[37] Results are expressed as means ± standard deviation or median (interquartile range; IQR) according to data distribution. Mean values were compared by analysis of variance and frequencies by chi-square test, according to data distribution, and differences mTOR inhibitor were considered significant when P ≤ 0.05 (two-tailed). Non-normally distributed variables were log-transformed before analysis. Our sample had >95% power of detecting an OR of 1.5 for steatosis, of the 148M PNPLA3 allele, with a significance of 5%. The

association between the PNPLA3 I148M polymorphism and steatosis (dependent variable) was evaluated by logistic regression analysis adjusted for confounding variables, which included those selected a priori for their biological relevance plus those that were found to be associated with the outcome of interest at univariate analysis (specified below). Analyses were carried out with JMP 9.0 statistical analysis software (SAS Institute Inc., Cary, NC). Clinical characteristics of CHB patients are summarized in Table 1. Most patients were HBeAg-negative men with normal body weight and no significant alcohol consumption. Mild steatosis (5%-33% of hepatocytes involved) was present in 146 (62%) patients, whereas severe steatosis (≥33% of hepatocytes) was present in 24 (10%) patients. Advanced fibrosis (METAVIR stage 3-4) was detected in 94 patients (40%). Variables significantly associated with steatosis severity are presented

in Table 2. As expected, severity of steatosis was significantly associated with older age, male sex, and higher BMI, whereas it was not significantly Staurosporine mw associated with regular consumption of any amount of alcohol. A higher prevalence of hyperglycemia was observed

in patients with mild steatosis, whereas TGs increased progressively with steatosis severity. There was also an increase in fibrosis stage associated with lower platelets in patients with steatosis. Oxalosuccinic acid Prevalence of the 148M PNPLA3 allele increased progressively with severity of steatosis (P = 0.020; Table 2). Clinical features of patients subdivided according to I148M PNPLA3 polymorphism are reported in Table 1. The 148M PNPLA3 allele was significantly associated with steatosis (P = 0.045), but, in particular, with severe steatosis (P = 0.005), whereas a trend was observed for association between the 148M allele and a NAS >2, consistent with the presence of steatohepatitis (P = 0.07). The 148M allele was not associated with fibrosis in the whole series of patients. There was a negative association between the 148M PNPLA3 allele and diabetes or impaired fasting glucose (IFG; P = 0.046) as well as between the 148M allele and HBeAg positivity (P = 0.046) and the precore mutation (P = 0.032). Independent predictors of steatosis, severe steatosis, and NAS >2 at multivariate logistic regression analysis are presented in Table 3. Steatosis of any degree was independently associated with older age (OR, 2.67; CI, 1.50-4.

[6] These hormones may partially be responsible for the catabolic response, because the administration of these hormones in normal human volunteers has been shown to reproduce many of the metabolic

alterations observed during critical illness.[34] Hyperglucagonemia was observed in patients with certain types of cancer.[35] Although stress hormones have clearly been shown to affect carbohydrate, lipid, and protein metabolism, the factors that Selleck INCB018424 cause net protein catabolism have yet to be identified; the catabolic changes in protein metabolism observed in stressed patients cannot precisely be reproduced by stress hormone infusion.[34] Aside from classical regulatory and counterregulatory Stem Cells antagonist hormones such as glucagon and catecholamines, inflammatory cytokines are independent factors that also affect substrate and protein metabolism.[36, 37] The evidence that the plasma concentration of tumor necrosis factor (TNF) is elevated in cancer patients also supports this theory,[38] although this evidence is still controversial. Therefore, it is reasonable to hypothesize that the changes in substrate metabolism in cancer patients are controlled by TNF. For example, TNF has been shown to cause cachexia,[39] which is similar to the conditions frequently observed in cancer patients. Furthermore, TNF

has also been shown to affect substrate and protein metabolism, causing

an increase in glucose production, glucose utilization, and essential amino acid oxidation, resulting in net protein catabolism.[37] However, TNF inhibits lipolysis and free fatty acid flux.[36, 37] Thus, TNF alone BCKDHA cannot account for all aspects of metabolic control, and other cytokines may contribute simultaneously to overall metabolic responses in stressed patients.[40] It has also been demonstrated that TNF causes changes in the hormonal milieu,[37, 41] causing an increase in plasma glucagon concentration in sublethal doses and increases in glucagon and catecholamine concentration in lethal doses.[41] Thus, alterations in substrate and protein metabolism seem to be controlled by complex mechanisms involving both classical regulatory and counterregulatory hormones and cytokines. Although the primary factors that control protein metabolism during critical illness have been identified,[33] a possible mediator and/or humoral factor that causes net protein catabolism during critical illness has not been identified. However, it has recently been demonstrated that cytokines are the substances that regulate substrate and protein metabolism.[37] Among the cytokines, TNF is the primary cytokine that plays a central role in the alteration in the overall systemic inflammatory response syndrome in critically ill patients.

No animals challenged with PH or CCl4 died before they were sacrificed at the indicated timepoints, regardless of

their genotypes. The ratio of liver weight / body weight (LW/BW) was calculated to demonstrate the regeneration of residual liver after PH. From 36 hours to 5 days after PH, the ratio of LW/BW was significantly lower in HDAC1/2-knockout mice. At 7 days all the livers were completely reconstituted, although some livers of the HDAC1/2-deficient mice appeared to weigh less (Fig. 2A). At 24 hours after CCl4 treatment, many hepatocytes that showed eosinophilic degeneration were visible around the portal areas. At 36 hours a similar degree of tissue MDV3100 order damage, characterized by massive periportal

necrosis, was observed in mice of all genotypes. At 72 hours the livers of the wild-type mice had almost completely recovered; Rucaparib cost however, the livers of the HDAC1/2-deficient mice, especially the Hdac1−/−,2−/− mice, were not completely repaired. The livers of these animals did not completely recover until 7 days after CCl4 injection (Fig. 2B,C). We assessed hepatocyte proliferation in the regenerating livers. Active hepatocyte mitosis emerged in the mice of all genotypes from 36 hours and reached a peak at 48 hours after PH or CCl4 injection. However, pathological mitotic figures, including multipolar division and from asymmetrical division, were observed substantially more frequently in the knockout mice, most notably in Hdac1−/−,2−/− mice, in which more than 10 defective mitotic figures were found per 1,000 hepatocytes (Fig. 3A,B). These

cells ruled out the possibility of dead cells for their prominent expression of phosphorylated histone H3 at Ser10 (p-H3S10), which appears specifically in M phase (Fig. 3C).[27, 28] We next counted the number of mitotic marker-positive cells at the indicated timepoints after PH or CCl4 treatment. No difference in the numbers of BrdU- or PCNA-positive cells was observed among the four genotypes (Supporting Figs. S1, S2). Surprisingly, however, Ki67, a mitotic marker normally expressed from mid-G1 phase to the end of mitosis, was decreased by ∼30%-70% in the Hdac1/2 knockout mice, especially in the Hdac1−/−,2−/− mice. Interestingly, a lack of Ki67 immunoreactivity, which was repeatedly confirmed with three different antibodies recognizing different epitopes of the Ki67 protein, was frequently observed in hepatocytes with abnormal mitosis (Fig. 3D,E; Supporting Fig. S3). Because HDAC1/2-knockout hepatocytes displayed similar BrdU uptake, we hypothesized that these hepatocytes would at least be able to enter the S phase of the cell cycle. We examined the expression of cell cycle markers in the regenerating livers after PH.

Methods: Male Sprague-Dawley rats were randomly allocated to 4 treatment groups (n = 10): water + water, indomethacin (8 mg/kg) + water, indomethacin + Olive Oil (OO) and indomethacin + EO. Rats were gavaged daily with water or oil from days 0–12 (0.5 ml) and water or indomethacin from days 5–12 (0.5 ml). Rats were euthanized on day 12 for intestinal tissue collection. Jejunal

and ileal samples (4 cm) were assessed for neutrophil infiltration indicative of acute inflammation using the colorimetric myeloperoxidase (MPO) assay (450 nm) expressed as units of MPO per gram of tissue (U/g). p < 0.05 was considered significant. Results: Jejunal MPO levels in indomethacin-treated rats were significantly greater compared with normal controls (208 ± 39 U/g and 62 ± 15 U/g, respectively; p < 0.01). Amongst indomethacin-treated groups, both OO (76 ± 21 U/g) and EO (76 ± 23 U/g) significantly BGB324 in vivo reduced levels of acute jejunal inflammation by 28% and 30% respectively, compared with indomethacin controls (p < 0.01). In the ileum, MPO levels were significantly greater in indomethacin-treated rats compared with normal controls (345 ± 40 U/g and 170 ± 29 U/g, respectively; p < 0.01). However, only EO (174 ± 28 U/g; p < 0.05), but not OO (285 ± 45 U/g; p > 0.05), significantly

reduced ileal MPO levels by 50% in indomethacin-treated rats, compared to the indomethacin control. Conclusions: Emu Oil reduced MPO levels Dasatinib purchase in the jejunum and ileum of rats with NSAID-induced enteropathy, indicative of decreased acute inflammation. This further suggests the therapeutic potential of Emu Oil to alleviate gastrointestinal symptoms associated with NSAID usage. AM FERGUSON,1 EG QUINN,1 J ROBERTS,2 C ROGGE,2 TW LEE2 1Department of Nutrition and Dietetics,

ISLHD, Wollongong, Australia, 2Department of Gastroenterology, ISLHD, Wollongong, BCKDHA Australia Introduction: Body composition and dietary behaviour changes occur in patients with IBD and when compared to healthy controls, consume altered macro and micronutrients. Blood tests alone cannot determine nutritional status; instead, several aspects including anthropometry and weight loss, dietary intake and nutrition assessment tools can establish existence of malnutrition. The aim was to examine risk and rates of malnutrition and weight loss in patients with IBD attending an outpatient clinic. Method: The clinic consisted of 2 gastroenterologists, an IBD nurse and a dietitian. All patients were prospectively screened for malnutrition using short nutrition assessment questionnaire (SNAQ) tool1 and referred to the dietitian if deemed at risk. Patients could also self refer or be identified by gastroenterologists to have nutritional concerns. Data collected over 6 months on anthropometry, usual and previous dietary intake and nutrition assessment score using subjective global assessment (SGA) tool2.

Methods: Male Sprague-Dawley rats were randomly allocated to 4 treatment groups (n = 10): water + water, indomethacin (8 mg/kg) + water, indomethacin + Olive Oil (OO) and indomethacin + EO. Rats were gavaged daily with water or oil from days 0–12 (0.5 ml) and water or indomethacin from days 5–12 (0.5 ml). Rats were euthanized on day 12 for intestinal tissue collection. Jejunal

and ileal samples (4 cm) were assessed for neutrophil infiltration indicative of acute inflammation using the colorimetric myeloperoxidase (MPO) assay (450 nm) expressed as units of MPO per gram of tissue (U/g). p < 0.05 was considered significant. Results: Jejunal MPO levels in indomethacin-treated rats were significantly greater compared with normal controls (208 ± 39 U/g and 62 ± 15 U/g, respectively; p < 0.01). Amongst indomethacin-treated groups, both OO (76 ± 21 U/g) and EO (76 ± 23 U/g) significantly C59 wnt cell line reduced levels of acute jejunal inflammation by 28% and 30% respectively, compared with indomethacin controls (p < 0.01). In the ileum, MPO levels were significantly greater in indomethacin-treated rats compared with normal controls (345 ± 40 U/g and 170 ± 29 U/g, respectively; p < 0.01). However, only EO (174 ± 28 U/g; p < 0.05), but not OO (285 ± 45 U/g; p > 0.05), significantly

reduced ileal MPO levels by 50% in indomethacin-treated rats, compared to the indomethacin control. Conclusions: Emu Oil reduced MPO levels Fulvestrant in vitro in the jejunum and ileum of rats with NSAID-induced enteropathy, indicative of decreased acute inflammation. This further suggests the therapeutic potential of Emu Oil to alleviate gastrointestinal symptoms associated with NSAID usage. AM FERGUSON,1 EG QUINN,1 J ROBERTS,2 C ROGGE,2 TW LEE2 1Department of Nutrition and Dietetics,

ISLHD, Wollongong, Australia, 2Department of Gastroenterology, ISLHD, Wollongong, Anidulafungin (LY303366) Australia Introduction: Body composition and dietary behaviour changes occur in patients with IBD and when compared to healthy controls, consume altered macro and micronutrients. Blood tests alone cannot determine nutritional status; instead, several aspects including anthropometry and weight loss, dietary intake and nutrition assessment tools can establish existence of malnutrition. The aim was to examine risk and rates of malnutrition and weight loss in patients with IBD attending an outpatient clinic. Method: The clinic consisted of 2 gastroenterologists, an IBD nurse and a dietitian. All patients were prospectively screened for malnutrition using short nutrition assessment questionnaire (SNAQ) tool1 and referred to the dietitian if deemed at risk. Patients could also self refer or be identified by gastroenterologists to have nutritional concerns. Data collected over 6 months on anthropometry, usual and previous dietary intake and nutrition assessment score using subjective global assessment (SGA) tool2.

Further investigation into this association is warranted to determine whether anticoagulant therapy or surveillance imaging is indicated in patients transplanted for PSC. Disclosures: The following people have nothing to disclose: Paul Reynolds, Elnaz Jafarimehr, Xiao Jing Wang, Ram M. Subramanian Introduction: Metabolic syndrome (MS) is a frequent condition after liver transplantation (LT). However, most of the studies are focused on the early years after LT, and only few data

are available on the long-term prevalence of this condition. Methods: Patients who underwent LT at Padua Liver Transplant Centre between January 2000 and March 2013 and who were followed up at the Multivisceral Transplant Unit (Padova University Hospital) were included in the analysis. Patients

<18 years old, who underwent re-LT, and patients who underwent multi-organ transplant were excluded from the PF-02341066 in vitro study. MS has been diagnosed according to the modified NCEP-ATP III criteria, and only post-LT “de novo” MS has been evaluated. Results: Overall, 165 patients were included in the analysis (74% male, mean±SD age at LT 52±8 years). Underlying liver disease was: HCV in 48.5% of patients, HBV in 11.5%, HBV and HCV in 3%, alcohol in 16.4%, alcohol and virus in 9.1%, and due to other causes in 10.3%. HCC was diagnosed in 59/165 (35.7%). After a median follow-up time of 6.4 years, prevalence of post-LT MS was 87/165 patients (52.7%): 80.5% male and with a mean±SD age at LT of 53.4±8.8 years. Underlying Opaganib nmr liver disease was HCV in 47% of patients, HBV in 12.6%,

HBV and HCV 2.3%, alcohol in 19.6%, alcohol and virus in 11.5%, and due to other causes in 6.9%. HCC was diagnosed in 28/87 (32%) patients. Immune system Patients with post-LT MS had a significantly higher pre-LT BMI (26.2±3.2 vs. 24±3; p<0.001), and higher prevalence of pre-LT diabetes (22.9% vs. 9.5%; p=0.039), post-LT hypertension (80.5% vs. 28.2%; p<0.001), and post-LT diabetes (59.8% vs. 15.4%; p<0.001) compared with patients without MS. Moreover, patients with post-LT MS presented hypertriglyceridemia (185.2±92 vs. 110.9±42.3; p<0.001) and significantly lower levels of HDL (38.8±14 vs. 53.3±16.9; p<0.001) compared with patients without MS. No differences in terms of liver disease etiology was found between patients with and without post-transplant MS, as well as in terms of immunosuppressive regimen (steroid use vs. no steroid use and cyclosporine-based vs. tacrolimus-based immu-nosuppression). At the multivariate analysis pre-LT diabetes (RR 9.16, 95% CI 1.09-76.9; p=0.04) and pre-LT BMI (RR per 5 unit increase 2.05, 95% CI 1.04-4.03; p=0.003) were identified as risk factors for post-LT MS. Conclusions: MS is a condition affecting more than the half of recipients in the long-term after LT. Pre-LT diabetes and pre-LT increased BMI are risk factors for the development of post-LT MS.

The peristalsis ratio of esophageal body reduced and the synchronous contraction ratio increased. The post-POEM systolic amplitude of esophageal body was lower than the pre-POEM one with significant difference (20.14 ± 12.92 vs 29.04 ± 5.23, P < 0.01). The average upper esophageal sphincter pressure decreased after POEM without statistical significance. After one month, the mean Eckhardt score was reduced by 5.45 score, Sirolimus in vitro with a total efficiency rate of 91.36% (74/81). 6 out 8 patients with refluxing symptom were diagnosed as GERD and resolved by PPI.

Conclusion: POEM via posterior wall could be a preffered choice for cardia achalasia patients with satisfying efficacy and safety. Key Word(s): 1. cardia achalasia; 2. POEM; Presenting Author: CHUNYAN PENG Additional Authors: XIAOPING ZOU Corresponding Author: XIAOPING ZOU Affiliations: Nanjing Drum Tower Hospital Objective: Achalasia

selleck products is an esophageal motility disorder of unknown cause, characterized by aperistalsis of the esophageal body and impaired lower esophageal sphincter relaxation. Endoscopic balloon dilatation and laparoscopic myotomy are established treatments for achalasia. Recently, peroral endoscopic myotomy (POEM) has been described as a new therapeutic option for achalasia. This study aims to investigate the effectiveness of POEM and characteristics of esophageal achalasia. Methods: The data on POEMs were collected prospectively. Pre- and postoperative symptoms were assessed with Eckardt scores. High-resolution manometry (HRM) was performed preoperatively and 3 days postoperatively. Pre-/postmyotomy data were compared using paired nonparametric statistics. Results: From 2012/09 to 2013/04, we enrolled 30 patients (18 women, 12 men; median age: 35.5 years), of whom 2 had type 1 (6.7%) click here and 28 had type 2 (93.3%) achalasia according to the Chicago classification. The median duration of symptoms was 24 months (3∼360 months). Before POEM, all the patients suffered from varying degrees of dysphagia, all had retrosternal pain (100%), and regurgitation (100%). Primary esophageal peristalsis was absent in all patients.

POEM was successfully performed in all patients. Compared with scores before POEM, patient symptom scores significantly dropped from 9 to 2 (P < 0.05). Also, the characteristics of esophageal motility had great changes. The resting lower esophageal sphincter (LES) decreased from median 33.2 mmHg to 18.5 mmHg (P < 0.05). Integrated relaxation pressure reduced from median 21.6 mmHg to 7.8 mmHg (P < 0.05). LES relaxation improved from median 18.9% pre- to 64.7% postoperatively and remained incomplete in response to swallowing in all patients. However, peristalsis of esophageal body still remained absent after POEM. No serious complications associated with POEM were encountered. No morbidity and no mortality occurred.

The peristalsis ratio of esophageal body reduced and the synchronous contraction ratio increased. The post-POEM systolic amplitude of esophageal body was lower than the pre-POEM one with significant difference (20.14 ± 12.92 vs 29.04 ± 5.23, P < 0.01). The average upper esophageal sphincter pressure decreased after POEM without statistical significance. After one month, the mean Eckhardt score was reduced by 5.45 score, Microtubule Associated inhibitor with a total efficiency rate of 91.36% (74/81). 6 out 8 patients with refluxing symptom were diagnosed as GERD and resolved by PPI.

Conclusion: POEM via posterior wall could be a preffered choice for cardia achalasia patients with satisfying efficacy and safety. Key Word(s): 1. cardia achalasia; 2. POEM; Presenting Author: CHUNYAN PENG Additional Authors: XIAOPING ZOU Corresponding Author: XIAOPING ZOU Affiliations: Nanjing Drum Tower Hospital Objective: Achalasia

Bioactive Compound Library concentration is an esophageal motility disorder of unknown cause, characterized by aperistalsis of the esophageal body and impaired lower esophageal sphincter relaxation. Endoscopic balloon dilatation and laparoscopic myotomy are established treatments for achalasia. Recently, peroral endoscopic myotomy (POEM) has been described as a new therapeutic option for achalasia. This study aims to investigate the effectiveness of POEM and characteristics of esophageal achalasia. Methods: The data on POEMs were collected prospectively. Pre- and postoperative symptoms were assessed with Eckardt scores. High-resolution manometry (HRM) was performed preoperatively and 3 days postoperatively. Pre-/postmyotomy data were compared using paired nonparametric statistics. Results: From 2012/09 to 2013/04, we enrolled 30 patients (18 women, 12 men; median age: 35.5 years), of whom 2 had type 1 (6.7%) Farnesyltransferase and 28 had type 2 (93.3%) achalasia according to the Chicago classification. The median duration of symptoms was 24 months (3∼360 months). Before POEM, all the patients suffered from varying degrees of dysphagia, all had retrosternal pain (100%), and regurgitation (100%). Primary esophageal peristalsis was absent in all patients.

POEM was successfully performed in all patients. Compared with scores before POEM, patient symptom scores significantly dropped from 9 to 2 (P < 0.05). Also, the characteristics of esophageal motility had great changes. The resting lower esophageal sphincter (LES) decreased from median 33.2 mmHg to 18.5 mmHg (P < 0.05). Integrated relaxation pressure reduced from median 21.6 mmHg to 7.8 mmHg (P < 0.05). LES relaxation improved from median 18.9% pre- to 64.7% postoperatively and remained incomplete in response to swallowing in all patients. However, peristalsis of esophageal body still remained absent after POEM. No serious complications associated with POEM were encountered. No morbidity and no mortality occurred.

Methods: Female Dark Agouti rats (n = 8/group) were gavaged with water, Olive Oil (OO) or EO once daily (1 ml), injected with 5-Fluorouracil (5-FU) or saline on day 5 and euthanized on day 8, 9, 10 or 11. Intestinal villus height (VH) and crypt depth (CD), neutral mucin-secreting goblet cell (GC) count, myeloperoxidase (MPO) activity and selected cytokines were quantified. p < 0.05 was considered significant. Results: 5-FU significantly decreased MK-8669 cell line small intestinal VH on days 8 and 9, compared to normal controls (p < 0.05). In 5-FU-injected rats, only EO administration significantly increased VH in the ileum (day 8; 33%), jejunum and jejunum-ileum (JI) junction (day 9; 29%

and 45%, respectively) compared to 5-FU controls (p < 0.05). JI CD was significantly increased by 5-FU on days 9 (20%) and 10 (26%), compared to normal controls. OO and EO administration further increased JI CD on days 9 and 10, compared to 5-FU controls (p < 0.01). GC count was significantly reduced by 5-FU (jejunum: days 8 [41%] and 9 [30%]; ileum: day 8 [47%]; p < 0.05) and EO increased ileal GC on days 10 (75%) and 11 (54%) compared to 5-FU controls (p < 0.05). MPO activity was significantly increased in jejunum (days 8 [277%] and 9 [137%]) and ileum (day 8; 6-fold) following 5-FU

injection, compared to normal controls (p < 0.05). Both EO and OO significantly reduced jejunal MPO on days 8 (OO: 45%; EO 62%) and 9 (OO: 71%; EO: 83%), however, only EO decreased ileal MPO

on day 8 (55%; p < 0.05). Cytokine levels were not significantly affected by either oil or 5-FU administration at the day 8 time Seliciclib ic50 point (p > 0.05). Conclusions: Promotion of repair from injury could represent a new mechanism of action Tenoxicam for Emu Oil, suggesting potential as an adjunct to conventional treatment approaches for cancer management. JE BAJIC,1 GS HOWARTH,1,2,3 EM PENASCOZA,1 SM ABIMOSLEH1,2 1Discipline of Physiology, School of Medical Sciences, The University of Adelaide, Adelaide, Australia, 2Centre for Paediatric and Adolescent Gastroenterology, Children, Youth and Women’s Health Service, North Adelaide, Australia, 3School of Animal and Veterinary Sciences, The University of Adelaide, Adelaide, Australia Introduction: Non-steroidal anti-inflammatory drug (NSAID) ingestion frequently manifests as inflammation and ulcerating lesions lining the gastrointestinal tract, which may result in fatal sepsis. To date, there are no effective treatment options. Emu Oil (EO) is extracted from emu adipose tissue comprising a fatty acid profile of oleic, palmitic, linoleic and stearic acids. The remaining composition remains undefined, although natural antioxidants such as carotenoids, flavones, tocopherols and phospholipids have been implicated. We have previously demonstrated the anti-inflammatory properties of EO in a rat model of ulcerative colitis (Abimosleh et al., Dig Dis Sci, 2012) and chemotherapy-induced mucositis (Abimosleh et al., Exp Bio Med, 2013; in press).

Methods: Female Dark Agouti rats (n = 8/group) were gavaged with water, Olive Oil (OO) or EO once daily (1 ml), injected with 5-Fluorouracil (5-FU) or saline on day 5 and euthanized on day 8, 9, 10 or 11. Intestinal villus height (VH) and crypt depth (CD), neutral mucin-secreting goblet cell (GC) count, myeloperoxidase (MPO) activity and selected cytokines were quantified. p < 0.05 was considered significant. Results: 5-FU significantly decreased click here small intestinal VH on days 8 and 9, compared to normal controls (p < 0.05). In 5-FU-injected rats, only EO administration significantly increased VH in the ileum (day 8; 33%), jejunum and jejunum-ileum (JI) junction (day 9; 29%

and 45%, respectively) compared to 5-FU controls (p < 0.05). JI CD was significantly increased by 5-FU on days 9 (20%) and 10 (26%), compared to normal controls. OO and EO administration further increased JI CD on days 9 and 10, compared to 5-FU controls (p < 0.01). GC count was significantly reduced by 5-FU (jejunum: days 8 [41%] and 9 [30%]; ileum: day 8 [47%]; p < 0.05) and EO increased ileal GC on days 10 (75%) and 11 (54%) compared to 5-FU controls (p < 0.05). MPO activity was significantly increased in jejunum (days 8 [277%] and 9 [137%]) and ileum (day 8; 6-fold) following 5-FU

injection, compared to normal controls (p < 0.05). Both EO and OO significantly reduced jejunal MPO on days 8 (OO: 45%; EO 62%) and 9 (OO: 71%; EO: 83%), however, only EO decreased ileal MPO

on day 8 (55%; p < 0.05). Cytokine levels were not significantly affected by either oil or 5-FU administration at the day 8 time Poziotinib mouse point (p > 0.05). Conclusions: Promotion of repair from injury could represent a new mechanism of action ADAM7 for Emu Oil, suggesting potential as an adjunct to conventional treatment approaches for cancer management. JE BAJIC,1 GS HOWARTH,1,2,3 EM PENASCOZA,1 SM ABIMOSLEH1,2 1Discipline of Physiology, School of Medical Sciences, The University of Adelaide, Adelaide, Australia, 2Centre for Paediatric and Adolescent Gastroenterology, Children, Youth and Women’s Health Service, North Adelaide, Australia, 3School of Animal and Veterinary Sciences, The University of Adelaide, Adelaide, Australia Introduction: Non-steroidal anti-inflammatory drug (NSAID) ingestion frequently manifests as inflammation and ulcerating lesions lining the gastrointestinal tract, which may result in fatal sepsis. To date, there are no effective treatment options. Emu Oil (EO) is extracted from emu adipose tissue comprising a fatty acid profile of oleic, palmitic, linoleic and stearic acids. The remaining composition remains undefined, although natural antioxidants such as carotenoids, flavones, tocopherols and phospholipids have been implicated. We have previously demonstrated the anti-inflammatory properties of EO in a rat model of ulcerative colitis (Abimosleh et al., Dig Dis Sci, 2012) and chemotherapy-induced mucositis (Abimosleh et al., Exp Bio Med, 2013; in press).