Objective To explore the correlation of electrophysiological features with clinical manifestation in patients with diabetic peripheral neuropathy (DPN).Methods The clinical data of 306 patients with DPN undergoing nerve conduction study (NCS) during May 2013 to June 2015 were retrospectively analyzed.Among 306 patients,304 were type 2,and 2 were type 1 diabetes with a mean age of 64.1 years and disease duration of 1 week-31 years.The relationship between the electrophysiological features and clinical manifestations was evaluated.Nerve conduction studies and F-wave and in sympathetic skin response were analyzed.Results ① NCS in lower limbs presented more abnormalities than that in upper limbs.There was the highest prevalence of not elicited sensory potential in Tibial nerve [56.9％(174/306),x2 =175.9] and the highest prevalence of not elicited motor potential in peroneal nerve [7.8％(24/306),x2 =1 103.1].Amplitude abnormality was more severe in sensory nerve than that in motor nerve[41.4％ (507/1 224) vs.10.8％ (132/1 224),x2 =559.2].The ratio of abnormal motor conduction velocity or distal latency was higher than that of amplitude decreased [22.9％ (280/1 224) vs.10.8％(132/1 224),x2 =1 077.4].② The abnormal ratios of the shortest F-wave latency was lower than that of the prolonged distal latency in median and tibial nerve [5.4％ (33/612) vs.20.6％ (126/612),x2 =607.6].③ The abnormal ratio of sympathetic skin response (SSR) in lower limbs were higher than that of upper limbs [40.2％ (246/612) vs.27.3％ (167/612),x2 =129.4,P ＜ 0.001],abnormal ratio of amplitude was higher than that of the prolonged latency [30.1％ (368/1 224) vs.4.7％ (58/1224),x2 =1040.5,P ＜0.001].Among the 99 cases presenting abnormal SSR in upper limbs,32 cases were normal in conventional NCS.Among the 127 cases presenting abnormal SSR in lower limbs,7 cases were normal in conventional NCS.④Disease course and glycosylated hemoglobin values were positively correlated with the distal motor latency,and negatively correlated with the nerve conduction velocity and amplitude.Conclusion Electrophysiological features of DPN is mainly shown in axon of the distal sensory nerve.Long duration and hyperglycemia may lead to more abnormalities in electrophysiological tests.

Objective To assess the irregular shape of hematoma with math methods,which is one of the risk factors of hematoma enlargement.Methods We reviewed images data of patients with spontaneous intracerebral hemorrhage treated nonsurgically who underwent initial computed tomography (CT) within 6 hours and repeated CT within 48 hours of onset.The area(s),the circumference(L),the greatest diameter(A)and the transverse diameter(B)of the greatest hemorrhage CT slice was measured.The formula X=L/S waft used to calculate the value.We calculated the area(S1)and the circumference (L1) of the ellipse with A as its long diameter and B as its short diameter.The formula X1=S1/L1 was used to calculate the value. We used formula R=X/X1 to assess the irregular hematoma shape.The relationships between hematoma enlargement and R was analyzed. Results Thirty-one patients(25.8%) showed enlarged hematomas after admission.The larger the value of R,the more irregular the shape of hematoma.When R≥1.3,the shape of the hematoma was significantly irregular.36.0% patients with R≥1.3 had hematoma enlarged.compared with only 18.6% those with R<1.3(χ2=4.62,P=0.032).Conclusions The irregular shape index R Can be used to assess the shape of a hematoma. A particularly high likelihood of hematoma enlargement is observed in patients with an irregularly shape index R≥1.3.

Objective To evaluate the effects of asymptomatic arteriovenous fistula closure on left ventricular morphology and function in renal transplant recipients.Methods Between March 2007 and March 2011,a total of 60 patients undergoing consecutive kidney transplantation with asymptomatic arteriovenous fistula were divided randomly into two groups: arteriovenous fistula closure group,and non-arteriovenous fistula closure group.By using echocardiography,the changes in CO,CI,EF,LVEDV and LVMI were analyzed.Results At 12th month after transplantation,the values of CO,LVEDV and LVMI were significantly lower than those before transplantation (P＜0.05).The value of CI also showed a tendency to decrease (P＞0.05),and the value of EF was increased significantly (P＜0.05).At 6th month after arteriovenous fistula closure (18 months after transplantation),the values of CO,CI,LVEDV and LVMI were significantly lower than those before arteriovenous fistula closure (12 months after transplantation) (P＜0.05),and the value of EF was increased significantly (P＜0.05),but the values of CO,CI,EF,LVEDV and LVMI remained unc(b)anged in controls (P＞0.05).At 18th month after transplantation,the values of CO (4.4 ±0.8 L/min),CI [3.0 ± 0.8 L·min-1·m-2],LVEDV (110.0 ± 17.4 ml) and LVMI (114.7 ± 42.5g/m2) in trial group were significantly lower than the values [CO: 5.1 ± 0.9 L/min,CI: 3.5 ± 1.0L·min-1·m-2,LVEDV: 121.4±19.3 mL,LVMI: 138.4±44.1 g/m2] in controls (P＜0.05),and the value of EF (75.2％ ± 7.4％ vs.70.5％ ± 8.2％) significantly higher (P＜005).Conclusion In both groups,kidney transplantation benefits significantly the regression of cardiac mass,cardiac index and left ventricular dimensions,but closure of asymptomatic AVF induces more significant regression.

AIM: To evaluate the implication of CXCL10-loop3-EGF fusion protein for the activities of targeting tumor and anti-angiopoiesis. METHODS: RT-PCR was preformed to amplify CXCL10 coding sequence from PBMC activated by IFN-γ. CXCL10-loop3-EGF fusion gene, which was conducted by Over-Lap Extention PCR, was hinged up with plasmid pTG19-T, transfected to E. coli DH5α and processed positive colony selection. After ligated with plasmid pET32a(+), recombinant CXCL10-loop3-EGF fusion gene was then transfected to E. coli Origami B (DE3) and induced to express its coding fusion protein his-CXCL10-loop3-EGF. The recombinant fusion protein CXCL10-loop3 -EGF was purified by His-bind affinity chromatograph, enterokinase cleavage, ultrafiltration and dislysis. The transwell chemotatic test and HUVEC angiopoiesis inhibition test were performed to determine the anti-tumor responses and anti-angiopoiesis activity of CXCL10-loop3-EGF fusion protein. RESULTS: CXCL10-loop3-EGF fusion protein was successfully constructed and confirmed by SDS-PAGE analysis and Western blotting. Significant PBMC chematatic activity and HUVEC anti-angiopoiesis activity were observed. CONCLUSION: CXCL10-loop3-EGF fusion protein, which has perfect anti-tumor activity, is successfully constructed.

AIM: To investigate the immunologic mechanism of CXC chemokine ligand 10(CXCL10) and its receptor CXC chemokine receptor 3 (CXCR3 ) involved in the process of endometriosis (EM). METHODS: Serum samples were collected from 3 groups; EM patients without operation (n = 76) , EM patients with operation (n = 10) and the normal control persons (n =76). CXCL10 and CA12S concentrations were detected by means of ELISA and chemilumino-metry. Cell surface antigens on the activated PBMC - CD3 and CXCR3, as well as CXCR3 subgene - CXCR3A and CX-CR3B were tested by flow cytometry (FC) and RT - PCR when PBMC was separated from women with EM ( n = 10) and without EM (n = 10), and then activated. RESULTS: Serum CXCL10 concentrations between three groups were signifi-canly different (P < 0.05). Compared to normal control group, although the supernatant CXCL10 concentration and CD3~+ /CXCR3~+ PBMC number in EM group has no significant difference (P >0.05) , highly expressed CXCR3B in EM group rather than CXCR3A was observed. CONCLUSION: CXCL10 in women with EM is low, indicating that it plays a vital role in the process of EM and immune system of the women with EM is defected and impaired. The immunoreactivity of PBMC from both EM patients and normal person is same to activated signal, but the productions are different: PBMC in EM group mainly express CXCR3B but PBMC in normal person mainly express CXCR3A after activation, which may be one of the immune mechanisms that EM escapes from immunological lethal effect of the infected host.

Objective To investigate the change of dynamic expression of t-PA and PAI-1 during early venous crisis after free perforator flap transplantation.Methods Thirty healthy New Zealand white rabbits weighed 2.5-3.0 kg were chosen and randomly divided into experimental group (n =15) and control group (n =15).Free transplantation of superficial epigastric artery perforator flap (SEAPF) was implemented in all rabbits firstly.Then the model of venous crisis was established by ligating the anastomosis vein in order to interrupt venous blood outflow in experimental group.The blood supply of all flaps was monitored by observing their color,swelling degree and the filling reaction of the capillaries after operation.Peripheral blood was drawn from femoral artery at different time point for measuring the concentration of t-PA and PAI-1 by Elisa.Partial flap tissue was harvested for pathological examination at corresponding time point.Data analysis was performed by using SPSS 17.0 statistical software.P ＜ 0.05 was considered statistically significant.Results One rabbit died of anesthesia,and the venous congestion was observed in 1 rabbit in control group.The models of free transplantation of SEAPF and venous crisis were established successfully in the remaining rabbits.No significant appearance change was observed within 1 h after the outflow vein being ligated,while typical appearance of venous crisis could be observed 2 hours after the outflow vein being ligated.Compared with the control group,the concentration of t-PA was lower,but the concentration of PAI-1 was higher in experimental group at 2 hours,4 hours,6 hours,8 hours after the outflow vein being ligated(P ＜ 0.05).However,there was no obvious differences between two groups at other time points (P ＞ 0.05).The pathological examination showed the red cells gradually got together and adhered to the venous wall,eventually the microcirculation had been blocked completely and theflap became necrosis after venous crisis being occurred.Conclusion t-PA and PAI-1 can't be used to diagnose early venous crisis of perforator flap transplantation.

Objective To explore the strategy and response of medical emergency centers to unexpected disaster,such as snowstorm in 2008.Method The response of Wuxi Medical Emergency Center to the snowstorm in 2008 was retrospectivey analyzed.Results Because of the disaster response plan in advance,preparation for the ambulance,and effective integration of pre-hospital care,pre-hospital tasks were completed successfully.But there existed some unsatisfied points,such as anti-skid chains wasn't fully prepared,and affected the efficiency of emergency treatment.Conclusions The increase of government input,good preparation,emergency network construction,scientific and timely disaster response plans are key to disaster events,such as snowstorm.

Based on the current status of allocation, demands and utilization of medical care resources and the needs for future development in Shanghai, the overall objectives, principles, key plans of allocation of medical care resources in the 12th Five-years Plan in Shanghai and the leading role of health bureaus at all levels were discussed.

BACKGROUND:Activation of Notch signaling plays a critical role in stem cel differentiation, and this effect seems to be cel-type dependent. Little is reported on the role of activation of Notch1 signaling in the differentiation of c-Kit+ bone marrow mesenchymal stem cels. OBJECTIVE:To analyze the influence of activation of Notch1 signaling on the differentiation of c-Kit+ bone marrow mesenchymal stem cels. METHODS:The Notch1 intracelular domain (N1-ICD) was obtained from the cDNA library by PCR and cloned intoBamHI/AgeI digested adenoviral GV314 plasmid to construct N1-ICD overexpressing shuttle plasmid, and the positive clones were verified by sequencing. N1-ICD shuttle plasmid and helper plasmids pBHGloxΔE1,3 Cre were used to co-transfect HEK293T cels to obtain N1-ICD overexpressing adenoviral particles (N1-ICD-Ad). The c-Kit+ subpopulation were isolated from bone marrow mesenchymal stem cels of the Sprague-Dawley rat femurviamagnetic activated cel sorting. After transfection of the c-Kit+ BMSCs with N1-ICD-Ad adenovirus, we assessed the activation of Notch1 signaling and differentiation in c-Kit+ bone marrow mesenchymal stem cels by quantitative RT-PCR and immunofluorescent staining. RESULTS AND CONCLUSION:N1-ICD coding sequence was successfuly generated from the cDNA library, and then was cloned into the linearized adenoviral vectors GV314. The resistant clones were verified by sequencing. With the assistance of packaging plasmids, recombinant N1-ICD-Ad adenovirus plasmids were successful packaged in HEK293T cels, and its title was 2×1012 PFU/L. c-Kit+ bone marrow mesenchymal stem cels with the purity of 91.6% were successfuly isolated from the bone marrow mesenchymal stem cels of the Sprague-Dawley rat femur. Compared with the blank and negative controls, N1-ICD-Ad infection in the c-Kit+ bone marrow mesenchymal stem cels led to substantial accumulation of N1-ICD in the cytoplasm and nuclei, significantly unregulated expressions of Hes1 (a downstream gene of Notch) and cardiomyocyte differentiation genes Nkx2.5 and cTnT, significantly increased the expression of von Wilebrand factor, an endothelial cel differentiation gene, and mildly increased the expression of smooth muscle22α, a smooth muscle cel differentiation gene. These experimental results indicate that the activation of Notch1 signaling contributes to multi-lineages differentiation of c-Kit+ bone marrow mesenchymal stem cels, and the construction of N1-ICD overexpressing adenoviral vector makes the foundation for further research on the role of Notch1 signaling in stem cel biology.

Objective To analyze the possibility of using TCR Vβsubfamily as the diagnostic in-dicators for major histocompatibility complex( MHC) deficiency-induced graft-versus-host disease( GVHD) . Methods The BALB/c mice were given 9.5 Gy (950 rad) of irradiation and transplanted with 106 of T-cell depleted (TCD) bone marrow cells from C57BL/6 and DBA/2 mice with MHC Ⅱ deficiency.Two control groups were set up accordingly by injection of TCD bone marrow cells from wild type ( WT) C57BL/6 and DBA/2 mice.Several parameters including the body weight, the GVHD clinical score and the survival time of the recipients were monitored.Flow cytometry analysis and mixed lymphocyte culture test were performed for the evaluation of autoimmune responses.Histological examination was used to analyze the severity of GVHD.Results The MHC deficiency-induced GVHD was successfully induced in the irradiated BALB/c mice receiving MHC mismatched allogeneic hematopoietic cell transplantation ( allo-HCT ) . The MHC matched DBA/2 mice with MHC deficiency could be used as the mice model of subclinical GVHD.Changes of the TCR Vβ6 were consistent with the results of histopathological examination.Conclusion Highly ex-pressed TCR Vβ6 could be used as indicators for the diagnosis of MHC deficiency-induced subclinical GVHD.