There is evidence to show that the treatment in a stroke unit reduces mortality in patients with stroke and improves neurological functional recoxery.Early mobilization is benefit to improve the prognosis in patients stroke,however,there is a lack of high-quality evidence.The term of"early mobilization"after stroke is not well defined now.A number of medical workers lack enough understanding of the early mobilization.How to perform the early mobilization to get the best benefit is unclear.This article reviews the related studies about the early mobilization after stroke.

AIM: To investigate the effects of p27kip1 ge ne on DNA replication and protein synthesis in esophageal carcinoma cells. METHODS: Recombinant adenovirus Ad-p27kip1 was constructed and transf ected into esophageal carcinoma cell EC-9706, and its effects on DNA replication , protein synthesis and the growth of esophageal carcinoma cells were explored b y means of cell growth count, -TdR, -Leucine incorporation meth od and flow cytometry. RESULTS: The growth of esophageal carcino ma cells was inhibited obviously. The radioactive intensity of -TdR and -Leucine in Ad-p27kip1 group decreased significantly than that in contr ol group after EC-9706 transfection (P

Objective Objective To study the influence of NS-398,a selective cyclooxygenase-2 inhibitor on the radiosensitivity of human esophageal carcinoma cell line EC9706 cell. Methods EC9706 cell, highly expressing COX-2, had been incubated with NS-398 at 10、20、50 and 100??mol/L for 24?h or 48?h before irradiation ranging from 0 to 10?Gy. Cell survival was measured by a standard clonogenic assay after 8 days of incubation. Apoptotic percentage was measured by FCM and DNA fragmentation by agarose electrophronesis. Results The senstization enhancement ratios (ratio of D_q) in EC9706 cell were 1.11, 1.24, 1.40, 1.54 at 10, 20, 50, 100??mol/L of NS-398 for 24?h pre-incubation and 1.11, 1.27, 1.58, 1.67 for 48?h pre-incubation, which showed a dose-dependant and time-dependant manner. FCM analysis revealed a higher sub-G_1 cell peak in NS-398 group after irradiation. Agarose electrophronesis showed a marked ladder. Radiation-induced apoptosis was enhanced by NS-398 (P

AIM: To investigate the effect on growth and activity of telomerase in esophageal carcinoma cells by inhibiting ubiquitin-proteasome pathway(UPP). METHODS: The esophageal carcinoma cell strain Eca9706 was treated with MG-132 to inhibit its UPP specially. The effect of growth suppression on cells was evaluated with MTT assay, morphologic changes of cells were observed under microscope, cell cycle and apoptosis were detected by flow cytometry (FCM). DNA fragment analysis was used to confirm the presence of apoptosis. The activity of telomerase was detected. RESULTS: MG-132 had obvious inhibitory effect on the growth of Eca9706 cells in a dose and time-dependent manner. Obvious pathologic change of cells were observed under microscope, cells became round, small and exfoliating. The FCM analysis showed that the ratio of esophageal carcinoma cells of G_1 phase increased and a obviously apoptotic sub-G_1 peak was found. Agarose electrophoresis showed marked ladder. The activity of telomerase was obviously inhibited. CONCLUSIONS: MG-132 significantly inhibits the growth and the activity of telomerase of Eca 9706 cells. These findings indicate that inhibiting UPP is a new strategy for the treatment of esophageal carcinoma. [

OBJECTIVE:To investigate effects of ubiquitin-proteasome inhibitor MG-132on apoptosis and survivin expression of esophageal carcinoma cells.METHODS:The esophageal carcinoma cells Eca9706were treated with MG-132,the growth inhibitory rate was determined with MTT assay,apoptosis was detected by flow cytometry,expression of survivin was detected by immunocytochemical technique.RESULTS:MG-132had obvious inhibitory effects on the growth of gastric car?cinoma cells,IC 50 of24hrs,48hrs,72hrs and96hrs were120.2,18.1,—12.2,and—16.9?mol/L respectively;Treated with5.0?mol/L MG-132for24hrs,48hrs,72hrs and96hrs,apoptotic rates of cells were(3.1?0.4)%、(31.7?3.5)%、(50.4?4.8)%and(66.6?6.2)%respectively;Expression of survivin was high in esophageal carcinoma cells and it was decreased in cells treated with MG-132.CONCLUSIONS:MG-132can significantly inhibit the proliferation of esophageal carcinoma cells and induce apoptosis,which might be associated with down-regulated expression of survivin.

Objective To observe the effect of hyperbaric oxygen (HBO) therapy on neurological functioning in rats modelling cerebral hemorrhage (ICH).Methods Sixty Sprague-Dawley rats had intracerebral hemorrhage induced by injecting autologous blood.They were then randomly divided into an HBO-free group and an HBO group,each of 30 according to a random number table.The HBO group was further divided into HBO 3 h,HBO 6 h,HBO 1 d,HBO 2 d and HBO 7 d groups which received HBO therapy for 3 hours,6 hours,1 day,2 days and 7 days respectively.Each had 6 members.The HBO-free rats were also divided into analogous HBO-free 3 h,HBO-free 6 h,HBO-free 1 d,HBO-free 2 d and HBO-free 7 d groups,and give no HBO intervention.All of the rats were evaluated for neurological impairment using the Longa scoring method before the treatment and 10 days,20 days and 30 days afterward.Results After 10,20 and 30 days of HBO treatment,there were significant differences in neurological functioning between each pair of HBO-free and HBO-treated groups.After 10 and 20 days of HBO treatment the average neurological function score of the HBO 3 h group was significantly different from that of the HBO 2 d group.The average score in the HBO 7 d group was also significantly different from that of the HBO 3 h,HBO 6 h,HBO 1 d and HBO 2 d groups after 10,20 and 30 days of HBO treatment.The average scores of the HBO 3 h,HBO 6 h,HBO 1 d and HBO 2 d groups improved significantly between 10 and 20 days after the treatment.The average score of the rats which received 30 days of treatment was also significantly different from those after 10 and 20 days.Conclusion HBO treatment can improve neurological function after cerebral hemorrhage,at least in rats.The best time to start HBO treatment is no later than 24 hours after the hemorrhage.The curative effect increases with extension of the treatment's duration.

Objective: To investigate the effect of sacubitril/valsartan on cardiac function in heart failure rabbits with preserved ejection fraction. Methods: Forty-five healthy adult male New Zealand rabbits were divided into sham operation group (n=12) and model group (n=33) by random number table method. HFpEF model was constructed by abdominal aortic constriction in model group. In sham operation group, 1 rabbit died due to anesthesia accident, and 1 rabbit in model group died of acute left heart failure. At 8 weeks of modeling, 3 rabbits were excluded due to the failure to establish the successful model. At the 8th week of modeling, 2 rabbits in sham operation group were selected and sacrificed by random number table method, and 3 rabbits in model group were selected and sacrificed for myocardial histological examination. Then, 9 rabbits in sham operation group and 26 rabbits in model group entered the subsequent experiment. The model group was randomly divided into untreated group (n=8), valsartan intervention group (n=9), and sacubitril/valsartan intervention group (n=9), respectively, drugs were applied per gavage. The feeding and exercise activity of rabbits in each group were evaluated by simple cardiac function classification at baseline, 4 and 8 weeks post intervention. Echocardiography was used to detect interventricular septal thickness at diastole(IVSd), interventricular septal thickness at systolic(IVSs), left ventricular posterior wall of diastolic(LVPWd), left ventricular internal diameter at diastolic(LVIDd), left ventricular internal diameter at systolic(LVIDs), and calculate the left ventricular ejection fraction(LVEF), mitral valve′s early diastolic flow velocity(E)/late mitral diastolic maximum flow rate ratio(A) and heart rate at baseline, 4 and 8 weeks post intervention. Serum N terminal B-type natriuretic peptide (NT-proBNP) and angiotensin (Ang)Ⅱ and soluble matrix lysin 2(sST2) content was determined by ELISA at baseline, 4 and 8 weeks post intervention. Eight weeks after intervention, the hearts of rabbits were taken and weighed, and heart mass index (HMI) and left ventricular mass index (LVMI) were calculated. Results: (1) Evaluation results of cardiac function: there were 2, 5, and 2 rabbits with cardiac function grade Ⅰ,Ⅱ and Ⅲ before the drug intervention, and 4, 4, and 1 rabbits with respective cardiac function grade after 8 weeks of intervention in valsartan group (P>0.05). There were 2, 4, and 3 rabbits with heart function gradeⅠ,Ⅱ and Ⅲ before the drug intervention, and 7, 2, and 0 rabbits with respective heart function grade after 8 weeks of intervention in sacubitril/valsartan group(P<0.05). (2) Echocardiographic results: at 8 weeks after drug intervention, IVSd and IVSs of rabbits in untreated group were significantly higher than those in sham operation group, and the ratio of E/A was significantly lower than that in sham operation group(all P<0.01). IVSs of the valsartan group was significantly higher than that of sham operation group, and the ratio of E/A was significantly lower than that of sham operation group(all P<0.01). The E/A ratio in the sacubitril/valsartan group was significantly lower than that in sham operation group(P<0.01). IVSd and IVSs in valsartan group were significantly lower than those in untreated group(all P<0.05), and IVSd in sacubitril/valsartan group was significantly lower than that in untreated group(P<0.01). The IVSd, IVSs, LVPWd, LVIDd, LVIDs, LVEF, E/A ratios were similar between sacubitril/valsartan group and valsartan group(all P>0.05). There was no significant difference in heart rate between the groups(P>0.05). (3) Serum NT-proBNP, Ang Ⅱ and sST2 levels: 4 weeks after drug intervention, untreated group, valsartan group, and sacubitril/valsartan group′s serum NT-proBNP levels were significantly higher than that of sham operation group(all P<0.01); serum NT-proBNP was significantly lower in sacubitril/valsartan group than that in untreated group(P<0.01). Four weeks after intervention, serum AngⅡ levels were significantly higher in untreated group, valsartan group, sacubitril/valsartan group than in sham group(all P<0.01), but there was no statistically significant difference between the modeling groups(P>0.05). Four weeks after drug intervention, the serum sST2 contents in untreated group, valsartan group, and sacubitril/valsartan group were significantly higher than in sham operation group(all P<0.01), and which was significantly lower in valsartan group and sacubitril/valsartan group than in untreated group(all P<0.01), which were significantly lower in sacubitril/valsartan group than in valsartan group(P<0.01). Eight weeks after drug intervention, serum NT-proBNP levels were significantly higher in untreated group, valsartan group, and sacubitril/valsartan group than in sham operation group(all P<0.01), which were significantly lower in valsartan group and sacubitril/valsartan group than in untreated group(all P<0.01), which were significantly lower in valsartan group than in sacubitril/valsartan group(P<0.01). Eight weeks after drug intervention, Ang Ⅱ levels were significantly higher in valsartan group and sacubitril/valsartan group than in untreated group(all P<0.01), which tended to be higher in untreated group and valsartan group, tended to be lower in sacubitril/valsartan compared to value at 4 weeks(all P>0.05). Eight weeks after drug intervention, serum sST2 was significantly higher in untreated group and valsartan group than in sham operation group(all P<0.01), which tended to be higher in sacubitril/valsartan group compared to sham operation group(P>0.05), which were significantly lower in valsartan group and sacubitril/valsartan group than in untreated group(all P<0.01), which was significantly lower in sacubitril/valsartan group than in valsartan group(P<0.01). (4) Comparison of whole-heart mass, left ventricular mass, HMI and LVMI: 8 weeks after drug intervention, the whole-heart mass, left ventricular mass, HMI and LVMI were significantly higher in untreated group than in sham operation group(all P<0.01), and the above indexes were also significantly higher in valsartan group than in sham operation group(all P<0.05), tended to be lower in valsartan group compared to untreated group (all P>0.05). HMI and LVMI were lower in sacubitril/valsartan group than in untreated group(all P<0.05). All the above indexes tended to be lower in sacubitril/valsartan group than in valsartan group(all P>0.05). Conclusion Sacubitril/valsartan is superior to valsartan alone on improving cardiac function in HFpEF rabbits.

Objective: To systematically evaluate the effects of hyperbaric oxygen on the hemodynamics and intracranial pressure of patients with severe craniocerebral injury (STBI). Methods: Reports of randomized and controlled trials applying hyperbaric oxygen in the treatment of STBI were retrieved from the Pubmed, Cochrane Library, Embase, CBM, CNKI, VIP and Wan Fang databases. Each report found was evaluated by two researchers independently applying pre-defined inclusion and exclusion criteria. The data were extracted and combined and a meta-analysis was performed. Results: Eight trials involving 725 patients were included in the meta-analysis. They combined to demonstrate that intracranial pressure, oxygen uptake and scores on the Glasgow coma scale improved significantly more in the hyperbaric oxygen group than in the control group after between 3 and 10 days of treatment. Conclusion Hyperbaric oxygen therapy is effective in treating severe craniocerebral injury and it is worthy of clinical application.

Cardiovascular disease is still the leading cause of mortality worldwide. Vascular endothelial dysfunction is viewed as the initial step of most cardiovascular diseases. Many studies have indicated that periodontal pathogens, especially Porphyromonas gingivalis, are closely correlated with vascular endothelial homeostasis, but the function of P. gingivalis and the underlying mechanisms are still elusive. To illuminate the effects and elucidate the mechanisms of P. gingivalis on endothelial structural integrity, we developed P. gingivalis infection models in vivo and in vitro. Endothelial cell proliferation, differentiation and apoptosis were detected. Here, we showed that P. gingivalis can impair endothelial integrity by inhibiting cell proliferation and inducing endothelial mesenchymal transformation and apoptosis of endothelial cells, which reduce the cell levels and cause the endothelium to lose its ability to repair itself. A mechanistic analysis showed that TLR antagonist or NF-κB signalling inhibitor can largely rescue the damaged integrity of the endothelium caused by P. gingivalis, suggesting that TLR-NF-κB signalling plays a vital role in vascular endothelial homeostasis destroyed by P. gingivalis. These results suggest a potential intervention method for the prevention and treatment of cardiovascular disease.