Helicobacter pylori Presenting Author: JAMSHID

VAFAEIMANESH Additional Authors: MOHAMMAD click here BAGHERZADEH Corresponding Author: JAMSHID VAFAEIMANESH Affiliations: Clinical Research Development Center Objective: Helicobacter pylori infection in gastric mucosa may cause systemic inflammatory reaction. We investigated the inflammatory effect of H pylori infection on nutritional factors such as serum albumin in hemodialysis patients and influence of eradication of H pylori on this association. Methods: Ninety-eight patients on hemodialysis were divided into 2 groups according to H pylori infection. Eradication of H pylori, 8 weeks after treatment, was confirmed by urease breath test and H pylori stool antigen. Serum albumin, lipid profile, and metabolite levels were checked before and after 8

weeks and 6 months of eradication of H pylori. Results: Thirty-nine patients (39.8%) were infected with H pylori. There were no significant differences between the two groups in age, dialysis duration, serum albumin, serum creatinine, blood urea nitrogen, hemoglobin, serum calcium, serum phosphorus, and lipid profile. Thirty-seven patients with H pylori completed the treatment period. Eradication was successful in 30 patients (81.1%). Eight weeks and 6 months after anti-H pylori drug therapy, the mean serum albumin level significantly decreased from 4.2 mg/dL to 3.6 mg/dL (P < 0.001) and 3.7 mg/dL (P < 0.001), respectively. Significant decreases were seen in serum cholesterol (P = 0.001), check details blood urea nitrogen (P = 0.005), and serum calcium level (P = 0.03) and a significant increase in hemoglobin level (P = 0.02). Conclusion: Our study did not demonstrate MCE公司 nutritional benefits after H pylori eradication treatment, as the level of nutritional markers reduced. This relationship needs to be confirmed by further

prospective studies. Key Word(s): 1. serum albumin; 2. Helicobacter pylori; 3. hemodialysis Presenting Author: JAMSHID VAFAEIMANESH Additional Authors: MOHAMMAD BAGHERZADEH Corresponding Author: JAMSHID VAFAEIMANESH Affiliations: Clinical Research Development Center Objective: Helicobacter pylori infection can be diagnosed by biopsy-based or noninvasive methods. Our aim was to identify H. pylori-positive patients on hemodialysis by the noninvasive method of H. pylori stool antigen (HPSA) and investigate its diagnostic accuracy for assessment of the eradication of infection after treatment in comparison with urea breath test (UBT). Methods: Serology, HPSA, and UBT were performed on 87 hemodialysis patients. Infection with H. pylori was confirmed if at least 2 tests were positive. Patients with H. pylori infection received a 2-week course of triple therapy. To evaluate success of eradication HPSA and UBT were done after 8 weeks. Results: Eighty-seven patients were enrolled in the study, of whom 39 (44.8%) were proved to have H. pylori infection. The HPSA was positive in the stool specimens of 37 patients (42.

Helicobacter pylori Presenting Author: JAMSHID

VAFAEIMANESH Additional Authors: MOHAMMAD Selleckchem Erastin BAGHERZADEH Corresponding Author: JAMSHID VAFAEIMANESH Affiliations: Clinical Research Development Center Objective: Helicobacter pylori infection in gastric mucosa may cause systemic inflammatory reaction. We investigated the inflammatory effect of H pylori infection on nutritional factors such as serum albumin in hemodialysis patients and influence of eradication of H pylori on this association. Methods: Ninety-eight patients on hemodialysis were divided into 2 groups according to H pylori infection. Eradication of H pylori, 8 weeks after treatment, was confirmed by urease breath test and H pylori stool antigen. Serum albumin, lipid profile, and metabolite levels were checked before and after 8

weeks and 6 months of eradication of H pylori. Results: Thirty-nine patients (39.8%) were infected with H pylori. There were no significant differences between the two groups in age, dialysis duration, serum albumin, serum creatinine, blood urea nitrogen, hemoglobin, serum calcium, serum phosphorus, and lipid profile. Thirty-seven patients with H pylori completed the treatment period. Eradication was successful in 30 patients (81.1%). Eight weeks and 6 months after anti-H pylori drug therapy, the mean serum albumin level significantly decreased from 4.2 mg/dL to 3.6 mg/dL (P < 0.001) and 3.7 mg/dL (P < 0.001), respectively. Significant decreases were seen in serum cholesterol (P = 0.001), PD0325901 clinical trial blood urea nitrogen (P = 0.005), and serum calcium level (P = 0.03) and a significant increase in hemoglobin level (P = 0.02). Conclusion: Our study did not demonstrate medchemexpress nutritional benefits after H pylori eradication treatment, as the level of nutritional markers reduced. This relationship needs to be confirmed by further

prospective studies. Key Word(s): 1. serum albumin; 2. Helicobacter pylori; 3. hemodialysis Presenting Author: JAMSHID VAFAEIMANESH Additional Authors: MOHAMMAD BAGHERZADEH Corresponding Author: JAMSHID VAFAEIMANESH Affiliations: Clinical Research Development Center Objective: Helicobacter pylori infection can be diagnosed by biopsy-based or noninvasive methods. Our aim was to identify H. pylori-positive patients on hemodialysis by the noninvasive method of H. pylori stool antigen (HPSA) and investigate its diagnostic accuracy for assessment of the eradication of infection after treatment in comparison with urea breath test (UBT). Methods: Serology, HPSA, and UBT were performed on 87 hemodialysis patients. Infection with H. pylori was confirmed if at least 2 tests were positive. Patients with H. pylori infection received a 2-week course of triple therapy. To evaluate success of eradication HPSA and UBT were done after 8 weeks. Results: Eighty-seven patients were enrolled in the study, of whom 39 (44.8%) were proved to have H. pylori infection. The HPSA was positive in the stool specimens of 37 patients (42.

Although involving a comparatively small number of subjects, Sesti et al.[21] conducted a cross-sectional study among 473 subjects, who participated in a study on metabolic risk factors, to examine the relationship between IR and NAFLD (Table 1). The subjects were divided into quartiles according to the three hepatic IR indexes (HOMA index: fasting insulin [mU/mL] × fasting glucose [mg/dL] / 405; hepatic IR index: glucose0–30 AUC × insulin0–30; and liver IR index: −0.091 + [log insulin AUC 0–120 min × 0.400] + [log fat mass% × 0.346] − [log HDL cholesterol × 0.408] + [log BMI × 0.435]). In a logistic regression model, adjusted for age and gender, subjects

in the highest quartile of the liver IR index had a 9.85-fold higher risk of having NAFLD than those in the lowest quartile (OR 9.85;

95% CI 5.33–18.20). Subjects in the highest quartile of the HOMA index had a 5.12-fold higher risk Barasertib supplier of having NAFLD than selleck chemicals those in the lowest quartile (OR 5.12; 95% CI 2.19–9.31). Further, subjects in the highest quartile of the glucose0–30 (AUC) × insulin0–30 (AUC) index had a 3.99-fold higher risk of having NAFLD than those in the lowest quartile (OR 3.99; 95% CI 2.30–6.92). After additional adjustment for a wide range of potential confounders, including WC, ALT level, AST level, GGT level, alkaline phosphatase level, high-sensitivity CRP level, insulin-like growth factor 1 level, 上海皓元 and glucose tolerance status, subjects

in both the highest quartile of the liver IR index and in the highest quartile of the hepatic IR index continued to have an increased risk of NAFLD as compared with those in the lowest quartile (OR 5.61, 95% CI 2.23–13.12 and OR 2.09, 95% CI 1.27–6.63, respectively), although the HOMA index was associated with a non-significant risk. White blood cell (WBC) count is a simple clinical marker of inflammation. Recently, elevated WBC levels have become useful predictors of CVD, diabetes, and metabolic syndrome.[22, 45] A cross-sectional study was conducted on 3681 healthy subjects (2066 men and 1615 women) undergoing medical checkups to determine the relationship between WBC counts and the presence of NAFLD.[46] After adjusting for age, smoking status, regular exercise, BMI, BP, FPG, TG, and HDL-c, multivariate logistic regression analysis showed that the ORs (95% CI) for NAFLD, according to WBC quartiles, were 1.00, 1.48 (1.10–1.98), 1.59 (1.18–2.14), and 1.84 (1.35–2.51) for men and 1.00, 1.15 (0.67–1.96), 1.88 (1.13–3.11), and 2.74 (1.68–4.46) for women (Table 1). These results show that WBC counts were independently associated with the presence of NAFLD regardless of the presence of classical cardiovascular risk factors or other components of metabolic syndrome. Proteomic methods were used to analyze 70 serum samples to identify potential new biomarkers for NAFLD.

Appreciating that the administration of 2-hydroxypropyl-β-cyclodextrin to mice can increase intracellular cholesterol transport,32 further study will be required to ascertain the specific influence of the vehicle on hepatic lipid distribution. We also noted tendencies toward increased hepatic and plasma concentrations of triglycerides and cholesterol in both wildtype and Pctp−/− mice treated with compound A1. The occurrence of these changes independent

of PC-TP expression is suggestive of an off-target effect of the small molecule, the mechanism for which is not yet understood. In summary, this study has served as proof of principle that genetic or chemical targeting of this website PC-TP in a mouse model can attenuate diet-induced glucose intolerance by sensitizing the liver to insulin action and reducing hepatic glucose production. If small molecule inhibitors of PC-TP prove to be capable of treating established type 2 diabetes, they could represent a novel approach to the management of

this common disorder. Moreover, these compounds should be of value in efforts to dissect the molecular mechanisms by which PC-TP regulates hepatic glucose metabolism. We thank Dr. Ji-Feng Liu at Aberjona Laboratories (Beverly, MA) for synthesizing inhibitor analogs PD0325901 datasheet and to Dr. Xin Teng, Brigham and Women’s Hospital, for preparing sufficient amounts of compound A1 (LDN-193188) for in vivo studies. The authors also thank Drs. Jorge Plutzky and Gabriela Orasanu for assistance with the experiment to test activation of PPARγ, Drs. Ross Stein, David Brooks, and David Silver for helpful discussions, and Mr. James Macdiarmid for editorial assistance with the article. Additional Supporting Information may be found in the online version of this article. “
“Aim:  The number of outpatients receiving systemic chemotherapy in Japan has recently increased. We retrospectively examined whether hepatitis B virus (HBV) carriers were safely treated and managed with systemic chemotherapy

or biologic agents as outpatients at our oncology center. Methods:  A total of 40 115 consecutive infusion chemotherapy or biologic therapies were administrated to 2754 outpatients in 上海皓元 the Chemotherapy and Oncology Center at Osaka University Hospital from December 2003 to March 2011. We first studied the prevalence of outpatients with hepatitis B surface antigen (HBsAg), and then retrospectively evaluated a database to determine the frequencies of testing for other HBV-related markers and the incidence of developing hepatitis or HBV reactivation in patients positive for HBsAg. As a control for comparison, we also examined these same factors in patients with hepatitis C virus antibody (anti-HCV). Results:  The majority of physicians at our hospital screened for HBsAg (95%) and anti-HCV (94%) prior to administrating chemotherapy. Of the 2754 outpatients, 46 (1.

Herein, we show that α4 integrin did not work in Con A-induced hepatitis but rather exacerbated symptoms perhaps by blocking MDSCs.

MDSCs are a heterogeneous family of cells that are in various stages of myeloid cell differentiation.[37] In mice, MDSCs are phenotypically characterized as CD11b+GR1+ coexpressing cells that represent a mononuclear CD49d+ MDSC subpopulation which strongly suppresses T-cell proliferation and activation through inducible NOS in tumor-bearing mice[28] but also in T-cell-mediated diseases. Importantly, our results show that Con A causes the recruitment selleck chemicals llc of monocytic MDSCs into the liver, which can be inhibited by anti-α4 integrin leading to increased IFN-γ production Dasatinib chemical structure in CD3 T cells. Although we previously blocked exogenous Th1 trafficking to the liver with anti-α4 integrin, the net effect of inhibiting α4 integrin recruitment of

endogenous cells including MDSCs caused more injury and increased recruitment of some cell types. Moreover MDSCs may stimulate Treg function and expansion[38] and Tregs are potent inhibitors of monocytic cells including effector T cells.[39, 40] Although blocking α4 integrin did not modify the number of Tregs in Con A-induced injured liver, we cannot exclude the possibility that a reduced number of MDSCs might cause a failure in stimulating Tregs and subsequent inhibitory cytokine production. Interestingly a 2-fold higher proportion of Tregs physiologically resides in the liver of VAP-1-deficient mice than of wild-type mice, which is augmented further in acute inflammation derived by Con A, suggesting that increased Tregs could also be contributing to benefits in VAP-1-deficient mice. Although SSAO inhibition alone did little to reduce inflammation blocking SSAO and adhesion

of VAP-1 was optimal. It has been reported that an SSAO inhibitor of VAP-1 reduced the recruitment of Gr-1+CD11b+ myeloid cells into tumor vasculature and attenuated the growth of tumor indicating that the SSAO activity of VAP-1 may be responsible for the recruitment of at least some leukocytes into the tumor.[41] In conclusion, VAP-1 plays a critical role in recruitment 上海皓元医药股份有限公司 of CD4 Th2 cells and inhibition of or lack of VAP-1 causes a decline in IL-4-producing T cells and subsequent improvement of the disease state. In various disease states ranging from sepsis to viral and autoimmune hepatitis, a very significant number of lymphocytes are recruited into the liver sinusoids. The strategy of inhibiting an inappropriate accumulation of inflammatory cells in liver microvasculature could improve the pathological state of a number of inflammatory diseases. Our data suggest that targeting VAP-1 has promise for the development of a potential antiinflammatory therapy. Anti-α4 integrin exacerbates the injury derived by Con A, which may be due to the inhibition of monocytic MDSCs, or indirect effects upon Tregs.

Herein, we show that α4 integrin did not work in Con A-induced hepatitis but rather exacerbated symptoms perhaps by blocking MDSCs.

MDSCs are a heterogeneous family of cells that are in various stages of myeloid cell differentiation.[37] In mice, MDSCs are phenotypically characterized as CD11b+GR1+ coexpressing cells that represent a mononuclear CD49d+ MDSC subpopulation which strongly suppresses T-cell proliferation and activation through inducible NOS in tumor-bearing mice[28] but also in T-cell-mediated diseases. Importantly, our results show that Con A causes the recruitment PF-02341066 chemical structure of monocytic MDSCs into the liver, which can be inhibited by anti-α4 integrin leading to increased IFN-γ production find more in CD3 T cells. Although we previously blocked exogenous Th1 trafficking to the liver with anti-α4 integrin, the net effect of inhibiting α4 integrin recruitment of

endogenous cells including MDSCs caused more injury and increased recruitment of some cell types. Moreover MDSCs may stimulate Treg function and expansion[38] and Tregs are potent inhibitors of monocytic cells including effector T cells.[39, 40] Although blocking α4 integrin did not modify the number of Tregs in Con A-induced injured liver, we cannot exclude the possibility that a reduced number of MDSCs might cause a failure in stimulating Tregs and subsequent inhibitory cytokine production. Interestingly a 2-fold higher proportion of Tregs physiologically resides in the liver of VAP-1-deficient mice than of wild-type mice, which is augmented further in acute inflammation derived by Con A, suggesting that increased Tregs could also be contributing to benefits in VAP-1-deficient mice. Although SSAO inhibition alone did little to reduce inflammation blocking SSAO and adhesion

of VAP-1 was optimal. It has been reported that an SSAO inhibitor of VAP-1 reduced the recruitment of Gr-1+CD11b+ myeloid cells into tumor vasculature and attenuated the growth of tumor indicating that the SSAO activity of VAP-1 may be responsible for the recruitment of at least some leukocytes into the tumor.[41] In conclusion, VAP-1 plays a critical role in recruitment MCE of CD4 Th2 cells and inhibition of or lack of VAP-1 causes a decline in IL-4-producing T cells and subsequent improvement of the disease state. In various disease states ranging from sepsis to viral and autoimmune hepatitis, a very significant number of lymphocytes are recruited into the liver sinusoids. The strategy of inhibiting an inappropriate accumulation of inflammatory cells in liver microvasculature could improve the pathological state of a number of inflammatory diseases. Our data suggest that targeting VAP-1 has promise for the development of a potential antiinflammatory therapy. Anti-α4 integrin exacerbates the injury derived by Con A, which may be due to the inhibition of monocytic MDSCs, or indirect effects upon Tregs.