Angiogenesis is an important link of tumor growth, invasion and metastasis. The tumor angiogenesis targeting strategy for the treatment of cancer has become a hot spot in oncology research currently. Signal transduction of tumor angiogenesis is a complex, multi-factor, multi-way and cross network system. Treatment for a single target is often not sufficient to halt or reverse its highly heterogeneous structure and abnormal shape. Therefore, it will be an important research direction that the combination of different pathways and mechanisms of medications effect on signaling pathway in tumor angiogenesis by multi-target. A number of experimental studies found that qi-reinforcing and blood-activating medication can play a regulating role of multiple targets, multiple pathways in tumor angiogenesis. It had different effect on tumor angiogenesis against tumor invasion and metastasis.Qi-reinforcing and blood-activating medication will have broad prospects in the treatment of tumor and angiogenesis.

Purpose:To assess the value of the sentinel lymph node by lymphoscintigraphy and gamma detector probe in early cervical cancer.Methods:22 patients with operable invasive early cervical cancer and clinically proven negative pelvic lymph nodes were included in the study. The 99m Tc-dextran ( 99m Tc-DX) of 74 MBq(2 mCi) was injected into the cervix at 2? and 10?. Lymphoscintigraphy and gamma probe detectors were used to detect the SLN. Results:The SLN was identified in 17 of the 22 patients. The sensitivity and the specificity of the SLN detection to predict the metastasis of the pelvic lymph node was 100% and 100% respectively. Conclusions:Identification of sentinel nodes using radionuclide is feasible and possible in women with early cervical cancer.

In the present study, the results were as follows: ( 1 ) Thyro-tropin-releasing hormone ( TRH ) injected into the intracerebroven-tricle increased intragastric pressure & evoked the phasic contraction of stomach significantly. ( 2 ) The increased response was decreased by bilateral destruction of dorsa. motor nucleus of vagus. ( 3 ) The increase was abolished completely by either vagotomy or atropine.The aforementioned results indicate that the action of dors. motor nucleus of vagus is partly involved the central mechanism of gastric movement induced by TRH & the vagal is the efferent pathway.

Objective To explore a best operative method in order to improve operative manipulated skill of simultaneous pancreas-kidney transplantation(SPKT),a model of SPKT was established in dogs.Methods 12 dogs of SPKT were performed in animal model.A renoportal end-to-end anastomoses between the renal and the spleen vein.Only two vascular end-to-side anastomoses between the donor portal vein and recipient ilio-vein,and between the donor celiac arteries and recipient abdominal aorta were constructed.Pancrease was placed in the right iliac fossa and kidney in the left.Pancreatic exocretion goes through bladder drainage.Results Combined resection was successfully performed in 6 dogs and the other underwent simultaneous pancreas-kidney transplantation.Satisfactory result was obtained in 5 survival dog for a mean of (1 5?0 8)days,although 1 dog died from hypopiesis.Conclusions The model is practically feasible and might be used in studying the problems involved in SPKT,which is effective for the treatment of end-stage diabetic nephropathy.

Jaundice is frequent clinic symptoms with high incidence especially among the critical patients. The sepsis complicated with jaundice has drawn more and more consideration. However, the pathogenesis about sepsis complicated with jaundice is not confirmed and it is sometimes identified incorrectly as cholestatic jaundice. This article summarises the pathogenesis and elucidate the management about sepsis complicated with jaundice.

ObjectiveTo investigate the effects of sevoflurane anesthesia on aquaporin-9 (AQP-9) expression in brain tissue after focal cerebral ischemia-reperfusion (I/R) in rats.MethodsSeventy-five male SD rats weighing 230-270 g were randomly divided into 3 groups ( n =25 each):group sham operation (group S) ; group I/R and group sevoflurane anesthesia (group SE).All the animals were tracheally intubated under 2.0％ sevoflurane and mechanically ventilated.Anesthesia was maintained with fentanyl infusion at 25 μg· kg-1 · h-1 after a bolus of fentanyl 10 μg/kg and inhalation of 65％ N2O in O2 in groups S and I/R and with inhalation of 2％ sevoflurane in 35％ O2 in group SE.Focal cerebral ischemin was induced by occlusion of middle cerebral artery for 2 h using a nylon thread with rounded tip which was inserted into the right internal carotid artery and advanced cranially until resistance was met.The neurologic function was assessed and scored (0=no deficit,4 =unable to move,unconscious) and brain edema rate (volume of ischemic hemisphere-volume of contralateral hemisphere ÷volume of contralateral hemisphere × 100％ ) and expression of AQP-9 were determined at 6 h,1,2,3 and 5 d of reperfusion.ResultsFocal cerebral I/R significantly increased neurologic deficit scores,brain edema rate and AQP-9 expression in brain tissue in group I/R as compared with group S.Sevoflurane anesthesia significantly attenuated the I/R-induced increase in neurologic deficit scores and brain edema rate and further increased I/R-induced increase in AQP-9 expression in brain tissue.ConclusionSevoflurane anesthesia can reduce focal cerebral I/R injury by up-regulating the expression of AQP-9 in brain tissue.

Objective To evaluate the effects of remifentanil post-conditioning on aquaporin-1 (AQP-1) expression during myocardial ischemia-reperfusion (I/R) injury in rats.Methods Twenty-four male.SpragueDawley rats,weighing 250-300 g,were randomly divided into 3 groups (n =8 each) using a random number table:sham operation group (group S),group I/R,and remifentanil post-conditioning group (group RP).Myocardial I/R was induced by 45 min occlusion of left anterior descending branch of coronary artery followed by 24 h reperfusion.Remifentanil 10 μg· kg-1· min-1 was infused over 10 min starting from 10 min before reperfusion in group RP,while the equal volume of normal saline was given instead in S and I/R groups.At the end of reperfusion,all the rats were sacrificed and their myocardial specimens from left ventricles were obtained for microscopic examination of thepathological changes and for determination of AQP-1 mRNA (using real-time fluorescent quantitative PC R) and AQP-1 protein (by Western blot) expression in the ischemic area and myocardial water content.Results Compared with S group,myocardial water content was significantly increased in the other two groups,AQP-1 mRNA and protein expression was up-regulated in group I/R,and no significant change was found in AQP-1 mRNA and protein expression in RP group.Compared with I/R group,myocardial water content was significantly reduced,and AQP-1 mRNA and protein expression was down-regulated in RP group.Conclusion Remifentanil post-conditioning reduces myocardial I/R injury possibly through down-regulating AQP-1 expression in myocardial tissues of rats.

Objective To evaluate the changes in the expression of spinal aquaporin-4 (AQP4) during remifentanil-induced hyperalgesia in a mouse model of incisional pain.Methods Seventy-two pathogen-free healthy adult male CD1 mice,weighing 25-30 g,were divided into 4 groups (n=18 each) using a random number table:control group (group C),incisional pain (group I),remifentanil group (group R) and remifentanil plus incisional pain group (group R+I).Normal saline was infused subcutaneously in group C.An incision was made in the left hind paw in group I.Remifentanil 80 μg/kg was subcutaneously infused for 30 min at a rate of 0.8 ml/h in group R.Remifentanil was infused subcutaneously before establishment of the model in group R+I.The thermal paw withdrawal latency (TWL) and mechanical paw withdrawal threshold (MWT) were measured at 1 day before establishment of the model (T0) and 6 h and 1,2 and 7 days after establishment of the model (T1-4).After measurement of the pain threshold at T3,12 animals were sacrificed randomly,and the lumbar segment of the spinal cord was removed for determination of the distribution and expression of AQP4 by Western blot.Results Compared with group C,the TWL was significantly shortened at T1-3,and the MWT was decreased at T2-4 in R and R + I groups,and the expression of AQP4 was significantly up-regulated at T3 in I,R and R+I groups (P＜0.05).Compared with group I,the TWL was significantly shortened at T2,3,and the MWT was decreased at T2.4 in group R,and the TWL was significantly shortened at T1-3,the MWT was decreased at T2.4,and the expression of AQP4 was up-regulated at T3 in group R+I (P＜0.05).Conclusion The mechanism by which remifentanil induces hyperalgesia is related to up-regulation of AQP4 expression in the spinal cord in a mouse model of incisional pain.

Objective:To study the epidemiology of attention-deficit hyperactivity disorder(ADHD) in pupils of Zhenjiang urban districts. Methods: Questionnaire was designed and employed for parents of 3 698 pupils at schools in Zhenjiang urban districts. ADHD was diagnosed according to the international DSM-Ⅳ scale. Differences were determined by Qi-square test and multiple regression analysis. Results: Prevalence of ADHD was 6.54% in pupils of Zhenjiang urban districts, and was 9.14% in male pupils and 4.01% in female. There was significant difference between 2 gender groups (? 2=34.933,P

Objective To explore the effect of remifentanil postconditioning on rats subjected to ischemia reperfusion injury and the relative mechanisms.Methods Seventy-eight Sprague-Dawley rats, weighing 200-250 g, were randomly divided into six groups (n=13): sham group (group S), ischemia/reperfusion group (group IR), naloxone group (group NAL), 5 μg·kg-1·min-1 remifentanil postconditioning group (group R1), 10 μg·kg-1·min-1remifentanil postconditioning group (group R2) and 20 μg·kg-1·min-1remifentanil postconditioning group (group R3).Group IR was given 45 min ischemia in the left descending anterior (LAD), followed by a 24-h period of reperfusion.Groups R1, R2, R3 received 10 min of remifentanil infusion of 5, 10 and 20 μg·kg-1·min-1 after 35 min ischemia followed by a 24 h period of reperfusion.Group NAL was given injection of naloxone 0.1 mg/kg at the point of 25 min myocardial ischemia, after 10 min, then remifentanil 10 μg·kg-1·min-1 for 10 min.The myocardial infarct size and pathological changes of myocardial tissue were observed, serum cTnI, LDH and CK-MB level were measured.Results Compared with group S, serum cTnI, LDH and CK-MB and myocardial infarct size were markedly increased in groups IR, NAL, R1, R2 and R3 (P<0.05), and pathologic injury of myocardial cells were augmented.In comparison with group IR, the indexes were decreased in groups R1, R2 and R3 (P<0.05).Conclusion Remifentanil postconditioning could protect against myocardial ischemia reperfusion injury in rats.The protection may be related to remifentanil activating the opioid receptors.There were ceiling effects of remifentanil postconditioning induced myocardial protection.