Recent studies have found that the incidence of diabetes with cognitive impairment increases significantly.This article reviews the clinical manifestation of diabetic cognitive impairment and expounds its potential pathogenesis from 4 aspects,including the toxic effect of hyperglycemia,and the changes of cerebrovascular pathology,neurotrophic factor and neuromodulation.

Objective To check the change of content of serum beta-apoliprotien(?-AP) and insulin(INS) in the patient with Alzheimer disease, and to reflect the effect of using different drug. Methods 60 cases of this disease and 30 cases of the control group were been detected by radioimmunoassay(RIA). Results The content of ?-AP in Alzheimer disease(AD) was obviously higher than that in control groups(P

Objective To evaluate the role and safety of continuous vano-venous hemofiltration(CVVH) in treating critical patients. Methods We summarized 109 cases of critical patients treated by CVVH in our ICU from 2002 to 2006. Results The therapy time ranged from 18 to 72 hours. Of all patients, there were 13 cases of hypotension, 5 cases of filter occlusion,2 cases of bleeding and 3 cases of local or blood infection. Conclusion CVVH can be appli-Gated in critical patients with good safety and efficiency. High-quality management plays an important role in the carry--out of CVVH.

Objective To investigate the mechanisms of methylglyoxal(MG)-induced injury of hippocam-pal neurons. Methods Primary cultured of hippocampal neurons from 1-day-old Sprague-Dawley rats were incuba-ted with MG for different time and dose period. Cells proliferation were assayed by methyl thiazolyl tetrazolium (MTT),and apoptosis was quantified by flow cytometer using annexin V-FITC and propidium iodide (PI) stai-ning. The protein and mRNA levels of brain-derived neurotrophie factor (BDNF) and tyrosine kinase B(TrkB) were assayed with Western Blotting and real-time PCR. Results Treatment with MG resulted in a concentration-dependent (r=0.946, P < 0.01) and time-dependent (r=0.993, P < 0.01) decreasing neurons viability. Com-pared with Oh group(1. 633±0. 153)%, 100 μM MG treatment for 2h,6h, 12h and 24h,the cellular apeptosis rate were significantly increased ((2. 833±0. 153)%, (3. 367±0. 153)%, (4. 433±0. 404)% and (8. 833± 0. 306)% respectivdy,all P<0.01). MG also increased the BDNF mRNA and protein expression after 12h treat-ment (P<0.05 or P<0.01),but decreased the TrkB mRNA and protein expression in the cells after 6h treatment (P<0.05 or P < 0.01). Conclusion MG has direct toxic effect on hippocampal neurons and can impaire the BD-NF-TrkB signal pathway by inhibiting the expression of TrkB,and increasing the apoptosis of hippocampal neurons.

Objective To investigate the relationship between methylenetetrahydrofotate reductase (MTHFR)C677T polymorphisms and H-type hypertension and increased plasma homocysteine (Hcy) levels. Methods From September 2013 to June 2014,4 012 permanent residents aged ≤30 year from 12 natural villages or communities in 6 regions of Hunan province were extracted according to the cluster random sampling method. Using computer random number table,571 residents were randomly selected as the research objects. According to the blood pressure and Hcy levels,571 residents were divided into 3 groups:a common hypertension group (n = 190),an H-type hypertension group (n = 94),and a normal blood pressure group (n = 287 ). Amplification refractory mutation system-polymerase chain reaction (ARMS-PCR)method was used to detect the MTHFR C677T polymorphisms in all the research objects and the penotyping was performed. Hcy levels were detected at the same time. Results There were significant differences in recessive model (CC + CT,TT)genotype frequencies among the H-type hypertension group (n = 66[70. 2%],n = 28[29. 8%]),common hypertension group (n = 156[82. 1%],n = 34[17. 9%]), and normal blood pressure group (n = 235[81. 9%],n = 52[18. 1%])(χ2 = 6. 797,P = 0. 033),and there were no significant differences in CC,CT,and TT genotype frequencies among the 3 groups (P >0. 05). In the recessive model,there were significant differences in TT genotype frequencies between the H-type hypertension group and the normal blood pressure group or the common hypertension group (χ2 = 5. 812,P = 0. 016;χ2 = 5. 212,P = 0. 022). There was no significant difference in TT genotype frequencies between the common hypertension group and the normal blood pressure group (P > 0. 05). The CC + CT and TT genotype Hcy levels of the MTHFR C677T recessive model in the H-type hypertension group were 17. 1 ±1. 6 and 19. 0 ±2. 9 μmol/ L respectively. There was significant difference between the genotypes (t = - 3. 115,P = 0. 004). The logistic regression analysis of MTHFR C677T recessive model genotype showed that after adjusting for sex and age,the residents with recessive model TT genotype had higher risk of H-type hypertension (OR,1. 946,95% CI 1. 172 -3. 232,P = 0. 01). Conclusion The TT MTHFR C677T gene mutation in this population may be an important genetic factor for the increased Hcy levels and the onset of H-type hypertension.

OBJECTIVE To establish a simple,sensitive method for detecting the double mutation of the basal core promoter(BCP) of HBV.METHODS FAM fluorescence-labeled TaqMan MGB and primers driving from the region containing the double mutation of BCP were designed for the real time PCR,then the standard positive control,standard negative control and HBV DNA were amplified and detected by the real time PCR.The results of detecting the double mutation of BCP were validated by the direct-sequencing analysis of PCR products.RESULTS The double mutation of BCP of HBV could be detected by the real time PCR.The sensitivity of the method was 3?100 copy templates and as few as 1% of mutant among wild-type virus sequence were detected.CONCLUSIONS The method can be used to detect the double mutation of BCP of serum HBV DNA.

OBJECTIVE To approach the pathogenic distribution of nosocomial infection and drug-resistance in tumor department to formulate the intervention strategy.METHODS Prospective monitoring and retrospective investigation were performed to analyze the 198 cases of nosocomial infection in tumor department.RESULTS The lower respiratory tract infection was the main infection in tumor department,accounted for 68.2%.The urinary tract infection rated the second,accounted for 16.7%.Pathogenic bacteria mainly included Pseudomonas aeruginosa(20.2%),Klebsiella pneumoniae(19.2%),Escherichia coli(16.2%),Staphylococcus aureus(10.6%),etc.Above pathogenic bacteria were all multidrug-resistant.Detection rate of extended spectrum ?-lactamases(ESBLs) producing Enterobacteriaceae strains was 45.7%.Detection rate of meticillin-resistant staphylococci(MRS) was 40.6%.CONCLUSIONS The drug-resistance status of nosocomial infection is very serious in tumor department.Comprehensive intervention strategy should be adopted to decrease the infection rate.

OBJECTIVE To investigate drug resistance status of the pathogens of nosocomial pulmonary infection in stroke patients and to provide the scientific reference for clinical prevention of nosocomial infections and reasonable use of antibiotics.METHODS By the methods combining prospective monitoring and retrospective review,patients′ clinical data were analyzed statistically.Referring to National Rules of Procedures in Clincal Laboratory,the strains were identified.The antibiotic susceptibility test was performed by K-B method and the results were read according to CLSI 2006.RESULTS The main pathogens of nosocomial pulmonary infection in stroke patients were Klebsiella Pneumoniae(22.0%),Pseudomonas aeruginosa(18.4%),Acinetobacter baumannii(12.7%),Staphylococcus aureus(12.3%) and Escherichia coli(11.4%).The detection rate of extensive-spectrum beta-lactamase(ESBLs) producing E.coli and K.pneumoniae was 43.2%.Meticillin-resistant S.aureus(MRSA) accounted for 39.0%.Pan-drug resistant strains were found in A.baumannii.CONCLUSIONS Drug resistance status of pathogens of nosocomial pulmonary infection in stroke patients is very serious.We should take intervention measures to prevent and control the onest and prevalence of resistant strains.

Objective To survey the prevalence of chronic obstructive pulmonary disease (COPD)in urban areas of Hunan province and relevant risk factors and provide a basis of the prevention and treatment for COPD. Methods A questionnaire survey was conducted among 4248 residents, aged over 15, by a simple cluster random sampling method in Changsha, Hunan, Wulipai street North Station community. All the respondents filled out an unified epidemiological survey questionnaire. All of the respondents received examination for lung function. Those respondents showed FEV1/FVC ＜70% were further examined by ECG,X ray inspection for differential diagnosis. The data of epidemiological survey was analyzed by multivariate logistic regression method. Results The response rate was 92%. The total prevalence of COPD was 4. 81%.The prevalence of COPD in the males was 6. 6%, and 3. 0% in the females. The prevalence of COPD in the males was significantly higher than that in the females (x2 = 29. 915, P ＜ 0. 01). The prevalence increased with age increasing (P ＜0. 01). The more the education was, the lower the prevalence of COPD was. Risk factors analyzed with non-conditional logistic were as follow. The odd ratio (OR) for COPD in the age was 1.92(P ＜0. 01) and the odd ratio (OR) for COPD in the sex was 1.81 (P ＜0. 01). The weak lighting in house increased the risk with the OR of 4. 25(P ＜0. 01) and pet feeding further increased the risk with the OR of 12.08(P ＜0. 01). The odd ratio (OR) for COPD in the smokers was 1.74(P ＜0. 01) and the prevalence of COPD was related with smoking intensity (branch years of cigarette). Smoking intensity above 500 increased the risk of COPD. The passive smoking increased the risk with the OR of 16. 39(P ＜0. 01). The odd ratio (OR) for COPD in the paternal family history with chronic pulmonary disease was 2. 13(P ＜0. 01) and 2. 11 (P ＜ 0. 01) in the maternal family history. The odd ratio (OR)for COPD in the education degree was 0. 52(P ＜ 0. 01). Conclusions The prevalence of COPD was high in Changsha city, which might be attributed to the risk factors such as house lighting, pet feeding, cooking,aged, male, smoking, passive smoking, and family history. The education degree was the protective factor of COPD. We should intervene the relevant risk factors of COPD so that the prevalence of COPD might be cut down.

Objective To observe the expression of Toll-like receptor(TLR) on peripheral blood dendritic cells(DC) in children with Henoch-Schtinlein purpura(HSP),and to investigate the pathogenesis of the abnormal expression of TLR in children with HSP.Methods Twenty hospitalized children with HSP in the Affiliated Hospital of Qingdao University Medical College from Dec.2011 to Jul.2012 were enrolled in the study(HSP group).Twenty agemetched healthy children were selected as a healthy control group.Peripheral venous blood was sampled under aseptic condition,peripheral blood mononuclear cells (PBMC) were isolated from density gradient centrifugation,and DC were generated by recombinat human granulocyte-macrophage colony-stimulating factor(GM-CSF),interleukin-4(IL-4) and tumor necrosis factor-α(TNF-α) in vitro.Expressions of CD83,CD86 and TLR2,TLR3,TLR4 in peripheral blood DC were examined by fluorescent activated cell sorter (FACS).Results 1.No significant distinction was found in the expression of the C Ds3 on peripheral blood DC between HSP group and healthy control group(t =0.80,P ＞ 0.05) ;in HSP group had remarkably increased expression of the CD86 on peripheral blood DC than that of the healthy control group (t =9.56,P ＜ 0.01).2.Expression rates of TLR2,TLR3,TLR4 on peripheral blood DC in the HSP group were higher than those in the healthy control group(t =1 1.79,13.29,9.45,all P ＜ 0.01).3.Expression rates of TLR2,TLR3 and TLR4 in HSP group had positive correlation with expression rates of CD86 (r =0.84,P ＜ 0.01 ; r =0.53,P ＜ 0.05 ; r =0.66,P ＜ 0.05).Conclusions Expressions of TLR2,TLR3 and TLR4 on peripheral blood DC significantly increased and were positively correlated with expression of CD86.This implies that TLR and co-stimulatory molecules might participate in the pathogenesis of HSP by mediating signal transduction,leading to abnormity of cytokines,then inducing Th1/Th2 immune imbalance by showing the advantage of Th2 function.