Objective:To investigate the demands for cardiac rehabilitation information in patients with coronary atherosclerotic heart disease (CHD) and influential factors.Methods:Information demands for cardiac rehabilitation in CHD patients were surveyed by questionnaire and the influential factors were analyzed by one-way ANOVA and multi-factor analysis of variance.Results:The score of demands for cardiac rehabilitation information in CHD patients was 3.86±0.53.Among them,the most urgent top 5 items were:drug knowledge,diagnosis and treatment,basic knowledge of the heart,emergency and safety and nutrition knowledge.The top 3-demand modes were:communication with medical workers,movies or videos to take home,and lectures.The score of demands for cardiac rehabilitation information was different in different age groups.The highest score was in the patients with age less than 60.There were different demands in different characteristic groups.Conclusion:The most urgent need and mode are drug knowledge and communication with medical workers,respectively.With the age increase,the demands for patients' cardiac rehabilitation information decrease.An individualized health education strategy should be developed according to the characteristics of CHD patients.

Objective To discuss the effects of Modic II changes on clinical outcomes of discectomy for lumbar disc herniation (LDH) with low back pain associated with unilateral sciatica. Methods Sixty-five cases of LDH with low back pain associated with unilateral sciatica received single segment discectomy during January 2007 to January 2009.There were 30 cases with Modic Ⅱ changes in group A, 35 cases without Modic Ⅱ changes in group B. Assessed the clinical outcomes by using MacNab analyzing system and visual analog scale (VAS). Results Two groups of the postoperative clinical symptoms had significant relief, the follow-up of 12 - 36 months, average (20.6 ± 7.5) months. MacNab efficacy evaluation by group A of optimal 10 cases (33.33%), good 17 cases (56.67%), general 3 cases (10.00%). Group B optimal 28 cases (80.00%), good 5 cases (14.29%), general 2 cases (5.71%), there was significant difference in fine rate (P<0.05). Preoperative group A VAS was ( 8.67 ± 0.30) scores, group B was (8.60± 0.32 ) scores (P>0.05). Postoperative group A VAS was (2.63 ± 1.30) scores,group B was (1.09 ±0.50) scores (P< 0.05). Conclusion Modic Ⅱ changes may be one of the reasons which cause the residual low back pain after the discectomy for LDH.

Aim To find out the relationship between muscarinic receptor and reactive oxygen species (ROS) and the probable differences between the four muscarinic receptor subtypes. Methods We transfected the plasmid encoding muscarinic receptor (including subtypes: M_1, M_2, M_3 and M_4) into PC12 cells. Then PC12 cells were exposed to hydrogen peroxide (H_2O_2), carbachol and other inhibitors such as atropine, LY294002 and PD98059. Results The results showed that activation of muscarinic receptor by carbachol protected PC12-M_1, PC12-M_2,PC12-M_3 and PC12-M_4 cells from apoptosis induced by H_2O_2. There was no statistical difference in the protective effect between these four muscarinic receptor subtypes. By using the inhibitors, we found that atropine and LY294002 blocked the protective effect of activation of muscarinic receptor on apoptosis induced by H_2O_2. Conclusion Activation of muscarinic receptor retarded the apoptosis induced by H_2O_2. There was no difference between the four muscarinic receptor subtypes. The protective effect was mainly mediated by the activation of muscarinic receptor and phosphatidylinositol-3 kinase (PI3K).

AIM: To study the changes of the sphingomylinase activity and ceramide content in rabbit aorta of experimental atherosclerosis and investigate the effects of emodin on them. METHODS: The qualified rabbits were fed with food containing 1% cholesterol and 5% lard for 10 weeks to establish the animal models. The concentration of cholesterol (TC) was assayed by a enzyme method. Trace-fast-test method was used to test the activity of superoxide dismutase (SOD) and motified-BAMuGuoFu methods was employed to assay the content of myocardial malondialdehyde (MDA). Radiolabeled-enzyme-tracing was used to detect the activity of the sphingomyelinase,and thin-layered scanning was conducted to analyze the content of the ceramide in aorta. RESULTS: The ceramide content in aorta and the sphingomyelinase activity were markedly increased in the rabbits with experimental atherosclerosis. The increase was positively correlated with the content of TC and MDA and negatively correlated with the activity of SOD in blood. Compared to the model animals, emodin at concentration of 5 mg?kg -1 , 10 mg?kg -1 and 20 mg?kg -1 respectively reduced the area of plague on endothelium in rabbit's aortic artery and elevated the activity of SOD (P

Objective To study the drug sensitivity of chemotherapeutic drugs by MTT method. Methods Twenty five lung cancer specimens obtained by operation were used for primary culture and the sensitivity of the cancer cells to four drugs, adriamycin(ADM), cis dichlorodiamine platinum(DDP), vincristine(VCR) and etoposide(VP16), was tested by MTT assay. TOPOⅡ, p53, bcl 2 and GST ? proteins in 10 cases of lung cancer tissue were determined by immunohistochemistry. Results The successfully obtained results in 21 cases showed that the effective rate of ADM, DDP, VCR and VP16 was 19.0%, 38.1%, 23.8% and 23.8% respectively. Positive expressions of TOPOⅡ, p53, bcl 2 and GST ? proteins were found in lung cancer tissue in the 10 cases which had different multi drug resistance(MDR) to the four drugs. Conclusion It is possible to test the drug sensitivity of the primary cultured lung cancer cells obtained from operation by MTT method and the results are useful for the selection of anticancer drugs. The expressions of TOPOⅡ, p53, bcl 2 and GST ? are factors to determine MDR for lung cancer cells.

Objective To evaluate the effect of intrathecal dexmedetomidine on the expression of G-protein-coupled inwardly rectifying K+ channel 1 (GIRK1) in dorsal root ganglia of rats with diabetic neuropathic pain (DNP).Methods A total of 144 healthy adult male SPF Sprague-Dawley rats,aged 8-10 weeks,weighing 200-220 g,were randomly divided into 4 groups (n =36 each) using a random number table:control group (group C),dexmedetomidine group (group D),group DNP,and DNP + dexmedetomidine group (group DD).DNP model was established by single intraperitoneal injection of streptozotocin (STZ) 60 mg/kg.In D and DD groups,dexmedetomidine 1.5 μg/kg was injected intrathecally at 14 days after citrate buffer or STZ injection,while the equal volume of normal saline was given in group C.The mechanical pain threshold was measured before STZ injection (T0),at 14 days after STZ injection (T1),and at 2,4 and 6 h after intrathecal injection (T:2-4).After measurement of the mechanical pain threshold at T2-4,the rats were sacrificed,and the dorsal root ganglia of the lumbar segment (L4-6) were removed for determination of the number of GIRK1 positive cells and expression of GIRK1 protein by immunofluorescence and Western blot,respectively.Results Compared with group DNP,the mechanical pain threshold was significantly increased,the number of GIRK1 positive cells in dorsal root ganglia was significantly increased,and the expression of GIRK1 was significantly up-regulated at T2-4 in group DD (P＜0.05).Compared with group D,the number of GIRK1 positive cells in dorsal root ganglia was significantly increased,and the expression of GIRK1 was significantly up-regulated at T2-4 in group DD (P＜0.05).Compared with group C,the mechanical pain threshold was significantly decreased at T1-4 in group DNP (P＜0.05).Conclusion Intrathecal dexmedetomidine attenuates DNP through up-regulating the expression of GIRK1 in dorsal root ganglia of rats.

Objective To evaluate the role of mammalian target of rapamycin (mTOR) signaling pathway in dexmedetomidine-induced reduction of renal ischemia-reperfusion (I/R) injury in rats and the relationship with hypoxia-inducible factor 1 (HIF-1α).Methods Seventy-two male Sprague-Dawley rats, aged 10-12 weeks, weighing 220-260 g, were randomly divided into 4 groups (n=18 each) using a random number table: sham operation group (group S), group I/R, dexmedetomidine group (group Dex) ,and rapamicyn + dexmedetomidine group (group Rpm+Dex).Renal I/R was produced by occlusion of bilateral renal pedicles for 35 min follow by reperfusion in anesthetized rats in I/R, Dex and Rpm+Dex groups.Bilateral renal pedicles were only exposed, and then the abdominal cavity was closed in group S.Dexdetomidine 50 μg/kg was injected intraperitoneally at 30 min before I/R in group Dex.In group Rpm+Dex, rapamicyn 1.5 mg/kg and dexdetomidine 50 μg/kg were injected intraperitoneally, and renal I/R model was established 30 min later.Immediately after onset of reperfusion, and at 4 and 24 h of reperfusion (T1-3) , blood samples were collected from the caudal vein for measurement of serum creatinine and blood urea nitrogen (BUN) concentrations.After blood sampling at T1-3, the rats were sacrificed, and the renal specimens were obtained for detection of HIF-1αt, erythropoietin (EPO) and mTOR expression by Western blot.Their kidneys were removed at T3, and cut into sections which were stained with haematoxylin and eosin and examined under microscope.Acute renal tubular necrosis was scored.The cell apoptosis in renal tissues was detected by TUNEL assay, and apoptosis index (AI) was calculated.Results Compared with group S,the concentrations of serum creatinine and BUN, expression of HIF-1α, EPO and mTOR at T2,3 , AI at T3 and acute renal tubular necrosis score were significantly increased in the other three groups (P＜ 0.05).Compared with group I/R, the concentrations of serum creatinine and BUN were significantly decreased, and the expression of HIF-1α, EPO and mTOR was up-regulated at T2,3 , and AI and acute renal tubular necrosis score were decreased in group Dex (P＜0.05) , and no significant change was found in the parameters mentioned above in group Rpm + Dex (P ＞ 0.05).Conclusion The mTOR signaling pathway is involved in dexmedetomidine-induced reduction of renal I/R injury, which may be related to dexmedetomidine-produced up-regulation of HIF-1α expression in renal tissues of rats.

Objective To investigate the effects of early continuous renal replacement thempy(CRRT)on correlation kidney injury and prognosis in patients with severe acute pancreatitis(SAP).Methods According to the digital table,40 SAP patients were randomly divided into two groups:the control group(21 cases)and CRRT treat-ment group(19 cases).The levels of serum creatinine,urea nitrogen,IL -1,IL -6,TNF -α,the APACHEⅡscore, the incidence of mechanical ventilation were compared between the two groups.Results The levels of serum creati-nine,urea nitrogen were significantly lower in the CRRT group than those in the control group in day 3(t =2.836, 2.952,P =0.003,0.004);The levers of IL -1,IL -6,TNF -αwere significantly lower in the CRRT group than those in the control group in day 3(t =2.376,2.414,2.197,P =0.351,0.028,0.042);The APACHE II score,inci-dence of mechanical ventilation,the fatality rate in the CRRT group were significantly lower than those in the control group in day 3[(20.16 ±5.23)points vs.(13.83 ±4.48)points,14 cases(66.7%)vs.6 cases(31.6%),8 cases (38.1%)vs.2 cases(14.3%),t =4.572,χ2 =4.912,4.043;P =0.0329,0.027,0.044].Conclusion Early CRRT therapy can eliminate the IL -1,IL -6 and TNF -αin SAP patients,can reduce the incidences of AKI,which may provide more clinical benefits in the early phase of SAP.

Background and purpose:It has been reported that gap junctional (GJ) function was signiifcantly decreased in hepatocellular carcinoma (HCC) tissues and cell lines. However, the increased GJ suppress tumorigenesis and the development of liver cancer. This study therefore aimed to examine the effect of simvastatin on GJ function between Hep3b cells. Thus, the exploition of drugs to increase GJ function between liver cancer cells will provide an efifcient approach to ifght against liver tumor as well as increase cytotoxicity of antitumor agents.Methods:SRB was used to assay the toxicity of simvastatin. The effect of simvastatin on GJ function was determined by “Parachute” dye-coupling assay and scrape loading/dye transfer assay.Results:Pretreated Hep3b cells with simvastatin at the concentration of 1, 5 or 10 μmol/L for 24 h did not induce the cytotoxicity. So simvastatin at the concentration of 5 and 10 μmol/L would not reduce the amount of GJ on cell membranes. “Parachute” dye-coupling assay showed that the treatment with 5 and 10 μmol/L simvastatin for 4 h enhanced the dye spread through GJ in Hep3b cells. Similarly, scrape loading/dye transfer assay showed that simvastatin could induce the increasing spread of lucifer yellow (Ly, Sigma) around the scoifng cells with increasing concentrations.Conclusion:Simvastatin could increase the GJ function of Hep3b cells.

Background and purpose:Gap junctions (GJ) could enhance cytotoxicity induced by chemo-therapeutic agents. Previous studies have showed that some of anesthetics exerted effect on GJ and thereby affected the cytotoxicity of X-ray. However, it is still unclear whether etomidate, a commonly used anesthesia adative agent, could alter GJ intercellular communication in tumor cells. This study explored the effect of etomidate on GJ composed of connexin 43 in U87 malignant glioma cells to provide mechanism clues for studies on the effect of anesthetics on the toxicity induced by chemotherapeutic agents.Methods:Sulforhodamine B was used to examine the toxicity of etomidate on U87 malignant gli-oma cells. The effect of etomidate on GJ function was determined by parachute dye-coupling assay.Results:Pretreatment of etomidate at the concentration of 0.1, 0.5, 1 or 5 μmol/L for 4 h did not induce cytotoxicity in U87 cells. So etomidate at these concentrations would not reduce the amount of GJ on U87 cell membranes. Parachute dye-coupling assay had showed that treatment with 0.5 and 1 μmol/L etomidate for 4 h significantly decreased the dye spread through GJ in U87 cells, while 0.1 μmol/L etomidate had no effect on dye spread of U87 cells through GJ.Conclusion:Etomidate inhibits GJ function in glioma cells.