Objective To study the relationships of Helicobacter pylori (Hp) infection and genetic polymorphisms of glutathione s-transferase P1 (GSTP1) with gastric cancer (GC). Methods The 98 patients with GC and 149 controls with normal finding at endoscopy were enrolled for this study. The rapid urease test (RUT), 13C- urea breath test (13C-UBT) and Giemsa staining of biopsy samples were used to check Hp infection. PCR-based restriction fragment length polymorphisms (PCR-RFLP) was used to detect GSTP1 genotype. Results The rate of Hp infection was higher in GC group than in control group (54.1% vs. 40.9%, x2 =4.11, P＜0. 05). The risk of GC would significantly increase in the GSTP1 homozygous mutant gene (MM) group with Hp infection (OR=5.44, 95%CI 1. 26-26. 79, x2=7.13, P＜0.05). Conclusions Hp infection and GSTP1 genetic polymorphisms are associated with gastric cancer risk in the elderly.

Objective To explore the potential genetic variants related with late-onset Alzheimer's disease(LOAD),and to broaden the AD genetic susceptibility factor profile.Methods We targetedly sequenced four lipids metabolism related genes including apolipoprotein E(APOE),sortilin-related receptor gene (SORL 1),apolipoprotein C-I (APOC1) and clusterin (CLU),validated these candidate variants in patients with LOAD and mild cognitive impairment (MCI)and the controls with normal cognitive function,and made a bioinformatic analysis.Results The mutation in the allele of CLU rs117389184,a low-frequency single nucleotide polymorphism,would increase the risk of LOAD and MCI[OR (95 ％ CI):3.56 (1.08-4.84),P =0.026;OR (95 ％ CI):3.06 (0.98-4.03),P =0.026],suggesting CLU rs117389184 gene variant was associated with cognitive impairment.This variation could affect CLU gene expression by interfering with the binding of transcription factors.Conclusions CLU rs117389184 is a new genetic risk variant for LOAD and MCI.

OBJECTIVE: To study the incidence of hearing loss at high frequency and the related influence factors among the flight cadets. METHOD: Using multi-stage sampling method, 312 flight cadets were randomly selected from grade 2011,2012,2013. The level of binaural hearing threshold at 4 kHz, 6 kHz, 8 kHz were measured by hearing-assistant evaluative apparatus. Whether or not have hearing loss was chosen as dependent variable. Territory, smoking, dietary habit, previous history of tinnitus, the noise exposure time, the vestibular function and the psychological quality were chosen as independent vailables. T test, ANOVA and accumulative logistic regression were performed to analyze the factors influence on hearing impairment by software SPSS 18.0. RESULT: The morbidity of hearing impairment among flight cadets was 18.9%. Results from single factor analysis showed that the levels of hearing thresholds at 4 kHz, 6 kHz frequency had statistically significant differences between smoking group and non-smoking group (P < 0.05). The levels of hearing thresholds at 4 kHz frequency had statistically significant differences between spicy diet group and not spicy diet group (P < 0.05). The levels of hearing thresholds at 4 kHz, 6 kHz, 8 kHz frequency had statistically significant differences among different strong noise exposure groups (P < 0.05), and that at a same frequency hearing loss increased when noise exposing increased. The levels of hearing thresholds at 4 kHz, 6 kHz frequency had statistically significant difference among different vestibular function groups (P < 0.05). Results of accumulative logistics regression showed that smoking and strong noise exposure were risk factors causing hearing impairment at 4 kHz frequency, and excellent vestibular function seemed to be a preventive factor. Smoking and strong noise exposure were also risk factors causing hearing impairment at 6 kHz frequency. CONCLUSION Hearing impairment appears higher morbidity among flight cadets, and it has statistical correlation with smoking, strong noise exposure and vestibular function.
Hearing Loss ; epidemiology ; Humans ; Logistic Models ; Male ; Risk Factors ; Space Flight ; Young Adult

Objectives To isolate cancer stem cells (CSCs) in pancreatic cancer cell lines PANC1 and ASPC-1 with serum-free medium( SFM ), and to detect the expression of miR-590-3p in CSCs. Methods PANC1 and ASPC-1 cells was cultured in serum-free medium. The monoclonal formation, differentiation and cell cycle, half inhibitory concentration ( IC50 ), and the expression of the surface markers CD24 + , CD44 + were detected. qRT-PCR was used to detect the expression of miR-590-3p. Results After SFM culture, (0.94 ±0.53 ) ％ of ASPC-1 and (0.57 + 0. 12 ) ％ PANC1 survived, and they formed spheres, and could continuously passage in vitro. Cell spheres differentiation recurred when serum was supplemented in SFM. The G0/G1 stage proportion, CD24+ , CD44 + , CD24+ CD44+ cells proportion, IC50 in ASPC-1 cell were (75.3 ± 5.4)％,0.96％ ～ 2.01％, 27.52％ ～ 34.47％, 0.35％ ～ 0.44％ and (224.37 ± 5.71 ) μg/ml, which were significantly higher than that those in parent cell [ (43.7 ± 3.8 ) ％, 0. 38％ ～ 0.42％, 17.65％ ～ 18.25％,0.05％ ～0.08％, (11.43 ±2.10)μg/ml, P＜0.05]. The G0/G1 stage proportion, CD24+ ,CD44+ ,CD24 +CD44 + cells proportion, IC50 in PANC 1 cell were ( 80. 1 ± 4.7) ％, 5.31％ ～ 9.84％, 72.05％ ～ 93.06％,4.91％ ～5.21％, (296.58±4.27) μg/ml, which were significantly higher than that those in parent cell [ (46.1 ±5.3)％, 4.09％ ～4.97％, 47.71％ ～55.66％, 1.48％ ～2.63％, (26.17 ±3.81)μg/ml, P＜0.05]. The expression of miR-590-3p in ASPC-1, PANC1 spheres was 4.67 and 4.52 times higher than the expression in parent cell lines. Conclusions Pancreatic cancer cell spheres can be isolated from ASPC-1, PANC1 by culture with SFM. miR-590-3p is up-regulated and may play an important role in regulating biological characteristics of pancreatic cancer stem cells.

ObjectiveTo investigate the methylation status in the promoter region of secreting frizzled related protein 2 (SFRP2) gene in patients with myelodyplastic sydrome (MDS) and to initially explore the relationship between the methylation of this gene and prognosis/survival time.MethodsMSP method was applied to examine the promoter methylation of SFRP2 gene in 43 bone marrow or peripheral blood samples of MDS patients.As controls,70 normal peripheral blood samples from volunteers of general outpatients were examined.Then some of the patients were followed up.ResultsIn 43 patients of MDS,10 samples (23.3 ％)showed SFRP2 gene methylation,and all of them were semi-methylation status.In 70 controls,no sample showed SFRP2 gene methylation.The frequency of SFRP2 gene methylation in MDS patients was significantly higher than that in controls (x2 =17.86,P ＜0.0001).Of the 10 SFRP2 gene methylation samples,5 were bone marrow samples and 5 were peripheral blood samples.In this group of patients,3 patients were diagnosed as RA,1 patient was diagnosed as RAS,2 patients were diagnosed as RCMD,3 patients were diagnosed as RAEB and 1 patient was diagnosed as MDS-U.There was no significant difference between the different sample source (bone marrow or peripheral blood) for the results of the methylation status (x2 =0.912,P ＞0.05).Either no significant difference between the different sex,age,type,chromosome and WPSS score (all P ＞0.05).The progress of disease didn' t influence the methylation rate (P ＞0.05).16 patients accepted follow-up and 11patients died,3 patients went to AML.2 died patients showed SFRP2 gene methylation.The survival analyses showed no relationship between the methylation of this gene and survival time(x2 =0.022, P ＞0.05).ConclusionIn this MDS group,there is a high level of methyl-modification in SFRP2 gene.The methylation of SFRP2 may be one of the molecular mechanisms that contribute to the progress of patients with MDS.The peripheral blood sample maybe a better substitute in detection of SFRP2 with MDS.

Objective: To explore the influencing factors affecting the cognitive impairment of the elderly population in China. Methods: A stratified multi-stage cluster sampling was used in 6 provinces (autonomous administrative regions and municipalities) to select the sample. A total 24 000 urban and rural residents aged 60 years and above received a set of standardized questionnaire interview, physical examinations, laboratory test of lipid and glucose levels of blood and apolipoprotein E (APOE) genotype. The primary screening of cognitive function was assessed by using the Chinese Version of Ascertain Dementia 8, and then suspicious cognitive impairment cases with more than two abnormal results would receive the further cognitive function assessment by using the Mini-Mental State Examination (MMSE). 1 300 cases with cognitive impairment and 2 600 controls without cognitive impairment were recruited and matched according to their age, gender and resident area in a 1∶2 case-control study. The conditional logistic regression model was used to analyze the association between relevant factors and cognitive impairment. Results: Factors negatively associated with cognitive impairment and their OR (95%CI) values were primary or middle school as 0.63 (0.51-0.77), high school and above as 0.59 (0.39-0.88), daily neighborhood communication as 0.61 (0.50-0.75), weekly participating in social activities 0.59 (0.44-0.79), daily tea drinking as 0.71 (0.58-0.88) and doing regular exercise as 0.71 (0.57-0.88), reading newspaper (occasional: 0.50 (0.37-0.67); frequent: 0.40 (0.28-0.57)), playing majiang or cards (occasional: 0.51 (0.34-0.74); frequent: 0.50 (0.36-0.68)) respectively. Factors positively associated with cognitive impairment and their OR (95%CI) values were APOE-ε4 heterozygote as 1.31 (1.08-1.58), homozygote as 2.74 (1.52-5.00), diabetes onset before 50 years of age and after as 9.03 (3.07-33.60) and 4.40 (3.18-6.17), stroke as 1.90 (1.35-2.69), asthma as 1.95 (1.11-3.42) respectively. Conclusion APOE-ε4 alleles, lower educational level, stroke, asthma, diabetes are risk factors of cognitive impairment in the elderly. Keeping a healthy lifestyle and preventing chronic diseases in the whole life course could significantly reduce the incidence of cognitive impairment in the elderly.

Time series model was developed to investigate the effect and contributions of related biomarkers on the cerebral endothelial dysfunction induced by beta amyloid(Aβ). HCMEC/D3 was incubated with 2. 5 μmol/L Aβ for 2, 4, 6, 8, 10, 12, 14, 16, 18, 20, 22 and 24 h, and biomarkers including cytosolic calcium ion, mitochondrial membrane potential(MMP), endothelial nitric oxide synthase(eNOS)and cell viability were determined. Time series model was established to assess the dynamic relationship between the related biomarkers and cell viability and the contribution of different biomarkers to cell damage. Impulse response analysis indicated that after a positive impact on cytosolic calcium ion, cell viability decreased and this impact continued to decline; after a positive impact on endothelial nitric oxide synthase and mitochondrial membrane potential, cell viability increases, which increased rapidly in the early stage, and the rate decreased in later stage. The result of variance decomposition showed that the cytosolic calcium ion played a major role in cerebral endothelial dysfunction induced by Aβ. Combined with the model study, it is concluded that the intervention on the level of cytosolic calcium ion at the early stage may be the possible way to slow the disease progression.

OBJECTIVETo study the baseline distribution of polymorphisms in the promoter of peroxisome proliferators activated receptor co-activator 1 (PPARGC1A) gene in ethnic Hans from Beijing, and to assess their association with type 2 diabetes (T2DM).

METHODSA 2-stage study was designed. Firstly, the promoter region of PPAGC1A gene was screened with PCRRFLP in a small population (n=216, T2DM/control: 104/112), which was followed by a replication study of a larger group (n=1546, T2DM/control: 732/814). Fasting plasma glucose, insulin, blood lipid, height, weight, waist circumference, and blood pressure were measured in all subjects. Potential association was assessed by logistic regression. Linkage disequilibrium and haplotype analysis were conducted with Haploview software.

RESULTSFive polymorphisms were identified with Sanger sequencing, among which T-2120C (rs3755857), -1999C/G (rs2946386) and -1437T/C (rs2970870) were included for genotypic analysis based on their moderate levels of heterozygosity. No significant difference was found between the two groups. When adjusted for age and gender confounding, we have combined the OR values from population 1 and population 2 based on Mantel-Haenszel fixed model, and recognized a mild contribution of C allele of -1999C/G (rs2946386) to the 1.18-fold risk of T2DM (P=0.03, OR=118). No haplotype was associated with T2DM after permutation correction.

CONCLUSIONThe C allele of -1999C/G ( rs2946386) in the promoter region of the PPARGC1A gene is mildly associated with T2DM. Variations in the promoter region of the PPARGC1A gene seem not to confer the risk of T2DM in our population.

Adult ; Aged ; Asian Continental Ancestry Group ; ethnology ; genetics ; Blood Glucose ; metabolism ; Case-Control Studies ; China ; ethnology ; Diabetes Mellitus, Type 2 ; blood ; ethnology ; genetics ; Ethnic Groups ; genetics ; Female ; Genetic Variation ; Humans ; Lipids ; blood ; Male ; Middle Aged ; Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha ; Polymorphism, Single Nucleotide ; Promoter Regions, Genetic ; Transcription Factors ; genetics

To assess relationships between xanthine oxidase (XOD) and nephropathogenic infectious bronchitis virus (NIBV) infection, 240 growing layers (35 days old) were randomly divided into two groups (infected and control) of 120 chickens each. Each chicken in the control and infected group was intranasally inoculated with 0.2 mL sterile physiological saline and virus, respectively, after which serum antioxidant parameters and renal XOD mRNA expression in growing layers were evaluated at 8, 15 and 22 days post-inoculation (dpi). The results showed that serum glutathione peroxidase and superoxide dismutase activities in the infected group were significantly lower than in the control group at 8 and 15 dpi (p < 0.01), while serum malondialdehyde concentrations were significantly higher (p < 0.01). The serum uric acid was significantly higher than that of the control group at 15 dpi (p < 0.01). In addition, the kidney mRNA transcript level and serum activity of XOD in the infected group was significantly higher than that of the control group at 8, 15 and 22 dpi (p < 0.05). The results indicated that NIBV infection could cause the increases of renal XOD gene transcription and serum XOD activity, leading to hyperuricemia and reduction of antioxidants in the body.
Antioxidants ; Chickens ; Glutathione Peroxidase ; Hyperuricemia ; Infectious bronchitis virus* ; Kidney ; Malondialdehyde ; RNA, Messenger* ; Superoxide Dismutase ; Uric Acid ; Xanthine Oxidase* ; Xanthine*

Objective To investigate serum levels of lipoprotein-associated phospholipase A2 (Lp-PLA2),high-sensitivity C-reactive protein (hs-CRP),complement component C1q (C1q) and homocysteine(HCY) in patients with Alzheimer's disease(AD),in order to provide a basis for establishing laboratory markers in AD patients.Methods One hundred AD patients and one hundred healthy controls from Beijing Hospital were selected.Serum levels of Lp-PLA2,C1q,hs-CRP and HCY were determined using a biochemistry analyzer.Serum levels of amyloid β-protein 40(Aβ40)and Aβ42 were measured using enzyme-linked immunosorbent assays.Results Serum levels of Aβ40,Aβ42,Lp-PLA2,hs-CRP,C1 q and HCY were higher in AD patients than in the control group[(66.0±14.0) pmol/L vs.(7.1±8.2) pmol/L,(7.2±1.4) pmol/L vs.(1.9±1.7) pmol/L,(510.6±140.1)U/L vs.(419.0±91.8) U/L,(2.8±3.4) mg/L vs.(1.2±0.7) mg/L,(218.0±58.4) mg/L vs.(194.8 ± 27.7) mg/L and (18.8 ± 9.3) μmol/L vs.(14.9 ± 5.2) μmol/L,all P ＜ 0.01],and the differences were greater in female subjects than in male subjectss.Conclusions High serum levels of Lp-PLA2,C1q,hs-CRP and HCY may be associated with Alzheimer's disease,while the exact relationships need to be further investigated.