Objective: To systematically review the association between apolipoprotein E (APOE) gene polymorphism and cerebral infarction in Chinese Han population. Methods: The pertinent literature of the gene polymorphism and the case control studies of cerebral infarction in Chinese Han population were researched comprehensively by combined application of 5 effective retrieval approaches. The odds ratio (OR) of the genotype distribution in cerebral infarction group and control group were calculated. Results: A total of 1986 patients with cerebral infarction and controls were included in the meta-analysis. After the data were pooled, the OR values of ApoE ε2/ε3, ApoE ε3/ε3, ApoE ε2/ε4, ApoE ε3/ε4, and ApoE ε4/ε4 were 0. 59 (95% CI, 0.44-0. 79), 0. 52 (95% CI, 0. 40-0.69), 2.00 (95% CI, 1.22-3.28), 2.77 (95% CI, 1.60-4.81 ), and 4. 66 (95% CI, 1.61-13.48), respectively. Conclusions: ApoE ε2/ε4, ApoE ε3/ε4 and ApoE ε4/ε4 genotypes are the risk factors of cerebral infarction. ApoE ε2/ε3 and ApoE ε3/ε3 genotypes are the protective factors of cerebral infarction.

To investigate the risk factors for intracerebral hemorrhage in general population.Methods:The related research was searched through English Medical Current Contents (EMCC),China Hospital Knowledge Database (CHKD),MEDLINE,and Chinese Biomedical Literature Database (CBM).The search terms were intracerebral hemorrhage,factor,and case-control study or cohort study.Results:There were 8 literatures with original data were in accordance with the inclusion criteria.All the data could not be combined because there were some differences in counting and metrology in the risk factors included in all the studies.Hypertension,family history of cerebrovascular disease,high salt diet,alcohol consumption,diabetes mellitus,high diastolic pressure,high systolic pressure,smoking,snoring disease,and increased weighted mean difference of body mass index (BMI) (95% confidence interval) were 5.71 (4.00-6.79),3.54 (2.44-5.14),2.58 (1.94-3.43),2.80 (2.29-3.43),2.78 (1.83-4.23,1.90 (1.35-2.70),17.76 (16.60-18.92),30.43 (28.61-32.25),5.42 (5.15-5.70),1.90 (1.34-2.69),6.88 (4.61-10.26,and 5.42 (5.15-5.70),respectively.There were significant differences between the patient groups and control groups among the above indexes (all P<0.000 01).Conclusions:The risk factors for intracerebral hemorrhage include hypertension,family history of cerebrovascular disease,high salt diet,smoking,alcohol consumption,snoring disease,diabetes mellitus,overweight,high diastolic blood pressure,high systolic blood pressure and increased BMI.

AIM To evaluate the integration method for analysis of voltage-dependent Ca2+-independent transient outward K+ currents (Ito) in pharmacology. METHODSThe inactivation phases of Ito were best fitted by the sum of two or three exponentials equations. The area under the raw current curves (AUC) was obtained by the integration of exponential equations. The AUC normalized to the cell capacitance represented the net K+ charge flow during any depolarized duration and was as the index for comparison. Calcineurin overexpression transgenic (TG) mice showed downregulation of Ito. These data were tested by the integration method. RESULTS AUC obtained from three or two exponentials fittings was calculated as: AUC=A1τ1+A2τ2+A3τ3+A0t-A1τ1e-t/τ1-A2τ2e-t/τ2-A3τ3e-t/τ3 or AUC=A1τ1+A2τ2+A0t-A1τ1e-t/τ1-A2τ2e-t/τ2. The 50% and 90% action potential duration (APD50, APD90) in ventricular myocytes of mice are about 10 ms and 30 ms, respectively. AUC at 10 ms (AUC50, AUC of 50% APD) and 30 ms (AUC90, AUC of 90% APD) in left ventricle cardiomyocytes of wild type (WT) and TG mice were normalized to the cell capacitance. The normalized AUC50 and AUC90 of WT group were significantly more than those of TG group, which was consistent to the prolongation of APD in TG mice and the previous published results(downregulation of components of Ito in TG mice). CONCLUSION The integration method was an ideal way for analysis of transient outward K+ currents in pharmacology.

Objective To investigate the Camtrylobacterjejuni's risk factors which were associated with the development of Guillain-Barre syndrome( GBS), the galE gene of C. jejuni strains were sequenced and the sequencing results were compared with other C. jejuni strains. Methods Selecting three GBS-asso-ciated C.jejuni strains isolated from stools of GBS patients who had been diagnosed as AMAN pattern by clin-ical and electrophysiological test from Hebei province, China. After sequencing galE gene, the results were spliced and assembled into a complete sequence by the terminals overlapped each other. The sequences of galE gene were compared with the corresponding sequences in GenBank to find the mutation and constructed the phylogenetic tree. Results The variation frequency of galE sequences of GBS-associated C. jejuni were higher than that of non-GBS-associated C. jejuni. The phylogenetic analysis demonstrated that each of the three C. jejuni strains was separately genetically closed to three strains which sequences have published in GenBank. The alignment with the related sequence of NCTC11168 shows that there are 4 same mutations in the galE gene of the three C. jejuni strains. The phylogenic tree reflected the regional feature of C. jejuni. Conclusion The probability of sequence variation of galE of GBS-associated C.jejuni is significantly higher than non-GBS-associated C. jejuni strains, the relation between the variation and GBS-pathogenesis remains to be further confirmed. The mutations found in the three C. jejuni strains established the foundation for ex-ploring the biologically characteristic of GBS-associated C. jejuni strains.

Objective To investigate microRNA expression profiles of colonic cancer without lymph node metastasis and identify the specific microRNAs associated with carcinogenesis of colon.Methods Cancerous and para-cancerous tissues (5 cm from cancer tissues of the colon) confirmed without lymph node metastasis were collected from 3 patients. The microRNAs were extracted and isolated by mirVana RNA kit. Hybridizations were made by applying the microRNAs to Agilent microRNA microarray. Data analysis was done by software of Feacture Extraction. The discovered microRNAs were confirmed by real time PCR assay. Results Twelve out of 14 microRNAs associated with colonic cancer were up-regulated in colonic tissues. They were miR-106b, miR-135b,miR-18a,miR-18b,miR-196b, miR-19a, miR-224, miR-335, miR-424, miR-20a' , miR-301b and miR-374a. The rest two of miR-378 and miR 378* were down-regulated. Two up-regulated microRNAs (miR-18a and miR-135b) were detected in 3 pairs of cancerous and para-cancerous tissues. The expression level of miR-18a and miR-135b were accordant with the results of real time PCR.Conclusions microRNA.such as miR-106b,miR-135b.miR-18a.miR-18b,miR-196b,ect,were differentially expressed between cancerous and para-cancerous tissues.Many of these target genes are supposed to participate in the process of multiple tunmorgenesis.These microRNAs play an important role in the carcinogenesis of colon.

OBJECTIVETo meet the needs of clinical practice of rescuing critical illness and develop the information management system of the emergency medicine.

METHODSMicrosoft Visual FoxPro, which is one of Microsoft's visual programming tool, is used to develop computer-aided system included the information management system of the emergency medicine.

RESULTSThe system mainly consists of the module of statistic analysis, the module of quality control of emergency rescue, the module of flow path of emergency rescue, the module of nursing care in emergency rescue, and the module of rescue training. It can realize the system management of emergency medicine and,process and analyze the emergency statistical data.

CONCLUSIONSThis system is practical. It can optimize emergency clinical pathway, and meet the needs of clinical rescue.

Objective: To study the effects p-phenylenediamine (PPD) on lung function and health-related quality of life of occupational exposed workers. Methods: This study was based on data from a company that produce hair dye containing PPD in China. Workers who exposed to PPD were selected as the study group, and workers un-exposed to PPD were selected as the control group. Questionnaires on health-related quality of life of workers using the 36-item Short Form Health Survey (SF-36) . Occupational health examination assessment results were tested in Taizhou Cancer Hospital. The lung function test includes forced vital capacity (FVC) , forced expiratory volume in one second (FEV_1.0) , and ratio of FEV_1.0 to FVC (FEV_1.0/FVC) . Results: The difference in systolic blood pressure between the PPD exposed group and the control group was statistically significant (P<0.05) . FVC, FEV_1.0, and FEV_1.0/FVC of the lung function indexes in the exposed group were lower than those in the control group (P<0.05) . In the health-related quality of life, body pain (P=0.002) , general health (P=0.029) , vitality (P=0.038) , and mental health (P=0.003) were lower in the exposed group than in the control group. Conclusion Occupational exposed to PPD may induce hazard to the workers’lung function and may cause detrimental effect on workers’ health-related quality of life.

Objective: To study the effect of p-phenylenediamine (PPD) on liver and kidney function in occupational exposed workers. Methods: Workers in a hair dye production enterprise which used p-phenylenediamine as a raw material for production were selected as the main research population. Then we conducted a questionnaire survey on the basic conditions of workers and conducted occupational health checkups on general health status, liver and kidney function. Occupational health examination assessment results were tested in Taizhou Cancer Hospital. All data was built using EpiData 3.1 software, and statistical analysis was performed using software SPSS 20.0. Results: The liver function indicators including direct bilirubin, prealbumin, total protein, and white protein, globulin, aspartate aminotransferase, glutamyl transpeptidase, and total bilirubin in the workers exposed to high concentration of PPD were at high normal values, and these indicators were significantly different from low PPD concentration group (P<0.05) . The serum creatinine and serum uric acid in the renal function index were significantly higher in workers exposed to PPD than in workers exposed to low concentrations and in the control group (P<0.05) . Conclusion Occupational exposed to PPD may have a hazard to the workers’ liver and kidney function. Long-term occupational exposure to PPD may lead to increased cumulative exposure of workers, which may cause potential chronic liver and kidney damage in occupationally exposed populations.

To investigate the effects of thanatos-associated protein 11 (THAP11) on the proliferation and apoptosis of esophageal cancer cell and the underlying mechanism.
 Methods: Expression of THAP11 in human esophageal epithelial cells (Het-1A) and esophageal cancer cells (Eca109, TE-1, Ec 9706) were detected by Western blotting. Esophageal cancer TE-1 cells were divided into 3 groups: a normal control (NC) group, a negative control (LV-NC) group and a THAP11 (LV-THAP11) group. Then the cell proliferation were detected by MTT assay, cell apoptosis were detected by flow cytometry, caspase-3 and caspase-9 levels were detected by caspases kits. Ubiquitination of p53 was determined in esophageal cancer TE-1 cells.
 Results: Expression of THAP11 was reduced in esophageal cancer cells compared with human esophageal epithelial cells (P<0.05). After transfection with LV-THAP11 in TE-1 cells, cell viability was reduced (P<0.05), while apoptosis rate and caspase-3 and caspase-9 levels were increased (P<0.05), indicating that THAP11 inhibited growth of esophageal cancer cells. In addition, the THAP11 increased the levels of p53 (P<0.05) and inhibited the ubiquitination of p53 regulated by MDM2. 
 Conclusion: THAP11 may inhibit the proliferation of esophageal cancer cells by inhibiting ubiquitination of p53.
Apoptosis ; Cell Line, Tumor ; Cell Proliferation ; Esophageal Neoplasms ; Humans ; Repressor Proteins ; metabolism ; Tumor Suppressor Protein p53 ; Ubiquitination