No such

No such Selleckchem Vemurafenib difference was found for birds and mammals. Second, the relative proportions of presumably more palatable and presumably less palatable prey differed. The relative proportions of mice and voles (the latter eaten more frequently) and the

relative proportions of soricomorphs and rodents (the latter eaten more frequently) were different. Finally, small prey items (i.e. invertebrates) were recorded incompletely for the brought-home method. Overall, the prey-brought-home method underrepresented small prey and underestimated the predation rate for cats, whereas the prey-eaten method was less likely to record unpalatable prey. We thus recommend to combine these two methods to obtain fuller and truer assessment of cat predation. “
“Rare and elusive species are seldom the first choice of model for the study of ecological questions, yet rarity and elusiveness often emerge from ecological processes. One of these processes is interspecific killing, the most extreme form of interference competition among carnivores. Subdominant species can avoid falling victim to other carnivores through spatial and/or temporal separation. The smallest carnivore species, including

members of the Mustelidae, are typically the most threatened by other predators but are also exceedingly challenging to study in the wild. As a consequence, we have only limited knowledge of how the most at-risk members of carnivore communities deal with being both hunters and hunted. We explored whether activity and space use of a little-known small carnivore, Liothyronine Sodium Erlotinib mw the Altai mountain weasel Mustela altaica, reflect the activity and distribution of its main prey, pika Ochotona sp., and two sympatric predators, the stone marten Martes foina and the red fox Vulpes vulpes. Spatial and temporal patterns of photographic captures in Pakistan’s northern mountains suggest that weasels may cope with being both predator and prey by frequenting areas used by pikas while exhibiting

diurnal activity that contrasts with that of the mostly nocturnal/crepuscular stone marten and red fox. Camera trap studies are now common and are staged in many different ecosystems. The data yielded offer an opportunity not only to fill knowledge gaps concerning less-studied species but also to non-invasively test ecological hypotheses linked with rarity and elusiveness. “
“Survival and consequent implications for population dynamics in the subtropical Striped Frog Hypsiboas leptolineatus was studied for 1 year in the southern Brazilian state of Paraná. By means of capture-marking-recapture, we estimated survival and capture probabilities in an open population. A total of 583 captures of 374 individuals, comprising 96% male (n = 353) and 4% females (n = 21), resulted in daily survival estimates ranging from 0.808 to 0.998 day−1.

Conclusion: Gastrointestinal

malignancy is 8-fold higher

Conclusion: Gastrointestinal

malignancy is 8-fold higher in PSC-IBD patients compared to those with IBD alone with up to 25-fold higher frequency of hepatobiliary cancers that include hepatocellular carcinomas. Hepatobiliary cancer screening in patients with PSC-IBD can be recommended. 1. Claessen M, Lutgens M, van Buuren H, Oldenburg B, Stokkers PC, van der Woude C, et al. More right-sided IBD-associated colorectal cancer in patients with primary sclerosing cholangitis. Inflamm Bowel Dis. 2009;15:1331–1336. MK SANDHU, W CUI, AE BLOCH, DM ISER, T NGUYEN, M RYAN, R CHEN, B DEMEDIUK, RG SHAW, SJ BELL, PV DESMOND, AJ THOMPSON St Vincent’s Hospital Melbourne, Victoria, Australia Background: Diagnostic criteria for PBC include elevated

serum ALP and positive AMA (titer ≥1:40). www.selleckchem.com/products/PD-0332991.html PBC is associated with progressive liver disease, but this may be prevented in responders to ursodeoxycholic acid (UDCA). The clinical significance of positive AMA serology with normal ALP is not clear. There are limited Australian data describing the natural history of PBC and no Australia data for patients with positive AMA serology but normal ALP. We therefore performed a retrospective Acalabrutinib mw analysis of the clinical features and outcomes of patients with positive AMA serology over a 10 year period at a large tertiary referral center. Methods: Patients were identified through hospital pathology (AMA) and pharmacy claims data (UDCA) between 2003 and 2013. The diagnosis of PBC was made in the setting of an elevated ALP and a positive AMA (titer ≥1:40). We performed a cross-sectional

comparison of the clinical characteristics of patients Oxymatrine with PBC vs. patients with positive AMA serology not meeting diagnostic criteria for PBC. Among patients with longitudinal data, we evaluated clinical outcome with a specific focus on the impact of therapy with UDCA. In patients meeting the criteria for PBC, treatment response was defined by >40% reduction, or normalization, of ALP at 1 year (Barcelona criteria). Results: 72 patients with positive AMA serology were identified. 33/72 (46%) patients met the diagnostic criteria for PBC, including 3 patients with PBC-AIH overlap. 7 patients had positive AMA, normal ALP, but characteristic histology and were classified as PBC for this analysis. 32/72 (44%) patients had positive AMA serology but normal ALP; 4 patients in this group had positive HCV serology. The majority of patients were female and Caucasian (>80%); PBC patients were older and more likely to have advanced liver fibrosis, but there were no other significant differences between the groups. Longitudinal follow-up was available for the majority (63 [88%], median duration 60 [24–120] months). 9 PBC patients were lost to follow-up after diagnosis. 29/31(94%) patients with PBC were treated with UDCA. 2 PBC patients did not receive UDCA – both presented with advanced disease and were palliated.

Similar quantities of mannans and SPs were reported previously in

Similar quantities of mannans and SPs were reported previously in the related seaweed C. fragile (Suringar) Hariot. Overall, both seaweed cell walls comprise ∼40%–44% of their dry weights. Within the SP group, a variety of polysaccharide structures from pyruvylated

arabinogalactan sulfate and pyruvylated galactan sulfate to pyranosic arabinan sulfate are present in Codium cell walls. In this paper, the in situ distribution of the main cell-wall polymers in the green seaweed C. vermilara was studied, comparing their arrangements with those observed in cell walls from C. fragile. The utricle cell wall in C. vermilara showed by TEM a sandwich structure of two fibrillar-like layers of similar width delimiting a middle amorphous-like zone. By immuno- and chemical imaging, the in situ Selleckchem Y 27632 distribution of β-(14)-d-mannans and HRGP-like epitopes was shown to consist of two distinct cell-wall layers, whereas SPs are distributed Vemurafenib mw in the middle area of the wall. The overall cell-wall polymer arrangement of the SPs, HRGP-like epitopes, and mannans in the utricles of C. vermilara is different from the ubiquitous green algae C. fragile, in spite of both being phylogenetically very close. In addition, a preliminary cell-wall model of the utricle moiety is proposed for both seaweeds, C. fragile and

C. vermilara. “
“GTPases of the Ras superfamily regulate a wide variety of cellular processes including vesicular transport and various secretory pathways of the cell. ADP –

ribosylation factor (ARF) belongs to one of the five major families of the Ras superfamily and serves as an mafosfamide important component of vesicle formation and transport machinery of the cells. The binding of GTP to these Arfs and its subsequent hydrolysis, induces conformational changes in these proteins leading to their enzymatic activities. The dimeric form of Arf is associated with membrane pinch-off during vesicle formation. In this report, we have identified an arf gene from the unicellular green alga Chlamydomonas reinhardtii, CrArf, and showed that the oligomeric state of the protein in C. renhardtii is modulated by the cellular membrane environment of the organism. Protein cross-linking experiments showed that the purified recombinant CrArf has the ability to form a dimer. Both the 20-kDa monomeric and 40-kDa dimeric forms of CrArf were recognized from Chlamydomonas total cell lysate (CrTLC) and purified recombinant CrArf by the CrArf specific antibody. The membranous environment of the cell appeared to facilitate dimerization of the CrArf, as dimeric form was found exclusively associated with the membrane bound organelles. The subcellular localization studies in Chlamydomonas suggested that CrArf mainly localized in the cytosol and was mislocalized in vesicle transport machinery inhibitor treated cells.

Using confocal microscopy, we corroborated the findings that acti

Using confocal microscopy, we corroborated the findings that activated EGFR was up-regulated in the bEnd3 cells and that EGFR activation was prevented with GM6001 (Fig. 3C). These findings confirmed that EGFR is transactivated by MMP-9 in bEnd3 cells. We then determined whether EGFR would directly influence the p38 MAPK activation with subsequent occludin alterations. As shown in Fig. 4, the specific EGFR inhibitor AG1478 significantly reduced the p38 MAPK activation and occludin loss in a dose-dependent manner. Importantly, p38 MAPK activation and suppression of occludin were similarly blocked by EGFR siRNA (Fig. 4). Overall, EGFR inhibition with AG1478 or

EGFR deletion with siRNA blocked p38 MAPK phosphorylation and restored occludin in brain EC. Apoptosis inhibitor Previously, we demonstrated that in ALF mice, occludin was significantly perturbed.5 In the present study, we assessed the role of EGFR activation and its associated p38 MAPK/NFκB signaling in brains of ALF mice. We showed by western blotting that occludin was significantly altered

in the brains of ALF mice and the alteration was restored with GM6001 treatment. These results are consistent with our previous report.5 Importantly, we observed Selumetinib datasheet EGFR activation along with p38 MAPK activation and IκBα degradation in the brains of ALF mice (Fig. 5A,B). With confocal microscopy, we substantiated that significant EGFR activation occurred in brains of ALF mice and that EGFR activation was attenuated with GM6001 treatment (Fig. 5C). In contrast, brains of normal control mice showed no EGFR activation. We observed spontaneous hypothermia in AOM-induced ALF mice (Fig. 6A). With heat support, the body temperature of AOM mice was maintained at normothermia.

Treatment with GM6001 did not Liothyronine Sodium alter the body temperature of the study mice (Fig. 6B). As shown in Fig. 6C,D, we observed that the occludin alteration in AOM-induced ALF mice was independent of body temperature and was reversed with GM6001. In addition, to investigate whether the occludin alteration occurs in other model of ALF, we employed a well-established model using tumor necrosis factor-alpha (TNFα) and D-galactosamine (Gal).36 We found that occludin was decreased in brains of the Gal/TNFα-induced ALF mice and that the occludin alteration was reversed with GM6001 treatment and was independent of body temperature (Fig. 6E,F). These results from AOM-induced ALF mice are consistent with the findings in vitro, suggesting that MMP-9 induced EGFR transactivation and that p38 MAPK/NFκB signaling plays an important role in regulating BBB TJ proteins in ALF. Collectively, our findings suggest that in addition to its direct proteolytic action,5 MMP-9 influences the TJ protein occludin in an indirect way through the following series of steps: first by transactivating EGFR on the bEnd3 cellular surface, second by up-regulating p38 MAPK, third by IκBα degradation and NFκB activation, and finally by suppressing occludin expression.

AMT, accurate mass and time; AUC, area under the receiver operati

AMT, accurate mass and time; AUC, area under the receiver operating characteristic curve; CBS, cystathionine beta synthase; selleck chemicals FAM3C, family with sequence similarity 3, member C; GST, glutathione S-transferase; HCV, hepatitis C virus; HDAC, histone deacetylase; HLA-C, major histocompatibility class 1 antigen C; IGFBP7, insulin-like growth factor binding protein 7; IPA, Ingenuity Pathways Analysis; LC-MS, liquid chromatography/mass spectrometry; LGALS3, galectin 3; MYH11, myosin, heavy chain 11; PRKAR2A, protein kinase A RII alpha; SVD-MDS, singular value

decomposition initialized multidimensional scaling; TPM1, tropomyosin 1. This study was approved by the Institutional Review Boards for Human Subject Review at both the University of Washington and Pacific Northwest National Laboratory in accordance with federal regulations. All percutaneous core needle biopsy and serum specimens were obtained with written informed consent from HCV-infected patients who underwent liver transplantation at the

University of Washington Medical Center during 2003-2004. No donor livers were obtained from executed prisoners or other institutionalized persons. For proteome analysis, the analyzed cohort contained a total of 24 biopsy specimens obtained from 15 patients (Supporting Table 1). Statistical comparisons of clinical covariates were performed using JMP version 6.0 (SAS Institute, Cary, NC) and are reported in Table 1. An independent Student t test was used for continuous variables and a two-tailed Fisher’s exact test buy MK0683 was used for categorical variables; P ≤ 0.05 was considered statistically significant. For metabolite analysis, the analyzed cohort contained serum samples from a total Montelukast Sodium of 60 patients, including six represented in our proteome analysis (Supporting Table 2). All patients underwent transplantation due to HCV-associated cirrhosis, and all developed recurrent HCV infection. Fibrosis stage was scored by histological evaluation performed by a single pathologist using the Batts-Ludwig

scoring system.11 At the time of biopsy, all research samples were collected at the bedside, flash frozen, and stored at −80°C until use. Peptide digests were prepared as previously described3, 5 and analyzed in triplicate utilizing a high mass accuracy liquid chromatography/mass spectrometry (LC-MS) Exactive platform (Thermo Electron Corporation, San Jose, CA). Identification of the detected peptide peaks was performed using the accurate mass and time (AMT) tag approach as described.3, 5, 12 Data quality was assessed at the technical replicate level via Pearson correlation. Mass spectrometry runs exhibiting considerable deviation based on both correlation and peptide coverage in comparison to technical and biological replicates were removed from the dataset.

IL-33 staining by IHC demonstrated strong nuclear positivity in K

IL-33 staining by IHC demonstrated strong nuclear positivity in Kupfer cells and venous endothelial cells, in only one of 5 subjects examined. No hepatocyte stained positive. Mice fed HFD developed significant steatosis and HFD feeding for 24, but not for 8 weeks, was associated with a 6-fold increase in hepatic Il33 expression. Conclusion: Steatosis causes an increase in IL-33 expression

in the liver and the expression seems to be limited to non-parenchymal cells. In patients with NASH, there is marked increase in circulating PD0325901 cost sST2 levels, which are associated with histological and biochemical disease activity. IL-33 levels are not detectable in these patients, possibly because of take-up by the sST2 over-abundance. Further studies to elucidate the mechanistic role of the IL-33/sST2 axis in the pathogenesis of NASH progression are warranted. Disclosures: The following people have nothing to disclose: Gihan Naguib, Jason L. Eccleston, Koji Fujita, Niharika Samala, Mary Walter, Yaron Rotman Non-alcoholic fatty liver

disease begins with liver accumulation of triglycerides, which eventually lead to non-alcoholic steatohepatitis (NASH) and finally to liver fibrosis. Also, ste-atosis-induced DNA damage is involved in this degenerative process. 5-methyl-1-phenyl-2- (1H)-pyridone (Pirfenidone, PFD) has been used for human chronic inflammation and fibrogenesis. Furthermore, pharmacological modulation of cannabinoid type 1 receptor by synthetic selleck compound antagonist SR141716A is associated with liver damage reduction. We aimed to determine the protective effect of PFD+SR141716A

in liver damage induced by experimental steatosis. Male C57/BL6 mice were fed with control diet (CD) or high-fat/carbohydrate diet (HFHC) (60% fat, 20% protein, 35% carbohydrate, and 55% fructose/45% sucrose in drink water) for 16 weeks (methionine/choline-deficient diet (MCD) was used as steatosis control), PFD 100 mg/ kg/d or SR141716A 3 mg/kg/d Methamphetamine was administered intragas- trically. Compared with HFHC mice, HFHC+PFD/SR141716A mice had significantly less weight gain, fat mass, lower blood glucose, insulinemia and hepatic steatosis and reduced circulating levels of triglycerides. However, triglycerides plasma levels in HFHC+PFD mice were similar. ALT and AST level caused by HFHC and MCD diets was significantly reduced by PFD+SR141716A regimen. PFD down-regulates mRNA expression of COL1A1 and TGFβ1 in HFHC mice, which is associated to lower liver histologic features of fibrosis. Additionally, PFD down-regulates serum IL1 β, IL6, IL17A and TNFα in HFHC mice, associated with decreased liver inflammation. PFD displayed a slight IL10 increase, which may explain reduction of inflammatory mediators and improvement of liver markers. Finally, Mice fed with HFHC diet develop a high number of micronuclei caused by DNA damage, fact prevented by PFD supplementation.

e , fitness) of the variants Conclusion: Although resistance eme

e., fitness) of the variants. Conclusion: Although resistance emerged during monotherapy with BMS-790052, the substantial anti-HCV effect of this compound makes it an excellent candidate for effective combination

therapy. (HEPATOLOGY 2011) The hepatitis C virus (HCV) nonstructural protein 5A (NS5A) is a multifunctional protein with key roles in HCV replication. NS5A has also been implicated in the modulation of cellular signaling pathways.1, 2 Because it is required in vivo and in vitro for viral replication and has no known human homologs, NS5A provides an attractive PLX4032 concentration target for therapeutic intervention.3 BMS-790052 is a potent HCV

NS5A replication complex inhibitor, with 50% effective concentration (EC50) values of 9 and 50 pM against genotype 1b and 1a replicons, respectively.4, 5 It is also potent against live virus (genotype 2a, JFH-1), with an EC50 of ∼28 pM.4 BMS-790052 has broad genotype coverage, with EC50 values ranging from pM to low nM for replicons with NS5A sequences derived this website from genotype 2a, 3a, 4a, and 5a.4 Proof of concept for BMS-790052 has been achieved clinically, where its exceptional in vitro potency translated to an in vivo effect in a single-ascending dose study.4 In this study, marked HCV RNA decline (∼2.9 log10) was needed for detection of resistant variants, suggesting that the variants were likely present as preexisting minor quasi species and were uncovered by the efficient suppression of wild-type

virus.4 However, the ability of BMS-790052 to further suppress viral replication with continuous dosing could not be assessed in the single-ascending Paclitaxel manufacturer dose study. In addition, analysis of specimens from the single-ascending dose study did not reveal whether the resistance detected clinically correlates with resistance observed in the in vitro replicon system. In the multiple-ascending dose (MAD) study reported here, a total of 24 chronically infected patients (4 active patients per cohort) were treated with BMS-790052 at 1, 10, 30, 60, and 100 mg once-daily or 30 mg twice-daily for 14 days. The treated patients generally experienced rapid, marked viral load declines. However, HCV RNA remained detectable in all genotype 1a–infected patients, and viral breakthrough was observed during the course of treatment in the majority of these patients. In contrast, viral breakthrough was observed less often in patients infected with HCV genotype 1b, and, in several patients, HCV RNA dropped below the level of quantitation (<25 IU/mL).

001) The mean fracture resistances (N) were: Gr1 = 1168 ± 157,a

001). The mean fracture resistances (N) were: Gr1 = 1168 ± 157,a check details Gr2 = 360 ± 110,d Gr3 = 1026 ± 188,b Gr4 = 887 ± 143,c Gr5 = 1007 ± 132,b Gr6 = 810 ± 164,c Gr7 = 1033 ± 218,a Gr8 = 955 ± 147,ab Gr9 = 780 ± 86c (groups with the same superscript letter indicate statistical similarity). Combining an OX with three resin cements

had a significant negative effect on the fracture resistance of premolars restored with composite inlay cemented with Panavia F2.0 and Variolink II, but it had no significant effect when cemented with Duolink. “
“Purpose: To investigate the reliability of titanium abutments veneered with indirect composites for implant-supported crowns and the possibility to trace back the fracture origin by qualitative fractographic analysis. Materials and Methods: Large base (LB) (6.4-mm diameter base, with a 4-mm high cone in the center for composite retention), small base (SB-4) (5.2-mm base, 4-mm high cone),

and small base with cone shortened to 2 mm (SB-2) Ti abutments were used. Each abutment received incremental layers of indirect resin composite until completing the anatomy of a maxillary molar crown. Step-stress accelerated-life fatigue https://www.selleckchem.com/btk.html testing (n = 18 each) was performed in water. Weibull curves with use stress of 200 N for 50,000 and 100,000 cycles were calculated. Probability Weibull plots examined the differences between groups. Specimens were inspected in light-polarized and scanning electron microscopes for fractographic analysis. Results: Use level probability Weibull plots showed Beta values HSP90 of 0.27 for LB, 0.32 for SB-4, and 0.26 for SB-2, indicating that failures were not influenced by fatigue and damage accumulation. The data replotted as Weibull distribution showed no significant difference in the characteristic strengths between LB (794 N) and SB-4 abutments (836 N), which were both significantly higher than SB-2 (601 N). Failure mode was cohesive within the composite for all groups. Fractographic markings

showed that failures initiated at the indentation area and propagated toward the margins of cohesively failed composite. Conclusions: Reliability was not influenced by abutment design. Qualitative fractographic analysis of the failed indirect composite was feasible. “
“The following article from Journal of Prosthodontics, “Effect of Chemical Disinfectants and Repair Materials on the Transverse Strength of Repaired Heat-Polymerized Acrylic Resin,”[4] by Ayman E. Ellakwa and Ali M. El-Sheikh, published online on September 4, 2006 in Wiley Online Library (http://wileyonlinelibrary.com), has been retracted by agreement between the authors, the journal Editor-in-Chief, Dr. David A. Felton and Wiley Periodicals, Inc.

Conversely, a higher level of education, fruit, and vegetable int

Conversely, a higher level of education, fruit, and vegetable intake were LEE011 associated with a decreased risk. The only region-specific factor was the positive association with chili pepper reported in at least five studies.

Competing interests: the authors have no competing interests. “
“Over the last 12 months, new insights into the association of non-Helicobacter pylori Helicobacters with a range of human diseases in children and adults, including hepatobiliary disease, Crohn’s disease, sepsis, and gastric disease were published. Studies investigating the presence of non-H. pylori Helicobacters in domestic animals reinforce previous findings that cats and dogs harbor gastric Helicobacter species and thus may be an important source of these organisms in humans. The confounding effect of enterohepatic Helicobacters on the outcome of biomedical research was investigated in several studies and led to recommendations that animals should be

screened prior to performing experiments. A number of important and novel investigations regarding pathogenic mechanisms and immune responses Autophagy Compound Library to enterohepatic Helicobacters were conducted. Genomic advances in non-H. pylori Helicobacters included description of the complete genome of Helicobacter canadensis, delineation of two Helicobacter bilis genomospecies, and identification of a novel cis-regulatory RNA. New insights concerning growth conditions, biochemical characterization, and the effect of certain dietary compounds on Helicobacter spp. have also been reported. In a study conducted in 77 children diagnosed with chronic liver disease, Casswall et al. using a Helicobacter genus-specific PCR, detected Helicobacter spp. Dichloromethane dehalogenase DNA in a liver biopsy from 1 child (4.2%) with autoimmune hepatitis (AIH), 3 children (11.1%) with primary sclerosing cholangitis (PSC) and 8.0% of controls. Sequencing of the PCR products

from AIH and PSC children showed these to be mostly similar to Helicobacter hepaticus, Helicobacter muridarum, Helicobacter canis and Helicobacter pylori, and to Helicobacter hepaticus, and Helicobacter pullorum in the controls [1]. Culture, nested PCR, and serology were used by Hamada et al. to determine the presence of enterohepatic Helicobacter spp. (EHH) in bile samples from patients with cholelithiasis (n = 60), cholecystitis and gastric cancer (n = 28), gall bladder polyps (n = 6), and 32 controls. Based on PCR and serology, H. hepaticus DNA was observed in 41% of cholelithiasis patients and 36% of cholecystitis and gastric cancer patients, which was significantly higher (p = 0.029) than in the two other groups. The authors concluded that H. hepaticus may be associated with diseases of the liver and biliary tract of humans [2]. In a further study, Kosaka et al. used Helicobacter bilis-specific primers to determine the presence of H.

In conclusion, the safety, effectiveness, and mechanism of action

In conclusion, the safety, effectiveness, and mechanism of action of intraportal-transplanted human BMSCs were demonstrated for the first time in a large animal (pig) model of FHF. The results suggest that immediate IPT of hBMSCs is a safe and effective treatment for FHF and that this method can possibly be used in future clinical therapy. We thank Yingjie Wang for helpful suggestions regarding the revised manuscript and Qiang Huang for helpful comments about animal experiments. Additional Supporting Information may be found in the online version of this article. “
“Background and Aim:  Endoscopic ultrasound

guided pancreatic pseudocyst drainage (EUS-PPD) is increasingly being used for management of pancreatic Rapamycin chemical structure pseudocysts.

We evaluated the outcome and complications of EUS-PPD with modified combined technique by inserting both endoprosthesis and naso-cystic drain. Methods:  Forty patients referred between August 2007 and January 2010 for EUS-PPD were prospectively studied. EUS-PPD was attempted for symptomatic pancreatic pseudocysts which were; (i) resistant to conservative treatment, (ii) in contact with the gastric or duodenal wall on EUS and (iii) having no bulge Copanlisib mw seen on endoscopy. Controlled radial expansion wire guided balloon dilation of the puncture tract was performed followed by insertion of a 10 French double pigtail stent and 7-Fr naso-biliary drain. The early and late outcome and complications of EUS-PPD were analyzed. Results:  Thirty-two patients had non-infected and eight had infected pseudocysts. EUS-PPD was technically successful in all. Pseudocysts resolved completely heptaminol in 39 patients, while one with infected pseudocyst underwent surgical resection for bleeding in the cyst. Naso-cystic drain was removed in 39 patients after median duration of 13 days. Thereafter, the double pigtail stent was removed in all cases after median duration of 10 weeks. Pseudocyst recurred in one patient requiring a second session of EUS-PPD. All 32 patients without cystic infection were successfully treated by EUS-PPD. Seven out of eight patients (87%) with cystic infection were successfully treated

by EUS-PPD. Conclusion:  Endoscopic ultrasound guided pancreatic pseudocyst drainage with modified combined technique is safe and is associated with high success rate. “
“Chronic pancreatitis (CP) is a disease characterized by irreversible destruction and fibrosis of the parenchyma, leading to pancreatic exocrine insufficiency. In developed countries, the etiology for 60% to 70% of CP amongst male patients is alcohol and 25% are classified as idiopathic chronic pancreatitis (ICP). The genetic predisposition to CP could be an inappropriate activation of trypsinogen in the pancreas. Two common haplotypes, c.101A > G (p.N34S) and c.−215G > A, and four intronic alterations of the serine protease inhibitor Kazal type 1 (SPINK1) gene have been found to increase the risk for CP in the Asia Pacific region.