“(Headache 2010;50:1262-1272) Objectives— To determine th


“(Headache 2010;50:1262-1272) Objectives.— To determine the prevalence, characteristics, impact, and treatment patterns of headaches after concussion in US Army soldiers returning from a deployment to Iraq or Afghanistan. Methods.— A cross-sectional study was conducted with a cohort of soldiers undergoing postdeployment evaluation during a 5-month period at

the Madigan Traumatic Brain Injury Program at Ft. Lewis, WA. All soldiers screening positive for a deployment-related concussion were given a 13-item headache questionnaire. Results.— A total of 1033 (19.6%) of 5270 returning soldiers met criteria for a deployment-related concussion. Among those with a concussion, 957 (97.8%) reported having headaches during the final 3 months of deployment. Posttraumatic headaches, defined as click here headaches

beginning within 1 week after a concussion, were present in 361 (37%) soldiers. In total, 58% of posttraumatic headaches were classified as migraine. Posttraumatic headaches had a higher attack frequency than nontraumatic headaches, averaging 10 days per month. Chronic Dabrafenib manufacturer daily headache was present in 27% of soldiers with posttraumatic headache compared with 14% of soldiers with nontraumatic headache. Posttraumatic headaches interfered with duty performance in 37% of cases and caused more sick call visits compared with nontraumatic headache. In total, 78% of soldiers with posttraumatic headache used abortive medications, predominantly over-the-counter analgesics, and most perceived medication as effective. Conclusions.— More than 1 in 3 returning military troops who have sustained a deployment-related concussion have headaches that meet criteria for posttraumatic headache. Migraine is the predominant headache

phenotype precipitated by a concussion during military 上海皓元 deployment. Compared with headaches not directly attributable to head trauma, posttraumatic headaches are associated with a higher frequency of headache attacks and an increased prevalence of chronic daily headache. “
“To evaluate the efficacy and safety of AVP-825, a drug–device combination of low-dose sumatriptan powder (22 mg loaded dose) delivered intranasally through a targeted Breath Powered device vs an identical device containing lactose powder (placebo device) in the treatment of migraine headache. Early treatment of migraine headaches is associated with improved outcome, but medication absorption after oral delivery may be delayed in migraineurs because of reduced gastric motility. Sumatriptan powder administered with an innovative, closed-palate, Bi-Directional, Breath Powered intranasal delivery mechanism is efficiently absorbed across the nasal mucosa and produces fast absorption into the circulation. Results from a previously conducted placebo-controlled study of AVP-825 showed a high degree of headache relief with an early onset of action (eg, 74% AVP-825 vs 38% placebo device at 1 hour, P < .01).

Hepatic lipid accumulation results from an imbalance between lipi

Hepatic lipid accumulation results from an imbalance between lipid availability and lipid disposal.[3] Several metabolic nuclear receptors (NRs) and transcription factors, such as peroxisome proliferator-activated receptors (PPARs), farnesoid X receptor (FXR), pregnane X receptor (PXR), and constitutive androstane receptor (CAR), have been reported to be critical for hepatic lipid homeostasis by controlling circulating lipid uptake, de novo lipogenesis, free fatty acid oxidation, and TG-rich lipoprotein secretion in the liver.[4, 5] Although liver X receptors (LXRs), comprising LXR-α

and LXR-β, mainly act as intracellular cholesterol sensors whose activation leads to protection from cholesterol overload,[6] their role in the regulation of fatty acid and TG metabolism is becoming clearer.[7] LXR isoform nonselective agonist TO901317 induces fatty liver and promotes the secretion of large, TG-rich selleck chemicals llc very-low-density selleck chemical lipoprotein particles in mice,[8] largely through the induction of lipogenic genes, including sterol

regulatory element-binding protein 1c (SREBP-1c), carbohydrate-responsive element-binding protein, stearoyl-CoA (coenzyme A) desaturase 1, and fatty acid synthase (FAS).[9] It has recently been reported that LXR activation may also regulate gene expression of thyroid hormone-responsive SPOT MCE 14 homolog (Thrsp),[10] a gene abundantly present in lipogenic tissues, where it is rapidly up-regulated by lipogenic stimuli, including thyroid hormone and a high-carbohydrate diet.[11] Previous studies demonstrate that Thrsp expression is directly under transcriptional regulation by the NRs, thyroid hormone receptor (TR) and CAR,[12, 13] and it may play an important role in lipogenic processes in the mammary gland.[14] However, Thrsp-null mice display a greater rate of hepatic de novo lipogenesis when exposed to long-term treatment with thyroid hormone or a

diet promoting lipogenesis, possibly because of compensation by a paralog of THRSP (MID1IP1, also named S14-R or Mig12).[15] Therefore, it remains unclear whether Thrsp promotes lipogenesis in the liver. In the present study, our aim was to elucidate the role of Thrsp in hepatic lipid homeostasis and the mechanism by which LXRs up-regulate Thrsp expression. We provide evidence that hepatic overexpression of Thrsp enhances lipogenesis in livers of C57Bl/6 mice and that hepatic knockdown of Thrsp attenuates liver steatosis in db/db mice. Thrsp expression is induced by LXR agonist TO901317 through an LXR-α–mediated, SREBP-1c–dependent mechanism. TO901317 was purchased from Cayman Chemicals (Ann Arbor, MI). TRIzol was purchased from Invitrogen (Carlsbad, CA). Reverse-transcription and probe-labeling kits were purchased from Promega (Madison, WI).

In human CCA samples, the IHC expression of Keratin-7, EpCAM and

In human CCA samples, the IHC expression of Keratin-7, EpCAM and CD133 did not differ between mixed-IHCCA, Muc-IHCCA and Muc-EHCCA. In contrast, CD1 3 positivity, considered as a marker of quiescent CSCs, was prevalent in Mixed-IHCCA while LGR5 positivity predominated in Muc-IHCCA or Muc-EHCCA. Moreover, in all CCA samples, CD90 expression was mostly restricted in tumor stromal cells (αSMA+/vimentin+). In all CCA samples, vimentin expression (western blot) largely predominates with respect to E-cadherin. In cultures of human CCA samples, RT-PCR showed how vimentin, CD90, CD44 and CD13 were largely (> 10-folds; p< 0.01) more expressed than

CD133, EpCAM and Lgr5. When the different CCA subtypes were compared, the CD13+ and CD44+ cell subpopulations MLN8237 nmr predominated (FC and RT-PCR) in Mixed-IH with respect to Muc-IHCCA or Muc-EHCCA (p< 0.01), while the opposite was found for CD90+ learn more cells. No difference was found between Muc-IH- or Muc-EHCCA. The tumorigenic potential (number, volume and growth curves of tumor xenografts) was: CD90+ > CD 13+ > CD133+; CD90+ and CD133+ cells from Mucin-CCA > Mixed-CCA. Conclusions:

the human CCA subtypes, Mixed and Mucin, show a different profile of CSCs further confirming their patho-biological diversity. The subpopulations of CD44+ and CD1 3+ cells were more represented in the Mixed-IHCCA, while CD90+ predominated in Muc-EH- or Muc-IHCCA. The CD90+ CSC subpopulation showed the highest tumorigenic potential and should be taken in great consideration for targeted therapies. Disclosures: The following people have nothing to disclose: Alessia Torrice, Guido Carpino, Alice Fraveto, Anastasia Renzi, Maria Consiglia Bragazzi, Felice Giuliante, Agostino DeRose, Vincenzo Cardinale, Rossella Semeraro, Paolo Onori, Chiara Napoletano, Antonio Franchitto, Alfredo Cantafora, Gian Luca Grazi, Eugenio Gaudio, Domenico Alvaro Background: Oval cells are adult liver progenitor cells whose role in hepatocarcinogenesis remains obscure. Wnt/β-catenin, reported MCE公司 to constitute a positive feedback loop with the differentiation monitor Bmi1,

contributes to hepatocarcinogenesis, while Notch 1 serves as its antagonizer. In this study, we tried to elucidate the multipotency of oval cells. Methods: Bmi1 was stably transfected into SD rat oval cells. The Bmi1 high oval cells were injected subcutaneously into Balb/c nude mice. The Bmi1 normal oval cells were used as control. Transplanted tumors were taken for pathological analysis and immunohisto-chemical assessment using monoclonal antibodies to CD34, AFP, CK18 and CK19. RT-PCR was applied to determine Wnt/β-catenin and Notch1 gene expression. Notch1 was silenced by siRNA. Tube formation assay was performed with Matrigel. Results: Bmi1high oval cells generated tumors in nude mice (9/14) and formed tube-like structures.

RT-PCR analysis showed that CK7 expression,

which was abs

RT-PCR analysis showed that CK7 expression,

which was absent in the beginning, first appeared around day 4, peaked on day 6, and then gradually declined and was undetectable in LDPCs by day 14. GGT first became detectable around day 6 and progressively increased in intensity, only to become undetectable in LDPCs on day 14 (Fig. 4A). IF DNA Damage inhibitor staining for these markers showed a very similar pattern to that seen with RT-PCR data, with the exception that some GGT protein expression was detectable in LDPCs on day 14. Oval-cell–specific protein OV-6, on the other hand, was first detected by IF staining on day 6 and reached a peak on day 8, after which it rapidly decreased, becoming virtually undetectable selleck chemicals llc in LDPCs (Fig. 4B). The expression pattern of these markers correlated well with the morphological changes we observed in culture. Oval cell markers were up-regulated as hepatocytes were in the process of transforming into progressively smaller cells and down-regulated as the LDPCs became the dominant cell type. To demonstrate that these changes took place in the same cell population, we performed costaining for oval cell marker OV-6 and LDPC markers CD45 and LMO2, and found that on day 8, most of

the cells coexpressed oval cell and LDPC markers (Fig. 4C). Taken together, these data strongly suggested that hepatocytes passed through an oval cell-like stage en route to becoming LDPCs. To provide additional evidence for the origin of LDPCs from hepatocytes in culture, we generated a double-transgenic mouse strain by crossing AlbCre and Rosa26 mouse strains. As predicted, the resulting AlbCreXRosa26 mice expressed the enzyme, β-galactosidase, only in the liver

by western blot analysis (Fig. 5A). The hepatocyte-specific expression of this medchemexpress marker, which labeled albumin-expressing cells permanently, was confirmed by X-gal staining and IF staining for β-galactosidase. Results showed that expression of the reporter construct was restricted to hepatocytes (Fig. 5B). The next step was to examine LDPCs generated from AlbCreXRosa26 mice for β-galactosidase expression. LDPC cultures of hepatocytes from double-transgenic mice were subjected to X-gal staining at various time points, which strongly suggested hepatocytes as the source of LDPCs (Fig. 6A). To ensure that the small, round cells that appeared in the cultures were LDPCs, we performed costaining for β-galactosidase and LDPC markers CD45 and LMO2. Virtually all cells coexpressed β-galactosidase and LDPC markers, thus confirming the identity of the mouse hepatocyte-derived LDPCs (Fig. 6B). To underscrore the biological relevance of LDPCs, we performed a transplantation experiment using rat LDPCs generated from male Fischer344 rats. We did a flow cytometric analysis of the harvested LDPCs using CD45 as a marker of LDPC purity, which was >97% (Supporting Fig. 4A).

Genotyping was performed with the Infinium HumanHap 550K chip Al

Genotyping was performed with the Infinium HumanHap 550K chip. All SNPs were in Hardy-Weinberg equilibrium. Linear regression models were used to assess associations, adjusting for age, sex, steatosis, ALT, type

of elastography probe, HOMA-IR, spleen size, presence of viral hepatitis and alcohol intake, using additive genetic models. Results: In 1037 participants (age 74.1±5.6 years; 50.7% males) reliable LSM and genetic data were obtained. Median LSM was 5.1 kPa (IQR 4.2-6.4). NAFLD was detected in 331 participants (31.9%). Two SNPs in the IFNGR2 gene, rs9976971 and rs2284553, were associated with LSM in the total cohort (p=0.018 and 0.011 respectively). This relationship remained selleck chemical significant in a multivariable model (p=0.043 and 0.010 respectively). A third polymorphism in the IFNGR2 gene, rs9808753, showed a trend towards significance in a multivariable model (p=0.08). In participants with NAFLD all three IFNGR2 SNPs were significantly associated with LSM (p=0.046; 0.044 and 0.003 respectively). In a multivariable model this relationship remained significant for rs9808753 (p=0.010). rs738409, rs12980275 and rs8099917, in the PNPLA3 and near the IL28B gene, were not associated with LSM in the total cohort, nor in participants

with NAFLD (all p-values >0.17). Conclusions: Two IFNGR2 SNPs GDC-0068 in vitro were associated with liver stiffness in this large population based cohort. In a subgroup of participants with NAFLD all three tested IFNGR2 variants showed an association with LSM. PNPLA3 and IL28B variants were not related to liver stiffness in the total cohort, nor in participants with NAFLD. These results suggest that IFNGR2 variants could not only

MCE公司 play a role in liver fibrogenesis in risk populations, but in the general population as well. Disclosures: Harry L. Janssen – Consulting: Abbott, Bristol Myers Squibb, Debio, Gilead Sciences, Merck, Medtronic, Novartis, Roche, Santaris; Grant/Research Support: Anadys, Bristol Myers Squibb, Gilead Sciences, Innogenetics, Kirin, Merck, Medtronic, Novartis, Roche, Santaris The following people have nothing to disclose: Elisabeth P. Plompen, Jeoffrey Schouten, Daan W. Loth, Bettina E. Hansen, Albert Hofman, Andre G. Uitterlinden, Bruno H. Stricker, Frank W. Leebeek Background: The response to chronic liver injury in hepatitis C (HCV) is fibrogenesis, which is characterized by the accumulation and reorganization of extracellular matrix. This extensive remodeling generates protein fragments originating from fibro-genesis or fibrosis resolution. These fragments may reflect the degree of fibrosis and/or the turnover of fibrotic processes and potentially serve as biomarkers that carry diagnostic and prognostic information. Aims: We aimed to evaluate the diagnostic and prognostic performance of two different sub-pools of type III collagen: Pro-C3, a cleavage specific formation biomarker and C3M, a biomarker for a MMP generated fragment.

Data were correlated with age, gender, symptoms and presence of c

Data were correlated with age, gender, symptoms and presence of concomitant colonic polyps. Results: Out of 8715

patients, 1043 (11.968%) had colonic diverticulosis (508 or 48.706% were females, 535 or 51.294% were males). There were 482 (46.2%) who had right sided diverticulosis, 308 (29.53%) had left sided, and 253 (24.257%) had bilateral disease. Most patients were in their 6th and 7th decades of life. Moreover, 45.254% of patients with colonic diverticulosis had concomitant colonic polyp. Conclusion: Among patients who underwent colonoscopy at Chinese General Medical Center from 2008 to 2012, 11.968% were found to have diverticulosis. Our study also showed a higher incidence of right sided disease, as well as correlation of colonic polyps with diverticular disease. Key Word(s): 1. diverticulosis; 2. Asia; 3. right sided; BGB324 4. colonic polyps; Table 1 Demographics, 2008–2012 Location Diverticulosis (n) Female (n) Male (n) B-Raf mutation Average Age Age Range Right 46.2% (482) 45.4% (219) 54.6% (263) 58 25–90 Left 29.5% (308) 48.7%(150) 51.3% (158) 70 28–92 Bilateral 24.3% (253) 54.9% (139) 45.1% (114) 65 41–89 All 100.0% (1043) 48.7% (508) 51.3% (535) 64 25–92 Presenting Author: MICHAL TICHY Additional Authors: JIRI STEHLIK, JIRI LASTUVKA, PETER KRISKA, VERA POKLUDOVA, DANIEL ADAMEK, PAVEL REITERER Corresponding Author: MICHAL TICHY Affiliations:

Krajska zdravotni, a.s.; Amedea, s.r.o.; VZP – pobocka Usti nad Labem Objective: Pneumatosis (cystoides) Intestinalis (PCI) is a relatively rare disorder. It is often incidental finding on the CT scan or colonoscopy. Only in minority of the cases the clinical symptoms are due to presence of PCI. The disorder is characterized by the presence of gas in the intestinal

wall or outside the wall. Pathogenesis is unclear. PCI is associated with numerous diseases. Chronic obstructive pulmonary disease (COPD) is one of them. Recommended MCE公司 treatment options are antibiotics, surgical treatment or hyperbaric oxygen therapy which is considered treatment of the first choice by more authors. Methods: Colonoscopy was performed in a 64-yers old woman presenting with abdominal pain and change in bowel habits. Colorectal cancer had been suspected. Total colonoscopy was done and 20 cm long segment in the left side colon with typical endoscopy PCI image was detected (figure 1). Lumen was partially obstructed. Subsequent CT scan confirmed the finding. There were no laboratory abnormalities. The patient had a history of a stroke years ago. Currently she was treated only for arterial hypertension and COPD. Hyperbaric oxygen treatment was started – 2 atmospheres/hour in 2 cycles with 15 sessions. Endoscopy after 3 months has shown significant regression. So did the CT scan. Pneumology consultation was performed and moderate COPD confirmed.After another 3 months CT scan showed relaps of PCI. Third cycle of hyperbaric oxygen therapy was started.

Nonetheless, it provides an important step forward in addressing

Nonetheless, it provides an important step forward in addressing this potentially important issue in a large, well-characterized cohort of patients and will hopefully Saracatinib order engender additional interest and research in this area. Taken together, the results from both studies also highlight the insensitivity of current highly sensitive methods of serum HBV DNA testing for the detection of OBI and the importance

of studies of HBV infection and replication in liver tissue samples for understanding the true prevalence and clinical relevance of OBI. In conclusion, to achieve a clear understanding of the role of OBI in LDE225 order the development of chronic liver disease and HCC, robust answers to the following research questions are needed. Is there a difference between OBI detected in low-prevalence versus high-prevalence HBV endemic regions? Do the samples and methods used for detecting OBI have adequate

sensitivity, specificity, and precision? Are the study designs free from unintended bias? Additional cohort, case-control, and population-based studies should shed additional light on the role of OBI in development of HCC in chronic HCV patients and those with cryptogenic liver disease and are urgently needed. These investigations will hopefully determine whether OBI is truly a significant, important

risk factor for advanced liver disease and HCC and what interventions, if any, are needed to mitigate medchemexpress this risk. “
“Fasudil, a Rho-kinase inhibitor, has been shown to reduce portal venous pressure in cirrhotic rats. However, its effects on portal and systemic hemodynamics have not been investigated in cirrhotic patients with portal hypertension. The aim of this study was to assess the effects of fasudil on the portal and systemic hemodynamics of cirrhotic patients with portal hypertension. Twenty-three patients with cirrhosis and portal hypertension were studied. Systemic and portal hemodynamics were measured prior to and 50 min after the initiation of intravenous administration of 30 mg fasudil (n = 15) or placebo (n = 8). After fasudil, there were significant decreases in both mean arterial pressure (P < 0.05) and systemic vascular resistance (P < 0.05), whereas the heart rate increased significantly (P < 0.05). There was a significant decrease in the hepatic venous pressure gradient (P < 0.05). Portal vascular resistance also decreased significantly (P < 0.01). Placebo caused no significant effects. There were no symptomatic reactions caused by changes in the mean arterial pressure or heart rate after fasudil.

32 Our current findings would suggest Oatp1b2 is an important reg

32 Our current findings would suggest Oatp1b2 is an important regulator of hepatic TH activity, and its absence results in the dysregulation of cholesterol homeostasis as a result of reduced TR-mediated expression of Cyp7a1. Down-regulation of Cyp7a1 in Slco1b2−/− mice has also been recently reported by Csanaky et al.,12 although in their study Slco1b2−/− mice exhibited higher serum BA levels. It is possible the marked age difference between the mice in that study relative to those reported here could be one explanation for the observed differences in BA levels. Indeed, developmental effects on BA pool

size in rodents AZD8055 has been reported.33 Similarly, the involvement of THs in regulation of glucose homeostasis has been widely appreciated for many decades. The understanding of TH effects has been supported by in vitro analysis,34 and there has been characterization of knockout mouse models linking THs to induction of hepatic gluconeogenic enzymes such as PEPCK and glucose 6-phosphatase, along with reduced insulin half-life

and sensitivity.35-37 Our findings in Oatp1b2-transporter–deficient mice support the linkage of hepatic TH status to glucose homeostasis resulting from reduced hepatic glucose uptake and gluconeogenesis. Dysregulation of Glut2 seems to be a major factor in TR regulation of glucose homeostasis. Indeed, Navitoclax it is becoming evident that glucose itself can function as a regulator of glycolysis.17 This mechanism of action appears to depend on the equilibration of glucose across the plasma membrane through glucose transporters.38Glut2−/− mice exhibit a diabetes phenotype characterized by hyperglycemia, relative hypoinsulinemia and high-circulating free fatty acids.39 This

phenotype results from impaired glucose-stimulated insulin secretion in 上海皓元医药股份有限公司 pancreatic β-islet cells.40 In Glut2-null mice, a marked increase in hepatic glycogen content was also noted. This appears to result from elevated cytosolic glucose concentrations due to the loss of Glut2-mediated cellular efflux.41 In humans, loss of function mutations in GLUT2 have been linked to Fanconi-Bickel syndrome, a rare autosomal recessive disorder in which one hallmark feature is hepatomegaly secondary to liver glycogen accumulation.42 Therefore, the mechanism by which L-thyroxine treatment results in significantly reduced hepatic glycogen content43 is likely in part mediated by induction of Glut2 expression. Interestingly, liver-specific reconstitution of Glut2 revealed that this transporter is responsible for the observed metabolic abnormalities noted in Glut2−/− hepatocytes.41 Consistent with our data suggesting Oatp1b2-dependent TR-mediated activation of Glut2, expression of GLUT2 in human liver has been noted to be modulated by THs.

5%) The YY1 mRNA positive rate of 40 tissues with esophageal squ

5%). The YY1 mRNA positive rate of 40 tissues with esophageal squamous cell carcinoma was 50% (20/40). The YY1 mRNA positive rate of 40 patients with esophageal squamous cell carcinoma in peripheral blood was 47.5% (19/40). With the increasing degree of malignancy and disease progression,

the positive rate rised gradually (P < 0.05). EPZ6438 Conclusion: The specific high expression of YY1 mRNA both in tissue and peripheral blood of patients with esophageal squamous cell carcinoma in Xinjiang Kazak. Which is closely relate to the incidence, development of esophageal cancer. YY1 mRNA is a good marker for micro-metastasis of esophageal cancer. It is expected to become a molecular markers of the census and screening with esophageal cancer in a high incidence. Key Word(s): 1. YY1 mRNA; 2. Kazakh; 3. micrometastases; 4. RT-PCR; Presenting Author: DONASUBANI JAYATUNGE Additional Authors: CHANDIKA LIYANAGE, N NAWARATNE Corresponding Author: DONASUBANI JAYATUNGE Affiliations: MBBS; MBBS, MS, MRCS. MPhil; MBBS, MS, MRCP Objective: Duodenal diveticuli are commonly found in the 2nd part of duodenum and majority are Juxta-papillary duodenal divericuli (JDPP) which are diverticuli

located within a radius of 2 cm from the ampulla. These JDPP are implicated in biliary stone formation. Alvelestat molecular weight This study analyses prevalence and disease pattern of JDPP in the Sri Lankan population. Methods: 640 consecutive patients who underwent ERCP at the National Hospital Sri Lanka from January 2011 to April 2013 were included in this study. The demographic data of individual with doudenal

diverticuli, the types of JPDD, its association with billiary stones and other pancreatobilliary disease were analysed. Results: 64 medchemexpress (10%) out of 640 patient had duodenal diverticuli (DD). The median age of presentation was 61 years (14–86) with female predominance [64% (n = 41)]. 91% (58) of DD were JPDD (8/58 were type 1, 16/58 were type 2 and 34/58 were type 3). Majority (63%) of the DD were associated with billiary stones and overall dilatation of the CBD was seen in 70% of the cases. 5 individuals had dilated CBD caused by the diverticula itself without obstruction from stones. When comparing data between the group with JPDD and without JPDD there was significant association between gender [female predominance (p = 0.002)], age [more in elderly population (p < 0.001) and billiary stone formation (p < 0.001). Conclusion: 10% of patients undergoing ERCP have duodenal diverticuli and there is significant association between JPDD and billiary stone formation. Key Word(s): 1. diverticuli; 2. billiary stones; 3. common bile duct; 4.

H pylori expressing high Trx1 significantly induced cell apoptos

H. pylori expressing high Trx1 significantly induced cell apoptosis, decreased the expression of cyclin D1 and up-regulated p21 in GES-1. However, in BGC823, it increased cell proliferation, and up-regulated cyclin D1. These imply

that the effects of H. pylori were different in the developing stages of gastric cancer. In vivo, we found that H. pylori expressing high Trx1 was much more high pathogenic. Mongolian gerbils were infected by H. pylori expressing high Trx1 for 91 weeks, resulting selleck screening library in significantly more serious pathological changes in the gastric mucosa, including gastric cancer and atypical hyperplasia. Conclusion: High Trx1 expression in H. pylori is associated with gastric carcinogenesis. In H. pylori, Trx1 likely participates in learn more the pathogenesis of gastric cancer and might be a novel risk marker for highly toxic H. pylori. Key Word(s): 1. Helicobacter pylori; 2. gastric cancer; 3. thioredoxin; Presenting Author: YANYAN SHI Additional Authors: MO CHEN, LINNA LIU, JING ZHANG, YE WANG, SHIGANG DING Corresponding Author: SHIGANG DING Affiliations: Peking University Third Hospital Objective: Helicobacter pylori (H. pylori) maintains long-term persistence in the host and combats oxidative stress via diverse antioxidant proteins, which are expected to be relevant to bacterial-associated diseases. The antioxidant system

in H. pylori is complex and has not been clear. We aim to investigate the expression of three essential antioxidants in H. pylori isolated from patients of different clinical outcomes. Methods: Forty H. pylori strains were isolated from endoscopic biopsy specimens of gastric mucosa from ten patients displaying gastric cancer, twelve patients displaying peptic ulcer, and eleven patients displaying gastritis. After RNA isolation and reverse transcription, the expressions of arginase (RocF), alkyl hydroperoxide reductase (AhpC) and thioredoxin 1 (Trx1) in H. pylori medchemexpress were

measured by real-time PCR. Comparisons between multiple sample sets were analyzed using a one-way ANOVA test. Pearson’s correlation test was used to assess relationships between multiple continuous variables. Results: RocF expression of H. pylori in gastric cancer tissues was higher than gastritis (P < 0.05). Trx1 expression of H. pylori in gastric cancer (P < 0.05) and peptic ulcer (P < 0.05) tissues was higher than gastritis. The expressions of RocF and Trx1 had positive correlation (r = 0.411, P < 0.05). These indicated that RocF and Trx1 might be related with each other and involved in gastric carcinogenesis. However, we did not find any difference of AhpC expression in different clinical outcomes and any correlation with other two genes. Conclusion: Trx1 and RocF expressions of H. pylori in clinical gastric cancer tissues were higher than in tissues with gastritis. In H. pylori, the members of antioxidant system likely correlate with each other and are relevant to gastric cancer. Key Word(s): 1.