This effort led to the development of OSU-2S, which exhibits higher potency than FTY720 in suppressing HCC cell growth through PKCδ activation. In contrast to FTY720, OSU-2S was not phosphorylated by sphingosine kinase 2 (SphK2) in vitro, and did not cause S1P1 receptor internalization in HCC cells or T lymphocyte homing in immunocompetent mice. Although devoid of S1P1 receptor activity, OSU-2S exhibited higher in vitro antiproliferative efficacy

relative to FTY720 against HCC cells without cytotoxicity in normal hepatocytes. Several lines of pharmacological and molecular genetic evidence indicate that ROS–PKCδ–caspase-3 signaling underlies OSU-2S–mediated antitumor effects, and that differences in the antitumor activity between FTY720 and OSU-2S were attributable to SphK2-mediated phosphorylation of FTY720, which represents a metabolic inactivation of its ICG-001 antitumor activity. Finally, OSU-2S exhibited high in vivo potency in suppressing xenograft tumor growth in both ectopic and orthotopic models without overt toxicity. Conclusion: Using the molecular

platform of FTY720, we developed OSU-2S, a novel PKCδ-targeted antitumor agent, which is devoid of S1P1 receptor activity and is highly effective in suppressing HCC tumor growth in vivo. These findings suggest that OSU-2S has clinical value in therapeutic strategies check details for HCC and warrants continued investigation in this regard. (HEPATOLOGY 2011;) Hepatocellular carcinoma (HCC) is a leading cause of cancer death worldwide, and is expected to become more prevalent in the United States over the next decade due to the dramatic rise in the incidence of hepatitis MCE公司 C virus infection. A major challenge in the systemic treatment of HCC is cellular resistance to conventional cytotoxic agents, which may be attributed to the heterogeneity of genetic abnormalities acquired during the course of hepatocarcinogenesis.1 Consequently, targeting molecular defects that allow HCC cells to evade apoptosis

represents a viable strategy to improve patient outcome. Accordingly, a number of therapeutic agents targeting aberrant cellular growth and survival signaling pathways have been investigated for the treatment of HCC.2 Recently, sorafenib, a multikinase inhibitor, was approved for the treatment of advanced HCC.3 This therapy, however, only works in a subset of patients and is not curative, which underlies the urgency in identifying new therapies. FTY720, a synthetic sphingosine immunosuppressant, was recently approved for the treatment of relapsing multiple sclerosis.4 Its immunosuppressive effect is attributed to the ability of its phosphorylated metabolite (p-FTY720) to induce T lymphocyte homing by targeting sphingosine-1-phosphate (S1P) receptors.

Sokal, Xavier Stephenne, Christophe Bourdeaux, Raymond Reding 3:45 PM 124: Serum microRNAs as Novel Non-invasive Diagnostic Biomarkers of Liver Disease in Children with Cystic Fibrosis

Naomi L. Cook, Tamara N. Pereira, Peter J. Lewindon, Ross Shepherd, Grant A. Ramm 4:00 PM 125: Identifying Frequency Of Inherited Metabolic Disorders In Patients With Infantile Liver Disease Zoe Gray, Kirsten McKay, Carla Lloyd, Jane Hartley, Fiona MacDonald, Christian J. Hendriksz, Paul Gissen, Deirdre A. Kelly 4.15 PM 126: Ascitic fluid infection in acute and chronic liver disease in children: Evaluation, comparative analysis and outcomes Surender K. Yachha, Rohan Malik, Rishi Bolia, Anshu Srivastava, Ujjal Poddar Parallel 18:

Complications of Cirrhosis Monday, November 4 3:00 – 4:30 PM Ballroom find more AB MODERATORS: Juan Carlos Garcia-Pagan, MD Theo Heller, MD 3:00 PM 127: Portal vein thrombosis (PVT) in compensated cirrhosis: A prospective cohort study on 898 patients Filipe G. Nery, Cendrine Chaffaut, Bertrand Condat, Emmanuelle de Raucourt, Larbi Boudaoud, GS-1101 mw Pierre-Emmanuel Rautou, Aurelie Plessier, Dominique Roulot, Jean Claude Trinchet, Dominique Valla, Sylvie Chevret 3:15 PM 128: Acute kidney injury (AKI) in patients with Acute on Chronic Liver failure (ACLF) is different from patients with cirrhosis Rakhi Maiwall, Suman Kumar, Chitranshu Vashishtha, Manoj Kumar, Hitendra K. Garg, Sumanlata Nayak, Sunil Taneja, Bhaskar Thakur, Shiv K. Sarin 3:30 PM 129: Diagnostic test accuracy of vWF for hepatopulmonary syndrome in patients with liver cirrhosis Thomas Horvatits, Andreas Drolz, Arnulf Ferlitsch, Christian Muller, Peter Schenk, Valentin Fuhrmann 3:45 PM 130: Stratification based on acute on chronic liver failure (ACLF) has greater prognostic accuracy than stratification based

on creatinine, Acute Kidney Injury (AKI), Encephalopathy or Child-Pugh Score. Prognostic relevance of 48 hour post-enrolment ACLF Stratification Paolo Angeli, Pere Gines, Salvatore Piano, Elisabet Garcia, medchemexpress Filippo Morando, Ezequiel Rodriguez, Xavier Ariza, Elisabetta Gola, Elsa Sola, Monica Guevara, Richard Moreau, Rajiv Jalan, Juan Cordoba, Marco Pavesi, Francois Durand, Thierry Gustot, Faouzi Saliba, Marco Domenicali, Alexander L. Gerbes, Julia Wendon, Carlo Alessandria, Wim Laleman, Stefan Zeuzem, Jonel Trebicka, Mauro Bernardi, Vicente Arroyo 4:00 PM 131: Predicting Presence of Clinically Significant Hepatic Involvement in Hereditary Hemorrhagic Telangiectasia using a Simple Clinical Scoring Index Siddharth Singh, Karen L. Swanson, Matthew Hathcock, Walter K. Kremers, John Pallanch, Michael J. Krowka, Patrick S. Kamath 4.15 PM 132: The Cirrhosis Dysbiosis Ratio Provides Insight into Gut Microbiome Changes Across the Spectrum of Cirrhosis: A Prospective Study of 250 Patients Jasmohan S. Bajaj, Phillip Hylemon, Douglas M. Heuman, Arun J. Sanyal, Patrick M.

87 NRTIs are implicated as causal agents, which subsequently served as motivation for the generalized black box warning for all NRTIs regardless of each drug’s potential for mitochondrial Decitabine in vivo toxicity. The pathogenesis of this syndrome has not yet been completely elucidated. Severe mitochondrial injury of the hepatocytes secondary to NRTIs has been reported in asymptomatic patients with normal

lactic acid levels and in the absence of steatohepatitis.88 The hepatic abnormalities in lactic acidosis secondary to NRTI toxicity have been described in a systematic review of cases reported in the literature which included 90 patients with lactic acidosis.85 Laboratory evidence of mild to moderate hepatic dysfunction was present in 41

of the 63 cases (65%) in whom information was given, with median (range) aminotransferase values between 1.5 and 2.5 (1.4-10.7) times above the ULN. Of 39 premortem or necropsy liver biopsies, 36 (92%) had hepatic steatosis: macrovesicular steatosis in 12 (31%), microvesicular steatosis in eight (21%), and with a mixed pattern in 16 (41%). this website The other three biopsies showed inflammation and hepatic fibrosis. Mortality was 48% in this review of cases. Lactic acidosis has been reported in persons receiving both single-NRTI and dual-NRTI regimens including combinations of zidovudine or stavudine with didanosine, zalcitabine, or lamivudine.86 The role of each specific NRTI in the development of lactic acidosis is often difficult to determine because the patients might have been exposed to several NRTIs and frequent changes in medications are made. Nevertheless, it is known that the dideoxynucleosides (d-drugs) have a higher potential for mitochondrial toxicity with greater ability to inhibit mitochondrial DNA synthesis in vitro and in vivo.30, 85, 86, 89 Several cohorts suggest that the coadministration of stavudine and didanosine is associated with 上海皓元 the greatest relative risk.40, 41 Of note, this drug combination is contraindicated by the guidelines due to high risk of lactic acidosis.9 Hydroxyurea, which was used in the past as adjuvant treatment with didanosine, increases its toxic

effect due to the rise of intracellular levels of 5′-triphosphate products.90, 91 Cumulative exposure to NRTI is another factor believed to be important for the development of lactic acidosis.85, 92 In addition, lactic acidosis appears to be more common in women and the obese.85, 86, 93 An increased risk of lactic acidosis among pregnant women being treated with didanosine and stavudine has been also reported.43, 46 A contribution to the pathogenesis of lactic acidosis of HIV and HCV has been suggested but it has not been established.30, 85, 93 In a retrospective and cross-sectional study in which liver biopsies from 152 HIV/HCV-coinfected patients were evaluated, associations between accelerated fibrosis progression and nevirapine, and between slower fibrosis progression and PI use were found.

To determine whether different genetic alterations influenced hepatocyte size within transplant foci, we measured microscopic hepatocyte cross-sectional area in foci

(Table 4). Mean hepatocyte area did not significantly increase for any genetic alteration, although in foci expressing TAg plus either c-myc or TGFα, hepatocyte diameter sometimes was smaller than control hepatocytes. Thus, changes in focus growth were associated with hyperplasia, not cellular hypertrophy. Mean focus area plots (Fig. 2) can be influenced by two aspects of focus growth. First, oncogene expression may alter growth of Selleckchem Smoothened Agonist all donor cells. Median focus size addresses this effect (Table 3) and reveals growth changes for which each oncogene or oncogene combination is sufficient. Second, oncogene expression

may cause development of a few exceptionally large foci (outliers), which will increase mean focus size (Fig. 2) but not affect the distribution median. To quantitate outliers in focus ratio distributions at 12 weeks posttransplantation (the end-stage for check details these studies), we used the method of Tukey.17 In this method, extreme outliers (EOs) are defined as 3 × the interquartile range or more above the third quartile of a distribution, where the interquartile range is the distance between the first and third quartiles. Among single oncogenes, only TAg expression was associated with a significant increase in outliers (Table 3). Coexpression of oncogenes increased

outlier frequency further (even by 2 weeks for TAg/c-myc hepatocyte foci). Note that, for foci coexpressing TGFα and c-myc, all of the mean focus area medchemexpress increase from 4 to 12 weeks (Fig. 2E) was due to outliers, because median focus size did not increase (Table 3). There was no effect of recipient sex on outlier frequency (data not shown), consistent with the slight to minimal gender differences in disease latency in these lines of donor mice. When examined microscopically, most TGFα/c-myc median (non-outlier) foci at 12 weeks posttransplantation resembled normal hepatic parenchyma: only 2 of 10 non-outlier foci displayed a mildly atypical hepatocellular phenotype (two-cell-thick hepatic plates). In contrast, 11 of 11 EO foci were composed of dysplastic hepatocytes that were clearly distinguishable from adjacent parenchyma, including thickened hepatic plates, basophilic, and clear cell phenotypes. In this regard, most resembled classic altered cell foci that develop after carcinogen administration. Transplanted hepatocytes enter the parenchyma by passing through or between endothelial cells to enter liver plates in the host liver, favoring transit and subsequent engraftment of single cells.

1999). The absorbance spectrum of cPPB-aE is identical to that of the new pigment (peak X) of dinoflagellates

and both pigments exhibit no chlorophyll fluorescence. These results indicate that the new dinoflagellate chlorophyll derivative is cPPB-aE. This represents the first report of cPPB-aE also being expressed in photosynthetic organisms. GW-572016 There are two hypotheses for the function of cPPB-aE in dinoflagellates. One is that cPPB-aE is a degradation product of chlorophyll a as detoxified catabolite, discussed by Kashiyama et al. (2012). It is reasonable to speculate that the conversion of a toxic chlorophyll molecule to a safe form of cPPB-aE is beneficial to dinoflagellates. However, most unicellular phototrophs, such as cyanobacteria, the chlorophyte Chlamydomonas Ehrenberg and diatoms, contain no or very low levels of chlorophyll degradation products (data not shown). In these organisms, chlorophyll might be converted to colorless small compounds or the chlorophyll degradation products might be excreted from the cells. Why only dinoflagellates retain the chlorophyll degradation product in large amounts is something that needs to be resolved. The second hypothesis is that cPPB-aE

is involved in the quenching of excess energy in photosystems. The wavelength of maximum absorbance of cPPB-aE is longer than that of chlorophyll a and the life time of cPPB-aE fluorescence is very short compared to that of chlorophyll selleck chemicals llc a (Akimoto, unpublished data). These optical characteristics of cPPB-aE support the second hypothesis that cPPB-aE is involved in quenching excess energy. We discovered cPPB-aE in six dinoflagellates belonging to four different lineages and this raises the interesting question as to the origin(s) of this molecule. There are two possible hypotheses. The first is that cPPB-aE was acquired independently in each of the four lineages. Interestingly, all the dinoflagellates possessing cPPB-aE are benthic. This suggests that the production of this particular pigment derivative might be related to their habitat

environments. However, other benthic dinoflagellates from the same habitat do not have this chlorophyll derivative (data not shown), so no such clear correlation can be MCE公司 seen between the presence or absence of this molecule and habitat at this stage. The second hypothesis is that all photosynthetic dinoflagellates possess the ability to produce cPPB-aE to quench excess light energy, but usually there is no need to produce it because light conditions normally suit these dinoflagellates. To understand the evolutionary or ecological significance of the possession of this pigment derivative, an extensive survey of dinoflagellates from various habitats is needed as well as biochemical, physiological, and photochemical experiments using strains under different culture conditions.

Lake, MD 8:00

– 8:10 AM Introduction and Why the First Quarter? John R. Lake, MD 8:10 – 8:30 AM Justification for Routine Intensive Care after Liver Transplantation Michael A. Ramsay, MD 8:30 – 8:50 AM Early Graft Dysfunction: Causes, Recognition and Management Marc Deschenes, MD buy PLX4032 8:50 – 9:10 AM Small-for-Size Syndrome: Recognition and Management Chung-Mau Lo, MD 9:10 – 9:30 AM How Relevant is Acute Cellular Rejection? Michael R. Charlton, MD 9:30 – 9:50 AM Hepatic Artery Thrombosis: Conservative Management or Retransplantation? Nigel Heaton, MB, FRCS 9:50 – 10:10 AM Discussion 10:10 -10:30 AM Break Session II: Quarter 1-Investigation of Graft Dysfunction MODERATOR: John R. Lake, MD 10:30 – 10:50 AM Systematic Investigation of Elevated Transaminases during the Third Posttransplant Month Michael P.

Curry, MD 10:50 – 11:10 AM Systematic Investigation of Elevated Cholestatic Enzymes during the Third Post-transplant Month Andrew L. Mason, MBBS, MRCPI 11:10 -11:25 AM Specific Contribution selleckchem of the Histopathologist Stefan G. Hubscher, MD 11:25 – 11:40 AM Specific Contribution of the Advanced Endoscopist Mustafa A. Arain, MD 11:40 AM – Noon Discussion Noon – 1:00 PM Lunch Session III: Second Decade MODERATOR: John O’Grady, MD 1:00 – 1:05 PM Why the Second Decade? John G. O’Grady, MD 1:05 – 1:20 PM Will Retransplantation be the Norm for Pediatric Recipients with Ambitions for Grand-parenthood? Deirdre A. Kelly, MD 1:20 -1:40 PM Adolescence – Challenges and Responses Sue

V. McDiarmid, MD 1:40 – 1:55 PM Long Term Quality of life in Transplant Recipients Patrizia 上海皓元 Burra, MD, PhD 1:55 – 2:15 PM Tolerance Profiles and Immunosuppression Alberto Sanchez-Fueyo, MD 2:15 – 2:25 PM Is Disease Recurrence Still Relevant to Graft Survival? James F. Trotter, MD 2:25 – 2:45 PM Extrahepatic Implications of the Metabolic Syndrome Kymberly D. Watt, MD 2:45 – 3:05 PM Malignant Disease – Risk and Surveillance Strategies Geoffrey W. McCaughan, MD, PhD 3:05 – 3:30 PM Discussion AASLD/NASPGHAN Pediatric Symposium Friday, November 1 Noon – 3:00 PM Room 150A New Insights and Controversies in Liver-based Metabolic Diseases COURSE DIRECTORS: Udeme D. Ekong, MD Simon Horslen, MD 3 CME Credits The purpose of the program is to review the advances made in the last 10-years within the field of metabolic liver diseases. This program will also offer the opportunity to review the pathophysiology of liver based metabolic disorders while gaining insights into the latest treatments available for management of these disorders. It will also specifically address candidacy for treatment and counsel.

The apical scimitar released the greatest number of meiospores (cells · mL−1 · cm−2) and the sporophylls the least. Meiospores produced from all types of fertile laminae were equally viable. This reproductive plasticity may enhance reproductive output, and contribute to short and long-distance BMS-777607 solubility dmso spore dispersal and the cryptic gametophyte propagule bank for the next generation of sporophytes.

“
“Environmental contaminants, including poly-chlorinated biphenyls (PCBs), are enriched in coastal sediments, and despite a 1977 moratorium by the United States Environmental Protection Agency on the production of PCBs, levels remain high, more so near former industrial plants. The effects of these contaminants on sessile species in the intertidal zone, particularly nonanimal species such as the ubiquitous fucoid brown algae, are not well known. We investigated the developmental effects of chronic PCB treatment beginning at fertilization on two species of marine rockweed, Fucus vesiculosus Linnaeus and

Silvetia compressa (J.Agardh) E.Serrão, SAR245409 purchase T.O.Cho, S.M.Boo & Brawley. A mixture of the most widely used PCB congeners, Aroclors 1221, 1242, and 1254, was delivered at concentrations well below levels found in contaminated sediments, and resulted in severely delayed mitosis and cytokinesis in both species. In F. vesiculosus, this delay was accompanied by abnormal spindle morphology. PCB treatment also dramatically slowed or arrested rhizoid growth after 2–4 d, and by 7 d F. vesiculosus embryos were dead; in contrast, polar secretion of adhesive, germination, and photopolar germination were not affected. The dramatic delay in the first cell division and reduction medchemexpress in tip growth within the first week of development are likely to compromise S. compressa’s ability to reproduce and establish new generations. Thus, the data presented here suggest that PCBs still present in coastal sediments may be inhibiting recruitment in these species. Moreover, as sediment dredging causes

temporary spikes in PCB concentrations, these kinds of bioremediation steps may exacerbate the disruption of fucoid development. “
“The diplobiontic–haplodiplontic life cycle with alternating isomorphic generations in Stigeoclonium tenue (C. Agardh) Kütz. is described for the first time. Sporophytes (2n = 10) arise from tetraflagellate zoospores that are produced by meiosis. Sporic meiosis might be inferred from the cruciform divisions formed during zoosporogenesis and is confirmed through observations of prophase I substages. Zoospores do not germinate directly but produce a haploid cyst that germinates to give rise to a gametophyte (n = 5). Gametophytes produce biflagellate isogametes, which fuse to produce zygotes that germinate by mitosis into the sporophytic stage.

It is likely that seabird species smaller than Cory’s shearwater formed a large part of the diet of cats on Corvo in the past (Monteiro, Ramos & Furness, 1996). As these seabird

species were not found in cat scats in our study, cats likely exterminated accessible colonies of these species (Fitzgerald et al., 1991). Without the availability of introduced rodents as alternative prey, the feral cat population would not have survived the extermination of an important food source, highlighting the adverse effect of introduced Acalabrutinib chemical structure rodents in supplementing predator populations on islands. We found no evidence that seasonally varying abundance of prey taxa explained variation in the home-range size of domestic cats. Instead, home-ranges were

extremely variable among individuals and seasons as has been found elsewhere (0.3–69.0 ha; Metsers, Seddon & van Heezik, 2010, 0.5–21.8 ha; van Heezik et al., 2010). While confined cats that receive sufficient food from human Pritelivir solubility dmso owners may not need to adjust their roaming behaviour to prey availability, even the unconfined cats in our study did not display a consistent response to the availability of prey that we measured. Because cats appear to be generalist predators, the roaming behaviour may be controlled by factors other than food requirements, such as temperature, photoperiod, precipitation or territoriality (Goszczynski, Krauze & Gryz, 2009). Overall, we found high individual variation in home-range size, and all our covariate subgroups therefore had small sample

sizes, rendering their mean size estimates less robust. medchemexpress We found a small positive effect of age on home-range size, possibly because young cats show reduced dispersal behaviour until they are 1–3 years old (Liberg, 1980). Confined cats had generally smaller home-ranges than unconfined cats, and tended to roam less far from their home (Fig. 3), therefore cat owners could be encouraged to confine the cat to the immediate vicinity of the house. If individual cats display consistent individual roaming behaviour, identifying and constraining the widest roaming cats may be easier to implement than other generally applicable cat constraint approaches (Calver et al., 2011). Another potential management option is to restrict cat ownership in human settlements that are too close to vulnerable native wildlife congregations such as seabird colonies. Our study shows that confined cats are less likely to roam very far, but that some unconfined cats can move >10 km in a single night. On average, however, movements were within a 1-km radius around the owner’s house, and impacts on native wildlife are presumably greatest within this radius. The tracking of cats with GPS loggers provided a great opportunity to assess the spatial impact of domestic cats on native wildlife.

At patient level, the data on joint outcome suggest that a proportion of patients are equally well-off with intermediate-dose

prophylaxis, while others need a high-dose regimen to control their bleeding. Pharmacokinetic information [26] in combination with bleeding frequency and individual circumstances, such as sports participation [27], can be used to assist decisions on prophylactic dosing. Continued follow-up of these cohorts will provide us with some of the answers needed. Until then, personalizing prophylactic treatment, including lower dosed regimens, appears the most cost-effective treatment strategy. Regular factor infusions to prevent bleeding have become the mainstay of treatment for many patients with haemophilia. Numerous find more observational studies and one randomized controlled trial have documented that the efficacy of

prophylaxis started early in life reduces bleeding and prevents joint damage [28, 29, 6, 30]. Even when instituted later in life, after joint damage has occurred, prophylactic Selumetinib factor therapy can significantly reduce the number of bleeds including into joints, although data on long-term joint outcomes are still limited [30, 8, 9]. These results have raised the question of whether prophylaxis could be effective in patients with haemophilia and inhibitors to FVIII or FIX. This question has been addressed in case reports, case series, and in randomized trials. Patients with haemophilia and persistent inhibitors are more likely to have disabling haemophilic arthropathy and other sequelae of bleeding [31]. While the use of bypassing agents [recombinant factor VIIa (rFVIIa) or activated prothrombin complex concentrates (aPCC)] has advanced care of patients with inhibitors, these products are not as effective overall as factor replacement therapy and bleeding results in persistent adverse effects. If

prophylactic therapy with bypassing agents could prevent bleeding, there is the potential for even more benefit in the inhibitor population from this approach. Multiple reports have relayed successful use of either MCE公司 rFVII or aPCC in a prophylactic regimen, although with varying dosing and treatment intervals [27, 32, 33]. In general, these reports document decreased bleeding, improved quality of life, and often the ability to support a rehabilitation regimen, albeit in small numbers of patients. Three randomized controlled trials which evaluated prophylaxis in inhibitor patients have now been reported, one with rFVIIa and two with aPCC [34-36]. In the study subjects, generally patients with a history of frequent bleeding episodes, there was a significant decrease in bleeding with prophylactic therapy. There were no thrombotic complications and two allergic reactions to the aPCC.

For the control models, saline was used instead of the trichinella spiralis. 40 NIH mice were randomly divided into five groups: normal controls of 2 weeks (NC-2w) group, 2 weeks after infection group (PI-2w), normal control of 8 weeks (NC-8w), 8 weeks after infection

group (PI–8w) and Bifidobacterium longum intervention group (PI-B). Mice were sacrificed at the 2th week after infection for the NC-2 w and PI-2 w groups and at the 8th week for the NC-8w and PI–8w groups. Mice of PI-B group were sacrificed after infection for eight weeks and then intervention with Bifidobacterium longum for one week. Visceral sensation evaluation of abdominal withdrawal reflex score was performed for find more all mice before they were sacrificed. The terminal ileum tissue of each mouse was removedfor detecting the expression of NLRP6 inflammasome related proteins AZD6244 chemical structure including NLRP6, ASC, CARD8, caspase-1, IL-18 and IL-1β. Results: (1) Immunohistochemical results showed that NLRP6, CARD8 and ASC only expressed in mucous membrane layer; (2) The statistical analysis results of Western

blot showed that the expression level of NLRP6, CARD8 and caspase-1 of PI – 8w group had no significant decline when compared to PI – 2 w group, but had an significant rise when compared to the NC – 8 w group; (3) The expression level of ASC of PI-8w group was declined significantly when compared to PI-2w group, but there was an striking increase when compared with NC-8w group; (4) The expression level of ASC and caspase-1 of PI-B group went down remarkblely compared with the PI – 8w group; (5) The expression of IL-18 which is a downstream cytokine of NLRP6 inflsmmasome significantly increased at the PI-2w and PI-8w groups compared with their control groups, while it significantly decreased in the PI-B group compared with PI-8w group; (6) IL-1β, the other one downstream cytokine of NLRP6 inflammasome, only increased MCE公司 remarkably in PI-2w group. Conclusion: NLRP6 inflammasome participates in immune activation of intestinal mucosa in PI – IBS models, and Bifidobacterium longum intervention can reduce the expression level of the major ligands (ASC, CAPASE-1)

and thedownstream cytokineIL-18 of NLRP6 inflammasome. Key Word(s): 1. NLRP6 inflammasome; 2. B longum; 3. PI-IBS; Presenting Author: HAO WANG Additional Authors: GUANGYING ZHOU, CHANG GAO, KE ZHAO, QIANG FU, TONG LIU, YONGCHENG LV, HONGQIU HAN Corresponding Author: HAO WANG, YONGCHENG LV, HONGQIU HAN Affiliations: Department of General Surgery, Tianjin Medical University General Hospital; Tianjin General Surgery Institute; ShunHo Cell Biotech (Tianjin) Co., Ltd. Objective: Novel immunotherapies that directly target ulcerative colitis (UC) are still lacking. Endometrial regenerative cells (ERCs) are mesenchymal-like stem cells that can be non-invasively obtained from menstrual blood and are easily grown/generated at a large scale without tumorigenesis.