Hepatic mRNA/miRNA profiles were generated with 17581 mRNAs and 504 miRNAs meeting array QC criteria. The transcriptome of control and drained groups was largely similar with only a single differentially expressed (DE) mRNA apparent (criteria: fold change >1.5 and adjusted P value <0.05). Cholestasis resulted in pronounced changes of the transcriptional landscape when compared with control (1353 DE mRNAs, 47 DE miRNAs) and drained

(111 DE mRNAs, 2 DE miRNAs) MS-275 price groups. Overrepresentation analysis indicated a multitude of pathways affected by cholestatic conditions including ECM organization, regulation of actin cytoskeleton and biotransformation. Alterations pertaining to BS homeostasis included downregulation of BS synthesis (CYP7A1), repression of BS uptake (SLCO1B1/3) and induction of basolateral efflux transporters (SLC51A/B) in cholestatic liver. Conclusions Extrahepatic cholestasis elicits large scale alterations in hepatic mRNA and miRNA expression. A notable difference in the number of DE mRNAs/miRNAs

was apparent when comparing cholestatic with control and drained groups, with the latter two having similar serum biochemistry and identical mRNA/ miRNA profiles. Follow-up studies are required to assess the interaction between miRNA and mRNA networks and the role of the identified pathways in cholestatic liver injury. Disclosures: The Torin 1 cell line following people have nothing to disclose: Frank G. Schaap, Marlon J. Jetten, Marcel H. Herwijnen, Maarten L. Coonen, Jos C. Kleinjans, Peter L. Jansen, Steven Olde Damink Background and aims: Sclerostin, an inhibitor of the Wnt pathway is involved in the regulation of osteoblastogenesis and its role in the development of bone disease in primary biliary cirrhosis (PBC), a disease characterized by low bone formation, is unknown. Therefore, we have assessed the circulating levels and the liver gene and protein expression of sclerostin

in this cholestatic disease. Methods: Serum sclerostin levels were measured in 83 women with PBC (mean age: 60 ± 12 years) and 101 control women of the same age. Lumbar and femoral bone mineral density (BMD) as well as parameters of mineral metabolism and bone remodeling (Ca/P, PTH, 25OHD, PINP, bone Celecoxib ALP, sCTX, NTX and osteocalcin) were measured. Moreover, sclerostin gene expression in the liver was assessed in samples of liver tissue taken by biopsy in 11 PBC patients and 5 healthy controls by real time PCR, and presence and distribution of sclerostin was evaluated in liver slices from 11 patients by immunohistochemistry. The presence and severity of histologic lesions were assessed semiquantitatively in the same liver samples. Results: Seventy-seven percent of patients had low BMD (22% osteoporosis and 55% osteopenia). PBC patients had higher sclerostin levels than controls (76.7±38.6 vs. 32.5±14.7 pmol/L, p<0.001). Serum sclerostin correlated inversely with markers of bone formation PINP (p=0.05) and osteocalcin (p=0.03), and bone resorption, NTX (p=0.01) and sCTX (p=0.

Its diagnosis requires a liver biopsy and it usually responds to increased immunosuppression. Immunosuppression predisposes to infections, cytomegalovirus infection/disease being one of the most important ones, and to malignancies, in particular Epstein–Barr virus associated post-transplant lymphoproliferative disorder. The individual immunosuppressive agents used have their individual side effect profile. Calcineurin inhibitors (cyclosporine A, tacrolimus), which

formthe backbone of maintenance immunosuppression, are, among others, associated with nephrotoxicity. Steroids and calcineurin inhibitors predispose to weight gain, hypertension, dyslipidemia, and insulin resistance/diabetes, which develop in 30–60% of patients. Thus, liver transplant recipients are at a threefold higher risk for fatal and non-fatal cardiovascular GSK-3 phosphorylation events than the normal population. Finally, some underlying liver disease may Proteases inhibitor recur with varying frequency and may impact, such as hepatitis C recurrence, on survival outcome. The internist/family physician and transplant hepatologist share

the long-term care for the liver transplant recipient, the former bringing his or her expertise with managing cardiovascular risk factors and many conditions common in the non-transplant population that may occur also in the liver transplant recipient, the latter his or her experience with managing immunosuppression and graft related issues. “
“Telomere shortening impairs liver regeneration in mice and is associated with cirrhosis formation in humans with chronic liver disease. In humans, telomerase mutations have been associated with familial diseases leading to bone marrow failure or lung fibrosis. It is currently unknown whether telomerase mutations associate with cirrhosis induced by chronic liver disease. The telomerase Pregnenolone RNA component (TERC) and the telomerase reverse transcriptase (TERT) were sequenced in 1,121 individuals (521 patients with cirrhosis induced by chronic liver disease and 600 noncirrhosis controls).

Telomere length was analyzed in patients carrying telomerase gene mutations. Functional defects of telomerase gene mutations were investigated in primary human fibroblasts and patient-derived lymphocytes. An increased incidence of telomerase mutations was detected in cirrhosis patients (allele frequency 0.017) compared to noncirrhosis controls (0.003, P value 0.0007; relative risk [RR] 1.859; 95% confidence interval [CI] 1.552-2.227). Cirrhosis patients with TERT mutations showed shortened telomeres in white blood cells compared to control patients. Cirrhosis-associated telomerase mutations led to reduced telomerase activity and defects in maintaining telomere length and the replicative potential of primary cells in culture. Conclusion: This study provides the first experimental evidence that telomerase gene mutations are present in patients developing cirrhosis as a consequence of chronic liver disease.

One other study looking at the effect of pretreatment with PPI on eradication rates did not find a benefit [11]. In addition to trials focussing on certain specific regimens, there were a number of studies that focussed on the processes of second- and third-line therapies over the last year. Regarding second-line therapy, one study from Japan revealed very high second-line eradication SCH772984 clinical trial rates with PPI, amoxicillin, and metronidazole for 1 week after failure of first-line eradication therapy with a PPI, amoxicillin, and clarithromycin and that the trend was stable over 5 years

with a reported overall second-line eradication rate of 92.4% [12]. Another group reported a prospective study of patients with antibiotic resistance and found excellent eradication Alvelestat chemical structure rates of 88.6% in this population when culture-based selection for second-line therapy was employed [13]. When treatment failure occurred, the interval between first-line H. pylori eradication treatment and second-line treatment may be critical to the second-line

therapeutic effect. A Japanese study reported an 88.6% ITT eradication rate for those treated with PPI, amoxicillin (1500 mg/day), and metronidazole (500 mg/day) for 1 week within 6 months of initial treatment failure compared with 68.8% when the second-line therapy was commenced after more than 180 days [14]. On the issue of third-line therapy, a multicenter study also from Japan compared several options for rescue treatment and found triple therapy with PPI, amoxicillin, and sitafloxacin as the best option with 70% eradication and only 7.7% resistance [15]. A very comprehensive review article this year suggested that in general clinical practice, levofloxacin–amoxicillin–PPI given twice daily, unless regional or new data show high quinolone resistance, is a good second-line combination [16]. In one other study, doxycycline was seen to have no efficacy against H. pylori in a series of 16 patients with multiresistant strains when used Bcl-w with PPI and amoxicillin [17]. There have been several studies again this year examining sequential and concomitant (non-bismuth quadruple) therapy, both in comparison with

standard triple therapy and each other. Sequential therapy consists of 5 days of PPI therapy plus amoxicillin, followed by a further 5 days of PPI with two other antibiotics, usually clarithromycin and metronidazole. By contrast, concomitant therapy involves maintaining three antibiotics along with the PPI for the duration of therapy. A very large and comprehensive meta-analysis and systematic review of studies looking at 5666 patients receiving sequential therapy compared with 7866 receiving other regimens concluded that the overall eradication rate of sequential therapy was suboptimal at 84.3% [18]. It was, however, superior to 7-day triple therapy (risk ratio (RR) 1.21, number needed to treat (NNT) of 6), and marginally superior to 10-day triple therapy (RR 1.

The results of an ELISPOT assay with more than 25 spots in the wells without peptides (control wells) were excluded from the analysis. IFN-γ ELISPOT assays were also performed

using PBMC-depleted CD4+ or CD8+ cells to determine what kind AZD3965 solubility dmso of T cell is responsive to the peptides. In the assay using PBMC-depleted CD4+ or CD8+ cells, the number of cells was adjusted to 3 − 105 cells/well after the depletion. Depletion of CD4+ or CD8+ cells was performed using the MACS separation system with CD4 or CD8 MicroBeads (Miltenyi Biotec, Auburn, CA) in accordance with the manufacturer’s instructions. For the detection of myeloid-derived suppressor cells (MDSCs), PBMCs were isolated from 20 randomly selected patients 2-4 weeks after HCC treatment. To determine the frequency of CD14+HLA-DR−/low MDSCs, two-color fluorescence-activated cell sorting analysis was performed buy GDC-0199 using the following antibodies: anti-CD14 and anti–HLA-DR (Becton Dickinson). Flow cytometry was performed using the FACSAria II system (Becton Dickinson). The frequency of CD14+HLA-DR−/low MDSCs was calculated as a percentage of HLA-DR−/low cells in CD14+ cells. Peptide MRP3765-,

AFP357-, AFP403-, and hTERT461-specific tetramers were purchased from Medical Biological Laboratories Co., Ltd. (Nagoya, Japan). PBMCs were stained with anti–CD8-APCAb (Becton Dickinson, Tokyo, Japan), anti–CCR7-FITCAb (eBioscience, Tokyo, Japan), anti–CD45RA-PerCP-Cy5.5Ab (eBioscience, Tokyo,

Japan), and tetramer-PE for 30 minutes at room temperature. Cells were washed, fixed with 0.5% paraformaldehyde/phosphate-buffered saline, and analyzed using the FACSAria II system. Data are expressed as the mean ± SD. The estimated probability of tumor recurrence-free survival was determined using the Kaplan-Meier method. The Mantel-Cox log-rank test was used to compare curves between groups. The prognostic factors for tumor recurrence-free Succinyl-CoA survival were analyzed for statistical significance using the Kaplan-Meier method (univariate) and the Cox proportional hazard model (multivariate). Linear regression lines for the relationship between the frequency of CD14+HLA-DR−/low MDSCs and the number of TAA-specific T cells were calculated using Pearson’s correlation coefficient. A level of P < 0.05 was considered significant. The clinical profiles of the 69 patients analyzed in the present study are shown in Table 1. HCC was histologically classified as well, moderately, and poorly differentiated in 7, 3, and 1 cases, respectively. In the other cases, HCC was diagnosed on the basis of typical CT findings and elevated AFP levels.

Our previous study using MEFs derived from CasΔex2/Δex2 mice showed that Cas Δex2 possesses reduced function in FN-mediated signaling.32 Thus, to examine the Cas requirement for SEC function, we first attempted to knock down endogenous Cas in NP31 cells by RNA interference. However, we found that NP31 cells rapidly lost fenestra formation when they were exposed to transfection reagents with nonspecific small interfering RNA Saracatinib ic50 or even no RNA (data not shown). We thus used an alternative Cas mutant overexpression approach. We used Cas ΔSH3 because the SH3 domain represents virtually the functional domain of exon 2 (Fig.

1) and other motifs in exon 2, YLVP and YQxPs, have been demonstrated to Ipatasertib clinical trial be redundant or dispensable for Cas-mediated signaling.34 In fact, Cas ΔSH3–expressing NP31 cells exhibited biochemical properties similar to those of

CasΔex2/Δex2 MEFs, such as impaired Cas tyrosine phosphorylation and reduced interaction of Cas with CrkII32 (Fig. 4). Thus, Cas ΔSH3 is biochemically equivalent to and functionally recapitulates Cas exon 2 deletion. In agreement with these biochemical alterations, we demonstrated that Cas ΔSH3 abolished reorganization of the actin cytoskeleton and critically inhibited the formation of fenestrae (Fig. 5). These findings strongly indicate that the Cas exon 2 deficiency affected actin cytoskeleton reorganization and SEC fenestration in CasΔex2/Δex2 embryos, and the impaired SEC fenestration subsequently induced massive hepatocyte apoptosis during liver development. Previous in vitro studies in SECs showed that

treatment of the cells with anti-actin agents and artificial modulation of Rho small GTPases impaired SEC fenestration35-40; in addition, SEC fenestration was required for hepatocyte survival.5, 6 These findings are consistent with the notion described previously. Monoiodotyrosine The current study highlights the importance of Cas in liver development. It also unveils an unexpectedly intimate interaction between SEC cytoskeletal turnover and hepatocyte development by illustrating the indirect influence of SEC fenestration on hepatocyte survival. It has previously been reported that the numbers and diameters of fenestrae are sensitive to growth factors such as vascular endothelial growth factor,41-43 endothelin-1,44-46 and transforming growth factor β.43 Intriguingly, these factors are known to tyrosine-phosphorylate Cas,47-49 and this strongly suggests that Cas tyrosine phosphorylation is involved in the induced changes of fenestrae. Defenestration has been reported in various liver diseases such as alcoholic liver damage,50, 51 hepatitis and liver cirrhosis,52, 53 and liver cancer54, 55 and causes portal hypertension and liver dysfunction.

To calculate net benefits, the quality adjusted life year, that significantly reflects such health gain, has to be compared with specific economic impacts. Differences in data sources, in medical practice and/or in healthcare systems and costs, imply that most current pharmacoeconomic analyses are confined to a narrow healthcare payer perspective. Long-term/lifetime prospective or observational studies, devoted to a careful definition of when to start a treatment; of regimens (dose and type of product) to employ, and of inhibitor population (children/adults, low-responding/high responding inhibitors)

to study, are thus urgently needed to allow for newer insights, based on reliable data sources into resource allocation, effectiveness and cost-utility analysis in the treatment of haemophiliacs with inhibitors. Trametinib “
“Therapy with fresh frozen plasma (FFP) confers serious

risks, such as contraction of blood-borne viruses, allergic reaction, volume overload and development of alloantibodies. The aim of this study was to apply principles SB203580 of pharmacokinetic (PK) modelling to individual factor content of FFP to optimize individualized dosing, while minimizing potential risks of therapy. We used PK modelling to successfully target individual factor replacement in an 8-month-old patient receiving FFP for treatment of a severe congenital factor V (FV) deficiency. The model fit for the FV activity vs. time data was excellent (r = 0.98) and the model accurately predicted FV activity during the intraoperative and postoperative period. Accurate PK modelling ID-8 of individual factor activity in FFP has the potential to provide better targeted therapy, enabling clinicians to more precisely dose patients requiring coagulation products, while avoiding wasteful and expensive product overtreatment, minimizing potentially life-threatening complications due

to undertreatment and limiting harmful product-associated risks. “
“Summary.  All UK patients with bleeding disorders treated with any UK-sourced pooled factor concentrates between 1980 and 2001 have been informed that they may be at an increased risk of infection with variant Creutzfeldt–Jakob disease (vCJD). We describe a study to detect disease-associated, protease-resistant prion protein (PrPres) in 17 neurologically aysmptomatic patients with haemophilia considered to be at increased risk of vCJD. Materials from 11 autopsy and seven biopsy cases were analysed for PrPres. The tissues available from each case were variable, ranging from a single biopsy sample to a wide range of autopsy tissues. A single specimen from the spleen of one autopsy case gave a strong positive result on repeated testing for PrPres by Western blot analysis. This tissue came from a 73-year-old male patient with no history of neurological disease, who was heterozygous (methionine/valine) at codon 129 in the prion protein gene.

(HEPATOLOGY 2011;.) Hepatocellular carcinoma (also called malignant hepatoma) is one of the most common malignant tumors and the third leading cause of cancer mortality worldwide.1 Despite many efforts to develop various classes of agents, systemic chemotherapy and hormone therapy have failed to significantly increase the survival of patients with advanced hepatoma. However, recent advances in the understanding of hepatoma progression have led to the development of novel molecularly targeted therapies.2 Because angiogenesis is pivotal for the development and progression of hepatoma,

key molecules Alectinib regulating angiogenesis are regarded as promising targets for treating hepatoma.3 Hypoxia inevitably develops in rapidly growing tumors and is an important microenvironment that forces changes in tumor behavior. In particular, hypoxia activates hypoxia-inducible factor-1α (HIF-1α), which promotes the progression of malignancy by stimulating angiogenesis and by augmenting the ability of tumors to survive.4, 5 The roles of

HIF-1α have been extensively investigated in cancer patients and in tumor-bearing mice.6, 7 Consequently, HIF-1α is believed to be a valid target for the treatment of aggressive tumors, and many efforts have been made to identify suitable HIF-1α inhibitors.8 Chaetocin, which is produced by Chaetomium sp., is an antibiotic having the thiodioxopiperazine structure (a disulfide-bridged Selleck MLN2238 piperazine).9 Other thiodioxopiperazines are known to have antimicrobial, antiviral, immunosuppressive, and antiinflammatory activities,10, 11 but the biological activity of chaetocin has been reported in relatively few reports. In one such report, it was suggested that chaetocin inhibits the histone methyltransferase suv39H1.12 Recently, it was also demonstrated that chaetocin induces apoptosis of myeloma cells and retards the growth of myeloma xenografts.13 Mechanistically, it was

proposed that chaetocin produces oxidative damage in myeloma cells by inhibiting the antioxidant enzyme thioredoxin reductase.14 However, little is known about the effects of chaetocin on solid tumors, and thus we tested the anticancer activity of chaetocin against solid tumors. Here we demonstrated that chaetocin has Coproporphyrinogen III oxidase antiangiogenic and anticancer activities in hepatoma and fibrosarcoma grafts, and that these actions of chaetocin are due to HIF-1α down-regulation caused by the deregulation of HIF-1α premessenger RNA (pre-mRNA) splicing. ATP, adenosine triphosphate; CA9, carbonic anhydrase 9; EPO, erythropoietin; HIF, hypoxia-inducible factor; MEF, mouse embryonic fibroblast; PDK1, pyruvate dehydrogenase kinase 1; PHD, prolyl-hydroxylase domain protein; RCC, renal cell carcinoma; VEGF, vascular endothelial growth factor; VHL, von Hippel-Lindau.

7). To validate our microarray data, we analyzed the expression patterns of a set of ERSR markers by ISH. Interestingly, these genes are selectively overexpressed in hi559 liver (Fig. 6A-F). Together, these data implicate lack of PtdIns synthesis in leading to hepatocellular ER

stress, causing the hepatic pathology in hi559 larvae.6 We performed transmission electron microscopy to analyze the ultrastructural pathology of hi559 hepatocytes. Wild-type hepatocytes exhibit a homogeneous, grainy cytoplasm, generally without clearing areas (Fig. 7A). By contrast, the hi559 hepatocytes have abnormal mitochondria, large cytoplasmic clearing areas with several membrane-bound structures containing granular materials (Fig. 7B). Irregularly shaped lipolysosomes containing lipid droplets of variable electron density are frequently Trichostatin A supplier seen in hi559 hepatocytes (Fig. 7F). Most strikingly, hi559 hepatocytes have large, excessively dilated (luminal swelling), abnormally

distributed ER (Fig. 7C,D). It appears that the prominent clearing areas in hi559 hepatocytes may be the sequelae Cytoskeletal Signaling inhibitor of excessive ER luminal swelling and vacuolation. The lumens of the expanded ER in hi559 hepatocytes are often filled with aggregates of variable electron density, suggestive of accumulated proteins (Fig. 7E). In some instances, the ER membranes are selectively sequestered and tightly packaged into autophagosome-like structures (Fig. 7G). Aggregates of macrophages are noticed adjacent to the necrotic hepatocytes, indicating mild inflammation (Fig. 7H.) These ultrastructural pathologies are consistent with chronic unresolved ER stress and resemble that seen in NAFLD. While analyzing the expression of ER stress markers, we noticed elevated expression of the crucial ER stress sensor http://www.selleck.co.jp/products/AG-014699.html hspa5 in hi559 livers at 4 dpf prior to onset of the hepatic phenotype (Fig. 8A). This implicates that hepatocellular ER stress may be a major contributor to the hepatic steatosis seen in hi559 larvae at 5 dpf. To test whether ER stress during this developmental stage could

cause hepatic steatosis, we treated wild-type larvae with tunicamycin, an inhibitor of protein N-glycosylation that induces ER stress. Chronic treatment with 1 μM tunicamycin from 3.5 dpf through 5.5 dpf induced defects similar to those seen in hi559 larvae in ≈90% of the treated larvae (Fig. 8B-E). Larvae subsequently die at 6 to 7 dpf, similar to hi559, when tunicamycin treatment was continued. Induction of ER stress upon tunicamycin treatment was confirmed by ISH with the crucial ER stress marker hspa5. The ubiquitously elevated expression of hspa5 was apparent in tunicamycin-treated larvae (Fig. 8C). Whole-mount ORO staining further confirmed the development of fatty liver in tunicamycin-treated larvae (Fig. 8D).

Key Word(s): 1. ulcerative colitis; 2. DAIKENCHUTO; 3. serum bile acid; Presenting Author: Cilomilast research buy ROBERTA PICA Additional Authors: ELEONORAVERONICA AVALLONE, CLAUDIO

CASSIERI, MADDALENA ZIPPI, PAOLO PAOLUZI Corresponding Author: ROBERTA PICA Affiliations: IG-IBD Objective: The true prevalence of colonic diverticulosis (CD) is difficult to measure because most individuals are asymptomatic. In literature, there are few study about the prevalence of CD in patients affected by ulcerative colitis (UC). Aim of this study has been to investigate the prevalence of CD in UC and in adult patients referred in a single centre. Methods: Computerized data of consecutive patients, referred to our Institution to undergo a colonoscopy for colorectal cancer screening (CCS) and/or for UC control, between January 1, 2009 and December 31, 2009, were retrospectively studied. Results: Six hundred and five consecutive patients were included in the study. Of these patients, 438 (72.4%) underwent colonoscopy for colorectal cancer screening (Group A) and 167 (27.6%) for UC control (Group B). In group A 224 patients (51.1%) were male (average age of 62.7 ± 14.2

SD years), in group B 102 (61.1%) were male (average age of 57.6 ± 12.1 SD years). Prevalence of CD was higher in group A (122 patients, 27.8%) than group B (18 patients, 10.8%) (p < 0.0001). Female gender in patients with CD was higher ACP-196 ic50 in group A than group B (68 patients, 55.7% and 4 patients, 22.2%, respectively) (p = 0.0106). In group A sigma and left colon was involved in 119 (97.6%) patients versus 12 (66.7%) of Group B (p = 0.0001), in Group B the right colon was involved in 4 (22.2%) patients versus 1 (0.8%) of Group A (p = 0.0009). Conclusion: Prevalence of CD was significantly lower in patients with UC than in adult population. Key Word(s): 1. ULCERATIVE COLITIS; 2. DIVERTICULOSIS; 3. IBD; Presenting Author: ANILK VERMA Additional Authors: URVASHIB SINGH, MANVI MISHRA, POOJA PANDEY, ASHA MISHRA, KAMLESH PANDEY, SIDDHARTHADATTA GUPTA GUPTA, VINEET AHUJA, HK PRASAD, GOVINDK MAKHARIA Corresponding

Cyclooxygenase (COX) Author: GOVINDK MAKHARIA Affiliations: All India Institute of Medical Sciences Objective: Similarity in the clinical, histological, endoscopic features between intestinal tuberculosis and Crohn’s disease (CD), mycobacterial pathogens, specifically Mycobacterium aviumparatuberculosis (MAP) has been thought to be a candidate pathogen for CD. The present study involves the detectionMAP in patients with CD and other inflammatory diseases such as ulcerative colitis (UC) and intestinal tuberculosis (ITB) and controls. Methods: Colonic biopsies from macroscopically affected and unaffected colonic mucosa and blood for buffy coat were obtained from 178 subjects (CD; n = 40), (UC; n = 48), (ITB; n = 46), and controls (n = 44).

Key Word(s): 1. ulcerative colitis; 2. DAIKENCHUTO; 3. serum bile acid; Presenting Author: Metformin concentration ROBERTA PICA Additional Authors: ELEONORAVERONICA AVALLONE, CLAUDIO

CASSIERI, MADDALENA ZIPPI, PAOLO PAOLUZI Corresponding Author: ROBERTA PICA Affiliations: IG-IBD Objective: The true prevalence of colonic diverticulosis (CD) is difficult to measure because most individuals are asymptomatic. In literature, there are few study about the prevalence of CD in patients affected by ulcerative colitis (UC). Aim of this study has been to investigate the prevalence of CD in UC and in adult patients referred in a single centre. Methods: Computerized data of consecutive patients, referred to our Institution to undergo a colonoscopy for colorectal cancer screening (CCS) and/or for UC control, between January 1, 2009 and December 31, 2009, were retrospectively studied. Results: Six hundred and five consecutive patients were included in the study. Of these patients, 438 (72.4%) underwent colonoscopy for colorectal cancer screening (Group A) and 167 (27.6%) for UC control (Group B). In group A 224 patients (51.1%) were male (average age of 62.7 ± 14.2

SD years), in group B 102 (61.1%) were male (average age of 57.6 ± 12.1 SD years). Prevalence of CD was higher in group A (122 patients, 27.8%) than group B (18 patients, 10.8%) (p < 0.0001). Female gender in patients with CD was higher check details in group A than group B (68 patients, 55.7% and 4 patients, 22.2%, respectively) (p = 0.0106). In group A sigma and left colon was involved in 119 (97.6%) patients versus 12 (66.7%) of Group B (p = 0.0001), in Group B the right colon was involved in 4 (22.2%) patients versus 1 (0.8%) of Group A (p = 0.0009). Conclusion: Prevalence of CD was significantly lower in patients with UC than in adult population. Key Word(s): 1. ULCERATIVE COLITIS; 2. DIVERTICULOSIS; 3. IBD; Presenting Author: ANILK VERMA Additional Authors: URVASHIB SINGH, MANVI MISHRA, POOJA PANDEY, ASHA MISHRA, KAMLESH PANDEY, SIDDHARTHADATTA GUPTA GUPTA, VINEET AHUJA, HK PRASAD, GOVINDK MAKHARIA Corresponding

Ergoloid Author: GOVINDK MAKHARIA Affiliations: All India Institute of Medical Sciences Objective: Similarity in the clinical, histological, endoscopic features between intestinal tuberculosis and Crohn’s disease (CD), mycobacterial pathogens, specifically Mycobacterium aviumparatuberculosis (MAP) has been thought to be a candidate pathogen for CD. The present study involves the detectionMAP in patients with CD and other inflammatory diseases such as ulcerative colitis (UC) and intestinal tuberculosis (ITB) and controls. Methods: Colonic biopsies from macroscopically affected and unaffected colonic mucosa and blood for buffy coat were obtained from 178 subjects (CD; n = 40), (UC; n = 48), (ITB; n = 46), and controls (n = 44).