrition support therapy for ICU critically ill patients with diabetes which had a considerable effect, but more cheaper,and practical compared to the enteral nutrition emulsions.

Objective To investigate the neuroprotective effect of escitalopram on focal cerebral ischemia/reperfusion in rats and its possible mechanisms.Methods Seventy-five male Sprague-Dawley rats were randomly divided into three groups:sham operation,saline control and escitalopram intervention groups (n =25 in each group).A focal cerebral ischemia reperfusion model in rats was induced by the intraluminal suture method.The modified neurological severity scale was used to evaluate neurological deficit in rats (n =5 in each group).Laser confocal technology was used to observe the microvascular diameter,density,and total area in ischemic region (n =5 in each group).Enzyme-linked immunosorbent assay was used to detect the plasma concentration of vascular endothelial growth factor (VEGF) (n =5 in each group).Immunohistochemical staining (n =5 in each group) and Western blotting (n =5 in each group) were used to detect the expression of VEGF in the ischemic brain tissue.Results At day 14 after modeling,the neurological deficit improved more significantly in the escitalopram intervention group than that in the saline control group (4.39 ±0.92 vs.6.57 ± 1.13; P =0.015).The 3D confocal vascular imaging showed that capillary diameter in the escitalopram intervention group was significantly smaller than that in the saline control group (2.93 ± 0.19 μm vs.3.56 ± 0.22 μm; P ＜0.01); the vascular density was significantly higher than that in the saline control group (232.68 ±12.54/0.002 mm3 vs.176.26 ± 10.87/0.002 mm3; P=0.000); the total microvascular area was significantly greater than that in the saline control group (89 154± 3 298 μm2/0.002 mm3 vs.75 368.14± 3 519 μm2/0.002 mm3; P=0.000).Enzyme-linked immunosorbent assay showed that the plasma VEGF concentration in the escitalopram intervention group was significantly higher than that in the saline control group (50.35 ± 5.44 pg/ml vs.13.75 ± 4.12 pg/ml; P =0.000).Immunohistochemical analysis showed that the VEGF expression in ischemic brain tissue in the escitalopram intervention group was significantly higher than that in the saline control group (P =0.000).Western blotting showed that the VEGF expression in ischemic brain tissue in the escitalopram intervention group was significantly higher than that in the saline control group (0.94 ±0.18 vs.0.62 ±0.22; P =0.006).Conclusions Escitalopram may reduce neurological deficit in cerebral ischemia/reperfusion in rats.Its mechanisms may be associated with VEGF-mediated angiogenesis.