As the subject of educational scientific research work,teachers are the first driving force of curriculum reform and specialty building in school.The deployment and quality of teachers are closely related to scientific research achievement.In order to ascertain their relationship the situation of articles published papers and scientific projects have been analysed combined with the age professional titles and educational background of teachers in our college,which may provide preferences for the sustainable development of the school.

Objective To investigate the relationships between serum osteocalcin levels of fasting plasma glucose(FPG),fasting serum insulin(FINS),insulin resistance,β-cell function as well as lipid metabolism in male traumatic patients.Methods A prospective cohort study was carried out in the Emergency Room of Shanghai Sixth People's Hospital from April to October of 2015.The male adult traumatic patients without traumatic brain injury,shock and the medical history such as the fractures,diabetes were enrolled as trauma group,and then patients' age,body mass index(BMI),injury severity score(ISS), admission time after trauma and fluid resuscitation volume before testing(FRVT) were recorded.A total of 80 heathly male adult subjects were enrolled from the physical examination center as control group with matched age and BMI.Comparison of biochemical characteristics were carried out between two groups, and relationships between serum osteocalcin levels and glycolipid metabolism in trauma group were analyzed.Insulin resistance and β-cell function were calculated by Homeostasis model assessment-insulin resistance(HOMA-IR)and Homeostasis model assessment of β-cell function(HOMA-β).Results A total of 102 male adult traumatic patients mostly subjected to traffic accident (56.9%) with FRVT (208.78±98.68)mL and ISS(9.30±3.67)were enrolled in trauma group.Serum OC levels,HOMA-β,total cholesterol(TC),high density lipoprotein(HDL-c)and low density lipoprotein(LDL-c) were lower,but FPG,FINS,C-peptide(C-P),HOMA-IR were higher compared with control group(P<0.05).Serum OC levels wer were negatively correlated with FPG and TC(P<0.05),and positively correlated with FINS,HOMA-IR,and HOMA-β(P<0.05),but there were no correlation of OC with FRVT and ISS.By multiple linear regression analysis after adjusting for age,BMI,FRVT and ISS,serum osteocalcin levels were significantly related to TC in traumatic patients (β=-0.812,P=0.024).Conclusion The glycolipid metabolism may be impacted by the serum level of osteocalcin after trauma.

Objective Objective To evaluate the effects and safety of total glucosides of paeony (TGP) in the treatment of patients with Sjogren syndrome.Methods The Cochrane Library,PubMed,EMBASE,CBM,VIP,CNKI,Wanfang databases were searched from their establishments up to September 30,2015.We used the method recommended by the Cochrane collaboration to perform a meta-analysis of randomized controlled trails (RCTs) of total glucosides of peony in the treatment of patients with Sjogren syndrome.Two reviewers analyzed these data independently.The Cochrane Collaboration's software RevMan 5.3 was used for meta-analysis.Results A total of 573 patients in 10 studies were finally included,and were divided into different subgroups.The results of subgroup-analysis showed that:①Schimer test:TGP group had a higher effective rate than the blank control group [MD=2.41,95%CI (0.08,4.74)],lower effective rate than Chinese herbal medicine [MD=-2.55,95%CI (-3.88,-1.22);②Salivary flow:TGP group had a lower effective rate than the control group [SMD=-0.87,95%CI (-1.20,-0.54)].③Rheumatic factors (RF):TGP group had a higher effective rate than Chinese herbal medicine [SMD=0.44,95%CI (0.06,0.82)] and Chinese patent drug [SMD=0.74,95%CI (0.36,1.12)],lower effective rate than the blank control group [SMD=2.23,95%CI (-2.79,-1.67);④ C-reactive protein (CRP):TGP group had a higher effective rate than the control group [MD=4.51,95%CI (1.75,7.26)];⑤IgG:TGP group had a higher effective rate than Chinese patent drug group [MD=2.73,95%CI (1.63,3.84)],lower effective rate than the blank control group [MD=-3.90,95%CI (-5.67,-2.13),but no statistical difference was noted when compared with Chinese herbal medicine and Western medicine groups;⑥ESR:TGP group had a higher effective rate than Chinese herbal medicine group [MD=12.73,95%CI (3.62,21.84)] and Chinese patent drug group [MD=7.82,95%CI (5.39,10.24)],lower effective rate than the blank control group [MD=-7.13,95%CI (-12.70,-1.56) and Western medicine group [MD=-12.19,95%CI (-24.19,-0.19)];⑦Safety:8 studies reported adverse effects in 41 patients.TGP group had a higher adverse reaction rate than the control group [OR=3.23,95%CI (1.60,6.50)].Conclusion Current evidence demonstrates that TGP can effectively improve CRP,but its effects on Salivary flow,Schimer test,IgG,ESR,RF were not significant.However,the heterogeneity and high risk of bias in the reports involved in this study limits the reliability of this conclusion.

AIM: To investigate the correlation between the expression of neuron-specific protein and apoptosis in the process of differentiation from rat bone marrow stromal cells into neuron with brain-derived neurotrophic factor (BDNF). METHODS: The 5th passage MSCs were induced by BDNF and 2-mercaptoethanol (?-ME), respectively. At 1 h, 6 h, 12 h and 24 h, nestin, neuron specific enolase (NSE), microtubulease associated protein (MAP)-2 and glail fibrillary acidic protein (GFAP) were detected by Western blotting. Cell cycle and apoptosis were examined by flow cytometry. RESULTS: Nestin and NSE of neuron-like cells induced by BDNF and ?-ME were all positive by Western blotting. At 12 h, nestin and NSE turned to negative and apoptosis was detected in ?-ME group, nestin and NSE still positive and apoptosis wasn't detected in BDNF group. Till 24 h, nestin and NSE in BDNF group were negative but apoptosis still not detected. Notably, GFAP (glial astrocyte marker) was detected and MAP-2 wasn't detected in the two induced groups. CONCLUSION: The down-expression of neuron-specific protein correspondingly with apoptosis in the process of differentiation from MSCs into neuron with ?-ME shows that apoptosis may be one of the causes of induced cell death. BDNF induction was not the cause of apoptosis. Other factors may include for the cell death in the presence of neuron-specific protein expression induced by BDNF.

Objective To investigate the incidence and risk factors of deep vein thrombosis (DVT) in a cohort of Chinese patients with traumatic spinal cord injury (TSCI),and in addition,to evaluate the effect of injury types and concomitant injuries of other parts of body.Method Records of 143 casualties admitted to our institute for TSCI were analyzed retrospectively.Both lower extremities of all casualties were examined routinely with color Doppler ultrasonography (CDUS) before major surgical treatment.None of these casualties received any thromboprophylaxis before CDUS.Logistic regression was used to analyze risk factors of DVT.Results Of the 143 patients,32.2％ (n =46) suffered from DVT (proximal n =15,distal n =31).All casualties were diagnosed within one week after injury (mean 3.35 ± 1.65 days).Risk factors associated with DVT induced complete motor paralysis (odds ratio [OR] 5.05,95％ CI 1.70-14.90),concomitant fracture of lower extremities (OR 4.30,95％ CI 1.34-17.64),and lumbar vertebra injury (OR 4.29.95％ CI 1.50-10.83).Conclusions Clinically detectable DVT in TSCI are not uncommon in the Chinese population.Casualties with multiple risk factors may be benefited from early administration of thromboprophylaxis.

Objective To investigate the expression of neuroprotective peptide [Gly14]-Humanin (HNG) in eukaryotic cells by gene engineering technique and analyze its biological activity. Methods By means of asymmetrical primer/template, double stranded cDNA of HNG with FLAG in its C-terminal was obtained, which was cloned into the plasmid pcDNA3.1(-), and the resultant recombinant vector pcDNA3.1(-)/HNG-FLAG was transfected into PC12 cells. At the same time, the recombinant vector pcDNA3.1(-)/EGFP was transfected to control the efficiency of transfection. The expression of HNG in the cells was determined by immunocytochemistry. In order to analyze the biological activity of the expressed HNG, 25μM Aβ25-35 peptide was added to the culture medium of the transfected cells for 24h, then cell morphology, MTT assay and Hoechst 33258 staining were observed. Results The eukaryotic expression vector of pcDNA3.1(-)/HNG-FLAG was identified by enzyme digestion and sequencing. HNG was highly expressed in PC12 cells. After exposure of PC12 cells to 25μM Aβ25-35 for 24h, cell viability decreased to (65.8±5.3)%, and the dystrophic changes of neuritis and nuclei condensation were obvious. When cells were pre-transfected with pcDNA3.1(-)/HNG-FLAG, Aβ25-35-induced cell death and morphological changes of cells and nuclei were suppressed. In contrast, pre-transfected with empty vector did not protect cells from Aβ25-35-induced toxicity. Conclusion The eukaryotic expression vector for FLAG-tagged HNG was successfully constructed and expressed in PC12 cells. Expressed HNG has biological activity.

Objective To obtain highly purified astrocytes and identify the cells in each stage to support further studies.Methods The cerebral cortex of a neonatal SD rat was isolated and prepared into single cell suspension.The obtained cells were purified by differential adherence and shook at a constant temperature.By inverted phase contrast microscopy and HE staining,cell morphology was observed.The immunofluorescence staining with anti-mouse GFAP was used to identify the cells.Results The primary cortical cells developed rapidly at 3 d after culture and covered the flasks at 9-12 d.At this time,the cells showed stratification and the astrocytes lay at the lower layer.GFAP positive rate was only about (67.2 ±7.1)%.After the first passage,GFAP positive rate increased obviously (84.0±6.0)%. However, oligodendrocytes and microglias could not be removed completely,and the cells also showed stratification.Through 3 times of passages,we obtained many single species of astrocytes showing satellite shape with 2 or 3 processes,big cell body and round or oval-shaped nuclei leaned to one side.Immunofluorescence staining showed that nearly all of the cells were strong positive and the positive rate reached as high as (97.6 ± 2.4 )%.Conclusion Through differential adherence and shaking at a constant temperature,more astrocytes of high purity and in good state can be obtained.

Objective:To explore the value of stress hyperglycemia ratio (SHR) in predicting the prognosis of patients with acute heart failure (AHF).Methods:AHF patients admitted to the Emergency Department of Shanghai Jiao Tong University Affiliated Sixth People's Hospital from December 2016 to January 2019 were retrospectively included. Clinical data were recorded and SHR was calculated. According to the survival of the patients within 1 year, they were divided into the death group ( n=89) and the survival group ( n=218). Logistic regression analysis was used to analyze the risk factors of mortality. Kaplan-Meier analysis was used to evaluate the correlation between SHR and the prognosis of AHF patients. Results:A total of 307 patients aged 83 ( range 74-87) years old who met the inclusion criteria were included in this study, including 153 males and 104 females. The age, SHR and N-terminal prohormone of brain natriuretic peptide (NT-proBNP) in the death group were higher than those in the survival group [84 (78, 88) vs 82 (72, 86), 1.11 (0.91, 1.51) vs 1.02 (0.86, 1.27), 5 351 (2 098, 14 039)μg/L vs 4 243 (2 294, 7 565)μg/L ]. The left ventricular ejection fraction (LVEF) in the death group was significantly lower than that of the survival group [53 (45, 57) % vs 58 (44, 64) %, P< 0.05]. Logistic regression analysis showed that SHR was an independent risk factor for death in AHF patients ( OR=2.397, 95% CI: 1.285-4.471, P< 0.05). Median SHR was used to draw the survival curve. Patients with high SHR had a lower cumulative survival rate, and the difference was statistically significant ( P<0.05). Conclusion:SHR can identify critically ill patients and is an independent risk factor for death in AHF patients.

Objeetive To construct the cell DNA damage models for the human CML K562 cell line before or after imarlnib mesylate treatment and observe the repairing process dynamically for investigating the iniluence of imatinib mesylate on the repair function of K562 cells after cell DNA danlage.Methods The MTT assay was used to estimate the optimal pretreatment concentration of imatinib mesylate in K562 cells and Western blot was employed to evaluate the phosphorylation status in K562 cells after imatinib mesylate treatment to estimate BCR/ABL tyrosine kinase inhibition by imatinib mesylate.The comet assay was used to detect the DNA damage induced by hydrogen peroxide at various concentrations in K562 cells with or without the pretreatment of imatinib mesylate.A dynamic observation on the repairing process after cell DNA damage was made by the comet assay.Results The pretreatment by imatinib mesylate for K562 cells was optimized to be at a final concentration of 1 μmol/L for 24 h as revealed by the MTT assay additionly imatinib mesylate treatment at this concentration could effectively inhibit the phosphorylation of the BCR-ABL fusion protein at Tyr177(Deusityrate 0.100±0.018).When compared with the control group(Deusityrate 0.425±0.039),the BCR/ABL phosphorylation at Tyr177 was significantly decreased by (77. 11±5.59) % (t=4. 57,P＜0. 05). The cell DNA damage models for both imatinib mesylate-nontreated and imatinib mesylate-pretreated K562 cell groups were constructed with hydrogen peroxide treatment at a final concentration of 10 μmol/L for 10 min at 4℃ as confirmed by the comet assay. When compared with the control imatinib mesylatenontreatod K562 cell group,the time duration required for the DNA repair in imatinib mesylate-pretreated K562 cell group was significantly prolonged (F= 97.79,P＜0. 05 ). Conclusions The cell DNA damage models for the leukemic K562 cell groups before or after imatinib mesylate treatment were successfully constructed and the tyrosine kinase inhibitor imatinib mesylate for BCR/ABL fusion protein was revealed to attenuate the DNA repair capacity of the K562 cells after DNA damage.

OBJECTIVE: To construct a recombinant prokaryoticexpression plasmid pET/ c-Aβ(15)-c, and evaluate the immunogenicity of its encoded fusion protein as expressed in E.coli. METHODS: The gene fragment HBc88-144 was amplified by PCR and subcloned to pUC19. The synthetic, double-strand Aβ(1-15) gene was inserted downstream of HBc1-71 in pGEMEX/c1-71. After restriction enzyme digestion, c1-71- Aβ(15) was spliced to HBc88-144, yielding the recombinant gene c-Aβ(15)-c; that gene was subcloned into pET-28a(+). The fusion protein (CA15C) expressed in the transformed E.coli BL21 was induced with isopropyl β-D-1-thiogalactopyranoside (IPTG) and analyzed by SDS-PAGE. The virus-like particle (VLP) formed by fusion protein CA15C was observed with transmission electric microscope (TEM). Four Kunming (KM) mice were given intraperitoneal injections of CA15C, and the anti-Aβ antibody elicited was detected by indirect ELISA. RESULTS: The sequence of the recombinant gene was confirmed by restriction enzyme digestion and DNA sequencing. After IPTG induction, the fusion protein was expressed, mainly in the sediment from the bacterial lysate. The expression level was 40% of total protein in the sediment. The CA15C could form VLP. After 5 rounds of immunization, the titer of anti-Aβ antibody in the sera of KM mice reached 1:10000, while the anti-HBc antibody was undetectable. CONCLUSION Recombinant c-Aβ(15)-c gene can be expressed in E.coli. The expressed protein can form VLPs and has a strong immunogenicity.
Alzheimer Disease ; prevention & control ; Amyloid beta-Peptides ; genetics ; Animals ; Base Sequence ; Genetic Vectors ; genetics ; Hepatitis B Core Antigens ; genetics ; immunology ; Humans ; Mice ; Molecular Sequence Data ; Peptide Fragments ; genetics ; Recombinant Fusion Proteins ; genetics ; immunology ; metabolism ; Vaccines, Virus-Like Particle ; genetics ; immunology ; metabolism