In contrast to TNF-α-mediated hepatitis, apoptosis caused by Fas-

In contrast to TNF-α-mediated hepatitis, apoptosis caused by Fas-ligand (FasL) is JNK-independent.36 Based on the crucial role of Fas- and TNF-mediated cell injury in a broad spectrum of immune-related liver diseases, TAT-ARC protein transduction or ARC-related small molecules could be of therapeutic benefit for preventing and treating acute Selleckchem Forskolin and chronic liver injuries.17, 18 A short-term application of an antiapoptotic approach would also limit the risk of developing cancer. Although we applied TAT fusion protein intraperitoneally

or intravenously, regional delivery of high TAT-ARC concentrations or small molecules by way of the hepatic artery or portal vein might be attractive this website in the therapeutic setting. We thank Katarzyna Pogodzinski, Marlies Grieben, and Nadine Weser for excellent technical assistance. pTAT-HA and pTAT-βgal vectors were kindly provided by S. Dowdy (Howard Hughes Medical Institute, La Jolla, CA). This article is dedicated to Prof. Dr. Michael P. Manns on the occasion of his 60th birthday. “
“Plasma cell hepatitis (PCH) is an idiopathic disorder characterized by plasma cell infiltration in the allografts of patients who have undergone liver transplantation. Although an increasing number of cases of PCH have

been reported in liver transplant recipients with hepatitis C recurrence treated with interferon, it is unclear whether PCH is induced by interferon itself. Here, we describe the cases of two patients who developed PCH just after the

termination of antiviral therapy for recurrent hepatitis C after living donor liver transplantation. Liver dysfunction appeared at 1 month in one patient and 2 months in the other patient after pegylated interferon plus ribavirin therapy, and liver histology showed interface hepatitis with plasma cell-rich lymphoid aggregates. Both patients 上海皓元 recovered after steroid therapy and achieved sustained virological response. These cases suggest that PCH could be induced by the alteration of the immune condition resulting from the termination of antiviral therapy. PCH should be considered when the transaminase levels increase after antiviral therapy, and it should be carefully distinguished from hepatitis C relapse. PLASMA CELL HEPATITIS (PCH), termed de novo autoimmune hepatitis (AIH), is an idiopathic disorder with the histological characteristics of AIH, showing interface hepatitis with a predominantly lymphoplasmacytic necroinflammatory infiltrate with or without lobular involvement and bridging necrosis in patients after undergoing liver transplantation for indications besides AIH.[1-4] Interestingly, an increasing number of PCH cases have been reported in liver transplant recipients infected with hepatitis C virus (HCV), including patients treated with interferon and ribavirin for recurrent hepatitis C.

In contrast to TNF-α-mediated hepatitis, apoptosis caused by Fas-

In contrast to TNF-α-mediated hepatitis, apoptosis caused by Fas-ligand (FasL) is JNK-independent.36 Based on the crucial role of Fas- and TNF-mediated cell injury in a broad spectrum of immune-related liver diseases, TAT-ARC protein transduction or ARC-related small molecules could be of therapeutic benefit for preventing and treating acute Dabrafenib in vivo and chronic liver injuries.17, 18 A short-term application of an antiapoptotic approach would also limit the risk of developing cancer. Although we applied TAT fusion protein intraperitoneally

or intravenously, regional delivery of high TAT-ARC concentrations or small molecules by way of the hepatic artery or portal vein might be attractive buy Kinase Inhibitor Library in the therapeutic setting. We thank Katarzyna Pogodzinski, Marlies Grieben, and Nadine Weser for excellent technical assistance. pTAT-HA and pTAT-βgal vectors were kindly provided by S. Dowdy (Howard Hughes Medical Institute, La Jolla, CA). This article is dedicated to Prof. Dr. Michael P. Manns on the occasion of his 60th birthday. “
“Plasma cell hepatitis (PCH) is an idiopathic disorder characterized by plasma cell infiltration in the allografts of patients who have undergone liver transplantation. Although an increasing number of cases of PCH have

been reported in liver transplant recipients with hepatitis C recurrence treated with interferon, it is unclear whether PCH is induced by interferon itself. Here, we describe the cases of two patients who developed PCH just after the

termination of antiviral therapy for recurrent hepatitis C after living donor liver transplantation. Liver dysfunction appeared at 1 month in one patient and 2 months in the other patient after pegylated interferon plus ribavirin therapy, and liver histology showed interface hepatitis with plasma cell-rich lymphoid aggregates. Both patients 上海皓元医药股份有限公司 recovered after steroid therapy and achieved sustained virological response. These cases suggest that PCH could be induced by the alteration of the immune condition resulting from the termination of antiviral therapy. PCH should be considered when the transaminase levels increase after antiviral therapy, and it should be carefully distinguished from hepatitis C relapse. PLASMA CELL HEPATITIS (PCH), termed de novo autoimmune hepatitis (AIH), is an idiopathic disorder with the histological characteristics of AIH, showing interface hepatitis with a predominantly lymphoplasmacytic necroinflammatory infiltrate with or without lobular involvement and bridging necrosis in patients after undergoing liver transplantation for indications besides AIH.[1-4] Interestingly, an increasing number of PCH cases have been reported in liver transplant recipients infected with hepatitis C virus (HCV), including patients treated with interferon and ribavirin for recurrent hepatitis C.

In contrast to TNF-α-mediated hepatitis, apoptosis caused by Fas-

In contrast to TNF-α-mediated hepatitis, apoptosis caused by Fas-ligand (FasL) is JNK-independent.36 Based on the crucial role of Fas- and TNF-mediated cell injury in a broad spectrum of immune-related liver diseases, TAT-ARC protein transduction or ARC-related small molecules could be of therapeutic benefit for preventing and treating acute PD0325901 cost and chronic liver injuries.17, 18 A short-term application of an antiapoptotic approach would also limit the risk of developing cancer. Although we applied TAT fusion protein intraperitoneally

or intravenously, regional delivery of high TAT-ARC concentrations or small molecules by way of the hepatic artery or portal vein might be attractive Epigenetics Compound Library in the therapeutic setting. We thank Katarzyna Pogodzinski, Marlies Grieben, and Nadine Weser for excellent technical assistance. pTAT-HA and pTAT-βgal vectors were kindly provided by S. Dowdy (Howard Hughes Medical Institute, La Jolla, CA). This article is dedicated to Prof. Dr. Michael P. Manns on the occasion of his 60th birthday. “
“Plasma cell hepatitis (PCH) is an idiopathic disorder characterized by plasma cell infiltration in the allografts of patients who have undergone liver transplantation. Although an increasing number of cases of PCH have

been reported in liver transplant recipients with hepatitis C recurrence treated with interferon, it is unclear whether PCH is induced by interferon itself. Here, we describe the cases of two patients who developed PCH just after the

termination of antiviral therapy for recurrent hepatitis C after living donor liver transplantation. Liver dysfunction appeared at 1 month in one patient and 2 months in the other patient after pegylated interferon plus ribavirin therapy, and liver histology showed interface hepatitis with plasma cell-rich lymphoid aggregates. Both patients MCE recovered after steroid therapy and achieved sustained virological response. These cases suggest that PCH could be induced by the alteration of the immune condition resulting from the termination of antiviral therapy. PCH should be considered when the transaminase levels increase after antiviral therapy, and it should be carefully distinguished from hepatitis C relapse. PLASMA CELL HEPATITIS (PCH), termed de novo autoimmune hepatitis (AIH), is an idiopathic disorder with the histological characteristics of AIH, showing interface hepatitis with a predominantly lymphoplasmacytic necroinflammatory infiltrate with or without lobular involvement and bridging necrosis in patients after undergoing liver transplantation for indications besides AIH.[1-4] Interestingly, an increasing number of PCH cases have been reported in liver transplant recipients infected with hepatitis C virus (HCV), including patients treated with interferon and ribavirin for recurrent hepatitis C.

[27] Fourth, it is possible that differences in baseline characte

[27] Fourth, it is possible that differences in baseline characteristics between the two cohorts may account for some of the associations found with IL28B. However, analyzing the cohorts separately ZIETDFMK yielded similar findings (Supporting Table S1). Finally, clinical outcomes are much better endpoints of disease progression than fibrosis staging, and therefore should be the more biologically relevant measure of phenotype-genotype correlation. IL28B

genotype CC was associated with a lower frequency of HCV genotype 1 infection and hepatic steatosis compared to IL28B genotypes CT or TT. These appear to be consistent findings among studies that have examined these relationships.[11, 28-30] The reason for the association with HCV genotype 1 is not clear but the findings suggest that either HCV non-1 genotypes preferentially

infect subjects with IL28B genotype CC or that HCV genotype 1 infections may be more effectively cleared by those with learn more IL28B CC genotype compared to non-1 HCV genotype. It is possible that prior therapy of the HALT-C cohort may have introduced bias into the analysis by enrichment of the HALT-C cohort (predominantly HCV genotype 1) with IL28B non-CC genotypes. However, when we examined the NIH cohort, all of whom were untreated, the same association with IL28B genotype and HCV genotype was found. This study has several strengths that are worth highlighting. Patients were derived from two pedigreed cohorts that encompassed a wide spectrum of disease severity. Liver biopsies were evaluated by a panel of expert hepatopathologists in the majority of cases and a robust definition of fibrosis progression was used,

a 2-point increase in 上海皓元 fibrosis score, that should limit the effect of sampling error on liver biopsy. No previous study has used paired biopsies, which we believe is the best approach to explore the relationship between IL28B and disease progression. Subjects in the HALT-C trial were prospectively followed every 3 months for the development of clinical decompensation and all events were adjudicated by a panel of three rotating investigators before being entered into the trial database. A potential limitation was that all the subjects in the HALT-C cohort had received a prior course of therapy that may have influenced liver histology such that patients with IL28B genotype CC with milder disease may have responded to therapy, thereby enriching the cohort with subjects with more severe activity and fibrosis. However, since response to interferon-based therapy is independent of baseline ALT level[31] (a surrogate marker of HAI score), this would likely be true for other IL28B genotypes with milder activity and fibrosis.

This study evaluated the efficacy of endoscopic submucosal dissec

This study evaluated the efficacy of endoscopic submucosal dissection for residual/locally recurrent lesions in comparison with primary lesions. Method:  This retrospective case-control investigated 34 residual/locally recurrent

lesions and 384 primary lesions treated using endoscopic submucosal dissection. Tumor size, resected specimen size, procedure duration, en bloc resection rate, curative resection rate, histology, associated complications, and recurrence rate were compared between groups. Results:  Procedure duration tended to be longer (85 ± 53 min vs 73 ± 55 min) Dasatinib cell line and tumors were significantly smaller (20 ± 13 mm vs 33 ± 20 mm; P < 0.001) in the residual/locally recurrent group, compared with primary lesions. Both groups showed similar percentages of en bloc (100% vs 97.4%) and curative resection (88.4% vs. 83.6%). Perforation rate was significantly higher in the residual/locally

www.selleckchem.com/products/PLX-4032.html recurrent group (14.7% vs 4.4%, P < 0.05). However, emergency surgery was only needed in 1 of 5 cases in the residual/locally recurrent group, with the remaining 4 cases conservatively managed using endoclips. Conclusions:  Endoscopic submucosal dissection for residual/locally recurrent lesions was curative and efficacy. This procedure could help to avoid surgical MCE resection and frequent follow-up examinations in many patients. Conventional endoscopic mucosal resection (EMR) is

frequently performed for epithelial colorectal lesions, but residual/locally recurrent lesions may occur after endoscopic therapy and the rate of recurrence is reportedly 5.9–17%.1–4 Conventional therapy for residual/locally recurrent lesions involves repeated EMR and incineration by argon plasma coagulation (APC).5 Lesions that show sufficient elevation after injection or are small can either be resected with a snare or treated by incineration. These treatments, when successful, may be curative for residual/locally recurrent lesions. However, residual/locally recurrent lesions generally show severe fibrosis and a non-lifting sign. Repeated EMR following endoscopic diagnosis of residual/locally recurrent lesions is often unsuccessful and is technically difficult to perform due to submucosal fibrosis.6 If a lesion is large, performing additional EMR with a snare and incineration by APC is difficult. Such lesions often need repeated therapy, and some cases might need surgical resection. Incineration by APC also cannot provide histological specimens to confirm complete resection. Endoscopic submucosal dissection (ESD) has been a standard therapy for epithelial esophagogastric tumors, particularly in Japan.

This study evaluated the efficacy of endoscopic submucosal dissec

This study evaluated the efficacy of endoscopic submucosal dissection for residual/locally recurrent lesions in comparison with primary lesions. Method:  This retrospective case-control investigated 34 residual/locally recurrent

lesions and 384 primary lesions treated using endoscopic submucosal dissection. Tumor size, resected specimen size, procedure duration, en bloc resection rate, curative resection rate, histology, associated complications, and recurrence rate were compared between groups. Results:  Procedure duration tended to be longer (85 ± 53 min vs 73 ± 55 min) check details and tumors were significantly smaller (20 ± 13 mm vs 33 ± 20 mm; P < 0.001) in the residual/locally recurrent group, compared with primary lesions. Both groups showed similar percentages of en bloc (100% vs 97.4%) and curative resection (88.4% vs. 83.6%). Perforation rate was significantly higher in the residual/locally

C59 wnt mw recurrent group (14.7% vs 4.4%, P < 0.05). However, emergency surgery was only needed in 1 of 5 cases in the residual/locally recurrent group, with the remaining 4 cases conservatively managed using endoclips. Conclusions:  Endoscopic submucosal dissection for residual/locally recurrent lesions was curative and efficacy. This procedure could help to avoid surgical medchemexpress resection and frequent follow-up examinations in many patients. Conventional endoscopic mucosal resection (EMR) is

frequently performed for epithelial colorectal lesions, but residual/locally recurrent lesions may occur after endoscopic therapy and the rate of recurrence is reportedly 5.9–17%.1–4 Conventional therapy for residual/locally recurrent lesions involves repeated EMR and incineration by argon plasma coagulation (APC).5 Lesions that show sufficient elevation after injection or are small can either be resected with a snare or treated by incineration. These treatments, when successful, may be curative for residual/locally recurrent lesions. However, residual/locally recurrent lesions generally show severe fibrosis and a non-lifting sign. Repeated EMR following endoscopic diagnosis of residual/locally recurrent lesions is often unsuccessful and is technically difficult to perform due to submucosal fibrosis.6 If a lesion is large, performing additional EMR with a snare and incineration by APC is difficult. Such lesions often need repeated therapy, and some cases might need surgical resection. Incineration by APC also cannot provide histological specimens to confirm complete resection. Endoscopic submucosal dissection (ESD) has been a standard therapy for epithelial esophagogastric tumors, particularly in Japan.

The extensive results included the prevalence of chronic migraine

The extensive results included the prevalence of chronic migraine (CM) at about 1%. CM prevalence is highest in middle-aged women and in households with the lowest annual income. Moving to a very useful and practical manuscript, we have

“The 2012 AHS/AAN Guidelines for Prevention of Episodic Migraine: A Summary and Comparison With Other Recent Clinical Practice Guidelines” from Drs. Loder, Burch, and Rizzoli.[9] This article summarizes key guideline recommendations and changes using materials from the American Headache Society/American Academy of Neurology, Canadian Headache Society and European Federation of Neurological Societies’ guidelines. Perhaps the most clinically useful, from my perspective at least, publication (actually a series of 3 articles) was the extensive review by Drs. Kelley and Tepper on rescue therapy for acute migraine.10-12 They performed a MEDLINE search of selleck compound the topic as well as hand searches of headache and emergency medicine journals. They used weighted averages for outcomes and have

generated a very large amount of efficacy data. Two other features within the journal merit special mention. First is Headache Currents, the “journal within the Journal.” Formerly shared by Cephalalgia and Headache, it now appears exclusively MLN2238 in Headache. Dr. David Dodick was the first Editor; subsequently, I was the editor, and now, Dr. Stewart Tepper has taken charge. Until this year, it was 6 issues per year; now, we have 1 in each issue of the main Journal. Topics covered in the past 2 years are Unanswered Questions in Headache (by Drs. Ahn and Brennan), Pediatric Headache, Genetics and Headache, What Happens

to Old Headache Medicines (dihydroergotamine, ergotamine, methysergide, sumatriptan), and Highlights of IHC Berlin and AHS Annual Scientific Meeting MCE公司 2011; and Clinical Review of QTc Prolongation, Torsade de Pointes, Myocardial Ischemia from Coronary Vasospasm; Pathophysiology of Migraine; Thunderclap Headache and RCVS, Neuro-Ophthalmology, Cluster Headache Management, Hemicrania Continua, and Stroke and Headache. Second, I want to remind our readers that Headache is online, with Dr. Todd Schwedt performing the role of the online editor. Featuring an array of ancillary content, the Journal can be accessed online at http://www.headachejournal.org/view/0/index.html. Perhaps the crowning achievement of all the various online efforts Dr. Schwedt and his team have assembled are the virtual issues. Virtual issues are collections of articles on a particular subject, published previously in Headache: The Journal of Head and Face Pain. The articles highlighted are selected by a guest editor to provide a rapid overview of the activity in a particular aspect of headache medicine. The virtual issues will be updated on a regular basis by the editor but will not be available as a paper publication.

pylori positive gerbils No Enterobacteriaceae were detected Pos

pylori positive gerbils. No Enterobacteriaceae were detected. Positive colonization gerbils showed a higher histopathologic score of gastritis and a similar score of duodenitis. Conclusions:  Long-term H. pylori colonization affected the distribution and numbers of indigenous microflora in stomach and duodenum. Successful colonization caused a more severe gastritis. Gastric microenvironment may be unfit selleck kinase inhibitor for lactobacilli fertility after long-term H. pylori infection, while enterococci, S. aureus, bifidobacteria, and bacteroides showed their adaptations. “
“Background:  Interaction of Helicobacter

pylori with gastric mucosa leads to marked cellular and humoral host immunologic responses. The signaling pathways initiated by bacteria–host interaction that result in perturbations in cell structure and function remain unclear. Forkhead transcription factors of class O (FoxO) are implicated in the regulation of apoptosis, cell survival, and pathogenesis. H. pylori infection of gastric epithelial cells induces phosphoinositide-3 kinase (PI3K)-dependent Akt activation and cell survival signaling. We investigated the role of H. pylori-activated PI3K/Akt in the regulation of FoxO1/3a in gastric cells. Methods:  Immunoblot,

immunoprecipitation, and fluorescence microscopy were used to assess the effect of infection of gastric epithelial cells with wild-type H. pylori and their isogenic cag pathogenicity island (PAI) or oipA mutants on the FoxO1/3a signaling pathways. Interleukin-8 release was determined by enzyme-linked immunosorbent assays. Results: H. pylori infection resulted in activation see more of the PI3K p85 subunit and inactivation of FoxO1 and FoxO3a by their phosphorylation MCE and translocation of from the nucleus to the cytoplasm. Inhibition of PI3K or Akt kinase activity reduced FoxO1/3a phosphorylation.

Akt, FoxO1, or FoxO3a siRNA reduced H. pylori-induced interleukin-8 production. Infection with oipA mutants reduced PI3K/Akt activation and inhibited FoxO1/3a phosphorylation, whereas infection with cag PAI mutants reduced PI3K/Akt activity but did not inhibit FoxO1/3a activation. Conclusions:  FoxO1 and FoxO3a are novel nuclear substrates of H. pylori-induced PI3K/Akt cell survival signaling pathways that partially control interleukin-8 production. OipA-regulated interleukin-8 release through PI3K/Akt is dependent on FoxO1/3a inactivation, whereas cag PAI-mediated interleukin-8 production employs FoxO1/3-independent signaling. “
“Background and Objectives:  We examined the dynamics of Helicobacter pylori infection between pre-school and school ages and compared the determinants of late acquisition of H. pylori infection with determinants of early and persistent H. pylori infection. Methods:  ELISA was used to detect H. pylori antigens in stool specimens collected from children at preschool age (3–5 years) and from their mothers and siblings in 2004. The children were tested again for H.

pylori positive gerbils No Enterobacteriaceae were detected Pos

pylori positive gerbils. No Enterobacteriaceae were detected. Positive colonization gerbils showed a higher histopathologic score of gastritis and a similar score of duodenitis. Conclusions:  Long-term H. pylori colonization affected the distribution and numbers of indigenous microflora in stomach and duodenum. Successful colonization caused a more severe gastritis. Gastric microenvironment may be unfit GPCR Compound Library for lactobacilli fertility after long-term H. pylori infection, while enterococci, S. aureus, bifidobacteria, and bacteroides showed their adaptations. “
“Background:  Interaction of Helicobacter

pylori with gastric mucosa leads to marked cellular and humoral host immunologic responses. The signaling pathways initiated by bacteria–host interaction that result in perturbations in cell structure and function remain unclear. Forkhead transcription factors of class O (FoxO) are implicated in the regulation of apoptosis, cell survival, and pathogenesis. H. pylori infection of gastric epithelial cells induces phosphoinositide-3 kinase (PI3K)-dependent Akt activation and cell survival signaling. We investigated the role of H. pylori-activated PI3K/Akt in the regulation of FoxO1/3a in gastric cells. Methods:  Immunoblot,

immunoprecipitation, and fluorescence microscopy were used to assess the effect of infection of gastric epithelial cells with wild-type H. pylori and their isogenic cag pathogenicity island (PAI) or oipA mutants on the FoxO1/3a signaling pathways. Interleukin-8 release was determined by enzyme-linked immunosorbent assays. Results: H. pylori infection resulted in activation Poziotinib clinical trial of the PI3K p85 subunit and inactivation of FoxO1 and FoxO3a by their phosphorylation MCE公司 and translocation of from the nucleus to the cytoplasm. Inhibition of PI3K or Akt kinase activity reduced FoxO1/3a phosphorylation.

Akt, FoxO1, or FoxO3a siRNA reduced H. pylori-induced interleukin-8 production. Infection with oipA mutants reduced PI3K/Akt activation and inhibited FoxO1/3a phosphorylation, whereas infection with cag PAI mutants reduced PI3K/Akt activity but did not inhibit FoxO1/3a activation. Conclusions:  FoxO1 and FoxO3a are novel nuclear substrates of H. pylori-induced PI3K/Akt cell survival signaling pathways that partially control interleukin-8 production. OipA-regulated interleukin-8 release through PI3K/Akt is dependent on FoxO1/3a inactivation, whereas cag PAI-mediated interleukin-8 production employs FoxO1/3-independent signaling. “
“Background and Objectives:  We examined the dynamics of Helicobacter pylori infection between pre-school and school ages and compared the determinants of late acquisition of H. pylori infection with determinants of early and persistent H. pylori infection. Methods:  ELISA was used to detect H. pylori antigens in stool specimens collected from children at preschool age (3–5 years) and from their mothers and siblings in 2004. The children were tested again for H.

pylori positive gerbils No Enterobacteriaceae were detected Pos

pylori positive gerbils. No Enterobacteriaceae were detected. Positive colonization gerbils showed a higher histopathologic score of gastritis and a similar score of duodenitis. Conclusions:  Long-term H. pylori colonization affected the distribution and numbers of indigenous microflora in stomach and duodenum. Successful colonization caused a more severe gastritis. Gastric microenvironment may be unfit LBH589 for lactobacilli fertility after long-term H. pylori infection, while enterococci, S. aureus, bifidobacteria, and bacteroides showed their adaptations. “
“Background:  Interaction of Helicobacter

pylori with gastric mucosa leads to marked cellular and humoral host immunologic responses. The signaling pathways initiated by bacteria–host interaction that result in perturbations in cell structure and function remain unclear. Forkhead transcription factors of class O (FoxO) are implicated in the regulation of apoptosis, cell survival, and pathogenesis. H. pylori infection of gastric epithelial cells induces phosphoinositide-3 kinase (PI3K)-dependent Akt activation and cell survival signaling. We investigated the role of H. pylori-activated PI3K/Akt in the regulation of FoxO1/3a in gastric cells. Methods:  Immunoblot,

immunoprecipitation, and fluorescence microscopy were used to assess the effect of infection of gastric epithelial cells with wild-type H. pylori and their isogenic cag pathogenicity island (PAI) or oipA mutants on the FoxO1/3a signaling pathways. Interleukin-8 release was determined by enzyme-linked immunosorbent assays. Results: H. pylori infection resulted in activation this website of the PI3K p85 subunit and inactivation of FoxO1 and FoxO3a by their phosphorylation 上海皓元医药股份有限公司 and translocation of from the nucleus to the cytoplasm. Inhibition of PI3K or Akt kinase activity reduced FoxO1/3a phosphorylation.

Akt, FoxO1, or FoxO3a siRNA reduced H. pylori-induced interleukin-8 production. Infection with oipA mutants reduced PI3K/Akt activation and inhibited FoxO1/3a phosphorylation, whereas infection with cag PAI mutants reduced PI3K/Akt activity but did not inhibit FoxO1/3a activation. Conclusions:  FoxO1 and FoxO3a are novel nuclear substrates of H. pylori-induced PI3K/Akt cell survival signaling pathways that partially control interleukin-8 production. OipA-regulated interleukin-8 release through PI3K/Akt is dependent on FoxO1/3a inactivation, whereas cag PAI-mediated interleukin-8 production employs FoxO1/3-independent signaling. “
“Background and Objectives:  We examined the dynamics of Helicobacter pylori infection between pre-school and school ages and compared the determinants of late acquisition of H. pylori infection with determinants of early and persistent H. pylori infection. Methods:  ELISA was used to detect H. pylori antigens in stool specimens collected from children at preschool age (3–5 years) and from their mothers and siblings in 2004. The children were tested again for H.