NuPathe Inc. announced on January 17, 2013 that the U.S. FDA had approved Zecuity (sumatriptan iontophoretic transdermal system) for the acute treatment of migraine with or without aura in adults. The product is a single-use, battery-powered patch that actively delivers sumatriptan through the skin, providing relief of both selleck migraine headache pain and migraine-related nausea. It is the first transdermal patch approved for the treatment of migraine. The company has also announced that it is planning for the market launch of the product by the end of 2013. 2014 should prove to be another lean year for new migraine products, as the only possible FDA approval would

be for inhaled dihydroergotamine. In January 2013, MAP Pharmaceuticals, Inc., the developer of dihydroergotamine inhalation aerosol Selumetinib manufacturer (Levadex), was acquired by Allergan, Inc. In April 2013, Allergan announced that the U.S. FDA had issued a Complete Response Letter to its New Drug Application for dihydroergotamine inhalation aerosol

for the acute treatment of migraine in adults. The company announced that it had met with the FDA to clarify their specific requirements for approval of the product. The company stated that it has agreed to these new requirements and that it planned to submit an amended file by the end of 2013. Based on these assumptions, possible FDA approval is expected in mid-2014. Merck initiated a large Phase 2 trial of MK-1602 entitled “A Dose-Finding Study of MK-1602 in the Treatment of Acute Migraine” (NCT01613248) in 2012. The study compared a 100-fold range of MK-1602 doses (ie, 1 to 100 mg) vs placebo. The planned 834 subject study was reportedly completed Liothyronine Sodium in late 2012. However, no results from this study have been disclosed, as of

late 2013. No further clinical development plans for MK-1602 have been announced by the company, and the drug no longer appears on the corporate listing of its products in development, as of late 2013. Bristol-Myers Squibb evaluated a small molecule CGRP antagonist (designated BMS-927711) in a large (n = 825) Phase 2 study entitled “Dose Ranging Study of a Drug for the Treatment of Acute Migraine” (NCT00216736). The objective of the study was to determine an effective and tolerable dose range of BMS-927711 for the acute treatment of migraine. In this randomized, double-blind, placebo-controlled, dose-ranging study, the subjects were randomized using an adaptive design to one of the following dose groups: BMS-927711 (10, 25, 75, 150, 300, or 600 mg), sumatriptan 100 mg (active comparator), or placebo. All subjects were treated for a single migraine attack. Pain freedom at 2 hours postdose, the primary end point, was significantly higher after doses of 75 mg (31%, P = .002), 150 mg (33%, P < .001), and 300 mg (30%, P = .002) BMS-927711, and after 100 mg (35%, P < .001) sumatriptan compared with placebo (15%).

Methods: ① The luciferease gene coding sequence was amplified from PMIR-luciferase using polymerase chain

reaction (PCR). The amplified product was digested with BamH1 and Kpn1 and cloned into the Bam H1 and Kpn1 sites in Psmp8 plasmid under an αSMA promoter component. Talazoparib The recombinant was sequenced to assess the orientation of the insert and the correctness of the sequence. We named this recombinant Psmp8+Luciferase. ② Mouse hepatic stellate cells (HSCs) were isolated from kunming mice’s livers using the way of density gradient centrifugation. Isolated HSCs were activated after being cultured and passaged numbers of days. Expression of αSMA was determined by western blot and immunofluorescence. ③ Psmp8+Luciferase and Renilla luciferase vector were co-transfected HSCs, hepatic cells and kuffer cells. PeGFP plasmid and Renilla luciferase vector were co-transfected the above cells as the negative control. Using Dual-Luciferase Reporter Assay System detected the expression of the two plasmids in HSCs, hepatic cells, kuffer cells. Results: ① The Psmp8+Luciferase sequence and the orientation of the insert were sequenced correct. ② The cells isolated from mice livers could

express αSMA determined by western blot and immunofluorescence. So the isolated cells were HSCs and had been activated. Roxadustat ③ The Psmp8+Luciferase could express luciferase in HSCs, but not in kuffer cells and hepatic cells detected by Dual-Luciferase Reporter

Assay System. Conclusion: The Psmp8+Luciferase containing the αSMA promoter could express specifically in activated HSCs. This suggested that Psmp8+Luciferase containing Hydroxychloroquine αSMA promoter could be used as an specific vector targeted activation HSCs, further more it may be recombined and used in the fibrosis gene therapy. Key Word(s): 1. targeted therapy; 2. HSCs; 3. αSMA promoter; 4. liver fibrosis; Presenting Author: WUPENG BO Additional Authors: TANSHI YUN, ZHANG BO Corresponding Author: WUPENG BO Affiliations: wuhan university; guangxi renmin hospital Objective: Objective To explore the effects of ursodeoxycholic acid in rats’ chronic hepatic injury and it’s mechanism. Methods: Methods Rat s’ chronic hepatic injury model was induced by subcutaneous inject ion of CCl4 for 6 weeks. Suspension of ursodeoxycholic acid preprared with normal saline was given orally to the rats, 20 mg●kg-1●d-1 for 4 weeks. HE staining was done to characterize the change of hepatic pathology. Masson staining was used to qualitatively analyse the accumulation of extracellular matrix. The levels o f serum ALT, AST, TBIL and MAO were detected. And western blotting was also performed to detect the expression level of autophagic molecular signals including ATG-5, beclin-1 and LC3 II.

Using an appropriate method it was demonstrated that EN, as produced by Nutricia, does not contain high fructan levels. 1Halmos EP, Liels KL, Rosella O: Enteral and oral nutritional supplement formulas deliver laxative doses of FODMAPs which cannot be predicted by ingredients lists. Journal of Gastroenterology and Hepatology 2011;26(suppl 4):73. 2Technical Note 20, LPN 032857–04, Dionex, 2004. Disclosure of Interest: E. Strebe, M Deetlefs, G Witte, S Hougee: Other: Employee of Nutricia Advanced

Medical Nutrition, H. van Westerop, J Kersten Other: Employee of TNO Triskelion, “
“Department of Visceral Surgery and Medicine, University Hospital Bern, Bern, Switzerland Division of Vascular Surgery, Massachusetts HSP inhibitor General Hospital, Boston, MA Liver Crizotinib regeneration is of major clinical importance in the setting

of liver injury, resection, and transplantation. A20, a potent antiinflammatory and nuclear factor kappa B (NF-κB) inhibitory protein, has established pro-proliferative properties in hepatocytes, in part through decreasing expression of the cyclin dependent kinase inhibitor, p21. Both C-terminal (7-zinc fingers; 7Zn) and N-terminal (Nter) domains of A20 were required to decrease p21 and inhibit NF-κB. However, both independently increased hepatocyte proliferation, suggesting that additional mechanisms contributed to the pro-proliferative function of A20 in hepatocytes. We ascribed one of A20′s pro-proliferative mechanisms to increased and sustained interleukin (IL)-6-induced

signal transducer and activator of transcription 3 (STAT3) phosphorylation, as a result of decreased hepatocyte expression of the negative regulator of IL-6 signaling, suppressor of cytokine signaling 3 (SOCS3). This novel A20 function segregates with its 7Zn not Nter domain. Conversely, total and partial loss of A20 in hepatocytes increased SOCS3 expression, hampering IL-6-induced STAT3 phosphorylation. Following liver resection in mice pro-proliferative targets downstream of IL-6/STAT3 signaling were increased by A20 overexpression and decreased by A20 knockdown. In contrast, IL-6/STAT3 proinflammatory targets were increased in A20-deficient either livers, and decreased or unchanged in A20 overexpressing livers. Upstream of SOCS3, levels of its microRNA regulator miR203 were significantly decreased in A20-deficient livers. Conclusion: A20 enhances IL-6/STAT3 pro-proliferative signals in hepatocytes by down-regulating SOCS3, likely through a miR203-dependent manner. This finding together with A20 reducing the levels of the potent cell cycle brake p21 establishes its pro-proliferative properties in hepatocytes and prompts the pursuit of A20-based therapies to promote liver regeneration and repair. (HEPATOLOGY 2013) The liver has a unique regenerative capacity, restoring liver mass after surgical resection or toxic/viral hepatocyte damage.

Using an appropriate method it was demonstrated that EN, as produced by Nutricia, does not contain high fructan levels. 1Halmos EP, Liels KL, Rosella O: Enteral and oral nutritional supplement formulas deliver laxative doses of FODMAPs which cannot be predicted by ingredients lists. Journal of Gastroenterology and Hepatology 2011;26(suppl 4):73. 2Technical Note 20, LPN 032857–04, Dionex, 2004. Disclosure of Interest: E. Strebe, M Deetlefs, G Witte, S Hougee: Other: Employee of Nutricia Advanced

Medical Nutrition, H. van Westerop, J Kersten Other: Employee of TNO Triskelion, “
“Department of Visceral Surgery and Medicine, University Hospital Bern, Bern, Switzerland Division of Vascular Surgery, Massachusetts Selleckchem BTK inhibitor General Hospital, Boston, MA Liver selleck chemical regeneration is of major clinical importance in the setting

of liver injury, resection, and transplantation. A20, a potent antiinflammatory and nuclear factor kappa B (NF-κB) inhibitory protein, has established pro-proliferative properties in hepatocytes, in part through decreasing expression of the cyclin dependent kinase inhibitor, p21. Both C-terminal (7-zinc fingers; 7Zn) and N-terminal (Nter) domains of A20 were required to decrease p21 and inhibit NF-κB. However, both independently increased hepatocyte proliferation, suggesting that additional mechanisms contributed to the pro-proliferative function of A20 in hepatocytes. We ascribed one of A20′s pro-proliferative mechanisms to increased and sustained interleukin (IL)-6-induced

signal transducer and activator of transcription 3 (STAT3) phosphorylation, as a result of decreased hepatocyte expression of the negative regulator of IL-6 signaling, suppressor of cytokine signaling 3 (SOCS3). This novel A20 function segregates with its 7Zn not Nter domain. Conversely, total and partial loss of A20 in hepatocytes increased SOCS3 expression, hampering IL-6-induced STAT3 phosphorylation. Following liver resection in mice pro-proliferative targets downstream of IL-6/STAT3 signaling were increased by A20 overexpression and decreased by A20 knockdown. In contrast, IL-6/STAT3 proinflammatory targets were increased in A20-deficient Thymidylate synthase livers, and decreased or unchanged in A20 overexpressing livers. Upstream of SOCS3, levels of its microRNA regulator miR203 were significantly decreased in A20-deficient livers. Conclusion: A20 enhances IL-6/STAT3 pro-proliferative signals in hepatocytes by down-regulating SOCS3, likely through a miR203-dependent manner. This finding together with A20 reducing the levels of the potent cell cycle brake p21 establishes its pro-proliferative properties in hepatocytes and prompts the pursuit of A20-based therapies to promote liver regeneration and repair. (HEPATOLOGY 2013) The liver has a unique regenerative capacity, restoring liver mass after surgical resection or toxic/viral hepatocyte damage.

Compared with wild-type animals,

BYL719 ic50 cirrhotic PlGF−/− mice showed a significant reduction in angiogenesis, arteriogenesis, inflammation, fibrosis, and portal hypertension. Importantly, pharmacological inhibition with anti-PlGF antibodies yielded similar results as genetic loss of PlGF. Notably, PlGF treatment of activated hepatic stellate cells induced sustained extracellular signal-regulated kinase 1/2 phosphorylation, as well as chemotaxis and proliferation, indicating a previously unrecognized profibrogenic role of PlGF. Conclusion: PlGF is a disease-candidate gene in liver cirrhosis, and inhibition of PlGF offers a therapeutic alternative with an attractive safety profile. (HEPATOLOGY 2011;) Chronic liver disease can be defined as a complex pathophysiological process of progressive destruction and regeneration of liver parenchyma, leading to fibrosis, cirrhosis, and increased risk of hepatocellular carcinoma. A profound alteration of the hepatic angioarchitecture due to induction of long-term structural vascular changes is underlying this remodeling process. Hepatic angiogenesis occurs

during the progression of several chronic liver diseases, including hepatitis B/C, biliary cirrhosis, alcoholic cirrhosis, and nonalcoholic steatohepatitis. The resulting neovasculature is mainly located in the fibrotic areas of the liver and induces the formation of arterio-portal and porto-venous systemic anastomoses.1 Preclinical studies Wnt pathway of this phenomenon have

demonstrated that angiogenic inhibitors interfere with the progression of fibrosis. In human and experimental liver fibrosis, neovascularization seems to be a process strictly related to progressive fibrogenesis.2 In this context, studies in experimental models of cirrhosis have shown that treatment with angiogenic inhibitors such as neutralizing monoclonal anti–vascular endothelial growth factor receptor (VEGFR) antibody, TNP-470, and adenovirus expressing the extracellular domain of Tie2 decreased liver fibrosis.3, 4 Other parallels between fibrosis and angiogenesis have been postulated, such as the promotion of different subpopulations of hepatic stellate cells (HSCs; angiogenic versus fibrogenic phenotypes), and of hepatic inflammation as a process linking new angiogenesis and fibrogenesis.2, 5 Consequently, multitargeted therapies acting against both angiogenesis and inflammation have been shown to be beneficial in inhibiting the progression of fibrosis to cirrhosis. The validity of the latter approach was demonstrated in cirrhotic rats in which sunitinib and sorafenib, two inhibitors of tyrosine kinase receptors (RTKs) that target the platelet-derived growth factor and vascular endothelial growth factor (VEGF) signaling pathways, produced a reduction in the degree of hepatic angiogenesis, fibrosis, and inflammation, as well as a significant decrease in portal pressure.

As these reactions may herald the immunological development of neutralizing antibodies to the anti-TNF agent, some patients may develop loss of response and require modification of anti-TNF dose, dose-interval or switch to a different agent altogether. Neurological complications.  Anti-TNF therapy has been associated with development and exacerbation of both central and peripheral demyelination. However, a definite causal link has not been established.87,88 Overall, the incidence of de-novo

demyelinating disease is low.89 The α4-integrin inhibitor, natalizumab, has been associated with PML.5 Other.  Anti-TNF therapy is contraindicated in patients with NYHA class III or IV heart failure due to an increased risk of death observed in trials of these Paclitaxel agents to treat heart failure.90 Hepatic dysfunction and rarely fulminant hepatic failure have been reported with anti-TNF therapy. Psoriatic eczema is the most common dermatological side effect; however, it rarely necessitates cessation of anti-TNF therapy.58 Immunomodulator co-therapy.  The SONIC trial demonstrated that co-immunosuppression with a thiopurine and anti-TNF agent is superior selleck compound library to either agent alone for achieving and maintaining remission in

CD.91 Similar results were not shown in the COMMIT trial for co-immunosupression with anti-TNF agents and methotrexate.92 There is speculation that the addition of azathioprine, 6-mercaptopurine or perhaps methotrexate to anti-TNF reduces anti-drug antibody formation, hence boosting trough levels of the biological agent and rendering Farnesyltransferase the anti-TNF response more durable.91 This effect is not reflected in the earlier anti-TNF literature. The benefits of immunomodulator plus anti-TNF treatment must be balanced against increases in the risks of infection and lymphoma. Co-therapy of thiopurine and anti-TNF should be recommended in those with severe disease where maximal efficacy is desired. This is particularly important if few alternative medical options are available including prior loss of response or non-response to an alternative

anti-TNF agent. In UC patients receiving infliximab, co-immunosuppression with azathioprine was superior to azathioprine or infliximab monotherapy.35 Screening and prophylaxis.  History, chest X-ray and IFN-γ release assay screening for TB as well as careful historical and serological screening for potential bacterial and viral pathogens can be recommended,58,75 with subsequent immunization where appropriate. These will likely be related to local practices. Hepatitis B virus, human papilloma virus, influenza (including H1N1), and pneumococcal vaccines are all safe in those on immunosuppressive therapy.93 Live vaccines (VZV, yellow fever, measles-mumps-rubella and oral polio) should be avoided 3 weeks before and 12 weeks after anti-TNF therapy94,95 and where possible given prior to the initiation of immunosuppression.

0001), and both 2-APB and SKF96363, store-operated calcium channels (SOCs) inhibitors, completely inhibited ATP-induced [Ca2+]i increases after restoration Crenolanib of extracellular Ca2+. ATP promoted the proliferation and migration of HCC cells and the growth of HCC in nude mice. Suramin, P2Y2R specific siRNA, and 2-APB inhibited ATP-induced HCC cell proliferation and migration and HCC growth (P < 0.05 and P < 0.01). Conclusion: P2Y2R was up-regulated in human HCC cells and mediated ATP-induced

human HCC cell proliferation and migration and HCC growth through SOCs-mediated Ca2+ signaling, suggesting that P2Y2R may play important role in the development and progression of inflammation-associated HCC and targeting P2Y2R may be a promising therapeutic strategy against human HCC. http://www.selleckchem.com/products/DMXAA(ASA404).html Key Word(s): 1. P2Y2 receptor; 2. HCC; 3. ATP; Presenting Author: HYE JIN KIM Additional Authors: BEOM YONG YOON, SE YOUNG PARK, SE WOONG HWANG, SUN HYUNG KANG, HEE SEOK MOON, JAE KYU SEONG, EAUM SEOK LEE, SEOK HYUN KIM, BYUNG SEOK LEE, HEON YOUNG LEE Corresponding Author: HYE JIN KIM Affiliations: Chungnam National University Objective: Transarterial chemoembolization (TACE) have been applied for treating hepatocellular carcinoma (HCC), but procedure-related complications can be a serious problem. Methods: Liver abscess is most common infectious complication

during post-TACE period. Results: We describe three cases of necrotizing liver abscess after TACE in hepatocellular carcinoma. First case, a 79-year-old man, with 2.6 cm sized HCC in S4, was treated by TACE for two times during 2 months. About 1 month after the last TACE, abdominal CT scan revealed a gas containing liver abscess. Antibiotics and percutaneous transhepatic drainage was performed. Chloroambucil Cholangiography via drainage catheter showed

findings of bile duct necrosis. The patient improved condition and removed the catheter. Second case, a 68-year-old man, with four HCC in S4, 5, 7, 8, was treated by TACE for three times during 2 years. Two new lesions was found in S6/7, was performed by TACE. About 2 days later the patient had a fever and abdominal pain. Abdominal CT scan reveal a necrotizing liver abscess and percutaneous transhepatic drainage was performed. Two month later, the abscess improved and catheter removed. Third case, a 75-year-old man was performed embolization due to HCC rupture. After 1 month, abdominal CT scan revealed necrotizing liver abscess. Antibiotics and percutaneous transhepatic drainage was performed. However, the abscess persisted despite of treatment for 5 months. Conclusion: Physicians should be alerted to necrotizing liver abscess after TACE in patient with variable clinical manifestations. Key Word(s): 1. TACE; 2. HCC; 3.

15 In this context, Hou and colleages identified the network of low miR-199a/b-3p expression, high PAK expression and consecutive

activation Target Selective Inhibitor Library purchase of the Raf/MEK/ERK cascade as a new key player in development and progression of HCC. Notably, most of the patients analyzed in their study suffered from hepatitis B virus–associated HCC, and further studies are needed to clarify whether these data can be transferred one-to-one to HCC caused by other etiologies. Interestingly, the authors further verified an increase of miR-199a/b-3p in nontumorous but fibrotic tissues, which is in line with previous array-based data from mouse models of liver fibrosis and from patients with liver cirrhosis6, 16, 17 and suggests that this specific miRNA might functionally be

involved in the processes driving the transition from fibrosis to HCC. Finally, in this elegant article, the authors provided evidence that genetic delivery of miR-199a/b-3p might represent a promising option for pharmacological manipulation of tumor progression in patients with HCC. However, major obstacles have to be overcome on the way to a successful miRNA-based therapy. First, Dinaciclib mouse the optimal way for an effective and safe delivery of miRNA into cancer cells or the tumor microenvironment still remains unclear. They can be delivered by retroviruses, adenoviruses, or adeno-associated viruses or injected in cholesterol-modified form to the tissue of interest.18 The authors and other groups demonstrated the feasibility of both approaches in rodents and nonhuman primates. Second, the high number of potential targets for each individual miRNA may give rise to unexpected and

fatal toxicity. If these concerns can be addressed, the promise of an miR-based anticancer therapy might become reality. “
“Intestinal failure (IF) occurs where absorption of nutrients and water from the gut is inadequate to provide sufficient nutrition for maintenance and growth, resulting in the need for parenteral nutrition (PN). PN should be administered when the gut is unable to provide nutrition for a period of at least a week. The nutrition support team (NST) provides support in the nutritional management of any child with complex nutritional needs, Vildagliptin especially where there are complicating factors. Short bowel syndrome (SBS) in children is most common in infancy and is defined as a bowel length of <80 cm, with very short bowel defined as <40 cm and extreme as <15 cm. Most congenital enteropathies present in the first 6 months of life, often in the first weeks. Primary chronic intestinal pseudo-obstruction syndrome (CIPOS) may be familial or sporadic, due to abnormalities in enteric smooth muscle or the enteric nervous system. "
“We read with interest the article by Kamiyama et al.

Dyn2, dynamin 2; GFP, green fluorescent protein; GTP, guanosine triphosphate; PM,

plasma membrane; TfR, transferrin receptor. MiniPrep Express Matrix and Luria-Bertani medium were from BIO 101 (Vista, CA). Restriction enzymes were from New England Biolabs (Beverly, MA). Both anti-clathrin (X22) and anti-α-AP2 antibodies were collected from the supernatant of the X22 hybridoma and AP.6 hybridoma cell lines (ATCC, Rockville, MD). TfR1 antibody was purchased from Zymed Laboratories (San Francisco, CA). Anti-TfR1-N, pan-dynamin (MC63 and MC65), and Dyn2 antibodies were as described.14, 15 An anti-TfR2 antibody was raised against the peptide sequence QWSPRPSQTIYRRVEGPQLENLEEEDREEGE, corresponding to amino acids 13-43 in full-length rat TfR2 (Accession

number XM_222022). Transferrin and secondary antibodies conjugated Selleck PS341 to Alexa Fluor 594 or 488 were from Invitrogen (Eugene, OR). Unless otherwise stated, all other chemicals and reagents were from Sigma (St. Louis, MO). Two TfR isoform complementary DNA (cDNA0 sequences were from GenBank (Accession numbers TfR1 NM_022712; TfR2 XM_222022). The primers designed for TfR1 were TfR1 5′, GCCGCTGCATTGCGGACAGAGG AGGTGCTT and TfR1 3′, GCACAACCAGCTCAA GTCTAGAAACAGACTACCC; and for TfR2 were TfR2 5′, ATGGTCCAAGAAATCCAGAGACCTGTT GCTGAG and TfR2 3′, TCAAAAGTTATTGTC Selleck AZD8055 GATGTTCCAAACGTCGCCACT. Full-length cDNA was amplified using the XL PCR kit (Applied Biosystems, Branchburg, NJ). The polymerase chain reaction (PCR) cycle conditions were as follows: for TfR1, 94°C for 1 minute and 62°C for 5 minutes for 28 cycles, followed by 72°C for 7 minutes; for TfR2, 94°C for 1 minute and 65°C for 5 minutes for 28 cycles, followed by 72°C for 7 minutes. The PCR fragments were ligated into TA vector pCR3.1 (Invitrogen, Carlsbad, CA). WT Dyn2(aa) -GFP

was as described.13 Avelestat (AZD9668) Clone 9 and Hep3b2 cells (ATCC CRL-1439, Rockville, MD) were as described13; HepG2 and HuH-7 cells were as described.16, 17 These cells are widely utilized to study hepatocyte function, although they are not polarized and do not express most hepatocyte-specific proteins. Primary rat hepatocytes18 in Williams medium E supplemented with ITS, dexamethasone, 10% fetal bovine serum (FBS), 100 U/mL penicillin, and 100 μg/mL streptomycin were incubated at 5% CO2 / 95% air at 37°C. Cells were cultured on 22-mm microscope cover slips for transfections and immunocytochemistry. Transfections were using the Lipofectamine 2000 Reagent kit (Invitrogen) with 1 μg plasmid DNA per transfection. The conditions for stable expression of TfR2 -pCR3.1 in Clone 9 cells are as described.13 Transferrin endocytosis assays were performed as described.

However, studies have not yet been conducted to ascertain its role in prevention of hepatotoxicity. Aim: This study was planned to elucidate the role of wheat grass if any on liver function tests (LFT), antioxidants enzymes and histoarchitecture in hepatotoxicity conditions induced by Carbon tetra chloride (CCl4). Methods: 42 female

Wistar rats were divided into 7 groups. Group 1 (Normal control): Rats were given normal saline subcutaneously (SC). Group 2: CCl4 was administered SC at a dose of 2 ml/kg b.wt twice/week for 4 weeks. Group 3–6: – Rats in these groups received orally wheatgrass dissolved in water at different doses of 20 mg, 40 mg, 60 mg and 80 mg/100 g b.wt and CCl4 as was given to group 2 animals. Wheatgrass was started 2 weeks prior to first injection of CCl4. Group 7- Animals in this group received wheatgrass alone Inhibitor Library ic50 at a highest dose of 80 mg/100 g b.wt. The effects of different treatments were studied on LFT, Glutathione (GSH), lipid peroxidation (LPO), Catalase and superoxide dismutase (SOD) at end of 2 weeks and 4 weeks. Histological studies were also conducted. Results: The enzyme activity of ALP, Adriamycin AST, and ALT

were increased significantly at 2 and 4 weeks as compared to values in control group. Interestingly, supplementation of wheat grass at all doses brought down the already increased activity of ALT but there was more pronounced decrease with 80 mg dose of wheat grass at both the time duration s of 2 and 4 weeks. However, AST and ALP activity was found to be decreased significantly at 4 weeks following supplementation of wheat grass at doses Suplatast tosilate ranging from 40–80 mg. Also, it was found that GSH level significantly decreased while LPO increased in CCl4 treated rats as compared to group1 (control).

In wheat grass treated groups, GSH level was increased while LPO decreased as compared to group 2. Histologically, there was necrosis, portal triaditis & lobular inflammation in CCl4 group. Therefore, protection was observed with wheat grass which may not be significant at 2 weeks but values were significant at 4 weeks. Conclusion: Wheat grass supplementation at a dose of 80 mg/100 g is effective in controlling hepatotoxicity induced by CCl4. Wheat grass and its extracts can be boon in preventing liver diseases Key Word(s): 1. Wheatgrass; 2. Carbon Tetrachloride; 3. Prevention; 4. Hepatotoxicity; Presenting Author: TAMSINNAOMI CARGILL Additional Authors: PREYA PATEL, LYNFA LANZON-MILLER, SANDRO LANZON-MILLER Corresponding Author: TAMSINNAOMI CARGILL, PREYA PATEL Affiliations: Milton Keynes Hospital Objective: Nasal bridle use is claimed to enable uninterrupted delivery of enteral nutrition and prevent unnecessary percutaneous endoscopic gastrostomies (PEGs). This study assesses the outcomes of patients fitted with nasal bridles at Milton Keynes Hospital.