Objective To observe the hemodynamic changes on right ventricular hypertrophy induced by monocrotaline in rats . Methods Male SD rats were given monocrotaline 60 mg/kg by a single intraperitoneal injection ,the mRNA expression of RV/BW , RVHI and ANF were took as the indicators .Intraperitoneal injection with 10% chloral hydrate was performed ,the artery cannulae and right ventricular catheter were inserted ,and the right ventricle pressure was measured .Results The RVHI and RV/BW were significantly increased in M2W and M4W groups ,compared with vehicle control (P<0 .01) ,and the ANF mRNA expression was significantly increased in both groups .Bp and HR did not change in model groups .RVEDP markedly decreased (P< 0 .01) and RVP ,± dp/dtmax ,t dp/dtmax and Vpm increased (P<0 .001) in M2W groups ;and all parameters increased significantly in M4W groups (P<0 .01) .Conclusion Monocrotaline can induce RVH ,which accompany hemodynamic changes and the systolic and dias‐tolic dysfunction in right ventricle may eventually cause right heart failure .

Aim To investigate the effect taurine on ischemia-induced neuron apoptosis and its mechanisms. Methods Focal cerebral ischemia was induced by middle cerebral artery occlusion (MCAO). After 6 h permanent MCAO, mRNA expressions of Caspase-3/8 of rat brain were detected with real-time quantitative reverse transcriptase-polymerase chain reaction (real-time QRT-PCR). Oxygen-glucose deprivation (OGD) was used to induce an in vitro ischemia model. Primarily cultured cortical neurons were exposed to 4 h OGD. Intracellular calcium concentrations([Ca~(2+)]_i) was measured with fluorescent Ca~(2+) sensitive probe fura 2 acetoxylmethyl ester (Fura 2/AM). Neuronal apoptosis was assayed with flow cytometry of FITC-annexinV/propidium iodide binding 24 h after OGD. Results mRNA expressions of Caspase-3/8 were upregulated in MCAO model. [Ca~(2+)]_i and neuronal apoptosis were markedly increased in OGD model. Taurine pretreatment reduced the upregulation of mRNA expression of Caspase-3/8 in vivo and ameliorated calcium overload and neuronal apoptosis in vitro. Conclusion Taurine has neuroprotective effect against ischema-induced neuronal apoptosis. This is partly due to its effects on Caspase-3/8 and [Ca~(2+)]_i

Objective: To explore effect of TfR on immune function after ionizing by investigating changes in TfR expression on splenic lymphocytes of mice after whole body irradiation (WBI) with different dose X-rays. Methods: Direct immunoflurescence antibodies and flow cytometry were used to examine the changes of TfR expression. Results: The cell number of TfR positive expression in spleens increased significantly at 24 hours and 72 hours after WBI with 75 mGy X-rays but the cell number of TfR positive expression in spleens decreased significantly at 24 hours after WBI with 1～6 Gy X-rays. The activity of IL-2, meanwhile, demonstrated a parallel change. Conclusion: These results suggest that the TfR enhances immune function in low dose ionizing radiation but suppresses immune function in high dose. The change of TfR expression may be due to the change of IL-2 activity caused by ionizing radiation.

AIM To observe the protective effect of taurine on focal cerebral ischemia in rats. METHODS Male SD rats were divided at random into three groups, i.e. sham-operated, control and treatment group respectively. Before ischemia impairment, taurine(250 mg?kg -1?d -1)was administrated ip for one week in treatment group. A nylon suture was inserted into internal carotid artery to occlude the beginning of middle cerebral artery(MCAO). After 3 h permanent occlusion, neurology deficit score was evaluated. At 6 h, all animals were decapitated rapidly to get brain tissue. Brain infarct region was stained by 2,3,5-triphenyltetrazolium(TTC) and the size was measured by AUTOCAD. Contents of malondialdehyde(MDA) and nitric oxide synthase(NOS) and activity of superoxide dismetase(SOD) in brain tissue were detected by spectrophotometer. Expressions of iNOS and inter-cellular adhesion molecule-1 (ICAM-1) were observed through immunohistochemistry method. RESULTS Compared with the control group:Taurine can ameliorate neurological deficit score and decrease infarct volume induced by MCAO. Taurine improved the activity of SOD, but did not affect NOS activity in the infarct without affecting MDA content after 6 h MCAO. Taurine decreased the positive expression of ICAM-1 significantly in brain slice. CONCLUSION The results suggest that taurine may reduce expression of ICAM-1 and improve activity of SOD, and play an neuroprotective effect against middle cerebral artery occulusion.

OBJECTIVETo study the effect of total flavanones of Sedum sarmentosum (SSTF) on the apoptosis of rat hepatic stellate cells (HSC-T6) and its mechanism.

METHODDifferent concentrations of SSTF and HSC-T6 cells were co-cultured for different period of time. The MTT assay was used to detect the inhibitory effect of SSTF on the proliferation of HSC-T6 cells. The flow cytometry Annexin-V/PI double staining method was adopted to detect SSTF's effect on HSC-T6 cell apoptosis. Western blotting and Real-time PCR methods were applied to observe the effect on the protein and mRNA expressions of apoptosis-related cytokines Bcl-2, Bax and Caspase-3.

RESULTSSTF significantly inhibited HSC-T6 cell proliferation and induced cell apoptosis in a dose and time dependent manner. According to Western blotting result, SSTF promoted apoptosis by inhibiting Bcl-2, Bax and promoting the protein expression of Caspase-3; according to a further Real-time PCR study, Bcl-2 mRNA levels can inhibit Bcl-2 and promote Bax and Caspase-3 expressions.

CONCLUSIONSSTF has the effect of promoting the apoptosis of HSC-T6 mainly by inhibiting Bcl-2 and promoting protein and mRNA expressions of Bax and caspase-3.

Animals ; Apoptosis ; drug effects ; Caspase 3 ; genetics ; metabolism ; Cell Line ; Cell Proliferation ; drug effects ; Drugs, Chinese Herbal ; pharmacology ; Flavanones ; pharmacology ; Hepatic Stellate Cells ; cytology ; drug effects ; metabolism ; Proto-Oncogene Proteins c-bcl-2 ; genetics ; metabolism ; Rats ; Sedum ; chemistry

Objective To explore the outcomes of surgery of hip fracture in elderly pafienta aged equal or greater than 80 years old.Method The data of totally 132 patients with hip fracture aged equal or greater than 80 years old were treated with surgery between January 2004 and December 2008 was analyzed retrospectively Results Of 132 cases,68 cases were femoral neck fracture,while 64 cases were intertroehanteric fracture.The average in.hospital time waft(17.2±4.6)d,and 2 cases died of cerebral embolism and respiratory dysfunction in perioperative period respectively.One hundred and eight cases were followed up for 6 months to 5 yeats,with an average of 3.2 years.According to Harris hip scores,the average score of femoral neck fracture at 1 year and at 2 years postoperatively were(77.6±10.2),(77.3±9.3)scores,respectively;while intertrochantefic fracture at 1 year and at 2 years postoperatively were(84.6±9.8),(83.9±10.1)scores,respectively.Conclusions Aged patients with hip fracture should receivesurgical treatment as early as possible.The reasonable perioperative treatment and operative method are the keys to gain good outcomes.

AIM Taurine was reported neuroprotective under several ischemic models in vivo. In this study, the direct effect of taurine against oxygen-glucose deprivation (OGD) inducing acute neuronal injury and the underlying mechanisms in vitro were investigated. METHODSFour hours OGD was used to induce in vitro ischemic injury in rat cortical neurons. Taurine 5, 10 and 20 mmol·L-1 was added 20 h before and during 4 h OGD period respectively. Mortality rate of neuron was assayed by MTT and flow cytometry methods. Level of neuronal [Ca2+]i was detected by Fura 2/AM loading. Amino acid concentrations in culture media were measured by high performance liquid chromatography. RESULTS Under OGD conditions, neuronal death was markedly increased, and the levels of neuronal [Ca2+]i and extracellular glutamate level were enhanced obviously. Taurine pretreatment obviously decreased the percentage of neuronal death induced by OGD. In addition, abnormal elevation of neuronal [Ca2+]i and extracellular glutamate level induced by OGD both were markedly repressed by taurine. CONCLUSION Taurine can alleviate rat cortical neuron injury induced by OGD, the mechanisms were likely due to repressing calcium overload and inhibiting excessive release or leakage of glutamate under such conditions.

Objective To discuss the anticancer role of arsenic trioxide (ATO) with cisplatin on human oral carcinoma HSQ-89 cells. Methods The human oral epidermoid HSQ-89 cells were chosen as the subjects. Different concentrations of ATO were added into Cisplatin(DDP)-treated cells. The inhibition rate of tumor cells was detected by MTT assay. Results Different concentrations of ATO (0,2.5,5,7.5,10,12.5 μmol/mL) were added into oral cancer HSQ-89 cells which have been treated with DDP (15 μg/mL). The inhibition rate of tumor cells were 26.9%, 67.5%, 73.0%, 88.5%, 90.4%, 98.7%respectively; The combined application of ATO with cisplatin could improve the inhibition rate of HSQ-89 cells in a dose-dependent relation. Conclusion The combined application of ATO and DDP can produce a synergistic action of inhibition on oral cancer cell.

Objective To investigate the effects of artesunate on human cervical cancer cell line HeLa.Methods The inhibitory effect on cell proliferation was assessed by MTT assay.Transmission electron microscopy and fluorescent staining were applied to demonstrate the presence of apoptosis.Cell cycle,reactive oxygen species(ROS) levels and mitochondrial membrane potential(??m) were examined by flow cytometry,respectively.Expression of caspase-3 was detected by immunohistochemical methods.Results Growth inhibition of ART on HeLa cells was time-and dose-dependent.Apoptotic feature was observed by transmission electron microscopy and fluorescent staining.The blocking of the cell cycle was in S-phase.The expression of caspase-3 in cytoplasm was positive.The generation of ROS increased obviously(P

Objective To analyze the clinical features of rapid eye movement sleep behavior disorder (RBD) in pa?tients with Parkinson’s disease (PD) and investigate correlative factors of RBD. Methods Sixty-three consecutive PD pa?tients were included and classified into PD+RBD group (n=28) and PD-RBD group (n=35) according to REM Sleep Be?havior Disorder Questionnaire (RBDQ-HK). The degree of motor symptoms was compared using Unified Parkinson Dis?ease Rating Scale (UPDRS) and Hoehn&Yahr (H-Y) grade, the incidence of non motor symptoms was compared using non motor symptoms questionnaire (NMSquest), and the cognitive function, anxiety, depression, daytime sleep were com?pared using Montreal Cognitive Assessment (MOCA), Beck Anxiety Inventory (BAI), Beck Depression Inventory (BDI), Epworth Sleep Scale (ESS) between the two groups. Results The incidence of RBD in PD patients was 44.4% (28/63). There were longer illness course ( χ2=12.733, P=0.002), older age (t=-2.292, P=0.025), and higher H-Y grades (χ2=7.014, P=0.008) in PD+RBD group, compared with those in PD-RBD group, but there were no significant differences in sex, onset age, onset form and levodapa dose equivalents (LDE) between the two groups. There were higher UPDRSⅡ,Ⅲ scores (t=-2.734, P=0.008; U=3.329, P=0.001) in PD+RBD group. Most of the non motor symptoms, including the gastrointestinal dysfunctions, psychiatric comorbidity and sleep disturbances were more frequent in PD+RBD group (P<0.05), and the incidence of anxiety and depression were higher (χ2=3.958, P=0.047; χ2=10.338, P=0.001), whereas there were no significant differences in cognitive function and daytime sleep between the two groups. In addition, constipation (OR=7.257), illness course (OR=5.389), UPDRS Ⅲ scores (OR=1.060) were correlative with RBD in PD patients. Con?clusion PD patients with longer illness course, older ages, and severe motor and non motor symptoms more likely suffer from RBD. Besides, constipation, long illness course and high UPDRSⅢscores may be risk factors of RBD.