BACKGROUND: With the development of China, quality of life (QOL) is getting more and more attention, however, there are few studies on QOL, especially in Mainland China.OBJECTIVE: To observe the situation of combinative application of Functional Independence Measure (FIM) and QOL assessment in rehabilitation clinical practice.DESIGN: Case analysis.SETTING: Zhongshan Hospital of Fudan University.PARTICIPANTS: Totally 83 rehabilitation patients selected from Shanghai Zhongshan Hospital from January to December 2003,consenting to take part in the study, were divided into 4 groups: bone & joint rehabilitation(n=42), stroke rehabilitation (n=17), internal medicine (n=15), and cancer rehabilitation (n=9).METHODS: Every patient carried out functional independence assessment and quality of life measurement within 24 hours of admission. FIM was adopted for functional independence assessment which included 13 items of motor (ranged from 13 to 91 points) and 5 items of cognition (ranged from 5to 35 points), and FAQ for quality of life included making telephone call,self-care economy, shopping, using vehicle, housework, jobs, entertainment,etc. with 100 in total. The author performed all the assessment.MAIN OUTCOME MEASURES: Every patient carried out FIM and FAQ assessment after admission and discharge.RESULTS: All data of totally 83 patients entered the final analysis. [1]The average age and length of hospital stay in stroke group were higher than those in other groups (P ＜ 0.01). [2] FIM motor and cognitive scores in stroke group were higher at discharge than those at admission (5.276,3.624;6.200,5.941,P ＜ 0.01), but scores of functional activity were lower at discharge than those at admission (1.253, 1.547, P ＜ 0.01). [3]In bone joint group, the FIM cognitive scores were coincidence in general, while motor scores were higher at discharge than those at admission (6.220,5.388, P ＜ 0.01), but scores of functional activity were lower at discharge than those at admission (0.610, 0.912, P ＜ 0.01). [4] Only scores of functional activity in tumor group were lower at discharge than those at admission (0.722, 0.989, P ＜ 0.05). [5] All items in internal medicine group were coincidence in general (P ＞ 0.05).CONCLUSION: FAQ is more sensitive than FIM in rehabilitation practice, but cannot replace FIM, and should be used with FIM.

Aim To explore the effect of N-acetyl-L-cysteine ( NAC ) on β amyloid peptide 25 - 35 ( Aβ25-35 )-induced the increase of calpain activity and its possible mechanism. Methods The activity of cal-pain was induced by 20μmol·L-1 Aβ 25-35 in primary cortical neuron. Neurons were incubated in the absent or present Aβ25-35 , or pre-incubated NAC ( 10 mmol ·L-1 ) , then co-incubated with Aβ25-35 . The meas-urement of calpain activity, H2 O2 level and mitochon-drial membrane potential was performed on a micro-plate fluorometer. The ATP level was detected using a luciferin/luciferase based ATP assay kit. Results In Aβ25-35 treated group, the activity of calpain and H2 O2 was obviously higher than that in control group. How-ever, in neurons pre-incubated in NAC and then co-in-cubated in Aβ25-35 , the calpain activity and H2 O2 level were significantly decreased compared with that in Aβ25-35 group. Upon Aβ25-35 exposure for 12 h, corti-cal neurons showed a significant decrease in mitochon-drial membrane potential and ATP level when com-pared to the control group. Pre-treatment with NAC showed an increase in mitochondrial membrane poten-tial and ATP level as compared to neurons treated with Aβ25-35 alone for 12h. Conclusion This result sug-gests that NAC can attenuate calpain activity induced by Aβ25-35 through protecting mitochondria.

Objective To study the effect improvation of lung function and prognosis of singulair and seretide for moderate to severe AECOPD . Methods 78 patients associated with moderate to severe AECOPD from January 2014 to June 2016 in our hospital were researched.They were divided randomly into observation and control groups according to the order of admission, 39 cases in each group.In the control group, they were treated by conventional anti-infective, expectorant, oxygen, suction seretide.In the observation group, using singulair on the basis of the control group.Clinical data, clinical efficacy, clinical symptoms begin to improve time, hospitalization time, blood gas analysis (PaO2, PaCO2) after five days and pulmonary function after treatment forced expiratory volume in one second ( FEV1 ) , call gas peak velocity ( PEF) , forced expiratory volume in one second than the forced vital capacity (FEV1/FVC), maximum mid-expiratory flow rate (MMEF) were compared with each other.Results Their clinical data of patients and other general information and basic condition had no significant difference between each other.The effective rate of observation group and control group were 97.44%and 87.18%, clinical effecicy of observation group was better than the control group, the difference was statistically significant (u=2.2805, P<0.05).Postoperative hospital stay, time of symptoms began to improve of the observation group were shorter than the control group, the difference was statistically significant (P<0.05), PaO2 of 5-day post-treatment of observation group was higher, and PaCO2 was lower, the difference was statistically significant (P<0.05).Lung function of two groups of patients had no significant difference before treatment, after treatment, pulmonary function in the observation group (including FEV1, PEF, FEV1/FVC, MMEF) was better than the control group, the difference was statistically significant (P<0.05).Conclusion Seretide combined with singulair to treat severe AECOPD has a good effect, it can significantly improve the therapeutic effect and improve the patient's lung function.

0.05) . Tube re-adhesion rate was 10.7% and 17.9% (P

Objective To investigate the impact of hypoxia on the expression of early growth response-1 (Egr-1) and monocyte chemoattractant protein-1 (MCP-1) in mouse aorta,and to probe the underlying mechanism involving receptor for advanced glycation end-products (RAGE).Methods 3-month-old C57BL/6 mice were subjected to hypoxia [(6.0±0.5) ％ oxygen] to establish the global hypoxia model(n=6 rats for each).Aortas were dissected,Egr-1 mRNA and MCP-1 mRNA were detected by real time RT-PCR,Egr-1 and RAGE proteins were tested by Western blot,and Egr-1 DNA binding activity was assayed by electrophoretic mobility shift assay (EMSA).For blockade of RAGE,mice were pretreated with soluble RAGE (sRAGE) for 1 h by intra-peritoneal injection before they were exposed to hypoxia.Mice with normoxia were used as controls.Results After 30 minutes of hypoxic exposure,Egr-1 mRNA in aorta was increased to (28.3±0.9)folds compared with normoxic controls (F=617.17,P＜0.01),and the induction persisted for at least 3 hours.After 45 minutes of hypoxic exposure,Egr-1 proteins in aorta was increased to (5.7 ± 0.3) folds compared with normoxic controls (F =57.18,P＜ 0.01); the enhanced DNA binding activity of Egr-1 by hypoxia was attenuated by pretreatment with anti-Egr-1 lgG.After 4 hours of hypoxic exposure,MCP-1 mRNA expression in aorta was increased to(4.0±0.3)folds compared with normoxic controls (F=30.68,P＜0.01).RAGE antigen was increased significantly within 30 minutes of hypoxic exposure,with the peak at 15 minutes; hypoxia-induced Egr-1 mRNA expression was significantly attenuated by pretreatment with sRAGE (3.3 ± 0.2) folds compared with normoxic controls (F =30.20,P＜0.01).Conclusions Hypoxia significantly induces Egr-1 and MCP-1 upregulation expressions in mouse aorta,and blockade of RAGE significantly attenuates hypoxia-induced Egr-1 expression.Thcsc findings suggest RAGE signaling is involved in hypoxia-induced vascular inflammatory stress,and highlight this receptor as a potential therapeutic target to protect tissues injured by hypoxia.

Objective To evaluate the application of modified Abbe flap in repairing moderate defects of the upper lip and time point to divide the pedicle.Methods Classic Abbe flap was modified in its design,pedicle cutting and dividing time,which was used to repair moderate defect of the upper lip in 12 cases.Surgery was divided into two phases:one with modified Abbe flap surgery was performed for the combined nasal deformity repair simultaneously,and then the pedicle was divided 9days after surgery.Results 12 patients underwent modified Abbe flap.No vascular complications were found in these flaps.Upper lip shape was well and satisfactory functional recovery,corresponding improvement in nasal appearance.Conclusions The surgery that the modified Abbe flap with the pedicle is divided 9 days after surgery is very simple.On one hand,it greatly improves the patient's appearance and function of the upper lip,improve the overall shape of midface,on the other hand,dividing pedicle time is significantly shorter than in the past,specially reducing the suffering of patients and duration.It is particularly suitable for unilateral and bilateral cleft lip of the upper lip on secondary moderate deformities and combined nasal deformities.

Aim To explore the possible protective effect of ginsenoside Rg1 on oligomeric Aβ1-42 induced apoptosis and its possible mechanism. Methods The damage was induced by oligomeric Aβ1-42 in primary cortical neurons. Cells were incubated in the absence or presence of Aβ, or co-incubated in sp600125 with Aβ, or pre-incubated in ginsenoside Rg1 then co-incu-bated in Aβ. The p-JNK, JNK, caspase-3 activity and TUNEL-positive cells were detected. Results In Aβ1-42 treated group, the ratio of p-JNK/JNK level was increased more than that in non-treated group for 15 min. However, in neurons preincubated with (2. 5, 5, 10 μmol·L-1 ) ginsenoside Rg1 and then co-incuba-ted with 5 μmol·L-1 oligomeric Aβ1-42 , the p-JNK/JNK ratio, caspase-3 activity and TUNEL positive neu-rons were significantly decreased compared with those of Aβ1-42 treated group. Conclusion Ginsenoside Rg1 can attenuate the oligomeric Aβ1-42-induced apop-tosis by JNK pathway.

Objective To systematically assess the efficacy of memantine on moderate to severe Alzheimer's disease (AD).Methods With the evaluation method of the Cochrane system,searches were made in the Cochrane Library,MEDLINE,Embase,Forest Laboratories,CNKI,Wanfang Data,and VIP Data up to February 2013 for double blind,randomized,and placebo-controlled trials (RCTs) evaluating the efficacy of memantine for moderate to severe AD.A meta-analysis of included clinical trials was conducted using the Revman 5.2 software to evaluate the efficacy of memantine on overall clinical status,cognitive function activities of daily living,and behavioral and psychological disturbances.Results A total of 8 RCTs were included (2 527 patients with moderate to severe AD).Results of the meta-analysis showed that,for patients with moderate to severe AD,memantine had better efficacy than placebo on overall clinical status,cognitive function,and activities of daily living (MD=-0.24,95％CI:0.340.15;SMD=-0.26,95％CI:-0.340.18;SMD=-0.13,95％CI:-0.21-0.05),but there was no significant difference in efficacy on behavioral and psychological function between memantine and placebo (P =0.08).Analysis of subgroups showed that memantine had better efficacy than placebo on cognitive function in moderate AD patients (SMD =-0.22,95％CI:-0.37 0.06) and on overall clinical status,cognitive function,and activities of daily living in severe AD patients (MD-0.29,95％CI:-0.40 0.18;SMD=-0.31,95％CI:0.46-0.15;SMD=-0.16,95％ CI:-0.25 0.06;MD=-3.13,95％ CI:-4.88-1.39;respectively).Conclusions Memantine has efficacy on overall clinical status,cognitive function and activities of daily living in patients with moderate to severe AD,especially in patients with severe AD.

Objective To explore the protective effects of adipose - derived stem cells (ADSCs) with phosphodiesterase 5 inhibition by lentivirus-mediated stable gene silencing on the proliferation and apoptosis of renal tubular epithelial cells induced by ischemia-reperfusion injury in vitro. Methods To isolate cultivate and indentify ADSCs from rats. Lentiviral expression vector of carrying PDE5 shRNA gene was transfected into ADSCs, and a negative control group was set up.Western blotting was used to detect PDE5 protein expression levels. ADSCs were co-cultured with NRK-52E in a transwell system, and NRK-52E cells were treated with ischemia/reoxygenation protocol. Edu assay was performed to evaluate the proliferation of NRK cells, flow cytometry to detect the apoptosis of NRK cells, and ELISA to quantify the protein expressions of fibroblast growth factor (FGF) and hepatocyte growth factor (HGF). The expression of E - cadherin and cytokeratin 18 (CK18) was quantified by real time PCR and flow cytometry. Results Western blotting for PDE5 protein indicated a significant reduction of PDE5 protein levels in PDE5 shRNA transduced population. After the treatment of ischemia/reoxygenation in vitro, the proliferative viability and apoptosis of NRK-52E cells co-cultured with ADSCs induced by PDE5 gene inhibition were significantly improved, compared to the normal group (all P<0.05). And the release of HGF, FGF were markedly enhanced (all P<0.05). Moreover, the NRK-52E cells survival, the expression of E-cadherin and CK18 on PDE5 inhibited ADSCs co-cultured with I/R injured NRK cells was significantly increased compared to that in the negative control group (all P<0.05). Conclusion ADSCs preconditioned by inhibition of PDE5 can be a powerful novel approach to improve the survival of renal tubular cells following ischemia-reperfusion injury, and have an obvious tendency to transform epithelial cells.

Objective To investigate the possible effect of ginsenoside Rg1 and oligo Aβ1-42 on PKA/CREB pathway.Methods The damage was induced by oligomeric Aβ1-42 in primary cortical neuron.Neurons were incubated with or without glutamate,or incubated in Aβ,or pre-incubated in Rg1 and then co-incubated in Aβ.The proteins of p-CREB,t-CREB,PKA Ⅱ α and BDNF were detected by Western blot.Results After the treatment with Oligo Aβ1-42 for 2 h,the p-CREB/t-CREB level induced by glutamate was obviously lower (P＜ 0.001).However,in neurons pre incubatedwith 2.5,5.0,10.0 μmol/L of ginsenoside Rg1 and then co-incubated with 5μmol/L of oligo Aβ1-42,the p-CREB/t-CREB induced by glutamate was significantly increased as compared with that of Aβ1-42 group (P＜0.05).Upon Aβ1-42 exposure for 2 h,cortical neurons showed a statistically significant increase in PKA Ⅱ α as compared to the control group (P ＜ 0.001).Pre-treatmentwith varying doses of ginsenoside Rg1 (2.5,5,10μmol/L) showed a decrease in PKA Ⅱ α as compared to neurons treated with Aβ1-42 alone for 2 h (P＜0.001).Furthermore,BDNF level significantly increased in Rgl-pretreated cells as compared to cells treated with Aβ1-42 alone for 24h (P＜0.05).Conclusions Ginsenoside Rg1 attenuates the oligo Aβ142 inhibition of PKA/CREB pathway.