Education on the risks and absolute unacceptability of re-using needles and syringes and of

inadequate hospital sterilization measures will be very important, preferably combined with governmental initiatives and mandates against these vectors of infection. In addition, clear guidelines on universal precautions can reduce risks for health-care workers, while guidelines regarding the management of health-care AG-014699 supplier workers who are infected with HBV, HCV, and/or HIV can protect patients.27 Screening for HIV, HBV, HCV, malaria and syphilis is compulsory for all blood donations. According to the World Health Organization (WHO), Viet Nam has made www.selleckchem.com/products/Staurosporine.html substantial progress on transmission of HBV or HCV via blood transfusions and other blood products, increasing the rate of voluntary blood donations, the safest source of blood, from less than 15% in 1994 to more than 65% currently.28 To further reduce risks, WHO recommends developing quality assurance systems in blood centers and blood banks nationwide and creating a national blood service and a national blood policy in Viet Nam.

Re-use of contaminated needles and syringes by injecting drug users (IDU) is another substantial risk factor, with the prevalence of HCV shown to be extremely high (87%) in IDU in Ho Chi Minh2 Cepharanthine and northern Viet Nam (74.1%).18 The prevalence of HBV among IDU in northern Viet Nam is also extremely high

(80.9%).18 Researchers have strongly recommended interventions that target new heroin users.29 A 1998 study indicated the feasibility of establishing needle/syringe exchange programs in Viet Nam.30 The Vietnamese government has supported harm-reduction through needle/syringe exchange,31 and a recent study has shown that it contributes to safe injecting practices as well as safe disposal of used needles/syringes.32 Alas, despite the government’s support, the overall access to clean syringes/needles nationwide remains quite limited, with one recent study showing that 90% of IDU in seven provinces had no access to sterile injection equipment,33 so substantial expansion of harm-reduction programs is needed. It is not uncommon for needles and knives to be re-used in tattoo shops. In one study, tattoos were one of the two main risk factors for HCV.21 Since household sharing of razors is a risk factor for HBV,4 the same risk would apply to commercial re-use. Educating barbers and tattoo shop personnel about such risks is very important. This is a developing country with a relatively low annual per capita income (approximately $US1024)34 and very limited annual per capita spending on health care (according to WHO, approximately 264 international dollars, 2006).

008). In the British cohort, there were significantly more male patients (P < 0.01). The characteristics of the study cohort are shown in Table 1. An independent confirmation cohort of 377 HCV type 1–infected

patients from Germany was additionally analyzed (for main characteristics, see Supporting Ivacaftor molecular weight Table 2). Chronic HCV infection was diagnosed by positive anti-HCV test and by HCV RNA presence in serum for more than 6 months. All patients were treated with the dual combination therapy of Peg-IFN and RBV. They received the recommended doses and were adherent. Treatment duration ranged from 48 to 72 weeks, depending on the individual treatment response. A standard treatment duration of 48 weeks was applied in 872 patients (93%). An individualized treatment regimen, according to early virologic response pattern with more than 48 weeks, was given to 70 patients (7%) being part of the INDIV-2 study, as described BAY 80-6946 solubility dmso previously.33 Four hundred and ninety-five (54%) patients had sustained virological response (SVR), determined as undetectable HCV RNA levels 6 months after completion of therapy. All other patients were classified as patients with nonsustained virological response (non-SVR). The non-SVR cohort included patients with either nonresponse (N = 336) or relapse (n = 113). Nonresponse was defined as either <2log decline at week

12 or detectable viremia at week 24. Relapse was characterized as HCV RNA undetectable at the end of treatment, but detectable after treatment completion. The study was approved by the local ethic committees, and written informed consent for genetic testing was obtained from all participants. Although data of some cohort parts were already available by GWAS,16 the patients’ DNA samples were analysed anew for the IL28B SNPs, rs12979860, rs8099917, rs12980275, and rs8103142. Genotyping of rs12980275 and rs8103142 was done in only 931 and 605 patients, respectively. For genotyping, Molecular motor we performed real-time polymerase chain reaction (PCR) and melting curve analysis in the Light Cycler 480 System (Roche,

Mannheim, Germany), or we sequenced the specific regions of the IL28B gene. DNA was extracted from whole blood samples with an extraction kit from QIAGEN (Hilden, Germany). Primers and hybridization probes were obtained from TIB MOLBIOL (Berlin, Germany). Primer and probe sequences and PCR conditions are presented Supporting Table 1. Sequencing was performed with the BigDye Terminator and a capillary sequencer from Applied Biosystems (Darmstadt, Germany). Statistical analysis was performed with SPSS 18.0 (SPSS, Inc., Chicago, IL) and R 2.11.0 (www.r-project.org). The significance of differences was assessed in contingency tables by Pearson’s chi-squared test and Fisher’s exact test. All tests were two-sided, and P values less than 0.05 were considered to be statistically significant. The odds ratio (OR) and the 95% confidence interval (CI) were calculated.

Next, coculture experiments indicated that HCC cell-derived exosomes promoted the cell growth, migration and invasion of HCC cells and had the ability to shuttle miRNAs to recipient cells. Further, our data showed that Vps4A, a key regulator of exosomes biogenesis, was frequently down-regulated in HCC tissues. The reduction of Vps4A in HCC tissues was associated with tumor progression and metastasis. In vitro studies revealed that Vps4A repressed the growth, colony formation, migration and invasion of HCC cells. We further investigated the role and involvement of Vps4A in suppressing the bioactivity of

exosomes and characterized its ability to weaken the cell response to exosomes. By small RNA sequencing, we demonstrated that Vps4A facilitated the secretion of oncogenic miRNAs in GS-1101 order exosomes, as well as accumulation and uptake of

tumor suppressor miRNAs in cells. A subset of Vps4A-associated miRNAs was identified. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis indicated that the phosphatidylinositol-3-kinase (PI3K) /Akt signaling pathway was the most likely candidate pathway for modulation by these miRNAs. Indeed, we proved that the PI3K/Akt pathway was inactivated by Vps4A-overexpression. Conclusion: Exosome-mediated miRNA transfer is an important mechanism of self-modulation of the miRNA expression profiles in HCC cells. Vps4A may function as a tumor suppressor, which utilizes exosomes as mediators to regulate the secretion and uptake of miRNAs in hepatoma cells. These observations provide new insights into the development of HCC. This Cobimetinib order article is protected by copyright. All rights reserved. “
“Death receptors, a subset of the tumor necrosis factor (TNF) receptor (TNFR) superfamily that includes TNFR1, CD95 (Fas, Apo-1),

and the TRAIL (TNF-related apoptosis-inducing ligand) receptors, transduce signals capable of engaging apoptosis or necrosis,1 depending on the status of signaling molecules in the cells. Ligation of one such receptor, cluster of differentiation 95 (CD95), has catastrophic consequences in vivo, because this results in lethal, fulminant liver destruction.2 In this issue Clomifene of HEPATOLOGY, Hikita et al.3 employ a conditional gene deletion model to explore the molecular mechanisms of this liver failure. CD95, cluster of differentiation 95; FADD, Fas-associated protein with death domain; TNF, tumor necrosis factor; XIAP, X-linked inhibitor of apoptosis protein. Upon ligation, CD95 rapidly recruits an intracellular adapter molecule, Fas-associated protein with death domain (FADD), which in turn binds to and activates the initiator caspase, caspase-8.1 The activation of caspase-8 requires two steps: dimerization of the inactive “pro-form” of the molecule, followed by autocleavage, which generates a stable, active protease.

Failure to observe a relationship between alcohol consumption selleck and advanced fibrosis may reflect the fact that these factors are likely to have influenced entry into HCV treatment. Patients with advanced fibrosis would have been encouraged

to seek treatment, whereas heavy drinkers may have been unwilling or too ill to commit to treatment. Integrated care and aggressive follow-up by phone and in the clinic may have contributed to the high treatment completion rates and SVR achieved in this cohort, but adherence may also have been, in part, the result of the patients’ stable life circumstances and support of the family. In addition to stable insurance coverage, over 60% were married and 80% were either employed or retired. We did not assess the prevalence or severity of alcohol dependence https://www.selleckchem.com/products/PF-2341066.html in this study, but it seems likely that both are lower in privately insured cohorts with high marriage and employment rates than among the inner-city clinic patients and veterans studied by Chang et al.17 and Anand et al.,9 respectively. Socioeconomic stability and less-severe alcohol dependence may have contributed, in part, to the rapid drop in regular drinking

observed in response to HCV diagnosis and the further decrease once HCV treatment was initiated. We do not believe that these findings were obtained because our cohort was unique. An increasing percentage of the U.S. population is enrolled in integrated health care plans. Except for extremes of income, membership of the Kaiser Sacramento Health Care Plan is representative of the total area’s population,19 and demographics of the Sacramento area are similar to those for the United States as a whole. This is

important, because, although HCV+ rates are relatively low among individuals who are privately insured or on Medicare, this is such a large population that it accounts for 46% of the HCV+ patients in the U.S. household population (Third National Health and Nutrition Survey, National Center for Health Statistics, 1994, unpublished data). Our finding that failure to abstain for Adenosine triphosphate 6 months before HCV treatment was related to significantly higher risk of treatment failure in moderate, but not heavy, drinkers was also unexpected. This finding is counterintuitive and is based on a relatively small sample. Therefore, it needs to be replicated in a larger sample to determine whether or not it may have occurred by chance. Meanwhile, the fact that pretreatment abstinence was not associated with treatment outcome in the cohort as a whole suggests that requiring 6 months of abstinence before treatment is less critical to outcome than ensuring that patients are committed to treatment and providing close monitoring and ancillary care.

2). In Mz-ChA-1 cells, miR-148a expression was decreased to 0.25- ± 0.03-fold, and miR-152 expression was decreased to 0.23- ± 0.02-fold relative to H69 nonmalignant human cholangiocytes. Similar reductions in expression were also seen in malignant KMCH and TFK cells. The reduced expression of this group of miRNAs is consistent with increased expression of DNMT-1 in cholangiocarcinoma, see more and suggests that this group of miRNAs may be involved in deregulation of genomic methylation in human cholangiocarcinoma. A recent study of miRNA expression in intrahepatic cholangiocarcinoma samples showed reduced expression of miR-148a and miR-152 in cholangiocytes compared with normal liver tissues,20 but these were not aberrantly

expressed in malignant tissues. These Midostaurin manufacturer may reflect differences in anatomical site of origin between these tumors and the cell lines used in our study. Notably, miR-148a expression is reduced in metastatic hepatocellular carcinoma supporting its potential as an oncosuppressor RNA gene. Chromosomal aberrations in genomic regions encoding miRNAs could contribute to altered expression in tumors. In order to evaluate the relationship between chromosomal aberrations and miRNA expression in biliary cancers, we evaluated the frequency

of chromosomal loss in the regions corresponding to miR-130a (11q12.1), miR-130b (22q11.21), miR-148a (7p15.2), miR-152 (17q21.32), and miR-301 (17q22) in intrahepatic and extrahepatic cholangiocarcinoma, using a comprehensive cytogenetic database (http://www.progenetix.de/∼pgscripts/progenetix). Chromosomal losses were observed in 11% in the sites of miR-152 and miR-301 and in 22% in the site of miR-130a of extrahepatic bile ducts tumors, while no losses were detected for the location of miR-148a and miR-130b. In

intrahepatic bile duct tumors, losses in both sites of chromosome 17 were detected in 6%, while no losses were observed in the sites of miR-148a and miR-130a. The highest frequency (11.8%) of losses was observed much for the site of miR-130b. Analysis of chromosomal changes in Mz-ChA-1 using a bacterial artificial chromosome array comparative genomic hybridization analysis did not show any significant changes in copy number for clones encompassing the genomic site of these miRNAs. Thus, chromosomal alterations do not account for altered expression of these microRNAs in Mz-ChA-1 cells. To determine the role of this specific group of miRNAs on IL-6–mediated DNMT-1 expression, Mz-ChA-1 human cholangiocarcinoma cells were stably transfected to overexpress IL-6 (Mz-IL-6 cells). When implanted as xenografts in athymic nude mice, the growth rate of Mz-IL-6 xenografts was increased compared with Mz-1 control cell xenografts, in conjunction with a decrease in the number of TUNEL-positive (apoptotic) cells.3 We used an miRNA microarray to assess the expression of human miRNAs in Mz-IL-6 cell lines overexpressing IL-6 and in Mz-IL-6–derived xenografts.

CAR−/− mice demonstrated NASH inspite of decreased bodyweight/adiposity. Thus, nuclear receptors

PXR and CAR interfere with energy metabolism and apparently play an important protective role in Ar-induced liver injury. Disclosures: The following people have nothing to disclose: Banrida Wahlang, Keith C. Falk-ner, Ming Song, Heather B. Clair, Russell A. Prough, Matthew C. Cave Aim; Nonalcoholic fatty liver disease (NAFL) morbidity rate in Western countries is close to 20–30%. Nonalcoholic fatty liver disease (NAFLD) can progress to nonalcoholic steatohepatitis (NASH), cirrhosis and hepatocellular carcinoma. In spite of its high prevalence, up till now here is no proven effective treatment for NAFLD. Along with the “obesity epidemic,” the worldwide prevalence of NAFLD is increasing selleckchem rapidly Palbociclib concentration and is generally assumed to be a consequence of obesity-induced insulin resistance. On the other hand, not all obese individuals are insulin resistant, nor are all insulin-resistant individuals obese. MicroRNAs (miRs) are a class of

small non-coding RNAs that function to control gene expression. Although miRs play a key role in the pathogenesis of nonalcoholic fatty liver disease (NAFLD) and diabetes mellitus (DM), detailed mechanisms of this pathogenesis remains unclear. We found that miR-27b increased in liver biopsy specimens of NAFLD patients with DM using microarray analysis, as compared with controls. The aim of this study was to investigate whether overexpression of miR-27b in liver could cause fatty liver formation and insulin resistance, and to examine mechanism of NAFLD and DM onset in murine model. METHODS; Five-week-old male C57BL/6J mice were randomized into 2 groups(n=16 mice): basal diet (BD)-fed control mimic (BD-Con, n=4), BD-fed miR-27b-mimic (BD-miR-27b, n=4).

In this study, miR-27b mimics is injected intravenously at 7mg/kg. We comfirmed the target genes of miR-27b using quantitative RT-PCR analysis. insulin serum concentrations were measured Galactosylceramidase by a local laboratory for clinical examinations. As an alternative method for assessing insulin resistance (IR), the homeostasis model assessment of IR (HOMA-IR) was calculated using the following formula: fasting insulin (mU/mL) plasma glucose (mg/dL) / 405. Result; BD-miR-27b significantly showed steatosis using oil red o staining and increased hepatic tryglyceride content, as compared BD-Con. In the analysis of fat accumulation related gene expression, hepatic Peroxisome proliferator-activated receptor α (PPARα) and Microsomal triglyceride transfer protein (MTTP) are significantly decreased. At the same time, BD-miR-27b showed hyperinsulinemia and insulin resistance. In the analysis of insulin resistance related gene expression, hepatic Insulin receptor substrate 1 (IRS-1) is significantly decreased.

Plasma cytokines levels (IL-6 and TNF-α) were higher in patients with RAI, although the difference was not statistically significant due to the high variation in cytokine levels. No significant differences were observed between groups regarding plasma levels of vasopressin and serum levels of nitric oxide. Table 3 shows serum total cortisol levels before and after the SST, transcortin, and albumin levels and serum cholesterol profile in patients with and without RAI. By definition delta cortisol and post-SST cortisol levels were significantly lower in patients with RAI. Baseline serum total cortisol levels,

serum levels of transcortin (the main cortisol binding protein), albumin, total cholesterol, and HDL were not significantly different between patients with normal and abnormal adrenal function. Ulixertinib LDL levels tended to be lower in patients with RAI. Estimated baseline free cortisol levels (FCI and cFC) were also similar between groups. In 18 patients this website (3 with and 15 without RAI) SST was repeated 153 ± 151 days after inclusion.

Two out of the three patients with RAI and 14 out of the 15 patients with normal adrenal function at admission showed normal delta values at follow-up. These data suggest that adrenal function in cirrhosis patients without RAI is relatively stable and that RAI is potentially reversible. Mean duration of hospitalization was 13 ± 12 days (from 2 to 83 days) with no significant differences between patients with and without RAI. Clinical outcome differed significantly between patients with

normal and abnormal adrenal function (Table 4). The probability of developing new bacterial infections (24% versus 9%; P = 0.01), new episodes of severe sepsis or septic shock (19% versus 4%, P = N-acetylglucosamine-1-phosphate transferase 0.008), and new type-1 HRS (11% versus 1%, P = 0.006) was significantly higher in patients with RAI than in those with normal adrenal function. The probability of death during hospitalization (16% versus 4%, P = 0.02) was also higher in patients with RAI. No new episodes of variceal bleeding occurred during hospitalization in either group. Mean follow-up was similar in patients with and without RAI (72 ± 30 versus 78 ± 25 days, respectively). Main outcomes at 3 months also differed between patients with normal and abnormal adrenal function (Table 4). The 3-month probability of developing new bacterial infections (41% versus 21%; P = 0.008), new severe sepsis, or septic shock episodes (27% versus 9%, P = 0.003, Fig. 1) and new type-1 HRS (16% versus 3%, P = 0.002) was higher in patients with RAI than in those with normal adrenal function. The probability of death was also significantly higher in patients with RAI (22% versus 7%, P = 0.01, Fig. 2).

Conclusion: Our novel findings document the key immune regulatory function of Gsk3β signaling in the pathophysiology of liver IRI, and provide a rationale to target Gsk3β as a refined therapeutic strategy to ameliorate liver IRI. (HEPATOLOGY 2011;) Ischemia and reperfusion injury (IRI) is a common clinical problem associated with liver transplantation, partial hepatic resection, or trauma. Although IRI significantly impacts both acute liver failure/graft rejection, as well as chronic liver dysfunction,1-4 no effective therapy is available to prevent or treat the clinical syndrome. The pathogenesis

of IRI is a two-stage process consisting of the initial cellular damage due to ischemia, followed by reperfusion-initiated inflammation-induced hepatocellular damage. Recently, host innate Toll-like receptor 4 (TLR4) activation by endogenous ligands has been identified as the key trigger in the liver immune response against IR.5-9 As cell surface TLR4 ligation activates RG7420 supplier Cell Cycle inhibitor multiple intracellular signaling pathways10, 11 leading to the induction of pro- and anti-inflammatory gene programs, our better appreciation of their regulatory mechanisms should identify novel therapeutic targets to selectively alleviate pro- while sparing or promoting anti-inflammatory immune responses and ultimately ameliorate tissue damage. Recent studies have revealed that glycogen synthase kinase 3β (Gsk3β) may represent such

a target. Indeed, inhibition of Gsk3β in vitro significantly increased interleukin (IL)-10 production while suppressing release of pro-inflammatory cytokines in macrophages stimulated with TLR ligands. TLR activation leads to Gsk3β phosphorylation by the phosphoinositide 3 (PI3) kinase-Akt pathway. The resultant increase of 3′-5′-cyclic adenosine monophosphate

(cAMP) response element-binding (CREB) but decrease of nuclear factor kappa B (NF-κB) activity diminish the expression of pro-inflammatory second genes, such as IL-12, tumor necrosis factor alpha (TNF-α), and IL-1β, while augmenting the expression of anti-inflammatory IL-10.12In vivo, Gsk3β inhibitors effectively protected mice from endotoxin shock.12 These data suggest the therapeutic potential of Gsk3β inhibition and warrant further confirmation in clinically relevant animal inflammatory disease models. Gsk3, a ubiquitously expressed serine/threonine kinase, was initially found to regulate glycogen synthesis.13, 14 There are two highly homologous Gsk3α and Gsk3β isoforms. Gsk3β, constitutively active (in dephosphorylated form) in resting cells, has a broad range of substrates regulating cell activation, differentiation, and survival. In heart IRI models, Gsk3β inactivation represents the convergence point for multiple cytoprotective signaling pathways.15 Gsk3β regulates the induction of the mitochondrial permeability transition pore (MPTP), a key step in triggering mitochondria-mediated cell death, which constitutes the critical IRI effector pathway.

[91, 92] Acute liver injury is associated with a spectrum of hemostatic changes including thrombocytopenia and reduced platelet function.[93] Sullivan et al. reported that severe thrombocytopenia induced peliosis hepatitis in a drug-induced liver injury model, whereas platelets contribute to hepatocyte necrosis by promoting buy Dorsomorphin neutrophil accumulation.[81] In this paper it is suggested that the increment of platelets in CLD and cirrhosis can play a pivotal role in ameliorating liver fibrosis and dysfunction, although the effect of thrombocytopenia in hepatic pathogenesis remains controversial. On the other hand, platelets can be recruited to the liver and play

a role in promoting immune and inflammatory cell recruitment, and the phenomenon subsequently will lead to the exacerbation of acute liver injury after acute viral infection or ischemia-reperfusion. Therefore, it is possible to say that an excessive increment of platelets might have harmful effects on acute liver injury. In summary, it is suggested that platelets can be characterized as a double-edged sword for the treatments of acute and chronic liver injury. Further studies

for the effect of platelets on the liver are essential for developing new approaches for the treatment of CLD and acute liver injury. “
“Hepatocyte growth factor (HGF) is a pleiotropic cytokine related with cell proliferation and survival; however, its role in viral Cobimetinib molecular weight Clomifene hepatitis is not elucidated. In this study, we studied HGF immune role in viral hepatitis. Mice received hydrodynamically delivered HGF plasmid or

control plasmid and then infected with adenovirus, and parameters of immune-mediated liver damage were evaluated. We studied dendritic cell (DC) activation in the presence of HGF. T cells collected from infected mice were restimulated with virally infected DC to measure cytokine production in vitro. HGF ameliorated the liver inflammation during viral hepatitis as alanine transferase, intrahepatic lymphocytes, and splenocyte counts were diminished by HGF. Lower histological scores of liver pathology were observed in the HGF group. DC from the HGF group expressed reduced CD40. The hepatic expression and serum concentration of IL-12p40 were diminished in HGF-transfected mice. In vitro experiments with DC confirmed that HGF diminished CD40 expression and IL-12p40 production. The expression and serum levels of IFN-γ, IL-6 and CXCL9 were significantly decreased in the HGF group. HGF overexpression diminished the expression and concentration of IL-10 and TGF-β. The frequency of PD-1+Tim-3+ in CD8 T cells was decreased by HGF overexpression. Moreover, T cells in the HGF group at day 14 secreted more IFN-γ and TNF-α than those in the control group when restimulated with virally infected DC.

0 software. Subgroup analysis and sensitivity analysis were also carried out. Results: 55 RCTs involving a total of 8449 participants met the inclusion criteria. Compared with the non-probiotics anti-H. pylori regimens, probiotics significantly mTOR inhibitor increased the eradication rate. The pooled RR by intention-to-treat and by perprotocol analysis in the probiotics supplementation versus without probiotics was 1.15[95% confidence interval (CI), 1.12–1.19]

and1.14 (95% CI, 1.11–1.17), respectively. And reduced the risk of overall H. pylori therapy related adverse effects (RR0.48, 95% CI,0.38–0.60). In addition, There are no significant differences for the eradication rate of H. pylori whenever you add probiotics. The pooled RR(itt) is 1.17 (95% CI, 1.09–1.26) (using probiotics as a pretreatment),1.14 (95% CI, 1.10–1.19) (using probiotics after regular non-probiotics selleck screening library therapy), 1.16 (95% CI, 1.10–1.21) (using probiotics in the same time with the regular non-probiotics therapy). Conclusion: The supplementation with probiotics during H. pylori eradication therapy may be effective in increasing eradication rates and decreasing therapy-related side effects. In addition, the probiotics may have similar effects on eradication rates whenever they are added. Key Word(s): 1. Meta-analysis; 2. Helicobacter pylori; 3. eradication; 4. probiotics; Presenting Author:

JINGTONG WANG Additional Authors: LAN YAO, XIANGHAI ZHOU, ZHENYU ZHANG, QIAN XUE, LINONG JI, YULAN LIU Corresponding Author: YULAN LIU Affiliations: Department of Gastroenterology, Peking University People’s Hospital; Department of Gastroenterology, Department of Gastroenterology, Peking University People’s Hospital Objective: At present,

the literature on the relationship between helicobacter pylori (Hp) infection and type 2 diabetes mellitus (T2DM) is inconsistent. We investigated serum Hp IgG positive rate and Hp infection rate in T2DM patients; we also explored the difference of related metabolic markers between Hp (+) group and Hp (−) group. Methods: 795 residents in Pinggu District, Beijing, China were selected and their socio-demographic factors, levels of serum Hp IgG, diagnosis of T2DM and related metabolic markers were investigated. Thiamet G Another 127 patients taking endoscopy examination in our hospital were also selected and we investigated their socio-demographic factors, rapid urease test, levels of serum Hp IgG, histopathological examination, diagnosis of T2DM and related metabolic markers. We used t test or non-parametric test, χ2 test and logistic regression to explore the association between Hp infection and T2DM. Results: By applying serous diagnostic criteria of Hp infection and excluding confounding or potential confounding factors, we find that there is no significant difference of Hp infection rate between T2DM patients and non-T2DM ones (p > 0.05, T2DM 32.47%, non-T2DM 42.