[27] found that resistance exercise activity, click here at least once a week, was associated with a lower proportion of subjects with NAFLD, independently of BMI, nutritional factors, insulin resistance, and some circulating adipokines, such as adiponectin and resistin. The underlying mechanisms by which exercise, particularly resistance training, may reduce hepatic fat content are not entirely understood. They probably include changes in energy balance, circulatory lipids, fat

oxidation, and insulin sensitivity.[24] In our study, we were careful to avoid a hypocaloric diet or dietary changes during the exercise intervention. Thus, the mild weight loss we observed in both groups is attributable to the effects of exercise and is actually a proof of patients’ compliance with Olaparib mw the training protocol. Although transferring the results

of randomized clinical trials, like ours, to “real-world” settings is not always easy, we believe that our data are clinically important, as they support a beneficial effect of exercise per se for the treatment of NAFLD in type 2 diabetic patients, which can be an adjunct to caloric restriction. Moreover, the finding that resistance exercise is as effective as aerobic exercise in improving hepatic steatosis provides a useful alternative in patients in whom aerobic training may not be accessible, as the high cardiorespiratory demand characteristic of this type of exercise is associated with fatigue and discomfort. Another interesting and MCE novel finding of our study is the close association between changes in hepatic fat content and changes in SSAT and DSAT. In multivariate regression analysis, the absolute reduction in hepatic fat content was best predicted by baseline hepatic fat content and changes in SSAT and DSAT. Whereas the relation between baseline hepatic fat content and its change after exercise intervention could be an expected finding, the independent and opposite associations between the absolute reduction in hepatic fat content and changes in SSAT and DSAT are intriguing. Evidence

indicates that these two subcutaneous fat depots differ in terms of structure and pathophysiology.[28] Interestingly, whereas VAT and DSAT correlate negatively with whole-body insulin sensitivity, SSAT does not.[29] Moreover, SSAT correlates with a more favorable cardiometabolic risk profile in type 2 diabetic patients, whereas DSAT behaves as a VAT depot.[30] Based on these findings, it was hypothesized that higher energy storage in SSAT might exert protective effects by decreasing fat deposition in the liver as well as in other ectopic fat depots. Our data further support this hypothesis, showing that the lower the reduction in SSAT following exercise-induced energy burning, the higher the reduction in hepatic fat content.

8%; 2 cases were positive for CHC, and 1 case was positive for GPC3), but they were never positive for two markers. As shown in Table 3, absolute specificity (100%) for HCC was obtained when staining with at least two markers was taken into account. With respect to the performance of staining with at least two markers in the detection of small and nonsmall HCCs, a four-marker (4M) panel with CHC was superior to a three-marker (3M) panel without CHC. In particular, a gain in sensitivity was seen for small HCCs with 4M staining (63.8%) versus 3M staining (46.8%). In small HCCs, the 4M panel showed an accuracy of 84.3%, which was superior

to the accuracy of the 3M panel (76.9%). Table 4 reports the accuracy in the detection of small G1 HCCs; HGDNs that did not transform into HCCs during follow-up were used MAPK Inhibitor Library cell assay as a negative control group. Absolute specificity was obtained when at least two markers were scored as positive, with 50% sensitivity for the 4M panel versus 33.3% sensitivity for the 3M panel Protease Inhibitor Library and with 67.4% accuracy for the 4M panel versus

56.5% accuracy for the 3M panel. Table 5 reports the performance of the 4M panel in the detection of HCCs with respect to the grade (G1 versus G2/G3) and the size (small versus nonsmall) when at least two markers or at least one positive marker was considered; HGDNs were used as a negative control group. When the staining involved two of the four immunomarkers (regardless of which ones), the accuracy of the panel was excellent in both small and nonsmall G2/G3 HCCs (93.9% and 97.4%) and in nonsmall G1

HCCs (93.9%; Table 5). In contrast, the accuracy of the same panel (two-marker staining) decreased in small G1 HCCs (67.4%) because the sensitivity of HCC detection dropped to 50%, although absolute specificity was retained. In the same group of tumors, the sensitivity and accuracy were partly restored (80% and 80.4%, respectively) when at least one immunomarker was considered (regardless of which one), but absolute specificity was not maintained (Table 5). The performance of the individual markers in the detection of small G1 HCCs is shown in Supporting Fig. 1. In this HCC subpopulation, CHC and GS appeared to be the most sensitive markers, whereas GS and HSP70 were the most specific markers. Pathologists today are asked to provide timely and 上海皓元 conclusive diagnostic reports for the management and therapy of radiologically equivocal hepatocellular nodules found in small biopsy samples. Although the traditional H&E-based morphology remains the milestone, integration with biological information is required to make biopsy interpretation more objective and reproducible. To support the morphological criteria, additional and more objective criteria of malignancy, such as stromal invasion and the composite expression of a number of tissue biomarkers (translated to clinical practice from expression studies of human hepatocarcinogenesis8-13), have been proposed.

In addition, HS may contribute to poorer response to interferon-based therapy against HCV. Cumulative exposure to dideoxynucleoside analogs and, perhaps, to efavirenz are factors Akt inhibitor associated with HS progression. Because of this, antiretroviral drugs with less potential impact on mitochondrial toxicity should be prioritized in HIV/HCV-coinfected patients. Finally, the natural history of HS and steatohepatitis in HIV/HCV coinfection needs further investigation, particularly in patients receiving the newer antiretroviral drugs. Additional Supporting Information may be found in the online version of

this article. “
“Human hematopoietic cell transplantation (HCT) is now a standard procedure for many patients with hematologic malignancy and genetic disorders. The path from experimental to standard procedure has been difficult, as mortality

in the early days was very high and the biology of transplant-related problems was so complex that improvement in outcomes had to wait for deeper scientific knowledge. Liver complications have become far less frequent because we now BVD-523 understand how to prevent and treat most of the serious hepatobiliary problems.1, 2 In the online Supporting Information, I have provided three color plates of histologic findings, a brief discussion of indications for transplant and how HCT is carried out (Supporting Appendix 1), a glossary of common terms (Supporting Appendix 2), a list of abbreviations (Supporting Appendix 3), and a topic-oriented reading list (Supporting Appendix 4). ALT, alanine aminotransferase; AML, acute myeloid leukemia; AST, aspartate aminotransferase; CY, cyclophosphamide; BCV, carmustine/cyclophosphamide/etoposide; BU, busulfan; EBV, Epstein-Barr virus; GVHD, graft-versus-host disease; HBsAg, medchemexpress hepatitis B surface antigen; HBV, hepatitis B virus; HCV, hepatitis C virus; HCT, hematopoietic

cell transplantation; MRI, magnetic resonance imaging; SOS, sinusoidal obstruction syndrome; TBI, total body irradiation; VZV, varicella zoster virus. Hepatic fungal infection should be sought in transplant candidates with tender hepatomegaly, fevers, and abnormal liver enzymes, using high-resolution computed tomography or magnetic resonance imaging, fungal biomarkers (galactomannan and glucan assays), and liver biopsy. Miliary fungal lesions are too small to be imaged. Fungal liver infection should be controlled before transplant with caspofungin, micafungin, or posaconazole until engraftment, which can then effect resolution of intractable fungal abscesses.3 Patients without evidence of fungal liver abscesses at baseline routinely receive fluconazole, itraconazole, or voriconazole to prevent liver infections. Hepatitis B and hepatitis C will be transmitted from viremic donors to transplant recipients.

6 per year post-RS. Similar results were obtained in cases with high radiographic scores

and in inhibitor patients. Pain reduction was observed in most cases. Average range of motion was maintained or increased 1 year post-RS in most joints. Extension was stable or increased in 88.2% of the knees and 86.5% of the elbows. Ankle plantarflexion was stable or increased in 90.9%, whereas dorsiflexion was maintained or increased in 87.9%. Worsening of the range of motion, when present, ranged from 14 to 17 degrees. We concluded that RS with C-Y90 represents an important resource for the treatment of chronic haemophilic synovitis, markedly reducing joint bleeding frequency and pain, irrespective of the radiographic stage and inhibitor status. “
“The most commonly performed assay for factor VIII:C worldwide for many years has been the one-stage assay. mTOR inhibitor The one-stage assay is based on the activated partial thromboplastin time (APTT) and depends selleck chemicals upon the ability of a sample containing factor VIII to correct or shorten the delayed clotting of a plasma which has a complete lack of FVIII (FVIII-deficient plasma). It should be noted however that mild haemophilia A is not excluded by the finding of a normal FVIII:C level by one-stage assay, for the reasons discussed below. Several groups have reported that a subgroup of mild haemophilia A patients have discrepancy between the activity of FVIII as determined using

different types of assay [1–3]. More than 20% of mild haemophilia A patients are associated with assay discrepancy, where a twofold difference between results obtained with different assay systems is considered as discrepant [1]. In some cases the one-stage assay result may be five times higher than the two-stage clotting or chromogenic assay [1]. The most common type of assay discrepancy is to have results of one-stage assays higher than results 上海皓元 of two-stage clotting or chromogenic assay. In more than three-fourths of such patients all assay results are reduced below the lower limit of the reference range so that a diagnosis may be reliably made irrespective of which method is employed for

analysis. However, a small proportion of patients have results by the one-stage assay which is well within the normal range with reduced levels by a two-stage clotting or chromogenic assay [3,4]. These patients have bleeding histories compatible with the lower levels obtained in a two-stage clotting or chromogenic assay. In many cases the genetic defect has been identified, so there is no doubt that these subjects do indeed have haemophilia [4,5]. In our experience about 5–10% of mild haemophilia A patients have a normal one-stage assay result. This is a prevalence similar to that described by other groups. As FVIII activity is normal in the one-stage APTT-based assay, it is not surprising that the APTT is also normal in such patients.

As illustrated in Fig. 3F, IFN-γ treatment inhibited the ZVADFMK expression of α-SMA and TGF-β1 in 2-week CCl4 mice but not in 10- or 12-week CCl4 mice. STAT1 was phosphorylated in isolated HSCs of the IFN-γ–treated 2-week group, but not in HSCs of the IFN-γ–treated

10- or 12-week groups. Finally, expression of SOCS1 protein, a negative regulator of STAT1,16 in HSCs was up-regulated in 2-week CCl4 mice after IFN-γ treatment. HSCs isolated from 10- or 12-week CCl4 mice had higher basal levels of SOCS1 protein than those from 2-week CCl4 mice, which were not further up-regulated after IFN-γ treatment (Fig. 3F). To further understand the underlying mechanism of suppressed NK cell function observed in advanced liver fibrosis, day 4 (D4) (early activated) or day 8 (D8) (intermediately activated) cultured HSCs were cocultured with liver NK cells for 24 hours. After coculturing with HSCs, IFN-γ

production by NK cells was significantly selleck chemicals llc increased in coculturing with D4 HSCs or with D8 HSCs. Higher levels of IFN-γ were observed when cocultured with D4 HSCs than those with D8 HSCs (Fig. 4A). Coculture studies of IFN-γ–deficient cells suggest that the source of IFN-γ production is from NK cells (Fig. 4B). Furthermore, incubation with NKG2D neutralizing antibody diminished IFN-γ production in the coculture experiments (Fig. 4C), suggesting that activated HSCs induce IFN-γ production by NK cells through an NKG2D-dependent mechanism. Expression of TGF-β protein was significantly higher in D8 HSCs compared with D4 HSCs (Fig. 4D). Because TGF-β is a potent inhibitor for NK cells,7, 17 we hypothesized that TGF-β1 produced by cocultured HSCs may inhibit IFN-γ production and cytotoxicity of NK

cells. As illustrated in Fig. 4E, incubation with TGF-β neutralizing antibody markedly enhanced NK cell cytotoxicity against D8 HSCs as well as D4 HSCs (albeit to a lesser extent). In addition, 上海皓元医药股份有限公司 TGF-β antibody treatment increased IFN-γ production by NK cells when cocultured with D8 HSCs but did not affect IFN-γ production in coculture experiment with D4 HSCs (Fig. 4F). Furthermore, the addition of TGF-β1 ligand suppressed the cytotoxicity of NK cells against D4 and D8 HSCs (Supporting Fig. 4). Although IFN-γ–mediated STAT1 activation has been well documented in HSCs,6, 11, 12, 18 the aforementioned experiments show that IFN-γ activation of STAT1 in HSCs from livers with advanced liver fibrosis appears to be disrupted (Fig. 3F). To study the underlying mechanisms responsible for the disruption, IFN-γ–mediated inhibitory cell proliferation and activation of STAT1 were compared on D4 and D8 HSCs. As shown in Fig. 5A, IFN-γ treatment suppressed cell proliferation of D4 HSCs, but not D8 HSCs. Western blotting showed that IFN-γ induced STAT1 activation (phosphorylated STAT1) in D4 HSCs, but this activation was markedly attenuated in D8 HSCs (Fig. 5B and Supporting Fig. 5A).

Because these results identify novel immune-mediated mechanisms that contribute to fibrosis progression in NAFLD, the findings have potential clinical implications for one of the

most common types of chronic liver injury. The authors thank Dr. Alisan Kahraman (Essen, Germany) for technical advice; Patrice McDermott (Human Vaccine Institute Flow Cytometry Core Facility, Duke University, NC) for help with primary mononuclear cell sort; selleckchem Dr. R.J. Wechsler-Reya (Duke University Medical Center, NC) for providing the Patched-deficient (Ptc+/−) mice; Dr. G.J. Gores (Mayo Clinic, Rochester, MN) and Yoshiyuki Ueno (Tohoku University, Sendai, Japan) for providing the murine immature ductular cell line (603B); Dr. M Rojkind (George Washington University, Washington, DC) for providing the rat hepatic stellate cell (HSC) line 8B; and Dr. A. Gemcitabine solubility dmso Bendelac (University of Chicago, Chicago, IL) for providing the mouse invariant hybridoma cell line (DN32). CD1d-tetramers were obtained through the NIH Tetramer Facility (NIAID, MHC Tetramer Core Facility, Atlanta, GA). The authors also thank Dr. Jiawen Huang for assistance with animal care and Mr. Carl Stone for administrative support. Additional

Supporting Information may be found in the online version of this article. “
“Aim:  To evaluate the usefulness of a platelet-derived growth factor (PDGF)-B specific monoclonal antibody (mAb) as

a therapeutic agent to treat chronic liver fibrosis. Methods:  Liver fibrosis was induced in medchemexpress ICR mice by bile duct ligation (BDL) or BALB/c mice by weekly injection of concanavalin A (ConA) for 4 or 8 weeks. A mAb specific for mouse and human PDGF-B chain, AbyD3263, was generated, tested in vitro and administered twice a week throughout the experimental period. Results:  AbyD3263 showed neutralizing activity against mouse and human PDGF-B chain in cell-based assays, as measured in vitro by inhibition of phosphorylation of PDGF receptor β and proliferation of hepatic stellate cells induced by PDGF-BB. The half life of AbyD3263 in mice exceeded 7 days and dosing of animals twice a week resulted in constant plasma levels of the mAb. Induction of liver fibrosis by BDL and ConA resulted in elevated levels of alanine aminotransferase (ALT) in plasma and hydroxyproline in the liver. Treatment with AbyD3263 did not modify ALT levels, but significantly reduced hydroxyproline content in the liver with a maximum reduction of 39% and 54% in the BDL and ConA models, respectively, compared to controls.

4A). Importantly, this Adeno-PLA2GXIIB virus but not the control virus elevated the rate of hepatic VLDL secretion in PLA2GXIIB−/− mice close to that of the wild-type level (Fig. 6A,B) and restored the decrease in serum TG level in PLA2GXIIB−/−

mice (Fig. 6C), strongly indicating that PLA2GXIIB functions to regulate lipid metabolism. Finally, to confirm that PLA2GXIIB functions down-stream of HNF-4α to control lipid metabolism, we injected into wild-type and PLA2GXIIB−/− mice the control Adeno-ΔE1E3 or Adeno-HNF-4α and measured the JQ1 changes in serum TG levels. We established that Adeno-HNF-4α was effective in overexpressing HNF-4α and inducing PEPCK, MTP, and PLA2GXIIB mRNA expressions in HepG2 cells (Supporting Information Fig. 4B,C). Although Adeno-HNF-4α elevated the serum TG level in wild-type mice compared to the control adenovirus (Fig. 6D), it failed to elevate serum TG level in PLA2GXIIB−/− mice (Fig. 6D). In all, our analysis strongly suggested that PLA2GXIIB is an important target of HNF-4α necessary for controlling lipid metabolism. We demonstrated Vemurafenib mw in this study that PLA2GXIIB is an HNF-4α target gene. First, close

to its transcriptional start site at positions −68 to −86, PLA2GXIIB promoter contains an HNF-4α response element composed of 5′-AGAGGACAAAGGTGAAAC-3′, representing a direct repeat with a 1 base pair spacer (DR1) of an imperfect nuclear hormone receptor consensus binding

sequence AGGTCA. Second, HNF-4α bound to this response element by EMSA analysis and that an anti-HNF-4α antibody immunoprecipitated a chromatin fragment spanning this response element from mouse liver. Third, HNF-4α modulators regulated PLA2GXIIB expression in HepG2 cells and fasting induces hepatic PLA2GXIIB expression similar to other HNF-4α target genes. Noticeably, HNF-4α overexpression by adenovirus or knockdown by small interfering RNA also regulated PLA2GXIIB expression.9 Moreover, PLA2GXIIB expression is strongly reduced in HNF4αLivKO mice.6 Importantly, medchemexpress PLA2GXIIB-null mice accumulated TG, cholesterol, and fatty acids in the liver and developed severe hepatosteatosis despite reduced serum TG and cholesterol levels, closely resembling some of the phenotypes of HNF4αLivKO mice.6 Because cholesterols, TGs, and phospholipids are first exported from the liver via VLDL-TG particles which then serve as key precursors for LDL and HDL cholesterol,13 we found that PLA2GXIIB-null mice are defective in hepatic VLDL-TG secretion, which is likely responsible for the hepatosteatosis and reduced serum total TG, cholesterol, and phospholipids levels observed. Critically, an adenovirus encoding HNF-4α failed to elevate serum TG levels in PLA2GXIIB-null mice.

000,

respectively) for patients with reduced serum zinc levels. Serum zinc levels remained an independent risk factor for development of hepatic encephalopathy (OR = .82 ; 95% CI: .73-.92; p = .001) and hepatorenal syndrome (OR = .79 ; 95% CI: .68-.91; p = .001) when subjected to multivariate analysis. Furthermore, actuarial survival free of liver transplantation was reduced for patients with low serum zinc levels (low zinc: 22.2 months; 95% CI: 17.4–27.0 vs. normal zinc: 30.1 months; 95% CI: 25.5–35.0; p = .003). see more Patients with primary sclerosing cholangitis (PSC) are particularly affected by reduced zinc levels (low zinc: 12.5 months ± 2.4; 95% CI: 7.7–17.2 vs. normal zinc: 39.1 months ± 4.7; 95% CI: 29.8–48.5) resulting in impaired survival (p =.001) while this was not the case for patients with viral liver disease (p =.294), alcoholic liver diseaes (p =.545) or patients classified with other Sorafenib in vitro hepatic disorder (p =.087). In PSC patients, serum zinc levels remained an independent predictor of survival when subjected to multivariate analysis (OR = .80; 95% CI: .64-.98; p = .038). Conclusions: We were able to identify serum zinc levels as a predictor

of reduced survival in ESLD patients, particularly in PSC patients. Whether zinc supplementation might be beneficial for patients on liver transplantation list needs to be further addressed. Disclosures: The following people have nothing to disclose: Kilian Friedrich, Christian Rupp, Andreas Wannhoff, Wolfgang Stremmel, Daniel Gotthardt

Background: Patients are prioritized for liver transplantation (LT) by their anticipated 90-day wait list mortality using the MELD score, but 上海皓元 the MELD underestimates wait list mortality when hyponatremia is present. A revised MELD that incorporates the added mortality due to hyponatremia, the MELD-Na, was shown to reduce wait list mortality in hyponatremic patients in a modeling study. In UNOS Region 6, regional agreement has resulted in prioritization of cirrhotic patients with hyponatremia for LT using a MELD-Na exception since 2008. Aims: (1) Determine if patients granted a MELD-Na exception in Region 6 have similar waitlist mortality compared to patients with similar MELD scores without hyponatremia. (2) Determine if patients granted a MELD-Na exception in Region 6 have similar post-transplant survival compared to patients with similar MELD scores without hyponatremia. Methods: In the UNOS registry, we selected all patients listed for LT in Region 6 from Jan 2008 to Mar 2014 who received a MELD-Na prioritization exception based on regional agreement. We compared their wait list mortality to a MELD-matched group listed for LT without hyponatremia using multiple Cox regression. We then compared post-LT mortality of MELD-Na prioritized patients who received LT with a MELD-matched group without hyponatremia who received LT using multiple Cox regression.

We aimed to determine correlations between LY2109761 cell line the CESI, clinical disease activity indices, and CRP in SBCD patients. A prospective study was conducted between October 2008 and February 2011 on 58 established SBCD patients and suspected patients who received a definitive SBCD diagnosis during study. Patients underwent

complete CE and were scored according to the CESI and Harvey–Bradshaw index (HBI). Statistical correlation among CESI, HBI, and CRP was assessed. Weak, but significant, correlations were found between CESI and HBI (r = 0.4, P < 0.01). The correlation between CESI and CRP was moderate (r = 0.58, P < 0.01). The median CRP value was significantly higher in patients with moderate to severe CESI compared with the mild group (22.60 ± 16.79 mg/L vs 11.88 ± 8.39 mg/L, P < 0.01). Changes between baseline and

follow-up CESI failed to correlate with the delta-HBI or delta-CRP (both, P > 0.05). In this cohort of SBCD patients, clinical disease activity index was not reliable predictors of mucosal inflammation. CRP, however, might be a useful inflammatory marker for evaluating the moderate to severe CE activity in SBCD patients. Furthermore, therapy-induced clinical and biological improvement was not associated with repair of SBCD mucosal lesions. “
“In 2009, a correlated set of polymorphisms in the region of the interleukin-28B (IL28B) gene high throughput screening compounds were associated with clearance of genotype 1 hepatitis C virus (HCV) in patients treated with pegylated interferon-alfa and ribavirin. The same polymorphisms were subsequently associated with spontaneous clearance of HCV in untreated patients. The link between IL28B genotype and HCV clearance may impact decisions regarding initiation of current therapy, the design and interpretation of clinical studies, the economics of treatment, and the process of regulatory approval for new anti-HCV therapeutic agents. (Hepatology 2011)

The current standard of care for chronic infection with hepatitis C virus (HCV) is 24 or 48 weeks of therapy with pegylated interferon-alfa (PEG-IFN) and ribavirin (RBV). Response to therapy is variable, and viral and host characteristics can influence whether patients achieve a sustained virological response (SVR), 上海皓元医药股份有限公司 defined as having undetectable serum HCV RNA at 24 weeks after cessation of treatment. Viral genotype is a predictor of response: patients infected with genotype 1 virus who are treated for 48 weeks with PEG-IFN and RBV have a 40%-50% likelihood of having an SVR, whereas patients with genotype 2 or 3 virus have an SVR rate of 70%-80% after only 24 weeks of PEG-IFN and RBV therapy. Patient genetic ancestry is also a factor in treatment outcome. African American patients with chronic HCV have an almost 50% reduction in SVR rates with PEG-IFN and RBV compared with non-Hispanic patients of European ancestry, and the difference is not explained by socio-demographic characteristics or compliance to treatment.

(p = 0.023). Prevalence of Barret’s oesophagus and oesophageal cancer was reported in 0.4% and 0.3% respectively. Comparing with historical data (1), prevalence of PUD continues to decline in keeping with reduction of H.pylori infection. Prevalence of EO increased steadily over the years in agreement with observations around the globe. Complications related to EO remains low. The decline of prevalence of GCA appears to correlate with an overall decrease in H.pylori infection with Chinese remains the highest ethnic group at risk. Conclusion: Further decline in H.pylori infection is associated with dramatic reduction in peptic ulcer disease and gastric cancer whilst in contrary a further increased

of erosive oesophagitis was observed in our population. Goh K.L., et al., Time trends in peptic ulcer, erosive reflux oesophagitis, gastric and oesophageal cancers in a multiracial BGB324 chemical structure Asian population. Aliment Pharmacol Ther, 2009.29(7):p.774–80. Key Word(s): 1. H. pylori; 2. endoscopy; 3. upper GI; 4. epidemiology Presenting Author: YAN PING LIANG Additional Authors: ZHI E WU, JIN TAO Corresponding Author: YAN PING LIANG Affiliations: The Third Affiliated Hospital of Sun Yat-Sen University, Third Affiliated click here Hospital, Sun Yat-Sen University Objective: To explore the related risk factors for gastroesophageal reflux disease

(GERD). Methods: Patients who were diagnosed as GERD on the basis of the Montreal Consensus guidelines (2006) from Jun 2011 to Jun 2013 in our hospital were enrolled as GERD group. Healthy people were selected to be served as control group. A questionnaire including lifestyle, dietary and demographic data was performed for each group. Univariate analysis was made to select the significant factors and the factors selected were brought into multivariate analysis of conditional logistic regression. Results: The risk factors of GERD included drinking distillate spirit, eating high fat and sweet food, overeating, spicy food, and strong tea. All these factors

were found to be correlated with GERD by univariate analysis (P < 0.05). Multivariate conditional logistic regression analysis appealed that fat food (OR: 3.123, 95% CI: 1.024–9.896, P < 0.05), sweet food (OR: 3.483, 95% CI: 1.102–10.296, P < 0.05), overeating (OR: 3.343, 95% CI: 1.432–9.897, P < 0.05), spicy food medchemexpress (OR: 3.163, 95% CI: 1.067–10.896, P < 0.01) and strong tea (OR: 2.343, 95% CI: 1.342–9.566, P < 0.01). Conclusion: Good and healthy eating habits and lifestyle would contribute to prevent and attenuate GERD. Key Word(s): 1. Gastroesophageal reflux disease; 2. questionnaire Presenting Author: YAN PING LIANG Additional Authors: ZHI E WU, LI TAO Corresponding Author: YAN PING LIANG Affiliations: The Third Affiliated Hospital of Sun Yat-Sen University, Third Affiliated Hospital, Sun Yat-Sen University Objective: To examine 24-h esophageal pH monitoring effectiveness in patients with laryngeal symptoms and without typical reflux symptoms.