Objective To evaluate the efficacy and safety of acupuncture as adjuvant treatment in the management of diabetic foot (DF).Methods We searched MEDLINE,Embase,CENTRAL,SinoMed,VIP,CNKI and WANFANG database.We also searched the bibliographies of retrieved articles and correlated proceedings and collected the literatures of DF of clinically randomized or quasi-randomized control trials of acupuncture as adjuvant treatment.After the data was extracted independently by 2 reviewers,we performed meta-analysis by using RevMan 5.1 software.Results Seven studies included 626 patients who met the inclusion criteria,and all employed clinical effects as evaluation indicator.Meta-analysis showed that acupuncture as adjuvant treatment could obviously improve the total effectiveness rate(RR =1.29,95％ CI:1.20,1.38,P ＜ 0.00001)and the recovery rate(RR =1.92,95％ CI:1.60,2.30,P ＜ 0.00001 ).No adverse reactions occured.Conclusions The limited current evidence shows that acupuncture as adjuvant treatment is safe and effective in the treatment of DF.Due to the poor quality of original studies,a prudent choice is suggested.Further studies with high quality and large samples according to CONSORT are also warrant.

Objective To identify the biological and molecular biological characteristics of SN7 virus isolated from Niviventer Confucianus in Sichuan province. Methods Monoclonal antibody, PRNT and PCR antigenicity analysis and genotyping of SN7 strain were performed. M and S segments of SN7 genome were also cloned and sequenced. The sequences were compared with those of other strains of Hantavirus. Results It was difficult to identify SN7 by using monocloncal antibody, PRNT and PCR. With sequence comparison, we found that strain SN7 had high homology(80.2%～87.1% of M segment and 76.6%～92.0% of S segment) with HTN type strains, and relatively low homology(70.0%～71.6% of M segment and 71.0%～72.2% of S segment) with SEO type strains. Strain SN7 was believed to belong to HTN type. Conclusions SN7 is a new subtype strain of HTN type viruses. It is possible that Hantavirus has immune escape in its natural hosts.

Objective To determine whether the inhibition of paxillin tyrosine residues 31 and tyrosine residues 118 (Pxn Y31 and Pxn Y118) phosphorylation via inhibition of c-Abl kinase will effectively block its downstream effector molecules vessel endothelium-cadherin (VE-cad), and whether Rho/Rho kinase activation which will induce the vascular barrier dysfunction. Methods Ninety healthy male Sprague-Dawley (SD) rats were randomly divided into nine groups (each n =10). Only tracheotomy was undergone in the sham group. Groups of protective ventilation were set at a volume tidal (VT) of 6 mL/kg, a positive end-expiratory pressure (PEEP) of 5 cmH2O (1 cmH2O =0.098 kPa) for 1 hour or 2 hours (namely group PVT 1 h and group PVT 2 h), respectively. Groups of high VT were put on mechanical ventilation (MV) at high VT 30 mL/kg, PEEP 0 for 1 hour or 2 hours (namely group HVT 1 h and group HVT 2 h), respectively. Groups UO126 and AG957 pretreatment were set on MV at HVT for 1 hour or 2 hour respectively, but they were given p42/44 mitogen-activated protein kinase (p42/44MAPK) inhibitor UO1261 mg/kg by intraperitoneal injection or c-Abl kinase inhibitor AG95710 mL/kg by intragastric injection 1 hour before HVT ventilation. All the animals were sacrificed after experiments and specimens of lung tissues and bronchoalveolar lavage fluid (BALF) were harvested. Pulmonary vascular permeability was measured by Evans blue (EB). The levels of tumor necrosis factor-α(TNF-α) in BALF were measured by enzyme linked immunosorbent assay (ELISA). Then the change of lung tissue pathology was observed with light microscope, diffuse alveolar damage system (DAD) score and lung wet/dry ratio (W/D) were estimated. The myeloperoxidase (MPO) activity was measured by colorimetric analysis, phosphorylations of c-Abl Y245, Pxn Y31, Pxn Y118, VE-cad Y658, p42/44MAPK Y202/Y204, myosin light chain (MLC) and myosin-associated phosphatasetype Y696 (MYPT Y696) were determined by Western Blot. Results ① There were no obvious pathological changes in the lung tissue in the sham group and PVT 1 h or 2 h group, and also there were no significant differences in all the parameters between above groups. However, the injury in lung tissue was severe in the HVT groups. In addition, DAD score, lung W/D ratio, EB content, the activity of MPO, and TNF-α in BALF in HVT groups were significantly higher than those in sham group and PVT groups. After pretreatment with AG957 or UO126, all the parameters were significantly decreased as compared with those of groups HVT. ② The levels of phosphorylation of the proteins in lung tissue in HVT groups were increased as compared with those of group sham and groups PVT, especially at 2 hours of MV. However, compared with groups HVT, the level of p-VE-cad Y658 in lung tissue decreased significantly in group AG957 and group UO126 at 2 hours after HVT. However, the levels of all phosphorylated proteins at 2 hours were significantly lowered in the AG957 group compared with those of the HVT group [p-c-Abl Y245 (gray value): 0.29±0.04 vs. 0.42±0.04, p-Pxn Y31 (gray value): 0.51±0.03 vs. 0.70±0.05, p-Pxn Y118 (gray value):0.65±0.04 vs. 0.91±0.04, p-VE-cad Y658 (gray value): 0.77±0.07 vs. 1.32±0.07, p-p42/44MAPK Y202/Y204 (gray value): 0.38±0.06 vs. 0.61±0.03, p-MLC (gray value): 0.37±0.04 vs. 0.77±0.05, p-MYPT Y696 (gray value):0.54±0.05 vs. 0.87±0.06, all P < 0.05]. After pretreatment with UO126, the phosphorylation level of VE-cad in lung tissue at 2 hours was significantly lower than that of HVT group (gray value: 0.74±0.04 vs. 1.32±0.07), and the phosphorylation levels of p42/44MAPK and its downstream effector molecules MLC and MYPT Y696 were also significantly decreased [p-p42/44MAPK Y202/Y204 (gray value): 0.38±0.07 vs. 0.61±0.03, p-MLC (gray value):0.37±0.04 vs. 0.77±0.05, p-MYPT Y696 (gray value): 0.55±0.05 vs. 0.87±0.06, all P < 0.05]. Conclusions Pxn Y31 and Pxn Y118 phosphorylation could be blocked by inhibition of c-Abl kinase, which could strengthen VE-cad at attachment junction and might block formation of Pxn-guanine nucleotide-exchange factor H1 (GEF-H1)-p44/42MAPK signalosome which induce activation local Rho signaling, lead to activation of MLC phosphorylation, actomyosin contraction, and increase endothelial permeability.

Objective To investigate the effects of insulin-like growth factor-1（IGF-1）on the cell proliferation of human non-small-cell lung cancer（NSCLC） and the possible molecular mechanism.Methods MTT assay was used to examine the effects of IGF-1 （0.1,1,10,100 ng/mL）on the cell proliferation of NSCLC cell lines（A549,LK2,H460）,Flow cytometry（FCM）and Western blot to ana-lyze the cell cycles and the protein expression of S-Phase Kinase-Associated Proteins 2（Skp2）and CDC20 homolog 1（CDH1）,respectively.Results The cell proliferation of NSCLC cell lines（A549,LK2,H460）could be promoted by the IGF-1 at different concentrations and the proliferation rate peaked when the cells were treated with 1 ng/mL IGF-1.Compared with control,the percentage of the S-phase cell population was significantly increased after the treatment of IGF-I（P 〈 0.01）and the protein expression of SKP2 also increased obviously（P 〈0.05）.However,there was no change in the CDH1 protein expression（P 〉 0.05）.Conclusion IGF-1 may accelerate the cell-cycle pro-gression of NSCLC cells by negatively modulating p27 protein via the up-regulation of SKP2 protein expression.

The article discusses the experiences of five-year minority medical students in internal medicine practice teaching.The content includes cultivating studnts’ ability of clinic thought,the application of casuistics methods,PBL method,combination of teaching and clinic,me-dia mix’s application,improving students’communication ability,adjusting teaching method in time,and so on.The purpose is to improve the effect of minority medical students in internal medicine practice teaching.

BACKGROUND: Based on a mouse model of tibial implantation, some scholars have found that the CaP-coated implant with recombinant human parathyroid hormone (1-34) (PTH(1-34)) shows strong osteogenesis effect at early stage, but this coating has not been applied in the oral environment.OBJECTIVE: To explore the role of local application of PTH(1-34) on immediate implant osseointegration . METHODS: Nine New Zealand white rabbits were randomly divided into two groups (six in experimental group and three in control group). All of the tooth sockets were filled with heterogeneous freeze-dried bone firstly after four incisors of each rabbit were extracted. In the experimental group, a titanium screw with PTH(1-34) loaded CaP coating was implanted into each tooth socket, while in the control group, a titanium screw with only CaP coating was implanted. The animals were executed respectively at 4, 8, 12 weeks after operation, and the intact maxillary and mandibular specimens were harvested and tested by gross observation, bone density analysis, torque test, histologic al observation, X-ray observation.RESULTS AND CONCLUSION: The gray value and maximum torque value of regenerated osseous tissue at different time points in the experimental group were significantly higher than those in the control group (P < 0.05). Within 4-12 weeks after implantation, regenerated and mature bone tissue appeared earlier in the experimental group than the control group. A large amount of new blood vessels were seen in the experimental group at 8 weeks after implantation, while in the control group, there were only few new blood vessels. To conclude, the local application of PTH(1-34) can promote bone formation, improve the implant-bone bonding strength, and enhance the stability of the implant.

Objective To study the effects of the interaction of advanced glycation end products (AGEs) and the receptor of AGEs (RAGE) on apoptosis of mice podocytes. Methods Podocytes were exposed to soluble AGEs such as bovine serum albumin (BSA), carboxymethyl-lysin (CML)-BSA, AGE-BSA and matrix-bound AGEs (AGE-modified collagen Ⅳ ), and to different concentrations of AGE, such as 10 mg/L, 50 mg/L, 100 mg/L. Apoptosis was assessed by TUNEL staining. Fluorescence-activated cell sorting (FACS) was used for the quantification of apoptotic andnecrotic podocytes after Annexin V-fluorescein isothiocyanate (FITC) and propidium iodide (PI) labeling. Apoptosis was described as the ratio of apoptotic cells to the total number cells under the high-power field, siRNA was transfected into podocytes through combining Dharmacon on Targetplus SMART pool siRNA reagents and Amaxa RNAi nucleofection kit. Results The apoptosis rate was higher in podoeytes exposed to either CML-BSA or AGE-BSA than that exposed to BSA. There was a two- to three-fold increase in apoptosis when podocytes were cultured in AGE-modified collagen Ⅳ as compared with native collagen Ⅳ. The apoptotic response of podocytes to AGE-BSA exposure occurred in a dose-dependent manner. Podocyte necrosis occurred only at the highest concentration of AGE-BSA(100 mg/L). AGE-BSA failed to induce apoptosis in podocytes transfected with RAGE siRNA. RAGE-specific gene knockdown did not significantly reduce the apoptosis of podocytes cultured in AGE-modified collagen IV. Conclusions The AGE-RAGE interaction plays a major role in the apoptosis of podocytes triggered by soluble AGEs, but not by matrix-bound AGEs. Reduction of AGE burden and RAGE expression may be important therapeutic approaches to prevent the progression of kidney disease.

Objective To investigate the resistant mechanism of carbapenem-resistant Escherichia coli and its relationship with endogenous infection. Methods Two carbapenem-resistant Escherichia coli strains were isolated from blood and stool of a same patient, respectively. The minimal inhibition concentrations (MIC) of the two isolates against imipenem and meropenem were determined by E-test. The susceptibility against other antimicrobial agents were done by disc diffusion method. Isoelectric focusing electrophoresis (IEF), polymerase chain reaction (PCR) amplification,cloning and sequencing, conjugation, Southern blotting were carried out to analyze the encoding gene of β-lactamases. Homology analysis of the two strains was done by pulsed field gel electrophoresis (PFGE). Results MIC against imipenem and meropenem of the two strains were both≥32 mg/L.Both strains produced KPC-2 (pI 6.7) and SHV-12 (pI 8.2) β-lactamases. blaKPC2gene was located on a 54 kb transferable plasmid. PFGE showed that the two Escherichia coli strains were derived from the same clone. Conclusions The resistance and enzyme digestion map of chromosome DNA of the two Escherichia coli strains are coincident. The Escherichia coli septicemia of this patient is probably an endogenous infection caused by the immigration of Escherichia coli from the gut.

Objective To investigate the antibiotic resistance of extended-spectrum-β-1actamases (ESBLs)-producing Escherichia coli (E.coli) and Klebsiella pneumoniae (K.pneumoniae) isolates and the risk factors of bloodstream infections caused by these strains.Methods Clinical data of 131 patients with E.coli or K.pneumoniae-induced bloodstream infections admitted in the Second Affiliated Hospital of Zhejiang Chinese Medical University during September 2009 and June 2014 were retrospectively analyzed.Species identification and antimicrobial susceptibility test were performed by Vitek 2 system,and ESBLs production was tested by standard disk diffusion method.Logistic regression analysis was performed to identify the risk factors of bloodstream infections induced by ESBLs-producing strains.Results Among 131 patients,65 were infected with ESBLs-producing strains,and 66 were infected with non-ESBLs-producing strains.The resistance rates of ESBLs-producing strains were above 50％ for penicillin,aztreonam and third/fourth generation cephalosporins,which were significantly higher than those of non-ESBLs producing strains.The resistance rates of ESBLs-producing E.coli and K.pneumoniae to carbapenems and piperacillin/tazobactam were 0-2.0％,2.3％ and 0-14.3％,26.7％,respectively.The univariate analysis revealed that patients with exposure to cephalosporins in recent 3 months (x2 =18.322,P ＜ 0.01),prior infection with ESBLs-producing strains (x2=14.610,P＜0.01),indwelling catheter in recent 3 months (x2 =13.016,P ＜ 0.01),history of hospitalization in recent 3 months (x2 =11.269,P ＜ 0.01),exposure to quinolones in recent 3 months (x2 =10.638,P ＜ 0.01),nosocomial infection (x2 =8.205,P ＜ 0.01),history of indwelling deep venous catheter or percutaneous central catheter in recent 3 months (x2 =4.817,P ＜ 0.05) and exposure to glucocorticoid hormone in recent 3 months (x2 =4.265,P ＜ 0.05) were associated with infection of ESBLs-producing strains.Multivariate Logistic regression analysis revealed that exposure to quinolones in recent 3 months (OR =6.851,P ＜ 0.01),prior infection with ESBLs-producing strains (OR =6.344,P ＜ 0.01),exposure to cephalosporins in recent 3 months (OR =3.719,P ＜ 0.01),and indwelling catheter in recent 3 months (OR =3.180,P ＜ 0.05) were independent risk factors for ESBLs-producing E.coli or K.pneumoniae infection.Conclusions ESBLs-producing E.coli or K.pneumoniae isolates are highly resistant to most antibiotics,and multidrug-resistance is common.Carbapenems were still the most effective antibiotics against ESBLs-producing E.coli or K.pneumoniae infection.Rational use of cephalosporins and quinolones,strictly following aseptic technique in operation,strict use of indications for indwelling catheterization,and completely eradicating ESBLs-producing strains in previous infections may be helpful in reducing bloodstream infections by ESBLs-producing E.coli or K.pneumoniae.

ObjectiveTo determine whether the inhibition of caveolin-1 tyrosine residues 14 (Cav-1-Y14) phosphorylation with protein tyrosine kinase inhibitors (PP2) will upregulate heme oxygenase-1 (HO-1) activity to protect against ventilation induced lung injury in vivo of an animal model.Methods Fifty-four male Sprague-Dawley (SD) rats were randomly divided into nine groups (eachn = 6). Group A served as normal control group, in which rats did not receive ventilation but tracheotomy. Groups B1 and B2 received lung protective ventilation respectively for 1 hour or 2 hours. Groups C1 and C2 received high tidal volume (40 mL/kg) ventilation for 1 hour or 2 hours, respectively. The group D1 or D2 also received high tidal volume ventilation for 1 hour or 2 hour respectively, but they were given PP2 1 hour before high tidal volume ventilation. The groups E1 and E2 also received high tidal volume ventilation respectively for 1 hour or 2 hours, but tyrosine kinase inhibitor PP2 and HO-1 inhibitor zinc protoporphyrinⅨ(ZnPPⅨ) were given to animals 18 hours before high tidal volume ventilation. All the animals were sacrificed after ventilation, and the specimens of lung tissues and bronchoalveolar lavage fluid (BALF) were harvested. Then the changes in pathology of lung tissue was observed, and diffuse alveolar damage scores (DAD) were calculated, myeloperoxidase (MPO) activity was measured by colorimetric analysis, lung wet/dry ratio (W/D) was estimated. The expressions of phosphorylated caveolin-1 (P-Cav-1-Y14), caveolin-1 (Cav-1) and HO-1 were determined by Western Blot. The expressions of high mobility group B1 (HMGB1) and advanced glycation end product receptor (RAGE) in lung tissues were assayed with immunohistochemistry staining. The levels of tumor necrosis factor-α(TNF-α) in BALF were measured by enzyme linked immunosorbent assay (ELISA).Results There was no significant difference in all the parameters between group A and groups B. Compared with group B1, DAD score, W/D ratio, the activity of MPO and the concentration of TNF-α in BALF in group C1 were significantly increased [DAD score:7.97±0.59 vs. 0.55±0.13, W/D ratio: 5.70±1.61 vs. 5.04±0.63, MPO (U/g): 1.82±0.14 vs. 0.77±0.26, TNF-α(ng/L): 370.10±29.61 vs. 54.38±8.18, allP< 0.05], and the injury in ventilation 2 hours group was more serious than that in ventilation 1 hour group. Compared with groups C, all the parameters in groups D were significantly decreased. The parameters in groups E were significantly higher than those in groups A, B, and D, but no significant difference was found as compared with groups C. Compared with groups B, the protein expressions of Cav-1 and P-Cav-1-Y14 (gray value) in groups C were significantly increased (1 hour: 1.49±0.02 vs. 1.26±0.13, 1.34±0.02 vs. 0.87±0.04;2 hours: 1.58±0.02 vs. 1.27±0.27, 1.31±0.01 vs. 0.95±0.02, allP< 0.05), and the expression of HO-1 protein (gray value) was significantly decreased (1 hour: 0.59±0.02 vs. 1.10±0.01, 2 hours: 0.49±0.01 vs. 1.20±0.02, both P< 0.05). No significant difference in Cav-1 protein expression between groups D as well as groups E and groups C. The protein expression of P-Cav-1-Y14 in groups D and E was significantly lower than that in groups C. The protein expression of HO-1 in groups D was significantly higher than that in groups C, but the phenomenon was not found in groups E as compared with groups C. Compared with group A, the positive expression of HMGB1 and RAGE in lung tissue in groups C and E was significantly increased, but no significant difference was found between groups B as well as groups D and group A.Conclusion Cav-1-Y14 phosphorylation is the key factor for ventilator induced lung injury, which can not only lead to a decrease in vascular barrier function, but also inhibit the activity of HO-1 enzyme, thus further aggravates inflammatory injury of the lung as induced by mechanical ventilation.