036; OR = 2.34; 95% CI = 1.0–5.1). Conclusion:  These results suggest that SLCO1B1 Exon4 C > A polymorphism confers increased risk for gallstone

MEK inhibitor disease in North Indian population. “
“We read with great interest the article by Ascha et al.1 on the incidence and risk factors for hepatocellular carcinoma (HCC) in patients with nonalcoholic steatohepatitis (NASH). The authors state that patients with NASH cirrhosis have a greatly increased risk of HCC and that the most significant factor related to this increase seems to be alcohol consumption. Although this study is important and intriguing in a number of ways and provides insight into the risk factors involved in HCC development, we would like to add one additional comment to the authors’ discussion that is noteworthy in several respects. In their article,1 the authors attempt to discuss comprehensively the incidence and risk factors for NASH-related and hepatitis C virus–related cirrhosis and HCC. Although it is obvious that evaluating the mechanisms for these diseases is beyond the scope of their study, it would have been worthwhile for the

authors to mention a potential underlying mechanism for these conditions that could lead to a better understanding of the results achieved in their report. For this reason, we would like to draw attention to the possible role of adipocytokines in the development of HCC, which could elucidate the risk factors associated with the development of HCC. Among the great number of mechanisms that have been proposed to explain the link ABT-263 solubility dmso between NASH-related cirrhosis and HCC, adipocytokine dysregulation offers new and promising perspectives for a wide range of liver diseases. Adipose tissue is a major source of bioactive substances learn more known as adipocytokines, which

include resistin, leptin, tumor necrosis factor α, and adiponectin.2 Hypertrophied adipocytes in obesity release chemokines that induce the accumulation of macrophages in visceral adipose tissue, which then produce nitric oxide and proinflammatory cytokines. These inflammatory changes induce adipocytokine dysregulation, which is characterized by a decrease in insulin-sensitizing and anti-inflammatory adipocytokines and an increase in proinflammatory adipocytokines.2 Disturbed adipocytokine secretion due to inflammatory changes in obese adipose tissue might, therefore, promote hepatic steatosis, inflammation, fibrogenesis, or hepatocarcinogenesis of the liver.3 Moreover, alcohol, which induces cell death and inflammation in the liver, can cause the development of HCC in NASH patients because of the liver injury already triggered by adipocytokine dysregulation. In conclusion, on the basis of the aforementioned mechanisms, it is reasonable to expect increased rates of HCC in NASH patients, especially those with increased alcohol consumption.

3C and 3B, respectively; Supporting Information Fig. 4). Quantification of platelet staining showed a statistically significant difference between seeded and

unseeded bioscaffolds HTS assay (Fig. 4F), confirming the antithrombogenic function of the ECs in the seeded bioscaffolds. We performed series of coseeding experiments of human umbilical vein endothelial cells (hUVECs) and freshly isolated human fetal liver cells (hFLCs), using the methods developed for re-endothelialization of the bioscaffolds. An initial indication of successful cell seeding of the bioscaffold was apparent by a macroscopic change in the bioscaffold appearance from transparent white to opaque yellow 3-4 days after seeding (Fig. 5A). DNA extraction from a small sample of the seeded scaffold after 7 days revealed a 10-fold increase in DNA concentration (P = 0.0061) compared to an acellular scaffold (Supporting Information Fig. 1A). These DNA amounts correspond to approximately 37% of the DNA present

in fresh ferret liver. H&E staining showed dense cellularity throughout the whole seeded bioscaffolds (Supporting Information Fig. 3D). Proliferation was assessed by immunofluorescence staining for Ki67 and revealed a high number of positive cells detected throughout the bioscaffold (Fig. 6A). Accordingly, TUNEL staining showed a low number of apoptotic cells (Fig. 6B). Quantitative selleck inhibitor image analysis confirmed a 3× higher number of proliferating versus apoptotic cells find more (Fig. 6C). Immunofluorescence staining showed hepatocytic lineage markers such as α-fetoprotein (Supporting Information Fig. 3E), CYP2A and CYP3A (Fig. 5B,C) were expressed by cells in the parenchyma. Double

immunostaining showed intense staining for cytokeratin 19 (CK19) in biliary tubular structures throughout the bioscaffold and clusters of albumin-expressing hepatocytes distributed in the parenchyma (Fig. 5D). There was very little coexpression of these markers by the same cells, suggesting that the bioscaffold contains discrete niches for bile duct and hepatocytes. A similar pattern was observed when sections were costained with CK19 (biliary epithelial cells) and CK18 (hepatocytes) (Supporting Information Fig. 3F). CK19 cells are seen in ductal structures and clusters of CK18 cells surrounding them and in the parenchyma. Some cells showed coexpression of CK19 and CK18, suggesting an immature hepatoblast phenotype.23 Endothelial cell markers such as Von Willebrand Factor (vWF) (Fig. 5E) and endothelial nitric oxide synthase (eNOS) (Fig. 5F) showed staining around the vascular structures of the bioscaffold.

275, P = 0.003) but not ulcers LBH589 purchase (RRR = 1.075, P = 0.444); with low MCV (RRR = 9.104, P = 0.036), low ferritin (RRR = 3.129, P = 0.016) and positive FOB (RRR = 2.7439, P = 0.007) individual predictors for carcinomas. Conclusion: Anaemic patients with a high total score, low MCV,

low ferritin and positive FOB are more likely to have carcinoma on endoscopy. Key Word(s): 1. anaemia; 2. lesion; 3. ulcer; 4. carcinoma; 5. endoscopy Presenting Author: JIN TAO Additional Authors: XIUQING WEI, YANPING LIANG, BIN WU Corresponding Author: JIN TAO Affiliations: 3rd Affiliated Hospital of Sun Yat-Sen University, 3rd Affiliated Hospital of Sun Yat-Sen University, 3rd Affiliated Hospital of Sun Yat-Sen University Objective: To study the effect of β-arrestin2 in radiation-induced progenitor/stem cells apoptosis by

mediating NF-B pathway. Methods: β-arrestin2 Knockout (KO) mice, stem cells marker Lgr5 knock-in (Lgr5-EGFP) and β-arrestin2 KO mice and their respective counterparts PD0325901 manufacturer were or were not injected with NF-B inhibitor of Bay117082 3 hour before exposure to radiation. Their small intestines were examined for histological and apoptosis and proliferation analysis. Intestinal epithelial cells were isolated for analyzing NF-B activity-related events. Moreover, β-arrestin2 and NF-B activity were down-regulated in vitro by RNA interference and chemical agent respectively following radiation. Cell apoptosis and NF-B activity-related events were investigated. Results: β-arrestin2 has a critical role in radio-sensitivity of intestinal injury and apoptosis. β-arrestin2 deficient mice exhibited decreased apoptosis in the intestinal progenitor/stem cells, promoted crypt proliferation and reproduction, and protracted survival following lethal doses of radiation. The intestinal radioprotection by β-arrestin2 deficiency depends on prolonged NF-B activation and

subsequent inhibition of PUMA mediated mitochondrial dysfunction. Unexpectedly, β-arrestin2 deficient selleck kinase inhibitor had little effect on radiation-induced intestinal vascular endothelial apoptosis. Consistently, β-arrestin2 knockdown also provided significant radio-protection through NF-B/PUMA in vitro. Conclusion: Our results suggest that β-arrestin2-mediated apoptosis in progenitor/stem cells compartments is crucial for radiation-stimulated intestinal injury and β-arrestin2 is a potential target for limiting the damaging effect of radiotherapy on the gastrointestinal system. Key Word(s): 1. ß-arrestin2; 2. progenitor/stem cells; 3. radiation-stimulated intestinal injury Presenting Author: JIN TAO Additional Authors: XIUQING WEI, YANPING LIANG, BIN WU Corresponding Author: JIN TAO Affiliations: 3rd Affiliated Hospital of Sun Yat-Sen University, 3rd Affiliated Hospital of Sun Yat-Sen University, 3rd Affiliated Hospital of Sun Yat-Sen University Objective: Intestinal mucositis is a common complication of chemotherapy.

Results: Sustained reduction in ALT level was similar to placebo (10/58; 17%; 95% CI, 9% to 29%) in both the vitamin E (15/58; 26%; 95% CI, 15% to 39%; P = .26) and metformin treatment groups (9/57; 16%; 95% CI, 7% to 28%; P = .83). The mean change in ALT level from baseline to 96 weeks was -35.2 U/L (95% CI, -56.9 to -13.5) with placebo vs -48.3 U/L (95% CI, -66.8 to -29.8) with vitamin E (P = .07) and -41.7 U/L (95% CI, -62.9 to -20.5) with

metformin (P = .40). The mean change at 96 weeks in hepatocellular ballooning scores was 0.1 with placebo (95% CI, -0.2 to 0.3) vs -0.5 with vitamin IWR-1 order E (95% CI, -0.8 to -0.3; P = .006) and -0.3 with metformin (95% CI, -0.6 to -0.0; P = .04); and in NAFLD activity score, -0.7 with placebo (95% CI, -1.3 to -0.2) vs -1.8 with vitamin E (95% CI, -2.4 to -1.2; P = .02) and -1.1 with metformin (95% CI, -1.7 to -0.5; P = .25). Among children with NASH, the proportion who resolved at 96 weeks was 28% with placebo (95% CI, 15% to 45%; 11/39) vs 58% with vitamin E (95% CI, 42% to 73%; 25/43; P = .006) and 41% with metformin (95% CI,

26% to 58%; 16/39; P = .23). Compared with placebo, neither therapy demonstrated significant improvements in other histological features. Conclusion: Neither vitamin E nor metformin was superior to placebo in attaining the primary outcome of sustained reduction in ALT level in patients with pediatric NAFLD. TRIAL REGISTRATION: clinicaltrials.gov FK228 research buy Identifier: NCT00063635. Nonalcoholic fatty liver disease (NAFLD) has rapidly become the most common form of chronic liver disease in children1 and is a major reason for referral to pediatric gastroenterologists and hepatologists. This dramatic increase in the prevalence of NAFLD is a direct consequence of the childhood obesity epidemic, with an estimated 10% of U.S. children having fatty liver.2 The spectrum

of NAFLD ranges from the benign form of hepatic steatosis, with the accumulation of lipids in the liver, to the progressive form of nonalcoholic steatohepatitis (NASH), which find more is characterized by steatosis along with inflammation, hepatocyte injury, and variable degrees of fibrosis.3 It is important to recognize that NASH may present with a distinct histological pattern in children, mainly characterized by increased portal inflammation and fibrosis, as opposed to the predominantly lobular inflammation and perisinusoidal fibrosis observed in adults.4, 5 The progression of NASH to cirrhosis that requires liver transplantation during childhood is well documented,6 making the identification of effective therapy for this condition a pressing issue. Weight loss may improve the liver disease or even lead to the resolution of NAFLD in some children,7 but other than lifestyle advice on diet and exercise, there are no approved therapies for pediatric NAFLD. Insulin resistance (IR) and oxidative stress (OS) play a significant role in disease development and progression (Fig.

Moreover, no association of p28GANK with those regulators was observed by immunoprecipitation

in MHCC-97L cells (data not shown). Through coimmunoprecipitation, we detected a complex consisting of p28GANK, RhoGDIα (RhoGDIa (Rho GDP dissociation inhibitor (GDI) α), and RhoA (ras homolog gene family, member A) proteins (Fig. 5E), which results in repression of ROCK2 (Rho-associated, http://www.selleckchem.com/products/LDE225(NVP-LDE225).html coiled-coil containing protein kinase 2) activity (Supporting Information Fig. 6). This result suggests a mechanism in which p28GANK activates p-AKT signaling through control of the RhoGDIα/RhoA/ROCK2 pathway. Consistent with this, Man et al. reported recently that AZD1208 cost p28GANK promoted

RhoGDIα interaction with RhoA, leading to inhibition of RhoA/ROCK2 activity, and prolonged AKT activation in NIH3T3 cells, human embryonic kidney 293 cells, and lung cancer cells.23 We further analyzed the expression levels of p28GANK, p-AKT, E-cadherin, TWIST1, HIF-1α, RB, and p53 in clinical HCC samples. Tissue microarray analysis of 130 patient specimens revealed a strong correlation of p28GANK expression with p-AKT levels (r = 0.2505, P = 0.0004) (Fig. 6A). Moreover, patients whose tumors expressed above-average levels of p28GANK or p-AKT exhibited significantly decreased trend in any of the prognostic indicators, including time to DFS and OS due to HCC-related death (Supporting Information Fig. 7A,B). For patients whose tumors had above-average levels of both p28GANK and p-AKT, adverse outcomes were exacerbated (Fig. 6B). Using the combination of these two parameters increased the prognostic value, as compared to p28GANK or p-AKT overexpression alone (Fig. 6B; Supporting Information Fig. 7A,B). In conclusion, evaluation of both p28GANK expression and p-AKT signal is a powerful predictor of poor prognosis, further supporting a model of p28GANK activation of PI3K–AKT–HIF-1α signaling, resulting in EMT

occurrence, learn more VEGF and MMP2 production, and thus metastases of HCC cells (Fig. 6C). Efforts to elucidate the molecular mechanism underlying HCC tumorigenicity, invasion, and metastasis of HCC are warranted in order to identify biomarkers for prediction and intervention. In this study, we determined the significance and underlying mechanism for p28GANK overexpression in HCC progression and metastasis. The p28GANK content was low in normal hepatocytes, increased in noninvasive and primary HCC cells, and reached the highest level in invasive HCC and PVTT cells. This progressively increased expression profile paralleled with deterioration of the disease, suggesting a role of p28GANK in progression of HCC.

Target sequences were FK228 mw amplified by means of polymerase chain reaction with specific primers. The nucleotide sequences of the amplicons were determined directly in both forward and reverse directions, using the ABI Prism BigDye Terminator cycle-sequencing ready reaction kit

on a fluorescent model 3100 DNA sequencer (Applied Biosystems). The amino acid sequences were deduced and aligned using Win software (version 7.0; Genetyx, Tokyo, Japan). Throughout this article, the amino acids are numbered according to the full-length genome sequence of isolate H77 (GenBank and DDBJ accession number AF009606).[16] Patients infected with HCV genotype-1 received treatment once per week for 48 weeks with recombinant peginterferon alfa-2b (Peg-intron, Schering-Plough Pharmaceutical, Osaka, Japan), at a dosage of 1.5 μg/kg body weight, in combination with oral ribavirin (Rebetol, Schering-Plough Pharmaceutical) as previously reported.[11] Those with HCV genotype-2 received the same treatment regimen for 24 weeks. Ribavirin was administered orally in a weight-adjusted dose given in two doses. The ribavirin dose was 15 mg/kg per day in patients

weighing ≤40 kg, 600 mg/day in patients weighing 40–60 kg, 800 mg/day in patients weighing 60–80 kg, and 1000 mg/day in patients weighing >80 kg. Blood tests and physical examinations were performed at 2, 4, 6, and 8 weeks after initiation of therapy, then every 4 weeks selleck inhibitor until

the end of treatment. After finishing treatment, blood tests and examinations were done at 12 and 24 weeks during the follow-up period. Adolescents among our patients were instructed to use birth control find more during the treatment and for 6 months after the end of treatment. Differences in mean values and the frequency of patients’ characteristics between groups were compared using the Mann–Whitney U-test and the Fisher’s exact test, respectively. All statistical analyses were performed using the SPSS V.12.0 statistical package, based on two-sided hypotheses tested with a significance level of P < 0.05. The study protocol complied with the ethical guidelines of the Declaration of Helsinki of 1975 (2004 revision) and was approved by the Ethics Committee of Osaka General Medical Center as well as by the respective organizations of each participating institute. The treatment response was evaluated 24 weeks after the completion of the prescheduled treatment period in 30 patients. The subjects’ average age was 10.9 years (range 3 to 17 years), the male-to-female ratio 16:14, transmission route was maternal infection in 26 patients and four infected from a blood transfusion, and the genotype-1: genotype-2 patient ratio was 16:14 (Table 1). The 30 patients in the study consisted of 17 children (3–11 years) and 13 adolescences (12–17 years).

2007) (Fig. 2). Here, we explore the hypothesis that Pleistocene

sea-level fluctuations have strongly influenced the phylogeography and demography of the dugong in Australian waters. Alternatively, it is possible that any phylogeographical patterns have been obscured as a consequence of movement of dugongs leading to a degree of genetic homogeneity in the ~7,000 yr since the most recent flooding of Torres Strait. In support of this possibility, satellite-tagging studies have shown that individual dugongs are capable of long-distance movement covering hundreds of kilometers (Sheppard selleck inhibitor et al. 2006). Knowledge of the extent to which dugong populations are interconnected will inform the debate about management of the species in Australia. Of particular interest is the spatial scale at which

it is legitimate to assess the eligibility of the species for listing under national and state legislation, which in turn determines the impact thresholds for government management action. The time-scales are within the reach of mitochondrial markers (Avise 1994) and we therefore present inferences from mitochondrial control region sequences. Mitochondrial sequence data constitute a single, maternally inherited marker. Ideally, biparentally inherited nuclear markers, such as microsatellites, should also be employed in a study like this. However, the material available to us, while adequate for amplification of the mitochondrial locus, often did not provide template selleck chemicals adequate for genotyping.

The work reported here extends that presented in two Ph.D. theses (Tikel 1997, STI571 in vivo McDonald 2005). These two authors each used DNA sequences from portions of the mitochondrial control region, as did we. Each found very strong evidence for the presence of two maternal lineages in Australia, as did we. One, the “widespread” lineage, occurs across the entire Australian range of the dugong, but is rare in southeastern Queensland. The “restricted” lineage was sampled primarily from the coast of Queensland. Samples were obtained opportunistically from dugongs from the full extent of the species’ range in Australia (Fig. 1, Table S1). Sources of material included dead stranded animals, animals taken by indigenous hunters, skin biopsies from live animals collected during satellite tagging experiments, and skin biopsies taken from free-ranging animals using a scraping device designed by Tikel (1997). Samples were also available from some dugongs from outside Australia (Table S1) to make a total of 188 (177 from Australia and 11 from elsewhere) for which a 411 bp portion of the control region was successfully sequenced (sequences with missing or ambiguous sites having been omitted). DNA extraction followed van Oppen et al. (1999) or used an Epoch GenCatch tissue kit (Epoch Biolabs Pty. Ltd.) following the manufacturer’s protocol. Initially, the “universal” forward primer L15926 (Kocher et al. 1989) and reverse primer A58 (5′ CCTGAAGTARGAACCAGATGTC 3′: Tikel et al.

2007) (Fig. 2). Here, we explore the hypothesis that Pleistocene

sea-level fluctuations have strongly influenced the phylogeography and demography of the dugong in Australian waters. Alternatively, it is possible that any phylogeographical patterns have been obscured as a consequence of movement of dugongs leading to a degree of genetic homogeneity in the ~7,000 yr since the most recent flooding of Torres Strait. In support of this possibility, satellite-tagging studies have shown that individual dugongs are capable of long-distance movement covering hundreds of kilometers (Sheppard AZD5363 cell line et al. 2006). Knowledge of the extent to which dugong populations are interconnected will inform the debate about management of the species in Australia. Of particular interest is the spatial scale at which

it is legitimate to assess the eligibility of the species for listing under national and state legislation, which in turn determines the impact thresholds for government management action. The time-scales are within the reach of mitochondrial markers (Avise 1994) and we therefore present inferences from mitochondrial control region sequences. Mitochondrial sequence data constitute a single, maternally inherited marker. Ideally, biparentally inherited nuclear markers, such as microsatellites, should also be employed in a study like this. However, the material available to us, while adequate for amplification of the mitochondrial locus, often did not provide template selleck chemicals adequate for genotyping.

The work reported here extends that presented in two Ph.D. theses (Tikel 1997, click here McDonald 2005). These two authors each used DNA sequences from portions of the mitochondrial control region, as did we. Each found very strong evidence for the presence of two maternal lineages in Australia, as did we. One, the “widespread” lineage, occurs across the entire Australian range of the dugong, but is rare in southeastern Queensland. The “restricted” lineage was sampled primarily from the coast of Queensland. Samples were obtained opportunistically from dugongs from the full extent of the species’ range in Australia (Fig. 1, Table S1). Sources of material included dead stranded animals, animals taken by indigenous hunters, skin biopsies from live animals collected during satellite tagging experiments, and skin biopsies taken from free-ranging animals using a scraping device designed by Tikel (1997). Samples were also available from some dugongs from outside Australia (Table S1) to make a total of 188 (177 from Australia and 11 from elsewhere) for which a 411 bp portion of the control region was successfully sequenced (sequences with missing or ambiguous sites having been omitted). DNA extraction followed van Oppen et al. (1999) or used an Epoch GenCatch tissue kit (Epoch Biolabs Pty. Ltd.) following the manufacturer’s protocol. Initially, the “universal” forward primer L15926 (Kocher et al. 1989) and reverse primer A58 (5′ CCTGAAGTARGAACCAGATGTC 3′: Tikel et al.

Ligation was performed by two experienced endoscopists who had performed more than 10 sessions of such procedures before the start of this study. Each varix was ligated with one to two rubber bands. Ligations with Selleckchem CP-673451 two to four rubber bands were employed in each session. Further sessions of treatment were performed at intervals of 4 weeks until all varices were obliterated or too small to be ligated. After obliteration, patients in the EVL group underwent follow-up endoscopy every 6 months. Repeat EVL was performed when varices recurred.

Among both groups, nadolol (E.R. Squibb) was administered from the start of enrollment. Nadolol was continued until the end of the study or death. Among the Combined group, nadolol was initiated 2 weeks before the first session of EVL. The dose of nadolol initially given was 40 mg once daily and then adjusted according to the dosage that reduced the resting pulse rate up to 25% or 55 beats per minute. Nadolol was usually administered once per day and compliance was assessed by a reduction of pulse rate and by quantifying the amount of tablets consumed. Patients in both groups were advised to receive follow-ups of abdominal sonogram, serum alpha-fetoprotein, and biochemistry at 3-month intervals. All patients suspected of upper gastrointestinal bleeding received emergency endoscopy within 12 hours of presentation. Supportive measures including blood transfusions,

vasoconstrictor infusion, and lactulose were administered Galunisertib ic50 to patients suspected of bleeding from esophageal varices. Esophageal variceal bleeding was defined as the appearance of hematemesis or melena, bleeding source was proven to originate from esophageal varices by emergency endoscopy, and requiring blood transfusion of greater than 2 units to maintain stable vital signs. Emergency EVL and prophylactic antibiotics with cefazolin were administered within 24 hours of esophageal variceal bleeding. Elective EVL for prevention of rebleeding was employed for check details patients of both groups if patients agreed. Quantitative data were summarized as means ± standard deviation, except for information on

the lengths of follow-up, which were summarized by median values. Quantitative variables were compared using Student’s t test and qualitative variables were compared using the chi-square test, employing Yates correction for continuity and Fisher’s exact test where appropriate. Kaplan-Meier estimation was applied to examine the time to first occurrence of variceal bleeding and the time to death. The log rank test was used to examine the variation of bleeding episodes and survival rate. Cox’s regression analysis was used to detect possible prognostic variables other than treatment modality on the bleeding and survival rates. All hypothesis tests were conducted against a two-sided alternative, where appropriate. Analyses were based on intention to treat and were performed using SPSS 10.0.5 (Chicago, IL).

8%(4/41) vs 41.7%(5/12),P < 0.05). No serious complications were encountered in both groups, such as pleural effusion, mediastinitis and digestive tract fistula. Conclusion: POEM with transverse entry incision can significantly decrease operation duration and reduce incidence of pneumatosis-related complication, while relieving symptoms dramatically. Key Word(s): 1. Achalasia; 2. POEM; 3. Transverse incision; Presenting Author: MENG LI Additional Authors: BIN

LU, LI CHU, HONG ZHOU, MINGYAN CHEN Corresponding Author: MENG LI, BIN LU Affiliations: selleck chemicals llc First Affiliated Hospital of Zhejiang Chinese Medical University Objective: Epidemiological studies suggest that uninvestigated dyspepsia (UD) is common. However, there is little data on the prevalence of UD and its overlap with other gastrointestinal diseases in the college student population. The aim of this survey was to investigate UD in college students in the Zhejiang province. Methods: A total of 2520 college students completed a questionnaire. The diagnosis of UD and irritable bowel syndrome (IBS) was based on the Rome-III criteria. Gastroesophageal reflux disease (GERD) was defined as episodes of heartburn

and/or acid regurgitation that occurred at least once a week. Results: A total of 1870 students (967 males, mean age 21.34 years) completed the questionnaire. The incidence of UD was higher in females and in senior students. The learn more prevalence of UD, IBS, GERD, UD + GERD overlap and UD + IBS overlap was 108 (5.67%), 129 (6.89%), 17(0.91%), 12 (0.64%) and 18 (0.96%), respectively. Conclusion: The incidence of UD is relatively low in Chinese college students. Overlap between UD and IBS or GERD is common, suggesting the involvement of common pathophysiological disturbances. Key Word(s): 1. college student; 2. Dyspepsia; 3. gastroesophageal; 4. prevalence; Presenting Author: HE DE-ZHIHE DE-ZHI MIDDLE NAME: Additional Authors: LI JIAN-SHENGLI JIAN-SHENG LI JIAN-SHENG Corresponding Author: HE DE-ZHIHE DE-ZHI MIDDLE NAME: Affiliations: Zhengzhou University Objective: to investigate the expression of IGFBP7 in gastric cancer and its

clinical selleck kinase inhibitor significance. Methods: Real-time quantitative PCR and Western blotting were employed to examine the expression of IGFBP7 in 73 paired normal gastric mucosa and adenocarcinoma tissues at mRNA and protein levels respectively. Another 281 paraffin-embedded gastric cancer blocks were used for immunohisochemical detection for IGFBP7 expression. The correlation of IGFBP7 expression and clinicopathological parameters and postoperational survival in gastric cancer was further explored by statistical analyses. Results: IGFBP7 expression was significantly reduced at both the mRNA (P < 0.001) and the protein (P < 0.001) levels in gastric cancer tissues. Immunohistochemical analysis revealed that IGFBP7 expression was completely lost in 169 out of the 281 (60.1%) patient samples.