The inflammation and Lapatinib clinical trial fibrosis score of each group: The score of blank group is lower than other experimental groups and has statistical significance (P < 0.05); TNBS group and MSODN I, II, III group have no statistical significance (P > 0.05); The scores of Decoy ODN I, II, III group are lower than TNBS group, MSODN I, II, III group and have statistical significance (P < 0.05); Decoy ODN I, II, III group have statistical significance among three groups (P < 0.05). 3. The expression level of IL-1β, TNF-α, Col-IIIα mRNA: Three mRNA expression level of blank group are lower than other experimental groups and

have statistical significance (P < 0.05); TNBS group and MSODN I, II, III group have no statistical significance (P > 0.05); Three mRNA expression level of Decoy ODN

I, II, III group are lower than TNBS group, MSODN I, II, III group and have statistical significance (P < 0.05); Decoy ODN I, II, III group have statistical significance among three groups (P < 0.05). 4. The protein expression change of NF-κB, TGF-β1: The NF-κB, Pexidartinib molecular weight TGF-β1 protein expression of blank group are lower than other experimental groups and have statistical significance (P < 0.05); TNBS group and MSODN I, II, III group have no statistical significance (P > 0.05);: The NF-κB, TGF-β1 protein expression of Decoy ODN I, II, III group are lower than TNBS group, MSODN I, II, III group and have statistical significance (P < 0.05); Decoy ODN I, II, III group have statistical significance among three groups (P < 0.05). Conclusion: 1. It confirms that medchemexpress TNBS/EtOH enema can induce the chronic intestinal fibrosis of mice by observing the disease activity index, colonic general observation, pathology and fibrosis of each group. 2. NF-κB Decoy ODN treat for 6 weeks is most significantly which can reduce intestinal inflammation and fibrosis in mice, NF-κB MSODN has no effective treatment. 3. The mechanism of NF-κB Decoy ODN for reducing intestinal inflammation and

fibrosis is to decrease the mRNA expression level of IL-1β, TNF-α, Col-IIIα and the protein expression of NF-κB, TGF-β1. NF-κB Decoy ODN can be a new effective drug for IBD therapy. Key Word(s): 1. IBD; 2. TNBS; 3. intestinal fibrosis; 4. NF-κB Decoy ODN; Presenting Author: JIANMEI YANG Additional Authors: XIAOJING LIU, YU FU, KAIFANG ZOU Corresponding Author: KAIFANG ZOU Affiliations: Huazhong University of Science and Technology; Union Hospital, Tongji Medical Collage, Huazhong University of Science and Technology Objective: Tfh cell plays an important role in humoral immunity. This study aimd at investigating the changes of Tfh cell numbers, plasma cell numbers and the titers of autoantibody in immune-complex induced colitis. Methods: Twelve male BALB/C mice were randomly divided into two groups: control group and model group.

Nevertheless, it is important to notice RAD001 that the aforementioned metabolic alterations presumably depend on, at least partly, different molecular mechanisms in preneoplastic and neoplastic rat liver lesions. Indeed, these metabolic changes can be easily explained for the preneoplastic foci, which are confined to the anatomic borders of the liver acinus and drain hyperinsulinemic blood from islet grafts. In HCC, however, the often scattered islet graft remnants can only be partly responsible for these metabolic alterations, although they can be regularly demonstrated

within tumors.21 Although the intralesional insulin concentration cannot be measured, it can be assumed that the former hyperinsulinemia, induced by the islet grafts, is significantly diminished within HCC. Thus, the metabolic alterations detected in the tumors cannot exclusively be explained as a consequence of increased insulin signaling. Previous

findings indicate that the IR is overexpressed in rat HCC, but not in preneoplastic foci.23 The latter finding might suggest that elevated levels of IR might provide a higher sensitivity for insulin signaling in HCC, despite the absence of elevated insulin levels. In the present study, we INCB024360 order show that suppression of the AKT inhibitors, TRB3, PHLPP1, and PHLPP2, and up-regulation of AKT and its upstream inducers, PIK3CA and PIK3CB, occur exclusively in rat HCC. These alterations, together with the peculiar up-regulation of the ACAC stabilizer, AKR1B10, in HCC, indicate the 上海皓元医药股份有限公司 existence in rat liver tumors of a complex genetic program leading to the perpetuation of the molecular mechanism that is solely dependent on insulin signaling in the preneoplastic foci. Additional molecular mechanisms might contribute to metabolic alterations in rat HCC and are currently under investigation. At the molecular level, in accord with

recent studies,29, 37, 38 we show that AKT signaling exerts its effects on metabolism through mTORC1-dependent and -independent mechanisms (Fig. 7). Under insulin growth-promoting stimuli, selective inhibition of mTORC1 by rapamycin triggered a significant decrease in glycolysis, a less pronounced reduction of lipogenesis, and no effect on both gluconeogenesis and some lipogenesis-related proteins (e.g., AKR1B10, USP2a, PRKCλ/ι, chREBP, AMPKα2, and INSIG2) in HCC cell lines. On the other hand, use of either the AKT1/2 inhibitor or concomitant suppression of PI3K and mTOR promoted a much stronger growth restraint, a more pronounced fall in lipid biosynthesis, and reactivation of gluconeogenesis in HCC cells supplemented with insulin. Besides their pathogenetic significance, the present results support the use of PI3K/mTOR and mTORC1/2 dual inhibitors, rather than mTORC1 single inhibitors, in the treatment of HCC with activated AKT.

Daly, Lucy Golden-Mason, Christopher P. Day Parallel 33: Experimental Cholestasis Tuesday, November 5 11:15 AM -12:45 PM mTOR inhibitor Room 152A MODERATORS: Jorge A. Bezerra, MD Cara Mack, MD 11:15 AM 223: SC-435, an Inhibitor of ASBT, Improves Liver Function in a Rat Partial Bile Duct Ligation Model of Cholestasis Bradley T. Keller, Svetlana Nikoulina, Nicolaus Nazarenkov, Bronislava Gedulin 11:30 AM 224: Nod2 deficiency protects mice from cholestatic liver disease by increasing renal excretion of bile acids Lirui Wang, Phillipp Hartmann,

Michael Haimerl, Sai P. Bathena, Yazen Alnouti, Alan F. Hofmann, Bernd Schnabl 11:45 AM 225: NHERF-1 Knockout Mice Have Lower Hepatic ICAM-1 Expression and Are Protected from Liver Injury Induced by Bile Duct Ligation Man Li, Albert Mennone, Carol J. Soroka, Kathy M. Harry, Edward J. Weinman, James L. Boyer 12:00 PM 226: Novel therapeutic implications of modulating β-Catenin during intrahepatic cholestasis Kari Nejak-Bowen, Michael Thompson, Satdarshan (Paul) S. Monga 12:15 PM 227: Secretion of gonadotropin-releasing Dabrafenib chemical structure hormone (GnRH) by cholangiocytes stimulates biliary proliferation via autocrine/paracrine mechanisms Debolina Ray, Sharon DeMorrow, Fanyin Meng, Julie Venter, Heather L. Francis, Laura Hargrove, Kelly McDaniel, Syeda H. Afroze, Paolo

Onori, Eugenio Gaudio, Shannon S. Glaser, Gianfranco Alpini 12:30 PM 228: PPARα positively regulates human MDR3/ABCB4 transcription and increases 上海皓元 biliary phosphatidylcholine secretion Nisanne Ghonem, Meena Ananthanarayanan, Carol J. Soroka, James L. Boyer Parallel 34: Experimental Hepatocarcinogenesis Tuesday, November 5 11:15 AM -12:45 PM Room 146A MODERATORS:

Satdarshan (Paul) S. Monga, MD Lopa Mishra, MD 11:15 AM 229: The Contribution of Toll-Like Receptor Signaling to the Development of Hepatic Fibrosis and Carcinogenesis in Hepatocyte Specific TAK1 Deleted Mice Jingyi Song, Sayaka Inokuchi, Yoonseok Roh, Ling Yang, Ekihiro Seki 11:30 AM 230: High Mobility Group Box 1(HMGB1) Triggers Progenitor Expansion and Hepatocarcinogenesis in the Chronically Injured Liver Peter Huebener, Pradere Jean-Philippe, Geum-Youn Gwak, Robert Schwabe 11:45 AM 231: Activated β-catenin and Yap Synergize to Promote Hepatoblastoma Formation in Mice Satdarshan (Paul) S. Monga, Lili Zhou, Kari Nejak-Bowen, Sarangarajan Ranganathan, Junyan Tao, DIego Calvisi, Xin Chen 12:00 PM 232: Novel Genetic Model of Cholangiocarcinoma in Mice Nataliya Razumilava, Daisaku Yamada, Steven Bronk, Jun Li, Jorge A. Bezerra, Xin Chen, Gregory J. Gores 12:15 PM 233: Genomics-based directions for targeted therapy in cholangiocarcinoma Jesper B. Andersen, Valentina M. Factor, Snorri S. Thorgeirsson 12:30 PM 234: SYK(L) and its splicing variant SYK(S) exert opposing roles in hepatocellular carcinoma Jian Hong, Yunfei Yuan, Jianping Wang, Yadi Liao, Ruhai Zou, Chuanlong Zhu, Binkui Li, Yi Liang, Pinzhu Huang, Wenyu Lin, Jia Le Dai, Raymond T.

Objective: Assess the feasibility, safety and risks of EUS-BD with intra-hepatic Alectinib datasheet biliary access and anterograde interventions using an algorithm to increase flexibility of interventions, limit adverse events and improve procedural time. Design: Prospective observational cohort study Patients: 23 consecutive patients underwent EUS-BD drainage for

failed ERCP. Main Outcome Measures: Technical and clinical success rates with adverse event rate using simplified algorithm. Results: Patient recruitment from June 2011-Feb 2014; mean age of 68.6 years, predominantly male (65.2%) with pancreatic cancer (52.4%), cholangiocarcinoma (17.4%), other malignant biliary obstruction (8.7%) and benign biliary obstruction (21.7%). Prior interventions included failed ERCP in 20/23 (87%) while 3/21 (13%) had

primary EUS-BD. Anterograde cholangiogram was achieved in all patients. Technical success was achieved in 22/23 (95.7%) with clinical success was achieved in 21/23 (91.3%). Placement of access wire was across the ampulla in 11/22 (50%) and into CBD or contra-lateral IHD in 11/22 (50%). Tract dilatation was accomplished in 18/22 (81.8%) but required completion using intra-hepatic needle knife in 3/22 (13.6%). Anterograde interventions were performed in 17/22 (77.3%) but crossover to rendezvous in 4/22 (18.2%) or choledochoduodenostomy 1/22 (4.5%). Three patients 3/23 (13%) also had endoscopic duodenal SEMS placement to relieve duodenal obstruction. Two patients (8.7%) had post-procedural bile leak and pain. Conclusion: EUS-guided anterograde biliary drainage CAL-101 chemical structure using the intra-hepatic access route has high technical and clinical success with low adverse rate. We would

promote a simplified standardized algorithm, which gives flexibility of direct anterograde interventions. G PUTT, A BLUETT, L IRVING, A IRETON Waikato Hospital Introduction: Pancreatic cancer and chronic pancreatitis are associated with severe pain requiring high dose narcotic analgesia. Endoscopic ultrasound (EUS)-guided coeliac plexus block (CB) or neurolysis (CPN) improves pain control and side effects of analgesia. We describe our initial 3-year experience, outcomes and adverse events. Methods: Retrospective analysis of 74 cases of EUS-guided CB/CPN performed between June 2011–May 2014 for MCE patients with chronic pancreatitis or pancreatic cancer. Coeliac axis and related structures were identified under EUS-guidance and confirmed on Doppler ultrasound. A standard 22G EUS needle was used to perform CB by injection of 20 ml 0.5% bupivacaine, while CPN involved injection of 20 ml 1:1 dilution of 0.5% bupivacaine and absolute alcohol. Pain scores were recorded prior to procedure and at one week, along with adverse events. Procedures were performed under conscious sedation or propofol-assisted anaesthesia when part of combined FNA or ERCP procedure.

However, there is little evidence for a clear dose-response relationship, and great heterogeneity of findings. We argue that dopaminergic state PARP inhibitor on its own

is an insufficient explanation, and suggest instead that there is now substantial evidence that both apathy and impulsivity are in fact multi-dimensional syndromes, with separate, dissociable mechanisms underlying their ‘surface’ manifestations. Some of these mechanisms might be dopamine-dependent. According to this view, individuals diagnosed as impulsive or apathetic may have very different mechanisms underlying their clinical states. We propose that impulsivity and apathy can arise from dissociable deficits in option generation, option selection, action initiation or inhibition and learning. Review of the behavioural A-769662 and neurobiological evidence

leads us to a new conceptual framework that might help understand the variety of functional deficits seen in PD. “
“Cognitive impairment occurs frequently in Parkinson’s disease (PD) and the concept of Mild Cognitive Impairment in PD (PD-MCI) has recently emerged. Patients with mild impairment are at risk of developing dementia, and thus it is a topic of growing interest. Many previous studies have investigated the neural correlates of cognitive impairment, in particular executive dysfunction, in PD patients without dementia using neuroimaging techniques including structural MRI, functional MRI and PET imaging. These studies, which have provided a foundation for understanding which brain regions and neurotransmitter systems may be involved in executive dysfunction in PD, will be reviewed. Recent neuroimaging studies that have used specific criteria to classify patients as PD-MCI, in the hopes of gaining further insight into the underlying neural mechanisms will also be discussed. In particular, this review will cover key findings

involving structural MRI investigating grey and white matter changes, functional MRI to examine changes in neural activation and PET imaging MCE公司 to investigate metabolic and neurochemical changes that have led to an improved understanding of pathology associated with executive dysfunction in PD without dementia and PD-MCI. “
“People with Parkinson’s disease (PD) exhibit slowed movements and difficulty in initiating movements. This review addresses the issue of whether or not cognitive representations of actions in PD are affected, alongside these motor problems. In healthy people, the motor system can be involved in tasks such as observing a graspable object or another person’s action, or imagining and naming actions, in the absence of overt movement. As described in this review, the fact that the slowed real movements exhibited by PD patients are coupled with slower motor imagery and verb processing provides additional evidence for the involvement of the motor system in these processes.

However, there is little evidence for a clear dose-response relationship, and great heterogeneity of findings. We argue that dopaminergic state Selleckchem PF-6463922 on its own

is an insufficient explanation, and suggest instead that there is now substantial evidence that both apathy and impulsivity are in fact multi-dimensional syndromes, with separate, dissociable mechanisms underlying their ‘surface’ manifestations. Some of these mechanisms might be dopamine-dependent. According to this view, individuals diagnosed as impulsive or apathetic may have very different mechanisms underlying their clinical states. We propose that impulsivity and apathy can arise from dissociable deficits in option generation, option selection, action initiation or inhibition and learning. Review of the behavioural selleck compound and neurobiological evidence

leads us to a new conceptual framework that might help understand the variety of functional deficits seen in PD. “
“Cognitive impairment occurs frequently in Parkinson’s disease (PD) and the concept of Mild Cognitive Impairment in PD (PD-MCI) has recently emerged. Patients with mild impairment are at risk of developing dementia, and thus it is a topic of growing interest. Many previous studies have investigated the neural correlates of cognitive impairment, in particular executive dysfunction, in PD patients without dementia using neuroimaging techniques including structural MRI, functional MRI and PET imaging. These studies, which have provided a foundation for understanding which brain regions and neurotransmitter systems may be involved in executive dysfunction in PD, will be reviewed. Recent neuroimaging studies that have used specific criteria to classify patients as PD-MCI, in the hopes of gaining further insight into the underlying neural mechanisms will also be discussed. In particular, this review will cover key findings

involving structural MRI investigating grey and white matter changes, functional MRI to examine changes in neural activation and PET imaging medchemexpress to investigate metabolic and neurochemical changes that have led to an improved understanding of pathology associated with executive dysfunction in PD without dementia and PD-MCI. “
“People with Parkinson’s disease (PD) exhibit slowed movements and difficulty in initiating movements. This review addresses the issue of whether or not cognitive representations of actions in PD are affected, alongside these motor problems. In healthy people, the motor system can be involved in tasks such as observing a graspable object or another person’s action, or imagining and naming actions, in the absence of overt movement. As described in this review, the fact that the slowed real movements exhibited by PD patients are coupled with slower motor imagery and verb processing provides additional evidence for the involvement of the motor system in these processes.

However, there is little evidence for a clear dose-response relationship, and great heterogeneity of findings. We argue that dopaminergic state find more on its own

is an insufficient explanation, and suggest instead that there is now substantial evidence that both apathy and impulsivity are in fact multi-dimensional syndromes, with separate, dissociable mechanisms underlying their ‘surface’ manifestations. Some of these mechanisms might be dopamine-dependent. According to this view, individuals diagnosed as impulsive or apathetic may have very different mechanisms underlying their clinical states. We propose that impulsivity and apathy can arise from dissociable deficits in option generation, option selection, action initiation or inhibition and learning. Review of the behavioural selleck compound and neurobiological evidence

leads us to a new conceptual framework that might help understand the variety of functional deficits seen in PD. “
“Cognitive impairment occurs frequently in Parkinson’s disease (PD) and the concept of Mild Cognitive Impairment in PD (PD-MCI) has recently emerged. Patients with mild impairment are at risk of developing dementia, and thus it is a topic of growing interest. Many previous studies have investigated the neural correlates of cognitive impairment, in particular executive dysfunction, in PD patients without dementia using neuroimaging techniques including structural MRI, functional MRI and PET imaging. These studies, which have provided a foundation for understanding which brain regions and neurotransmitter systems may be involved in executive dysfunction in PD, will be reviewed. Recent neuroimaging studies that have used specific criteria to classify patients as PD-MCI, in the hopes of gaining further insight into the underlying neural mechanisms will also be discussed. In particular, this review will cover key findings

involving structural MRI investigating grey and white matter changes, functional MRI to examine changes in neural activation and PET imaging 上海皓元医药股份有限公司 to investigate metabolic and neurochemical changes that have led to an improved understanding of pathology associated with executive dysfunction in PD without dementia and PD-MCI. “
“People with Parkinson’s disease (PD) exhibit slowed movements and difficulty in initiating movements. This review addresses the issue of whether or not cognitive representations of actions in PD are affected, alongside these motor problems. In healthy people, the motor system can be involved in tasks such as observing a graspable object or another person’s action, or imagining and naming actions, in the absence of overt movement. As described in this review, the fact that the slowed real movements exhibited by PD patients are coupled with slower motor imagery and verb processing provides additional evidence for the involvement of the motor system in these processes.

Also, it appears that overproduction of ROS by the damaged mitochondria could play a salient role. Factors that may be involved in the precipitation of alcoholic hepatitis are briefly discussed later. Only about 2–10% of the absorbed alcohol KU-57788 order is eliminated via the lungs and kidneys; the remaining 90% is metabolized mainly by oxidative pathways in the liver and by nonoxidative pathways in extrahepatic tissues. Oxidative metabolism in the liver results in extensive displacement of the liver’s normal metabolic substrates, the production of acetaldehyde and ROS, and an increase in the NADH/NAD+ ratio (Fig. 2). The major pathway of oxidative metabolism of ethanol in the

liver involves multiple isoforms of cytosolic ADH, which results in the production of acetaldehyde. Accumulation of this highly reactive and toxic molecule contributes to liver damage. The oxidation of ethanol is accompanied by the reduction of NAD+ to NADH and, thereby, generates a highly selleckchem reduced cytosolic environment in hepatocytes. The cytochrome P450 isozymes, including CYP2E1, 1A2, and 3A4, which are predominantly localized to the ER, also contribute to ethanol’s oxidation to acetaldehyde in the liver. CYP2E1 is induced by chronic ethanol consumption and assumes an important role in metabolizing ethanol to acetaldehyde at elevated alcohol concentration. It also produces ROS, including hydroxyethyl, superoxide anion, and hydroxyl radicals.

Acetaldehyde, produced by ethanol oxidation, is rapidly metabolized mainly by mitochondrial ALDH2 to form acetate and NADH. Mitochondrial NADH is reoxidized by the electron transport chain (ETC). Most of the acetate resulting from ethanol metabolism escapes the liver to the blood and is eventually metabolized to CO2 by way of the tricarboxylic acid cycle in tissues such as heart, skeletal muscle, and brain, where mitochondria are

capable of converting acetate to the intermediate acetyl coenzyme A. a)  Acetaldehyde generation/adduct formation: if accumulated to high concentrations, acetaldehyde can form adducts with DNA and RNA, and decrease DNA repair. It also has the capacity to react with lysine residues on proteins including enzymes, microsomal proteins, microtubules, and affect their function. MCE Formation of protein adducts in hepatocytes may contribute to impaired protein secretion, resulting in hepatomegaly. In addition, acetaldehyde and malondialdehyde (a by-product of lipid peroxidation) can combine and react with lysine residues on proteins, giving rise to stable malondialdehyde-acetaldehyde-protein adducts that are immunogenic and, thus, can contribute to immune-mediated liver damage. Nitric oxide (NO), an RNS critical for hepatocyte biology, can interact with peroxides to generate peroxynitrite, which could be detrimental to the liver depending on the amount and duration. NO is produced by inducible nitric oxide synthase which is expressed in all liver cells (i.e.

CRP activates the complement pathway. It is a pattern recognition receptor with a pentameric polypeptide structure, which binds to a variety of intrinsic and extrinsic ligands. CRP’s highest affinity is towards phosphocholine residues. CRP is produced only in hepatocytes under the transcriptional control of interleukin-6 (IL-6).1 Circulating levels of CRP increase hundred-fold in response to infections and inflammation. Determination of CRP levels is one of the most solicited laboratory tests. The literature documents an increase

in CRP levels in cancer patients. High CRP levels INCB024360 datasheet may be of prognostic value since they are associated with poor survival. Among gastrointestinal tumors, esophageal,2 gastric,3 colorectal,4 and pancreatic cancers5 have reported this association. Mechanistically, high CRP levels are either a marker of reactive inflammation to a tumor or a marker of an ongoing inflammatory process that favored tumor development.

Tumors frequently show histological evidence of intratumoral and/or peritumoral inflammation. Necrotic cells release proinflammatory signals, which attract inflammatory cells from the surrounding tissue. This inflammatory response may foster the tumoral process rather than contain it. Inflammatory cells help to stimulate and to sustain angiogenesis and promote invasiveness by degrading the extracellular matrix. Inflammation is Midostaurin now recognized as an enabling characteristic of tumors.6 CRP has gained prognostic value in hepatocellular carcinoma (HCC). In a cohort of 90 HCC patients, Nagaoka et al.7 found that CRP levels above 3 mg/dL were predictive of poor prognosis and a decreased survival rate. In patients undergoing resection for HCC, MCE preoperative CRP levels correlated with tumor size and vascular invasion and were predictive of early recurrence.8 In the transplantation

setting, high preoperative CRP levels were related to tumor recurrence and poor overall survival; in those specific patients with HCC beyond Milan criteria, high CRP levels were an independent predictor of poor outcome.9 Finally, in a prospective evaluation of a cohort of 133 patients with newly diagnosed HCC, Kinoshita et al.10 reported that CRP levels above 1 mg/dL predicted a shorter survival and were characteristic of high Child-Pugh, CLIP, and JIS scores. In this issue of Hepatology, Peck-Radosavljevic and co-workers11 investigated the value of serum CRP levels in a large cohort of 615 HCC patients who were not amenable to surgery. The hazard ratio of death increased with CRP values up to 2.5 mg/dL, but not beyond. CRP levels above 1 mg/dL were significantly and independently associated with poor survival upon multivariate analysis in the discovery and in the validation cohorts. Patients with a CRP above 1 mg/dL at diagnosis had a survival of 4 months compared to 20 months for patients with a CRP below 1 mg/dL.

The

novel findings of this study help to dissect out the role of the complex cellular interactions BI 6727 nmr occurring in I/R, with the potential to develop therapeutic interventions to abrogate the sterile inflammatory response. The authors thank Nicole Hays and Junda Chen for their technical assistance in preparing this manuscript. Additional Supporting Information may be found in the online version of this article. “
“Background and Aims:  Non-steroidal anti-inflammatory drugs (NSAIDs) are among the most significant causative factors of gastroduodenal ulcers. Recent reports have demonstrated that NSAIDs can also frequently induce ulceration and erosions of the small intestine. The aim of this study was to examine whether or not roxatidine (an H2 receptor antagonist), which is known to increase gastric mucus in addition to inhibiting gastric acid, might suppress indomethacin-induced small intestinal mucosal injury, through an increase AZD6738 in mucus in rats. Methods:  Rats were given two p.o. doses of roxatidine, famotidine or cimetidine before and after the s.c. indomethacin injection. The injured area of the small intestine was analyzed. To examine effects of drugs on small intestinal mucus, rats were also given two p.o. doses of roxatidine, famotidine or cimetidine, and the ratio of the periodic

acid Schiff (PAS)-positive

area to the area of the mucosa in the small intestine was analyzed. In addition, we evaluated the involvement of nitric oxide (NO) and prostaglandins (PG) in the effect of roxatidine on small intestinal MCE mucus. Results:  Roxatidine significantly ameliorated indomethacin-induced small intestinal injury and increased the PAS-stained areas in the small intestinal mucosa, while cimetidine and famotidine had no significant effect. Pretreatment with N-nitro-L-arginine methyl ester but not with indomethacin, suppressed the effect of roxatidine on small intestinal mucus, suggesting that the effect is mediated by endogenous NO but not by PG. Conclusion:  Roxatidine suppressed indomethacin-induced small intestinal injury in rats. One possible mechanism is an increase of small intestinal mucus, mediated by NO. “
“Surgery remains an important treatment modality for many aspects of gastrointestinal cancer. In particular, it is the only definitive treatment for esophageal, gastric, and colorectal cancer, although the outcomes in esophegeal and gastric cancer remain modest. Recent developments in surgery for colorectal cancer, however, have resulted in improved outcomes, particularly with the introduction of mesorectal excision for rectal cancer. Surgery is also indicated for cancers of the liver, biliary tract, and pancreas.