PubMed,Embase,Cochrane Library,and ISI web were searched without any limitations with regard to publication date or language,as well as the references of qualifying articles.All kinds of cohort studies comprising the risk of gastric cancer between diabetic patients and control subjects were included.We excluded studies that investigated only mortality but not incidence.25 studies met our criteria,and the qualities of these studies were evaluated using the Newcastle-Ottawa Quality Assessment Scale.Statistical analyses were carried out with STATA software version 12.0.A random-effects model meta-analysis showed an increased risk of gastric cancer in diabetic patients (RR =1.20,95 ％ CI 1.12-1.28).Subgroup analyses indicated that this result persisted in studies of both male(RR =1.15,95％ CI 1.02-1.29) and female (RR =1.29,95％ CI 1.09-1.53) subjects,in studies of European countries(RR =1.25,95％ CI 1.07-1.46) and Asia countries (RR =1.18,95％ CI 1.09-1.28).Compared with nondiabetics,the incidence of gastric cancer may be increased by approximately 20％ in diabetics.Thus diabetes may be an independent risk factor for gastric cancer.This effect tends to be more significant in type 1 and female patients.

Adult ; Female ; Hepatitis B, Chronic ; blood ; pathology ; Humans ; Liver Cirrhosis ; blood ; pathology ; Liver Function Tests ; Male ; Middle Aged ; Transforming Growth Factor beta ; blood ; Transforming Growth Factor beta1

Objective To investigate the drug resistance of pseudomonas aeruginosa changes in the Sixth Hospital of Ningbo, Zhejiang province, in order to provide a basis for clinical rational use of antimicrobial drugs. Methods The clinical distribution and drug resistance to commonly used antimicrobial agents in 1970 strains of pseudomonas aeruginosa from the Sixth Hospital of Ningbo in 2014 －2016 were retrospectively analyzed. The data were statistically analyzed using WHONET 5. 6 software, excel software, SPSS17. 0 software. Results Clinical specimens isolated 15 963 strains of pathogenic bacteria,including 1 970 strains pseudomonas aeruginosa,accounted for 12. 34% . The detection rate of multi－drug resistance pseudomonas aeruginosa( MDRPA) reduced year by year, the detection rate in 2014 was 60. 95% ,which in 2015 was 58. 00% ,which in 2016 was 45. 58% . Pseudomonas aeruginosa was mainly isolated from sputum(67. 16% ),followed by wound secretion(23. 05% ). The detection rate of pseudomonas aeruginosa in ICU and geriatric department was higher,accounted for 20. 25% and 25. 28% respectively. The resistance of pseudomonas aeruginosa to many kinds of antimicrobial agents was increased from 2014 to 2016,the resistance rates to cefoperazone/ sulbactam were＞30% in 3 years,the resistance rate to imipenem was higher than meropenem. The drug resistance of pseudomonas aeruginosa isolated from sputum in ICU was higher than that in geriatric department(all P＜0. 05). Conclusion Pseudomonas aeruginosa nosocomial infection in the Sixth Hospital of Ningbo is severe,the infection rate and drug resistance monitoring should be strengthened,in order to reduce the infection rate and drug resistance.

OBJECTIVETo establish a comprehensive analytical method based on SPE-UPLC-MS for the simultaneous determination of bisphenol A (BPA), nonylphenol (NP), and octylphenol (OP) in urine samples.

METHODSSixty urine samples collected from healthy subjects were analyzed for BPA, NP, and OP concentrations. The samples were de-conjugated by adding β-glucuronidase and sulfatase. After the enzymatic treatment, the samples were subjected to the OASIS HLB column solid phase extraction cartridges so as to be cleaned and concentrated. The UPLC separation was performed on a Acquity UPLCTM BEH C18 column (2.1×100 mm, 1.7 μm) with a gradient elution system of methanol-water as the mobile phase. Triple-quadrupole mass spectrometry analyzer was used for the qualitative and quantitative analysis of UPLC-MS/MS system.

RESULTSThe limit of detection of BPA, NP, and OP was 0.10, 0.10, and 0.15 ng/mL, respectively. The recoveries of BPA, NP and OP were 80.1%-108%, 81.3%-109%, and 81.5%-98.7%, respectively. Among the 60 urine samples, BPA was detected in 8 samples at the level of 0.297-32.7ng/mL, NP was detected in 29 samples at the level of 1.69-27.8 ng/mL, and OP was detected in 17 samples at the level of 0.407-11.1 ng/mL.

CONCLUSIONThe method is simple with high sensitivity and selectivity, and is suitable for the determination of BPA, NP, and OP in urine. As shown by our analysis, BPA, NP, and OP appear to be prevalent in human urine. This is particularly true for NP. The results from our study is therefore valuable for future studies to assess the exposure to BPA, NP, and OP in the general population.

Benzhydryl Compounds ; Chromatography, Liquid ; methods ; Humans ; Mass Spectrometry ; methods ; Phenols ; urine ; Reference Values ; Solid Phase Extraction ; methods

OBJECTIVETo investigate the efficacy and safety of telbivudine for blocking mother-to-child transmission of hepatitis B virus (HBV) in pregnant women with high viremia.

METHODSA total of 128 pregnant women with high HBV load (HBV DNA ≥ 1.0*10⁷ copies/ml and positive for hepatitis B surface antigen (HBsAg)) were enrolled in the study from January 2009 to January 2013 and divided into the following three groups:group A (n=42) treated with telbivudine at 12 weeks of gestation until postpartum 12 weeks; group B (n=41) treated with telbivudine at 20 to 28 weeks of gestation until postpartum 12 weeks; group C (n=45; control group) with no telbivudine treatment.All study participants were given compound giyeyrrhizin for liver protection. All infants born to the women from the three groups were vaccinated with hepatitis B immunoglobulin (200 IU) and the HBV vaccine (20 tg) ager birth. The mother-to-infant transmission of HBV was indicated by the presence of HBsAg in infants at 7 months after birth.The maternal HBV DNA levels of the women in the three groups were statistically compared with the HBsAg positive rates in their neonates.

RESULTSThere were no significant differences in the HBV DNA levels between the three groups before treatment (P more than 0.05). The pre-delivery level of HBV DNA in group A (0.553 ± 1.588 log10 copies/ml) and in group B (0.486 ± 1.429 log10 copies/ml) was significantly decreased compared to that in group C (7.698 ± 0.255 log10 copies/ml) (both P < 0.01).The post-delivery (12 weeks) level of HBV DNA in group A (0.381 ± 1.116 log10 copies/ml) and in group B (0.335 ± 1.073 log10 copies/ml) was significantly decreased compared to that in group C (7.728 ± 0.277 log10 copies/ml) (both P < 0.01).There were no significant differences in the HBV DNA levels between group A and group B (P > 0.05). No infants in group A or group B were HBsAg-positive,while the HBsAg-positive rote was 17.4% in group C (P=0.012; P=0.015).

CONCLUSIONSTelbivudine treatment starting from the 12th week of gestation or from the 20-28th week of gestation can significantly decrease the serum HBV DNA level in peripheral blood of pregnant women with high viremia and reduce the infection rate of HBV in their neonates.

Female ; Hepatitis B Surface Antigens ; Hepatitis B Vaccines ; Hepatitis B virus ; Humans ; Immunoglobulins ; Infant, Newborn ; Infectious Disease Transmission, Vertical ; Mothers ; Pregnancy ; Pregnancy Complications, Infectious ; Thymidine ; analogs & derivatives ; Viremia

ObjectiveTo investigate the association of peroxisome proliferator-activated receptor gamma coactivator 1 alpha (PPARGC1A) rs8192678 single nucleotide polymorphism (SNP) with the risk of nonalcoholic fatty liver disease (NAFLD) and the influence of PPARGC1A rs8192678 SNP on NAFLD-related biochemical parameters. MethodsA total of 119 NAFLD patients who attended Qingdao Municipal Hospital Affiliated to Qingdao University from December 2017 to December 2018 were enrolled as NAFLD group, and 213 individuals who underwent physical examination during the same period of time were enrolled as control group. Clinical data and blood samples were collected from all subjects to measure related biochemical parameters and detect PPARGC1A rs8192678 SNP. The chi-square test was used to determine whether the genotype distribution of samples was in accordance with the Hardy-Weinberg equilibrium. The t-test or the Wilcoxon rank-sum test was used for comparison of continuous data between two groups, and the chi-square test was used for comparison of categorical data between two groups. A binary logistic regression analysis was used to investigate the risk factors for NAFLD. ResultsThere were no significant differences in the genotype and allele frequencies of PPARGC1A rs8192678 between the NAFLD group and the control group (χ2=0.011 and 0.015, P=0.918 and 0.904). The binary logistic regression analysis showed that CT genotype of PPARGC1A rs8192678 was not a risk factor for NAFLD (odds ratio=0.951, 95% confidence interval: 0.368-2.457, P=0.918). In the NAFLD group, the patients carrying CT genotype had a significantly higher level of gamma-glutamyl transpeptidase (GGT) than those carrying CC genotype (Z=-2.331, P=0.020). ConclusionPPARGC1A rs8192678 SNP does not increase the risk of NAFLD, while NAFLD patients carrying CT genotype tend to have a higher serum level of GGT.

OBJECTIVE To explore the effects and mechanisms of cycloartenol on myocardial ischemia-reperfusion injury in mice.METHODS In vitro experiments,primary cardiomyocytes were extracted from 1-3 days SD mice.The hypoxia/reoxygenation model was established by incubating cells in a hypoxic culture box for 3 hours followed by reoxygenation in a normal culture box for 3 hours.The primary cardiomyocytes were divided into Control group,H/R group,low-dose(3 μmol·L-1)and high-dose(10 μmol·L-1)cycloartenol groups,and SB203580 group.CCK-8 was used to detect cell viability,the apoptosis rate was detected by flow cytometry,and Western blot was used to detect the expression levels of p38 MAPK and p-p38 MAPK in each group.In an in vi-vo experiment,7-week-old male C57BL/6J mice were randomly divided into a Control group,an I/R group,and three doses of cyclo-artenol(0.2,0.5,1.0 mg·kg-1)groups.The mice were continuously administered for seven days before the surgery.The model was prepared by ligation of the left anterior descending coronary artery(LAD)for 30 minutes,followed by reperfusion for 24 hours to in-duce myocardial ischemia-reperfusion injury.Left ventricular ejection fraction(LVEF),cardiac output(CO),left ventricular fractional shortening(LVFS)of each group of mice were detected by small animal ultrasound.TTC staining was used to detect the changes of is-chemic infarct size in each group.The changes of myocardial tissue in each group were observed by HE staining.The expression levels of p38 MAPK,p-p38 MAPK,IL-6 and TNF-α in myocardial tissue of mice were detected by Western blot.Serum levels of creatine ki-nase isoenzyme(CK-MB),lactate dehydrogenase(LDH),cardiac troponin I(cTnI),interleukin-6(IL-6),and tumor necrosis fac-tor-α(TNF-α)were measured using ELISA kits.RESULTS In vitro experiments demonstrated that compared with the H/R group,both the cycloartenol and SB203580 pretreatment groups showed a significant increase in myocardial cell viability and the apoptosis rate decrease,which can downregulate the protein expression level of p-p38 MAPK and decrease the ratio of p-p38 MAPK/p38 MAPK(P<0.05).In vivo experiments confirmed that compared with the I/R group,cycloartenol pretreatment significantly improved LVEF,LVFS,and CO values(P<0.05),reduce myocardial ischemic infarct size,thereby enhancing myocardial function.The protein ex-pression level of p-p38 MAPK in myocardial tissue was down-regulated,the ratio of p-p38 MAPK/p38 MAPK was decreased,and the expression levels of IL-6 and TNF-α were decreased.Additionally,cycloartenol pretreatment reduced the levels of CK-MB,LDH,cT-nI,IL-6,and TNF-α in mouse serum(P<0.05).CONCLUSION Pre-treatment with cycloartenol can protect mouse cardiac func-tion and alleviate myocardial ischemia-reperfusion injury.Its mechanism of action may be related to the inhibition of p38 MAPK phos-phorylation,reducing inflammatory reactions.

Transmembrane 6 superfamily member 2 (TM6SF2) is a recently discovered gene,which is located on the chromosome 19 (19p12) and encodes a protein consisting of 351 amino acids.Presently,many studies have reported that the single-nucleotide polymorphism of TM6SF2 rs58542926 and plasma lipids are closely related to the incidence and development of diseases,such as non-alcoholic fatty liver disease (NAFLD),cardiovascular disease (CVD),liver cancer,and hepatitis C.This review will summarize the research progress conducted in these areas.

Background: s/Aims: Transmembrane 6 superfamily member 2 (TM6SF2) E167K variant is closely associated with the occurrence and development of metabolic dysfunction-associated steatotic liver disease (MASLD). However, the role and mechanism of TM6SF2 E167K variant during MASLD progression are not yet fully understood. Methods: The Tm6sf2167K knock-in (KI) mice were subjected to high-fat diet (HFD). Hepatic lipid levels of Tm6sf2167K KI mice were detected by lipidomics analysis. Thin-layer chromatography (TLC) was used to measure the newly synthesized triglyceride (TG) and phosphatidylcholine (PC). Results: The TM6SF2 E167K variant significantly aggravated hepatic steatosis and injury in HFD-induced mice. Decreased polyunsaturated PC level and increased polyunsaturated TG level were found in liver tissue of HFDinduced Tm6sf2167K KI mice. Mechanistic studies demonstrated that the TM6SF2 E167K variant increased the interaction between TM6SF2 and PNPLA3, and impaired PNPLA3-mediated transfer of polyunsaturated fatty acids (PUFAs) from TG to PC. The TM6SF2 E167K variant increased the level of fatty acid-induced malondialdehyde and reactive oxygen species, and decreased fatty acid-downregulated cell membrane fluidity. Additionally, the TM6SF2 E167K variant decreased the level of hepatic PC containing C18:3, and dietary supplementation of PC containing C18:3 significantly attenuated the TM6SF2 E167K-induced hepatic steatosis and injury in HFD-fed mice. Conclusions The TM6SF2 E167K variant could promote its interaction with PNPLA3 and inhibit PNPLA3-mediated transfer of PUFAs from TG to PC, resulting in the hepatic steatosis and injury during MASLD progression. PC containing C18:3 could act as a potential therapeutic supplement for MASLD patients carrying the TM6SF2 E167K variant.

Background: s/Aims: Transmembrane 6 superfamily member 2 (TM6SF2) E167K variant is closely associated with the occurrence and development of metabolic dysfunction-associated steatotic liver disease (MASLD). However, the role and mechanism of TM6SF2 E167K variant during MASLD progression are not yet fully understood. Methods: The Tm6sf2167K knock-in (KI) mice were subjected to high-fat diet (HFD). Hepatic lipid levels of Tm6sf2167K KI mice were detected by lipidomics analysis. Thin-layer chromatography (TLC) was used to measure the newly synthesized triglyceride (TG) and phosphatidylcholine (PC). Results: The TM6SF2 E167K variant significantly aggravated hepatic steatosis and injury in HFD-induced mice. Decreased polyunsaturated PC level and increased polyunsaturated TG level were found in liver tissue of HFDinduced Tm6sf2167K KI mice. Mechanistic studies demonstrated that the TM6SF2 E167K variant increased the interaction between TM6SF2 and PNPLA3, and impaired PNPLA3-mediated transfer of polyunsaturated fatty acids (PUFAs) from TG to PC. The TM6SF2 E167K variant increased the level of fatty acid-induced malondialdehyde and reactive oxygen species, and decreased fatty acid-downregulated cell membrane fluidity. Additionally, the TM6SF2 E167K variant decreased the level of hepatic PC containing C18:3, and dietary supplementation of PC containing C18:3 significantly attenuated the TM6SF2 E167K-induced hepatic steatosis and injury in HFD-fed mice. Conclusions The TM6SF2 E167K variant could promote its interaction with PNPLA3 and inhibit PNPLA3-mediated transfer of PUFAs from TG to PC, resulting in the hepatic steatosis and injury during MASLD progression. PC containing C18:3 could act as a potential therapeutic supplement for MASLD patients carrying the TM6SF2 E167K variant.