The IL28B polymorphism did predict for short duration in the RGT arm, with 90% of good-responder patients qualifying for 28 weeks of therapy. Poor-response IL28B patients PD0332991 research buy gained the most from the addition of BOC, with SVR rates increasing approximately twofold.74 The RESPOND-2 trial included only patients with prior relapse and partial response, that is, primary non-responders with a < 2log10 drop in HCV—RNA at week 12 were excluded.73 In this more difficult-to-treat population with a well-documented treatment

history, major improvements were seen in SVR rates irrespective of IL28B genotype. The IL28B genotype was not an independent predictor of SVR. Despite not predicting for SVR, the IL28B genotype did identify patients who were more likely to be eligible for short-duration therapy (36 weeks in total). The ADVANCE trial assessed TVR and peg-IFN/RBV in comparison with peg-IFN/RBV control.77 Patients were randomized to receive either standard of care, or 24 or 48 weeks of peg-IFN or RBV in combination with either 8 or 12 weeks of TVR. A total of 454 Caucasian patients or 42% of the overall trial cohort were genotyped, with improvements compared to control across all IL28B genotypes, but greater than twofold in poor-response genotypes.76 Again, the association between the IL28B genotype and treatment response was attenuated with TVR regimens, and the major SVR increment was noted in patients

who carried the poor-response IL28B genotypes. In contrast to SPRINT-2, SVR rates did increase compared to control PF-562271 ic50 in patients with the good-response IL28B genotype. The IL28B genotype identified patients more likely to be eligible for short-duration therapy. The REALIZE study included patients who failed to achieve SVR from prior treatment (i.e. patients with prior primary non-response were included), with patients receiving either 48 weeks of peg-IFN/RBV (control) or 12 weeks of combination triple therapy with TVR, and then another 36 weeks of peg-IFN/RBV.78 Absolute increases in SVR rate of 40–50% were seen with TVR, irrespective of IL28B genotype.75

Again, however, there remained a 18–19% difference in SVR rates observed between the good- and poor-response genotypes, even with the addition of TVR (SVR by IL28B genotype for TVR12/PR48: CC 79% vs CT 61% Orotic acid vs TT 60%). The IL28B genotype remains relevant to treatment outcomes in the setting of TVR/BOC therapy for treatment-naïve patients, but the strength of the association is attenuated. The major benefit of DAA is in poor-response IL28B genotype patients, where SVR rates are dramatically increased. In good-responder IL28B patients, the SVR benefit of DAA therapy is less clear. We feel that DAA therapy is likely to be associated with a small increase in SVR rate, but that the major benefit of DAA therapy in these patients will be to allow short-duration therapy. SVR rates were not increased in good-responder IL28B patients in SPRINT-2 (BOC), but were in ADVANCE (TVR).

Methods:

Twelve healthy male volunteers received a single oral dose of 800 mg [14C]-DLV (100 μCi). Blood, plasma, urine, feces and saliva were collected for 6 to 10 days and analyzed for radioactivity. Metabolite profiling was performed using plasma, urine and fecal samples by radiochromatography, and metabolite identification was based on LC/MS/MS. Quantitation of DLV and its major plasma metabolites, was performed using synthetic standards. Exposure of the major metabolites in humans was compared to that in rats and mice. In vitro studies with recombinant CYP450 enzymes, UGT enzymes and gut bacteria were performed to identify enzymes responsible for the metabolism of DLV. Results: Mean selleck chemicals recovery of radioactivity was high (93.4% over 216 h). Most of the radioactivity was recovered

in feces (93.3%), with minimal excretion into urine (0.146%). DLV represented the major circulating species in plasma (∼63.0% of total AUC). There were two major circulating metabolites, BI 208333, an acyl glucuronide conjugate representing 20.2% of total AUC, and CD 6168, an alkene reduction metabolite, representing 15.3% of total AUC. DLV, BI 208333 and CD 6168 demonstrated similar time courses of plasma exposure, with median tmax values in the range of ∼3 to 6 h and geometric mean terminal half-life of ∼3 h. DLV and CD 6168 were also the predominant components buy ZD1839 in feces representing 30.4% and 34.6% of radioactivity dose, respectively. Other fecal metabolites included three hydroxylated metabolites, which are most likely secondary metabolites of CD 6168, each representing <10% of the radioactive dose. In vitro data indicated that UGT1 A1 was predominantly responsible for formation of BI 208333, whereas gut bacteria, but not microsomal or cytosolic hepatic enzymes, were responsible for the reduction of DLV to form CD 6168. Conclusions: DLV demonstrated good recovery and mass balance in healthy male volunteers. Two major circulating

metabolites of DLV were identified, BI 208333 and CD 6168, which had similar pharmacokinetic profiles to that of the parent. Both metabolites were adequately represented in the nonclinical toxicity studies. Metabolism and excretion into feces are to the major elimination routes for DLV. Disclosures: Lin-Zhi Chen – Employment: Boehringer Ingelheim Pharmaceuticals Sean Regan – Employment: Boehringer Ingelheim Pharmaceuticals Inc. Hongbin Yu – Employment: Boehringer Ingelheim Pharmaceuticals, Inc. John P. Sabo – Employment: Boehringer Ingelheim Pharmaceuticals, Inc. The following people have nothing to disclose: Rucha S. Sane, Elsy Philip, Hlaing Maw, Arti Mathur, Yongmei Li, Debra A. Mandarino Background: MK-5172, a reversible, noncovalent, competitive inhibitor of the hepatitis C virus (HCV) NS3/4A protease, is being developed for the treatment of chronic HCV infection.

Methods:

Twelve healthy male volunteers received a single oral dose of 800 mg [14C]-DLV (100 μCi). Blood, plasma, urine, feces and saliva were collected for 6 to 10 days and analyzed for radioactivity. Metabolite profiling was performed using plasma, urine and fecal samples by radiochromatography, and metabolite identification was based on LC/MS/MS. Quantitation of DLV and its major plasma metabolites, was performed using synthetic standards. Exposure of the major metabolites in humans was compared to that in rats and mice. In vitro studies with recombinant CYP450 enzymes, UGT enzymes and gut bacteria were performed to identify enzymes responsible for the metabolism of DLV. Results: Mean MI-503 recovery of radioactivity was high (93.4% over 216 h). Most of the radioactivity was recovered

in feces (93.3%), with minimal excretion into urine (0.146%). DLV represented the major circulating species in plasma (∼63.0% of total AUC). There were two major circulating metabolites, BI 208333, an acyl glucuronide conjugate representing 20.2% of total AUC, and CD 6168, an alkene reduction metabolite, representing 15.3% of total AUC. DLV, BI 208333 and CD 6168 demonstrated similar time courses of plasma exposure, with median tmax values in the range of ∼3 to 6 h and geometric mean terminal half-life of ∼3 h. DLV and CD 6168 were also the predominant components Dabrafenib in feces representing 30.4% and 34.6% of radioactivity dose, respectively. Other fecal metabolites included three hydroxylated metabolites, which are most likely secondary metabolites of CD 6168, each representing <10% of the radioactive dose. In vitro data indicated that UGT1 A1 was predominantly responsible for formation of BI 208333, whereas gut bacteria, but not microsomal or cytosolic hepatic enzymes, were responsible for the reduction of DLV to form CD 6168. Conclusions: DLV demonstrated good recovery and mass balance in healthy male volunteers. Two major circulating

metabolites of DLV were identified, BI 208333 and CD 6168, which had similar pharmacokinetic profiles to that of the parent. Both metabolites were adequately represented in the nonclinical toxicity studies. Metabolism and excretion into feces are before the major elimination routes for DLV. Disclosures: Lin-Zhi Chen – Employment: Boehringer Ingelheim Pharmaceuticals Sean Regan – Employment: Boehringer Ingelheim Pharmaceuticals Inc. Hongbin Yu – Employment: Boehringer Ingelheim Pharmaceuticals, Inc. John P. Sabo – Employment: Boehringer Ingelheim Pharmaceuticals, Inc. The following people have nothing to disclose: Rucha S. Sane, Elsy Philip, Hlaing Maw, Arti Mathur, Yongmei Li, Debra A. Mandarino Background: MK-5172, a reversible, noncovalent, competitive inhibitor of the hepatitis C virus (HCV) NS3/4A protease, is being developed for the treatment of chronic HCV infection.

32 (95% CI: 0.11-0.94) for adipsin to 96.4 (95% CI: 11.8-785.4) for IL-8 in serum and from 0.17 (95% CI:

0.06-0.54) for MIP1d to 54.8 (95% CI: 6.9-432.5) for IL-8 in bile. Conclusion: Using multiplexed technology, we were able to identify a number of inflammatory and angiogenic markers selleck products in serum and bile associated with GBC risk. These results provide biological evidence for the role of inflammatory/immune processes involved in GBC and may offer a first step toward identifying biomarkers that could help identify gallstone patients at high risk of developing gallbladder cancer. Disclosures: The following people have nothing to disclose: Jill Koshiol, Troy J. Kemp, Felipe A. Castro, Yu-Tang Gao, Leticia Nogueira, Asif Rashid, Ann W. Hsing, Allan Hildesheim, Ruth M. Pfeiffer, Ligia Pinto Janus kinase-signal transducer and activator of transcription (JAK/STAT) signaling pathway has been implicated in a variety of cellular functions, playing important roles in controlling immune-mediated liver injury. The functions of STAT1 and STAT3 in the pathogenesis of liver diseases have been extensively investigated;

however, the role of STAT4 remains largely unknown. Here we demonstrated that STAT4 activation was detected in liver immune cells from patients with viral hepatitis, autoimmune hepatitis, nonalcoholic steatohepatitis, and alcoholic liver diseases, as well as in a mouse model of con-canavalin A (Con A)-induced T cell hepatitis. Flow cytometric and immunohistochemistry analyses Selleck Kinase Inhibitor Library revealed that STAT4 activation was mainly detected in T and NKT cells in Con A-induced T cell hepatitis model,

such activation was diminished in IL-12a-/- and IL-12b-/- mice. As expected, disruption of the STAT4 reduced the production of both Th1 and Th2 cytokines, but surprisingly exacerbated Con A-induced liver injury. In agreement with these findings, ablation of IL-12a or IL-12b also augmented Con A-induced hepatocellular damage. Further studies showed that hepatic NKT cells from Con A-treated STAT4-/- mice had higher levels of FasL expression and cyto-toxicity against hepatocytes than those from Con A-treated WT mice. In vitro studies revealed that blocking FasL by antibodies on NKT cells attenuated hepatic NKT cytotoxicity against hepatocytes. Our results Diflunisal suggest that IL-12 activation of STAT4 up-regulates expression of Th1 and Th2 cytokines but inhibits the expression of FasL on NKT cells. The suppression of FasL expression contributes to the protective effects of IL-12/STAT4 on Con A-induced T cell mediated hepatitis. Disclosures: The following people have nothing to disclose: Yan Wang, Dechun Feng, Hua Wang, Ming-Jiang Xu, Ogyi Park, Yongmei Li, Bin Gao Background CBLB502 (aka Entolimod) is a pharmacologically optimized derivative of bacterial protein flagellin, an agonist of toll-like receptor 5 (TLR5). Stimulation of TLR5 with CBLB502 was shown previously to have a radioprotective property in mouse and primate models.

32 (95% CI: 0.11-0.94) for adipsin to 96.4 (95% CI: 11.8-785.4) for IL-8 in serum and from 0.17 (95% CI:

0.06-0.54) for MIP1d to 54.8 (95% CI: 6.9-432.5) for IL-8 in bile. Conclusion: Using multiplexed technology, we were able to identify a number of inflammatory and angiogenic markers EX 527 manufacturer in serum and bile associated with GBC risk. These results provide biological evidence for the role of inflammatory/immune processes involved in GBC and may offer a first step toward identifying biomarkers that could help identify gallstone patients at high risk of developing gallbladder cancer. Disclosures: The following people have nothing to disclose: Jill Koshiol, Troy J. Kemp, Felipe A. Castro, Yu-Tang Gao, Leticia Nogueira, Asif Rashid, Ann W. Hsing, Allan Hildesheim, Ruth M. Pfeiffer, Ligia Pinto Janus kinase-signal transducer and activator of transcription (JAK/STAT) signaling pathway has been implicated in a variety of cellular functions, playing important roles in controlling immune-mediated liver injury. The functions of STAT1 and STAT3 in the pathogenesis of liver diseases have been extensively investigated;

however, the role of STAT4 remains largely unknown. Here we demonstrated that STAT4 activation was detected in liver immune cells from patients with viral hepatitis, autoimmune hepatitis, nonalcoholic steatohepatitis, and alcoholic liver diseases, as well as in a mouse model of con-canavalin A (Con A)-induced T cell hepatitis. Flow cytometric and immunohistochemistry analyses buy Gefitinib revealed that STAT4 activation was mainly detected in T and NKT cells in Con A-induced T cell hepatitis model,

such activation was diminished in IL-12a-/- and IL-12b-/- mice. As expected, disruption of the STAT4 reduced the production of both Th1 and Th2 cytokines, but surprisingly exacerbated Con A-induced liver injury. In agreement with these findings, ablation of IL-12a or IL-12b also augmented Con A-induced hepatocellular damage. Further studies showed that hepatic NKT cells from Con A-treated STAT4-/- mice had higher levels of FasL expression and cyto-toxicity against hepatocytes than those from Con A-treated WT mice. In vitro studies revealed that blocking FasL by antibodies on NKT cells attenuated hepatic NKT cytotoxicity against hepatocytes. Our results Uroporphyrinogen III synthase suggest that IL-12 activation of STAT4 up-regulates expression of Th1 and Th2 cytokines but inhibits the expression of FasL on NKT cells. The suppression of FasL expression contributes to the protective effects of IL-12/STAT4 on Con A-induced T cell mediated hepatitis. Disclosures: The following people have nothing to disclose: Yan Wang, Dechun Feng, Hua Wang, Ming-Jiang Xu, Ogyi Park, Yongmei Li, Bin Gao Background CBLB502 (aka Entolimod) is a pharmacologically optimized derivative of bacterial protein flagellin, an agonist of toll-like receptor 5 (TLR5). Stimulation of TLR5 with CBLB502 was shown previously to have a radioprotective property in mouse and primate models.

Lesions in the small and large bowel are usually hemorrhagic or infiltrative. Infiltration of lymphoreticular organs, mainly spleen, liver, and lymph nodes, is more prominent in chronic than acute leukemia. Neutropenic enterocolitis,

a necrotizing process involving the cecum, ascending colon, and terminal ileum, is increasing in incidence due to greater intensity of chemotherapy. Distension of bowel leads to mucosal breaches, permitting Napabucasin entry of organisms that grow profusely in the absence of neutrophils. Ischemic necrosis follows, leading to perforation and/or peritonitis. Patients present with fever, abdominal pain, diarrhea, nausea, vomiting, abdominal distension and tenderness. Ultrasound and computed tomography scans show thickening of the bowel wall. Treatment is supportive with surgery for necrosis and perforation. The main GI causes of death in leukemia are hemorrhage, infection, and necrotizing enterocolitis. This is a review of the gastrointestinal (GI) manifestations

of leukemia. It is based on the 153 articles found in the English literature using a Medline search since 1965 coupling “leukemia” with “esophagus,”“stomach,”“gastric,”“small bowel,”“colon,”“pancreas,” and “gallbladder” and by reviewing the reference lists of the articles found. Also articles were found through the search engine Google scholar. There is a discussion of the main types of involvement

buy Ibrutinib in the esophagus, stomach, and intestine, with emphasis on neutropenic enterocolitis and its differential diagnosis. Acute lymphoblastic leukemia (ALL), which accounts for 80% of leukemias in children, is due to an arrest of the lymphoid precursor cells (lymphoblasts) at an early stage of development. These cells invade the bone Mephenoxalone marrow resulting in a marked decrease in normal blood cells; they also enter other organs, particularly liver, spleen, and lymph nodes. Patients present with fever, infection in the presence of neutropenia, symptoms of anemia, bleeding from thrombocytopenia, bone pain, and lymphadenopathy. Acute myelogenous leukemia (AML), the most common acute leukemia affecting adults, is a maturational arrest of hematopoietic precursors with at least 20% blasts in the bone marrow. The result is leukemic infiltration of the bone marrow that reduces normal bone marrow cells and proliferates in the blood and frequently in liver and spleen. Symptoms include fatigue, bleeding, infection, and shortness of breath. Chronic lymphocytic leukemia (CLL) is the most prevalent form of leukemia in adults, peaking in the fifth to eighth decades. It is characterized by a progressive accumulation of mature and immunoincompetent lymphocytes in bone marrow and lymphoid organs. Patients may be asymptomatic, complain of vague symptoms or fatigue, and develop splenomegaly and adenopathy.

In addition, unlike HCC, EpCAM is not a good prognostic biomarker for

ICC because its expression is highly elevated in both HpSC-ICC and MH-ICC (data not shown). Further studies involving in-depth analyses Lenvatinib of miR-200c and EMT signaling and using relevant animal models would be needed to test the therapeutic relevance of these targets for ICC. Human adult livers are believed to be comprised of maturational lineages of cells beginning intrahepatically near the portal triads referred to as canals of Hering.45 This region is close to intrahepatic bile ducts and is believed to contain liver stem cells. It is suggested that liver stem cells may give rise to bipotent progenitor cells, which have the potential to differentiate into both hepatocytic and cholangiocytic lineages. In principle, hepatic stem/progenitor cells could be the common DAPT concentration cellular origin for both HCC and ICC. It is hypothesized that cancer progression is driven by the presence of CSC, which is also responsible for treatment resistance and tumor relapse.46 CSCs have been demonstrated in a growing range of epithelial and other

solid organ malignancies, suggesting that the majority of malignancies are dependent on such a compartment.47 This model is attractive because it may help to address the heterogeneity of HCC and ICC, and could facilitate research strategies to define novel and effective therapies.48 Consistently, studies on clinicopathological features of ICC suggest that some ICCs could arise from liver stem cells rather than from mature cholangiocytes.49, 50 Moreover, gene

expression profiling revealed that some HCC cases contain ICC-like gene expression see more trait and embryonic stem cell-like traits.15 These results suggest that certain types of ICC could be derived from the same cell origin that leads to HCC, whereas distinct mechanisms may be involved in the genesis of ICC. CHC has been traditionally classified into three subtypes based on the histological description by Allen and Lisa in 1949.51 These subtypes include type-A (collision or double cancer, which is referred to as separate HCC and ICC arising in the same liver), type-B (contiguous mass, which is referred to as admixed HCC/ICC such as fibrolamellar tumors), and type-C (transitional tumors, which are referred to as a tumor mass with cellular features of both HCC and ICC). In type-A tumors, the HCC and ICC lesions could be interpreted as originating separately from hepatocyte and bile duct epithelium. Type-B tumors could follow the same mechanism as type-A because it is difficult to distinguish them based on histological data. Because both HCC and ICC cellular features are intimately associated with the type-C tumors, they have been interpreted as arising from the same site and sharing the same cell origin. In our study, two Chinese and five Japanese CHC cases belong to type-B and seven Korean CHC cases15 belong to type-C.

In addition, unlike HCC, EpCAM is not a good prognostic biomarker for

ICC because its expression is highly elevated in both HpSC-ICC and MH-ICC (data not shown). Further studies involving in-depth analyses Forskolin price of miR-200c and EMT signaling and using relevant animal models would be needed to test the therapeutic relevance of these targets for ICC. Human adult livers are believed to be comprised of maturational lineages of cells beginning intrahepatically near the portal triads referred to as canals of Hering.45 This region is close to intrahepatic bile ducts and is believed to contain liver stem cells. It is suggested that liver stem cells may give rise to bipotent progenitor cells, which have the potential to differentiate into both hepatocytic and cholangiocytic lineages. In principle, hepatic stem/progenitor cells could be the common selleck cellular origin for both HCC and ICC. It is hypothesized that cancer progression is driven by the presence of CSC, which is also responsible for treatment resistance and tumor relapse.46 CSCs have been demonstrated in a growing range of epithelial and other

solid organ malignancies, suggesting that the majority of malignancies are dependent on such a compartment.47 This model is attractive because it may help to address the heterogeneity of HCC and ICC, and could facilitate research strategies to define novel and effective therapies.48 Consistently, studies on clinicopathological features of ICC suggest that some ICCs could arise from liver stem cells rather than from mature cholangiocytes.49, 50 Moreover, gene

expression profiling revealed that some HCC cases contain ICC-like gene expression DNA ligase trait and embryonic stem cell-like traits.15 These results suggest that certain types of ICC could be derived from the same cell origin that leads to HCC, whereas distinct mechanisms may be involved in the genesis of ICC. CHC has been traditionally classified into three subtypes based on the histological description by Allen and Lisa in 1949.51 These subtypes include type-A (collision or double cancer, which is referred to as separate HCC and ICC arising in the same liver), type-B (contiguous mass, which is referred to as admixed HCC/ICC such as fibrolamellar tumors), and type-C (transitional tumors, which are referred to as a tumor mass with cellular features of both HCC and ICC). In type-A tumors, the HCC and ICC lesions could be interpreted as originating separately from hepatocyte and bile duct epithelium. Type-B tumors could follow the same mechanism as type-A because it is difficult to distinguish them based on histological data. Because both HCC and ICC cellular features are intimately associated with the type-C tumors, they have been interpreted as arising from the same site and sharing the same cell origin. In our study, two Chinese and five Japanese CHC cases belong to type-B and seven Korean CHC cases15 belong to type-C.

This has been observed after accidental injuries with nonsterile needles29

or in chimpanzee studies.16 Two conclusions can be drawn from these observations: (1) the majority of the genome containing HBV and HDV particles is infectious; (2) HBV and HDV must have evolved a mechanism that efficiently promotes them to the liver. The molecular basis for this liver tropism is unknown. The work presented here suggests a mechanism on the level of receptor recognition. The data were acquired through application of chemically synthesized lipopeptide fragments of the HBV L-protein that interact selleck products with and inactivate an unknown HBV receptor. We provide evidence that the ability of HBV to address hepatocytes with high efficacy is triggered by the myristoylated N-terminal preS1-subdomain of L. The exclusive targeting of the respective

lipopeptides to the liver suggests that the HBV-receptor is liver-specific and not expressed in substantial amounts in other organs. The most remarkable finding of our study is the observation that wildtype HBVpreS1-lipopetides accumulate in livers of animals that are not susceptible for HBV. Using 26 peptides with different mutations, including exchanges of single L-amino acids with their respective D-enantiomers we demonstrated a tight correlation between the liver tropism in mice and the potency to inhibit HBV infection in vitro. Thus, receptor recognition of the HBVpreS-ligand is indistinguishable between mice and humans (and according selleck chemicals to the

data presented in Fig. 4A,B, also rats and dogs). The presence of an HBVpreS-receptor in rodents was unexpected and questions the hypothesis that the refractiveness of mice against HBV infection is caused by a deficiency in receptor-binding. However, the previous identification of Tupaia belangeri as a model for HBV infection30 implied that receptor expression is not limited to only closely related human species. The presence of an HBVpreS-specific receptor in mice and rats has important implications for the systematic development of immune competent small animal models for HBV and/or HDV. Since resistance Fossariinae against infection cannot solely be explained by the lack of an HBV-specific binding receptor it is probably related to the lack of either a cofactor, involved in membrane fusion (which could even be functionally associated with the same molecule), or a factor controlling a subordinated step after the release of the nucleocapsid or both. Using the transplanted uPA-SCID mouse model Lutgehetmann et al.31 demonstrated that mouse hepatocytes are not susceptible to HDV infection in vivo. Given that mouse hepatocytes bind HDV we conclude that a factor/activity required for triggering membrane fusion is missing. The presence of an HBVpreS-specific receptor in mice should also be considered when using transplanted uPA/RAG2 mice as an in vivo infection model.32 These mice are susceptible to HBV and HDV.

3–93.6% and 94.9%. Negative predictive values were very high (100%, 100% and 98.7% respectively). But positive predictive values were lower, ranging from 62.5 to 71.4%. Conclusion:  All monoclonal fecal tests in this series presented similar performance in the post-treatment setting. A negative test after treatment adequately predicted cure of the infection. However, nearly a third of tests were false positive, showing a poor predictive

yield for persistent infection. “
“Background: Helicobacter pylori-associated disease has led to aggressive diagnostic and eradication protocols that are partially responsible for www.selleckchem.com/screening/selective-library.html the decrease in prevalence of H. pylori carriage. Recent evidence indicates that in low-prevalence populations, H. pylori may have protective effects on allergic diseases. The aim of this study was to explore the relationship between pediatric asthma and H. pylori infection in a population with high

prevalence of H. pylori infection. Materials and Methods:  A national referral laboratory was screened for all 13C urea breath tests performed in children aged 5–18 years between 2007 and 2008, for patient demographics and physician-diagnosed asthma. Data concerning asthma-associated medication usage were extracted from electronic medical records and databases. Data were analyzed using a stepwise logistic regression model. Results:  During the study period, 6959 patients underwent urea breath testing (average age 12.4 ± 3.5 years). Of these, 3175/6959 (45.6%) were positive for H. pylori, and 578/6959 (8.3%) had asthma. Rates of asthma in H. pylori-positive and H. pylori-negative buy BAY 57-1293 children were 7.3 and 9.1%, respectively (odds ratio 0.82; 95% confidence interval

(CI) 0.69–0.98; p = .032). We also confirmed that male gender, urban residence, and age are associated with childhood asthma. Conclusions:  We demonstrate an inverse association between H. pylori and pediatric asthma in a population with a high prevalence of H. pylori. “
“Recent studies found that gastric cancer patients with Helicobacter pylori infection had a better response to chemotherapy and had an improved overall prognosis compared with those without. However, the underlying mechanism remains unknown. Quantitative real-time PCR (qRT-PCR) was utilized to determine the expression profile of miR-141 in H. pylori infected cells and tissues and their cAMP respective controls. qRT-PCR and Western blot were used to determine the expression level of KEAP-1. Luciferase reporter assays were used to determine whether KEAP-1 was a direct target of miR-141 in the gastric cancer cells. MTT and apoptosis assay were performed to detect the survival of cells under cisplatin treatment. We found that H. pylori infection can significantly down-regulate miR-141 expression. Knockdown miR-141 expression in 7901/DDP and 7901 cells could significantly improve cisplatin sensitivity. Over-expression of miR-141 resulted in enhanced resistance to cisplatin in both gastric cancer cells.