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.

BACKGROUND: It is reported that ceramide signal pathway may play an important role in the apoptosis of vascular endothelial cell and then lead to the progress of atherosclerosis, such as the formation of foam cells and the proliferation of smooth muscular cells.OBJECTIVE: To study the changes of the sphingomylinase activity and ceramide content in aorta of rabbits with experimental atherosclerosis and investigate the regulative effects and mechanism of emodin on them as compared with positive fenofibrate.DESIGN: Completely randomized controlled design.SETTING: Laboratory of Pharmacology & Toxicology, School of Pharmaceutical Science of Sun Yat-sen University.MATERIALS: The experiment was completed at the Laboratory of Pharmacology & Toxicology, School of Pharmaceutical Science of Sun Yat-sen University from July to December 2003. Totally 48 New Zealand male rabbits were selected. Forty animal models of atherosclerosis were made with high cholesterol feed, and the other 8 rabbits were selected as the normal controls. Model animals were divided randomly into model group, 5 mg/kg emodin group, 10 mg/kg emodin group, 20 mg/kg emodin group and 25mg/kg fenofibrate group with 8 in each group.METHODS: At the seventh weeks of model duplication, 5 mg/kg, 10 mg/kg and 20 mg/kg emodin were perfused in rabbits of emodin groups respectively, and 25 mg/kg fenofibrate was perfused in rabbits of fenofibrate group. Emodin and fenofibrate were diluted or suspensed with 2 mL saline once per day respectively. Rabbits in normal control group and model group were administrated with the same volume of saline for 4 weeks. The rabbits were raised separately and were fed with 135-150 g food per day.MAIN OUTCOME MEASURES: [1] The area of the lipid plaque in aortal intima; [2] the content of serum TC and TG; [3] SOD activity and MDA content; [4] SMase activity and CER content in aorta.RESULTS: Totally 48 rabbits entered the final analysis. [1] Area of the lipid plaque: Area of the lipid plaque was (48.87±15.5) % in the model group, which was larger than that in each emodin group (P ＜ 0.05 or 0.01),especially larger than that in the 10 mg/kg emodin group (22.19±12.9)%while that in the fenofibrate group was similar to that in the model group (P ＞ 0.05). [2] Content of serum TC and TG: The anrtal intima of control was smooth. Content of serum TC and TG in each emodin group were similar to those in the model group (P ＞ 0.05), but those in the 25 mg/kg fenofibrate group were lower than those in the model group (P ＜ 0.05). [3]Content of SOD and MDA in plasma: SOD activity of rabbits in each emodin group was higher than that in the model group (P ＜ 0.05, P ＜ 0.01),but the MDA activity in the 10 mg/kg and 20 mg/kg emodin group was lower than that in the model group (P ＜ 0.05). The MDA activity in the25 mg/kg fenofibrate group was similar to that in the model group (P ＞ 0.05).[4] Content of SMase and CER: Those in the model group were higher than those in the normal control group, but those in the 5, 10 and 20 mg/kg emodin groups were lower than those in the model group; those in the 25 mg/kgfenofibrate group were similar to those in the model group (P ＞ 0.05). [5]Analysis of correlation: Content of SMase was in positive relation with blood cholesterol (r=0.542, P ＜ 0.01), in positive relation with blood MDA (r=0.789, P ＞ 0.01), and in negative relation with blood SOD(r=-0.936, P ＞ 0.01); content of CER was in positive relation with blood cholesterol (r=0.433, P ＞ 0.05), in positive relation with blood MDA (r=0.673, P ＞ 0.01), and in negative relation with blood SOD (r=-0.876, P ＞ 0.01).CONCLUSION: The study finds that emodin, despite its insignificant effects on decreasing TG or TC, can protect vascular endothelial cells and reduce the area of lipid-laden plague of aortal intima by antioxidation, inhibition of the sphingomyelinase activity and reduction of the content of ceramide. It is suggested that moderate dosage of emodin employed in the study may be most appropriate to atherosclerosis treatment.

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 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.

Background and purpose: Gap junctions(GJ) could enhance cytotoxicity induced by chemotherapeutic agents. However, whether or not GJ composed of connexin 43 (Cx43) could increase etoposide cytotoxicity remains unclear. The aim of this study was to explore the effect of GJ composed of Cx43 on etoposide cytotoxicity in testicular cancer cells. Methods: Eighteen-glycyrrhetinic acid and siRNA were used to inhibit GJ function. Retinoid acid was used to enhance GJ function.“Parachute”dye-coupling assay was used to examine dye spread through GJ composed of Cx43 in MLTC-1 cells. “Standard colony-forming assay” was used to examine cell survivals of MLTC-1 cells treated with etoposide. Results: Assayed by “parachute” dye-coupling assay, the dye spread through GJ in MLTC-1 cells was significantly decreased by 18-glycyrrhetinic acid however increased by retinoid acid. Cx43 expression and GJ function in MLTC-1 cells were inhibited by Cx43-siRNA. Results from “standard colony-forming assay” showed that etoposide cytotoxicity was decreased by 18-glycyrrhetinic acid and siRNA, however enhanced by GJ function enhancer retinoid acid. Conclusion:The function inhibition of Cx43 composed GJ in MLTC-1 cells could decrease etoposide cytotoxicity. The enhancement of GJ composed of Cx43 in MLTC-1 could increase etoposide cytotoxicity.