Objective To investigate whether functional electrical stimulation (FES) can improve the expression of proteins in the NMDAR1-pGLuR1 pathway so as to promote the recovery of motor function and sensation after stroke.Methods Eighty-one Wistar rats were used to make a photochemical brain model of local ischemia.Rats were randomly assigned into a sham, placebo stimulation or FES group.Rats in the placebo and FES groups had local ischemia induced in the M1 zone of the brain using the photosensitive dye Bengal rose.It was administered intravenously and a laser beam was then stereotactically positioned on the skull.The rats in the FES groups were stimulated for 30 minutes (10 minutes on, 10 minutes off, then 10 minutes on).The placebo group's treatment was similar, but without the electric current.The rats in the sham group received no intervention.The cylinder test and the adhesive-removal test were used to test the rats' motor function and sensation before the operation and before they were sacrificed.Cohorts were sacrificed after 3, 7 and 14 days of intervention.NMDA receptor and AMPA receptor were detected in the peri-ischemic cortex using western blotting.Results After 7 and 14 days the index of forelimb motor function in the cylinder test of the FES group was significantly better than that of the placebo group.The average adhesive-removal time of the FES group was also significantly faster compared with the placebo group.After 7 days the average expression of NMDAR1 in the FES group was significantly higher than in the placebo group.The average expression of GluR1 and pGluR1 in the FES group was significantly higher than in the placebo group after 14 days.Conclusion Functional electrical stimulation can improve motor function after ischemia through the NMDARAMPAR signal pathway, at least in rats.

Objective To explore the role of apoptosis and the expression of X-linked inhibitor of apoptosis protein(XIAP) in polymorphonuclear neutrophils(PMNs) during acute pancreatitis(AP).Methods Blood from normal control(NC,n=15),mild acute pancreatitis(MAP,n=15) and severe acute pancreatitis(SAP,n=15) were collected.PMNs apoptosis was detected by flow cytometry.PMNs were isolated from each group and XIAPmRNA and protein levels were assessed by RT-PCR and Western Blotting.Results PMNs apoptosis in SAP group was(2.15?0.40)%,MAP group was(4.16?0.14)%,NC group was(4.31?0.12)%.PMNs apoptosis rate in SAP and MAP groups was decreased compared to NC group(P

Community-based rehabilitation (CBR) is positioned to provide various strategies for people with disabilities for achieving the embracing development of the community. CBR is also the terminal of the three-level rehabilitation service system. This paper analyzed the status of domestic community-based rehabilitation based on the document, discussed the possible problems referred to the international concepts about CBR, and suggested a new service pattern of CBR based on the internet and information technology.

Objective To evaluate effects of camptothecin on the autophagy of HaCaT cells.Methods Some cultured HaCaT cells were divided into several groups to be treated with camptothecin at concentrations of 5,10,25,50,100 and 200 nmol/L,and 0.1％ dimethyl sulfoxide (DMSO) (control group),respectively.Cell counting kit-8 (CCK-8) assay was conducted to estimate the proliferative activity of HaCaT cells after 24-and 48-hour treatment,flow cytometry to evaluate cell apoptosis after 24-hour treatment,and Western blot analysis to measure the expression of autophagy-related proteins microtubuleassociated protein 1 light chain 3 (LC3) and p62.Some HaCaT cells were divided into 2 groups to be treated with 10 nmol/L camptothecin and 0.1％ DMSO for 24 hours,respectively.Then,indirect immunofluorescence assay (IFA) was performed to determine the LC3 expression.Results Camptothecin at low concentrations of 5 and 10 nmol/L had no significant effects on the proliferation and apoptosis of HaCaT cells.Compared with the control group,the cellular proliferative rates were significantly inhibited by (31.23 ± 1.00)％,(54.21 ± 8.10)％ and (66.75 ± 10.70)％ in the 50-,100-and 200-nmol/L camptothecin groups after 24-hour treatment respectively,and by (25.81 ± 5.99)％,(44.35 ± 5.32)％,(65.81 ± 8.28)％ and (73.23 ± 9.59)％ in the 25-,50-,100-and 200-nmol/L camptothecin groups after 48-hour treatment respectively (all P ＜ 0.001).After 24-hour treatment,the apoptosis rates were significantly higher in the 50-,100-and 200-nnol/L camptothecin groups (14.46％ ± 2.38％,19.15％ ± 1.59％,29.88％ ± 1.37％,respectively) than in the control group (3.80％ ± 0.13％,all P ＜ 0.001).After 24-hour treatment with 5 and 10 nmol/L camptothecin,the protein expression of LC3 Ⅱ was significantly up-regulated,while p62 protein expression was significantly down-regulated:IFA showed that the percentage of autophagosome-positive cells was significantly higher in the 10-nmol/L camptothecin group than in the control group after 24-hour treatment (36.67％ ± 4.55％ vs.6.23％ ± 0.92％,t =6.546,P =0.003).Conclusions Camptothecin at low concentrations of 5 and 10 nmol/L can induce autophagy of HaCaT cells,but has no obvious effects on cell proliferation and apoptosis.Camptothecin at concentrations of 50,100 and 200 nmol/L can inhibit cell proliferation,promote cell apoptosis,and decrease autophagy levels.

Objective To study the effects of different types of exercise training on learning and memory, as well as on the expression of synaptophysin (SYP) and on postsynaptic density protein 95 (PSD-95) in rats in which a model of vascular dementia had been created.Methods Forty male Wistar rats were divided randomly into a voluntary exercise group (V-EX) , a forced exercise group (F-EX) , an involuntary exercise group (I-EX) , a vascular dementia group (VD) and a sham-operation group (Sham) , with 8 rats in each group.Two-vessel occlusion (2-VO) of the arteria carotis communis was used to create a model of vascular dementia in all of the rats except those in the sham-operation group.Beginning one week after the surgery, the V-Ex rats were free to run in a running wheel.The F-EX rats were forced to run 270 m a day in an electric wheel.The I-EX rats were stimulated to imitate the gait pattern of their forelimbs running at 9 m/min three times a day for l0 minutes each time.No special training was given to the rats in the other 2 groups.Three weeks after the surgery, their learning and memory were tested using a novel object recognition test.Immediately after the test, their prefrontal cortex was sampled and the expression of SYP and PSD-95 was detected using western blotting.Results The average novel object recognition indices of the rats in the V-EX, F-EX and I-EX groups were all significantly higher than that of the VD group.Average PSD-95 expression was also significandy higher than in the VD group.Conclusion Exercise, whether voluntary, forced or induced by functional electrical stimulation can improve learning and memory in vascular dementia, at least in rats.The mechanism is possibly that the training can increase the expression of PSD-95 in the prefrontal cortex, though not SYP.

Objective To observe the changes of the cells of human hepatocellular carcinoma (HepG2)using RNA for silencing the expression of COMMD7 gene,and investigate related mechanism of COMMD7 gene promoting HepG2 proliferation.Methods COMMD7 gene shRNA was designed and constructed into COMMD7-shRNA plasmid.HepG2 cells were divided into the HepG2 group,control-shRNA group (empty vectors were infected) and COMMD7-shRNA group (positive vectors were infected).Cells shapes were observed by fluorescence microscope after infecting.The expression of COMMD7 and expression and phosphosylation of extracellular regulated protein kinase1/2 (ERK1/2) and MEK1/2 protein were measured by Western blot.The cell vitality was measured by cholecystokinin octapeptide (CCK-8),and the apoptosis of cell was detected by flow cytometry.The measurement data with normal distribution were presented as (x) ± s.The comparisons among groups were evaluated with the one-way ANOVA,and pairwise comparison was analyzed by the LSD-t test.Results The cells were oval or spindle shapes and displayed green fluorescent after infected successfully.The results of Western blot showed that the relative quantitative expression of COMMD7 protein in the HepG2 group,control-shRNA group and COMMD7-shRNA group were 0.90 ±0.18,1.03 ±0.05 and 0.23 ±0.03,respectively,with a significant difference among the 3 groups (F =152.08,P ＜ 0.05),and the expression of COMMD7 protein in the COMMD7-shRNA group was significantly lower than those in the other 2 groups (t =20.74,21.16,P ＜ 0.05).The results of CCK-8 showed that the scores of the HepG2 vitality in the HepG2 group,control-shRNA group and COMMD7-shRNA group were 1.193 ±0.024,1.225 ±0.034 and 1.147 ±0.021,respectively,with a significant difference among the 3 groups (F =6.90,P ＜ 0.05),and the HepG2 vitality in the COMMD7-shRNA group was significantly lower than those in the other 2 groups (t =3.53,3.69,P ＜ 0.05).The results of flow cytometry showed that the apoptosis rate of HepG2 in the HepG2 group,control-shRNA group and COMMD7-shRNA group were 6.1％ ± 0.3％,7.8％ ± 0.5％ and 20.9％ ± 1.4％,showing a significant difference among the 3 groups (F =270.80,P ＜0.05),and the apoptosis rate of HepG2 in the COMMD7-shRNA group was significant higher than those in the other 2 groups (t =21.77,19.36,P ＜0.05).The results of Western blot showed that the relative quantitative expression of phosphorylation (p)-ERK1/2 and p-MEK1/2 in the HepG2 group,control-shRNA group and COMMD7-shRNA group were 0.932 ±0.046,0.945 ±0.017,0.553 ±0.052 and 0.452 ±0.031,0.468±0.027,0.263 ± 0.022,respectively,showing significant differences among the 3 groups (F =93.61,49.16,P ＜ 0.05),and the relative quantitative expression of p-ERK1/2 and p-MEK1/2 in the COMMD7-shRNA group were significantly lower than those in the other 2 groups (t =11.94,12.17,9.33,8.65,P ＜ 0.05).Conclusions COMMD7 gene can promote HepG2 proliferation via activating ERK/mitogen-activated protein kinase (MAPK) signaling pathway,and its mechanism may be promoting the phosphorylation of expression of ERK1/2 and MEK1/2.

Objective To investigate the expression of Ki-67,Survivin,Livin in dysplasia,colon carcinogenesis and para-carcinoma tissues,and to discuss the variation of cell proliferous capability in colon carcinogenesis and antiapoptosis factors.Methods 219 specimens were composed of mild,moderate and severe atypical hyperplasia,well,moderately,poorly differentiated adenocarcinoma,para-carcinoma tissues of 36,34,18,35,27,35 and 34 cases.Detected the expression of Ki-67,Survivin and Livin with tissue microarray and immunohistochemical methods.All data were statistically analyzed by SPSS 17.0.Results In mild,moderate and severe atypical hyperplasia,well,moderately,poorly differentiated adenocarcinoma and para-carcinoma tissues the expression of Ki-67 were (21.56 ± 19.20)％,(37.44 ± 17.41)％,(36.17 ± 17.41)％,(55.29 ± 16.13)％,(44.89 ± 29.67)％,(45.11 ± 29.24)％,(43.94 ± 28.84)％,Survivin were 13.8 ％,44.1％,77.8 ％,85.7 ％,85.1％,91.4 ％,91.1％,and Livin were 2.7 ％,38.2 ％,55.6 ％,100.0 ％,77.8 ％,80.8 ％,79.4 ％.The differences of Ki-67,Survivin and Livin expression in each group were statistically significant (F =6.796,X2 =81.754,X2 =95.200,all P ＜ 0.05).Ki-67 was significantly correlated with expression of Livin (r =0.360,P ＜ 0.05) and no correlated with expression of Survivin (r =0.044,P ＞ 0.05).Conclusion Colonic epithelium from mild atypical hyperplasia to proliferation of well-differentiated adenocarcinoma cells formed a peak,and gradually down to poorly differentiated adenocarcinoma formed a platform.When the colon epithelial cells to become cancerous,the capability of cell proliferation will significantly enhance,apoptosis inhibition will reach the peak and the tumor cell will happen the changes of malignant biological behavior.Tumor microenvironment may promote the cell proliferation in para-carcinoma tissues and the development of colon cancer.Livin may inhibit apoptosis and promot the progression in synergistic mechanism importing with Survivin,which play a role in the development of colonic adenocarcinoma.

Objective To characterize the changes in the dimensions during systolic and diastolic periods in the aorta with ECG-gated multi-detector CTA scans.Methods The CT angiograms of 115 patients (78 males,mean age 55.2 ± 9.4 years;37 females,mean age 60.1 ± 8.5 years) both in systolic and diastolic periods were obtained on a 64-slice ECG-gated multi-detector CT scanner.The diameters were measured at four anatomic levels of the aorta.(Level A:1 mm proximal to the innominate artery;Level B:1 mm distal to the left common carotid artery;Level C:1 mm distal to the left subclavian artery;Level D:10cm distal to the left subclavian artery).On each level,the maximal and the minimal diameters were measured both in systolic and diastolic periods.Results The paired sample t test results showed a significant difference between the systolic and diastolic diameters in all individual subjects on every level (P ＜0.001).The mean maximum diameter changes were 1.95％ (range-2.0％ to 7.0％),2.12％ (range-3.0％ to 6.0％),1.88％(range-1.0％ to 8.0％)and2.47％(range-3.0％ to 10.0％)at level A,B,C and D,respectively.The mean minimum diameter changes were 1.43％ (range-3.0％ to 5.0％),2.67％ (range-2.0％ to 11.0％),1.75％ (range-14.0％ to 9.0％)and 2.99％ (range -2.0％ to 11.0％) at level A,B,C and D,respectively.Conclusions The differences of the aortic diameters between systolic and diastolic periods are significant.The pulsatility of aorta in Chinese population may be different from published Western literature.

Objective To explore the function of ERCC2/XPD polymorphisms in the repair of DNA damage induced by UVC. Methods Plas?mids stably expressing ERCC2/XPD rs13181 AA(Lys751)and ERCC2/XPD rs13181 CC(Gln751)were transfected into Chinese hamster ovary cells,and the stable ERCC2 transfected cell lines were obtained. MTT assay was used to compare the inhibitory rates of the transfected cells treated with UVC at different irradiation intensity. The DNA damage repair ability of the transfected cells treated with UVC for 1,3,6 and 24 h was detected by modified comet assay. Results Compared with UV5ERCC2(CC),UV5ERCC2(CC) was more sensitive to UVC with decreased cell viability. DNA damage level of UV5ERCC2(CC) cells was more serious than UV5ERCC2(CC). Conclusion DNA repair capacity of ERCC2/XPD rs13181A allelic is lower than its wild?type,suggesting that ERCC2/XPDpolymorphisms play a critical role in UVC?induced DNA damage repair.

Objective:To analyze the changes of mean arterial pressure (MAP) and end expiratory carbon dioxide (ETCO 2) in patients after emergency endotracheal intubation (ETI). To explore the values of MAP and ETCO 2 monitoring in early prediction of severe cardiovascular collapse (CVC) after emergency ETI. Methods:The clinical data of adult patients who underwent ETI from March 2015 to May 2020 were collected consecutively in the emergency departments of Peking Union Medical College Hospital. The values of MAP and ETCO 2 were observed and recorded at 5, 10, 30, 60 and 120 min after intubation. According to whether severe CVC occurred after ETI, the patients were divided into the severe CVC group and non-severe CVC group. The values of MAP and ETCO 2 were compared at the same time points between the two groups and the adjacent time points within the groups. The correlation between MAP and ETCO 2 after ETI was also analyzed. ROC curve was used to analyze the ability of MAP and ETCO 2 at 5 min and 10 min after ETI to predict severe CVC. Results:Totally 116 patients were enrolled in this study, among them 75 (64.7%) cases had severe CVC after ETI. The majority were male and elderly patients in the severe CVC group. The values of MAP and ETCO 2 in 5, 10, 30, 60 and 120 min after ETI in severe CVC group were significantly lower than those in the non-severe CVC group. The values of MAP and ETCO 2 in the two groups showed simultaneous decrease from 5 min to 30 min after ETI, reached the lowest value at 30 min after ETI, and appeared the synchronous recover from then to 120 min after ETI. After ETI, the changes of MAP was correlated with that of ETCO 2 ( rs = 0.653, P<0.01). At 5 min after ETI, MAP could predict severe CVC (AUC=0.86, P<0.01), MAP≤72 mmHg was the best cutoff value (sensitivity 78.7%, specificity 87.8%); ETCO 2 could also predict severe CVC (AUC=0.85, P<0.01), and ETCO 2≤35 mmHg was the best cutoff value (sensitivity 77.3%, specificity 85.4%). At 10 min after ETI, MAP could predict severe CVC (AUC = 0.90, P<0.01), MAP≤67 mmHg was the best cutoff value (sensitivity 89.3%, specificity 85.4%), ETCO 2 could also predict severe CVC (AUC=0.87, P<0.01), and ETCO 2≤33 mmHg was the best cutoff value (sensitivity 81.3%, specificity 78.0%). There was no significant difference in the ability of prediction between any two indexes of the MAP and ETCO 2 at 5 min and 10 min after ETI ( P>0.05). Conclusions:Patients with severe CVC after ETI have early signs of decreased MAP and ETCO 2, but the delayed recognition and insufficient intervention may be related to the occurrence and development of severe CVC. MAP and ETCO 2 at the early stage after ETI have high accuracy in predicting severe CVC. MAP≤72 mmHg, ETCO 2≤35 mmHg at 5 min after intubation, MAP≤67 mmHg and ETCO 2≤33 mmHg at 10 minutes after intubation all suggest the possibility of severe CVC.