6A,B) To exclusively determine that IL30 inhibits IFN-γ expressi

6A,B). To exclusively determine that IL30 inhibits IFN-γ expression, the levels of IFN-γ in the blood and in the liver

were measured. Although coadministration of IL12 and IFN-γ induced higher levels of IFN-γ in both serum and the liver, the presence of IL30 resulted in no detectable IFN-γ in either serum or liver (Fig. 6D,E). These results suggest that IL30 is a potent inhibitor of IFN-γ expression and IL12- and IFN-γ-mediated GSK2118436 nmr liver toxicity. The preventive role of IL30 against IL12-induced toxicity described above encouraged us to study whether IL30 also has a therapeutic potential to repair the liver injury once initiated. In this regard, IL30 was administered 2 days after the IL12 treatment and liver toxicity was determined. Two independent methods of gene delivery, electroporation and hydrodynamic delivery, showed that IL30 administration postinjury selleck chemical heals liver injury and reduces the level of toxic IFN-γ expression (Fig. 7A,B). Because chronic inflammation causes liver fibrogenesis, the effect of IL30 was also assessed on hepatic fibrosis during chronic administration of ConA. Treatment with

IL30 by way of gene therapy reduced collagen depositions (Mason’s trichrome staining) (Fig. 8A). Such data reveal that IL30 has therapeutic potential in a clinical setting to reduce liver pathology. To determine how IL30 reduces toxic IFN-γ expression, we determined the transcriptional activity of IL-12-induced IFN-γ in the presence or absence of IL30 over time. Two days after the first treatment, IL30 raised IFN-γ levels, but 5 days after the second treatment IL30 reduced these levels by 10-fold (Supporting Fig.

7). IL30 does not affect the ability of IL12 to produce IFN-γ, nor does it affect cytomegalovirus (CMV)-promoter driven of IL12 ID-8 or IFN-γ expression (Supporting Fig. 8A-C), but instead disrupts constitutive IFN-γ expression once it is initiated, possibly posttranslationally. To better characterize the cellular source of IL30 in the liver, specimens from patients (with or without disease) were stained by way of immunohistochemistry. Interestingly, and never reported before, in normal patients IL30 is highly expressed in the hepatocytes, whereas the levels of expression are lower in the fibrous/connective tissue, further suggesting a protective role of IL30 (Fig. 8B). Although the staining intensity between normal hepatocyte, cirrhosis, and hepatocellular carcinoma (HCC) are similar (Fig. 8B), the data reported previously34 (Supporting Fig. 9) shows that IL30 messenger RNA (mRNA) levels were lower in patients with liver disease (HCC, dysplasia, or cirrhosis) than in healthy livers. The discordance between immunostaining and mRNA detection among patients is associated with the absolute tissue area that expresses IL30.

Thus, the infection of H pylori would

Thus, the infection of H. pylori would Dinaciclib manufacturer strongly affect the mRNA expression of AQP4 rather than H+/K+-ATPase nevertheless the aberrant differentiation of parietal cells. The mRNA expression of Shh was significantly decreased by the H. pylori infection in the wild type. In addition, in the H2R knockout mouse, the Shh expression was further decreased nevertheless the infection of H. pylori. Moreover, the mRNA expression of TFF2 was significantly increased in the H2R knockout mouse with H. pylori

infection compared with wild type, wild type with H. pylori infection, and H2R knockout mouse without H. pylori infection. We previously reported that the decreased expression level of Shh was observed in the H2R knockout mouse showing the

formation mTOR inhibitor of SPEM.[18] Since abnormal TFF2 expression has been reported in gastric cancer,[29] an increase in TFF2 expression may be a subtle indicator of potential malignancy. We also reported that suppressed Shh expression caused abnormal mucous neck-to-zymogenic cell lineage differentiation in the H. pylori-colonized stomach of Mongolian gerbils.[15, 30] SPEM is thought to be an early change of gastric metaplasia and then it gradually develops to intestinal metaplasia.[31] The present study demonstrated that SPEM was formed in the H2R knockout mouse at the age of 20 weeks. However, no malignant lesions such as gastric adenocarcinoma were observed even at the age of 60 weeks, while high ratio between AQP4 and H+/K+-ATPase mRNA expression was preserved. On the other hand, the H2R knockout mouse with H. pylori infection showed the highest mRNA level of TFF2 and suppressed expression of AQP4. Only in the H2R knockout mouse, the ratio between AQP4 and H+/K+-ATPase mRNA expression was suppressed by H. pylori infection. Previous report showed that decrease of AQP4 was observed in gastric PD184352 (CI-1040) adenocarcinoma tissue.[23] In this study, while the expressions of both AQP4 and H+/K+-ATPase mRNA are decreased in old age of the H2R knockout mouse and H2R knockout

mouse with H. pylori infection, the ratio between AQP4 and H+/K+-ATPase was decreased only in the H2R knockout mouse with H. pylori infection which is the most prominent for SPEM. Taken together, the ratio between AQP4 and H+/K+-ATPase mRNA expression might be a possible biomarker for the severe SPEM, which would be more likely to link to the gastric cancer development (Fig. 6). In conclusion, although AQP4-positive parietal cell is localized in the basal side of gastric mucosa in wild type, acid suppression like H2R knockout mouse causes the disturbance of parietal cell. Extended distribution of AQP4-positive cells in H2R knockout mouse is not preserved by H. pylori infection. As the expression of TFF2, a marker of SPEM, is elevated in the H2R knockout mouse with H.

4D, lanes 3 and 4) or S509 (S509A) (Fig 4D, lanes 5 and 6) was m

4D, lanes 3 and 4) or S509 (S509A) (Fig. 4D, lanes 5 and 6) was mutated to A, suggesting that the up-regulation effect of HBx on WT AIB1 is mainly the result of its inhibition of Fbw7α function. It is known that full-length AIB1 contains five functional domains: basic-helix-loop-helix domain; serine/threonine (S/T) domain; receptor interaction domain (RID);

CBP/P300 interaction domain; and histone acetyltransferase (HAT) domain (Fig. 5A). To identify which domains of AIB1 interact with Fbw7α or HBx, each of these five domains of AIB1 was coexpressed with Fbw7α or HBx in 293T cells, and Co-IP assays were performed. Western blotting analysis revealed that AIB1 interacted with HBx through its S/T and HAT domains (Fig. 5B) and interacted with Fbw7α through its S/T and RID domains (Fig. 5C). Because the S/T domain of AIB1 not only interacted with Fbw7α, selleck chemicals but also interacted with HBx,

it is possible that HBx inhibits the interaction between AIB1 and Fbw7α through the S/T domain. To test this hypothesis, Fbw7α was selleck kinase inhibitor coexpressed with full-length AIB1, S/T domain, or RID of AIB1 alone or in combination with HBx in 293T cells; then, Co-IP assays were performed. In the presence of HBx, the amount of Fbw7α protein coimmunoprecipitated with full-length AIB1, as well as the S/T domain of AIB1, was significantly reduced (Fig. 5D, lane 9 versus lane 8, and lane 11 versus lane 10), whereas the amount of Fbw7α protein coimmunoprecipitated with RID of AIB1 was comparable in the absence or presence of HBx, as expected (Fig. 5D, lane 13 versus lane 12), because RID could not interact with HBx. Taken together, these data indicate that HBx inhibits the Fbw7α-mediated ubiquitination and degradation of AIB1 by competitively inhibiting Suplatast tosilate the interaction between Fbw7α and the S/T domain of AIB1. It has been reported that AIB1 plays an important role in the transactivation process mediated by transcription factors, such as NF-κB and AP-1, which can also be activated by HBx.10, 12 Thus, we hypothesized that HBx and AIB1 can

cooperatively promote the transactivation activities of these transcription factors. To test this hypothesis, we cotransfected HBx and AIB1 with p65 or c-jun together with NF-κB reporter or AP-1 reporter into HepG2 cells, respectively. Compared to control transfection, the NF-κB reporter activities induced by HBx and AIB1 alone were 3- and 2-fold, respectively, whereas it was induced more than 5-fold by the coexpression of HBx and AIB1 (Fig. 6A). Similarly, the AP-1 reporter activities induced by HBx and AIB1 were less than 15- and 2-fold, respectively, whereas the coexpression of HBx and AIB1 dramatically increased AP-1 reporter activity more than 30-fold (Fig. 6B). These results suggest that HBx cooperates with AIB1 to promote the activities of NF-κB and AP-1.

However, this ability is of special significance in the Spanish r

However, this ability is of special significance in the Spanish ribbed newt due GSK-3 activation to the newly gained function in defence. A smooth and stable movement of the ribs, enabled by two-headed costo-vertebral joints, may be advantageous

when ribs are rotated forward to stretch the skin – in the case of P. waltl– to the point of piercing it. The proximal three-fourths of the ribs in Pleurodeles are filled with fat tissue, but the protrusible distal one-fourth is built up by massive bone, possibly to improve mechanical stability and decrease the probability of fractures. The protrusible tip is also coated with a thick periosteum. This tough sheath could also function as a physical barrier

against pathogens when the rib is protruded. Amphibians have an extraordinary ability to repair their skin, whereby antimicrobial peptides provide direct protection against certain bacterial, fungal and protozoan pathogens (for an overview, see Zasloff, 1987, 2002; Schadich, 2009). Pleurodeles BMS-777607 purchase waltl not only lives in a wet, microbially contaminated environment but also lacerates its skin during defence. Antimicrobial peptides, released from specialized cutaneous glands (Schadich, 2009), could be of special importance because dangerous infections through the wounds caused by rib protrusions seem to be avoided. The skin secretion of P. waltl also contains some poisonous components (Nowak & Brodie Jr, 1978; Heiss et al., 2009) that passively may seep into the body through the self-induced wounds, and yet we observed no self-intoxication by the newts. We therefore assume that P. waltl is immune against its own toxins. The high tolerance of urodeles against their own toxins has been demonstrated Acetophenone by Brodie Jr & Gibson (1969). They showed that Ambystoma

gracile and Taricha granulosa were tolerant to the intraperitoneal injection of their own skin secretion, but reciprocal injections were lethal even in small amounts for both species. The clade within the Salamandridae that comprises the three genera Pleurodeles, Echinotriton and Tylototriton is known to be monophyletic – with Pleurodeles as a sister group to the branch that includes Echinotriton and Tylototriton (Weisrock et al., 2006). Interestingly, while Pleurodeles and Echinotriton protrude their ribs, Tylototriton does not (Nowak & Brodie Jr, 1978; Brodie Jr, 1983; Brodie Jr et al., 1984). It seems, therefore, that the use of ribs as concealed weapons within this monophyletic clade is ancestral rather than derived. Only Tylototriton has lost this ability through time. However, to confirm this statement, the detailed mechanisms in Echinotriton and Tylototriton need to be studied similarly.

pylori-infected children with malaria or helminth infections Sym

pylori-infected children with malaria or helminth infections. Symptoms were generally not associated with levels of circulating peripheral cytokines irrespective of co-morbid infection diagnosis. Conclusions:  There is a high prevalence of asymptomatic H. pylori

infection in recently resettled African refugee children. Gastrointestinal symptoms were not predictive of H. pylori nor of helminth infections. Serum cytokines, particularly IL-5, IL-10, and TNFα, were significantly elevated in children with malaria and helminth infections but not in those with H. pylori infection. buy Y-27632
“Background: Helicobacter hepaticus, the prototype for enterohepatic Helicobacter species, colonizes the lower intestinal and hepatobiliary tracts of mice and causes typhlocolitis, hepatitis, and hepatocellular carcinoma in susceptible mouse strains. Cytolethal distending toxin (CDT) is the only known virulence factor found

in H. hepaticus. CDT of several Gram-negative bacteria is associated with double-stranded DNA breaks resulting in cell cycle arrest and death of a wide range of eukaryotic cells in vitro. We previously observed H. hepaticus CDT (HhCDT) mediated apoptosis in INT407 cells. However, the exact mechanism for the induction of the apoptotic pathway by HhCDT is unknown. The objective of this study was to identify the apoptotic signaling pathway induced by HhCDT in INT407 cells. Materials and Methods:  INT407 cells were incubated with or without recombinant HhCDT for 0–72 hours. H2AX phosphorylation Urease and apoptotic parameters were analyzed. Results:  H2AX was phosphorylated 24 hours postexposure to HhCDT. Expression of mTOR inhibitor pro-apoptotic Bax protein was upregulated after 24 hours, while Bcl2 expression decreased. Cytochrome c was released from mitochondria after 12–24 hours of exposure. Concurrently, caspase 3/7 and 9 were activated. However, pretreatment of INT407 cells with caspase inhibitor (Z-VAD-FMK) inhibited the activation of caspase 3/7 and 9. Significant activity of caspase 8 was not observed in toxin treated cells. Activation of caspase

3/7 and caspase 9 confirms the involvement of the mitochondrial apoptotic pathway in HhCDT-treated cells. Conclusion:  These findings show, for the first time, the ability of HhCDT to induce apoptosis via the mitochondrial pathway. “
“Background:  Nowadays, there is an increasing interest in noninvasive methods to diagnose Helicobacter pylori infection. Indeed, they can profitably replace endoscopy in predicting the diagnosis. The stool antigen test for H. pylori is a noninvasive immunoassay to diagnose active infection with this bacterium in human fecal samples. The aim of this study was detection of alkyl hydroperoxide reductase protein (AhpC) antigen by immunoblotting in stool samples for diagnosis of H. pylori. Materials and Methods:  Chromosomal DNA from H. pylori was isolated.

In conclusion, we

demonstrate that the mesodermal STM giv

In conclusion, we

demonstrate that the mesodermal STM gives rise to MC/SubMCs. Y 27632 Moreover, MC/SubMCs give rise to both HSCs and PMCs, including PFBs, SMCs, and FBs during liver morphogenesis. Further studies on the mechanisms underlying a transition from MC/SubMCs to HSCs and PMCs may lead to better understanding of cell fate regulation of HSCs and PFBs in both embryonic and adult livers. The authors thank Peng Li and Henry Sucov for providing MesP1Cre mice and Raul Lazaro, Kiki Ueno, and Bin Xie for technical assistance. Additional Supporting Information may be found in the online version of this article. “
“We previously reported that forced expression of Bmi1 (B lymphoma Moloney murine leukemia virus insertion region 1 homolog) in murine hepatic stem/progenitor cells purified from fetal liver enhances their self-renewal and drives cancer initiation. In the present study, we examined the contribution of the Ink4a/Arf tumor suppressor gene locus, one of the major targets of Bmi1, to stem cell expansion and cancer initiation. Bmi1−/− Delta-like protein (Dlk)+ hepatic stem/progenitor cells showed de-repression of the Ink4a/Arf locus and displayed Roxadustat price impaired growth activity. In contrast, Ink4a/Arf−/− Dlk+ cells gave

rise to considerably larger colonies containing a greater number of bipotent cells than wild-type Dlk+ cells. Although Ink4a/Arf−/− Dlk+ cells did not initiate tumors in recipient nonobese diabetic/severe combined immunodeficiency mice, enforced expression of Bmi1 in Ink4a/Arf−/− Dlk+ cells further augmented their self-renewal capacity and resulted in tumor formation in vivo. Microarray analyses successfully identified five down-regulated genes as candidate downstream DOK2 targets for Bmi1 in hepatic stem/progenitor cells. Of these genes, enforced expression of sex determining region Y-box 17 (Sox17) in Dlk+ cells strongly suppressed colony propagation and tumor growth. Conclusion: These results indicate that repression of targets of Bmi1 other than the Ink4a/Arf

locus plays a crucial role in the oncogenic transformation of hepatic stem/progenitor cells. Functional analyses of Bmi1 target genes would be of importance to elucidate the molecular machinery underlying hepatic stem cell system and explore therapeutic approaches for the eradication of liver cancer stem cells. (Hepatology 2010) Polycomb group (PcG) proteins operate as the cellular memory machinery through epigenetic chromatin modifications and are indispensable to the maintenance of cellular identity.1, 2 In particular, Bmi1, a core molecule of polycomb repressive complex 1 (PRC1), plays an important role in the self-renewal of various stem cell systems, including hepatic stem cells.

In addition, the importance of continual swallowing training and

In addition, the importance of continual swallowing training and rehabilitation for these patients to resume adequate oral intake is emphasized. However, identifying definitive clinical characteristics of older adults likely to benefit from PEG tube feeding will require larger prospective cohort studies. In conclusion, further research is needed to refine guidelines that will minimize the risks and maximize the benefits for those patients who require enteral feeding via PEG to meet their basic nutritional needs. Sanders et al.10 have shown that guidelines help to improve the appropriateness of patient selection

and play a proactive role click here in the decision making for medically adequate PEG insertion with a consecutively improved outcome. Allowing patients and clinicians to incorporate unbiased, objective information alongside their individual

culture, personal and religious beliefs regarding PEG placement, should be considered as implementing the best evidence-based this website medicine (Table 1). “
“Salicylates have been used since antiquity to relieve pain and inflammation. However, it has been only in the last half century that evidence has emerged that aspirin causes reproducible acute and superficial injury to the gastric and duodenal mucosa, and is an important cause of complicated and uncomplicated peptic ulcer. Superficial damage to the mucosa occurs rapidly and reproducibly and acid and pepsin then produce a second wave of deeper injury. Most of the time this heals rapidly, but some focal deeper mucosal lesions (erosions) occur frequently and the point prevalence of frank ulcers in low dose aspirin users is around 10%. It is even more recently that aspirin’s unique antiplatelet action has been recognized, with long-lasting inhibition of platelet aggregation due to irreversible inactivation of the cyclooxygenase-1 mediated Adenosine production of thromboxane. It has now become the mainstay of pharmacological reduction of thrombotic risk in patients

with cardiovascular diseases. In addition, evidence is accumulating about the cancer-reducing effects of blocking cyclooxygenase in a number of tissues. For example, recent data indicate that even at a 75-mg/day dose, it may reduce colorectal cancer risk after a lag of a year or so. Because of its widespread use for cardiovascular protection, aspirin is now one of the most frequently prescribed drugs—and gastroenterologists regularly need to deal with its ulcerative complications along the whole length of the gastrointestinal tract. Strategies that can be used to reduce these risks include using the lowest effective aspirin dose and co-prescribing acid suppressants. The salicylates are a very old family of drugs.

7B,C) These results indicate that overexpression of both Cryab a

7B,C). These results indicate that overexpression of both Cryab and 14-3-3ζ promotes the progression of HCC. Here, the majority of our data reinforce the notion that Cryab is a positive regulator of HCC growth and aggressiveness. First, Cryab promoted HCC progression in Tamoxifen chemical structure vivo and in vitro. Second, functional and genetic screens demonstrated that Cryab overexpression fostered HCC progression by inducing EMT. We also demonstrate for the first time that Cryab complexed

with 14-3-3ζ, and elevated expression of Cryab up-regulated 14-3-3ζ protein, which relayed the signal from Cryab to activate the ERK1/2. Clinically, we found that Cryab expression correlated with BCLC staging, patients’ overall survival, and disease recurrence. Moreover, we demonstrated that Cryab overexpression activated the ERK1/2/Fra-1/slug signal to induce HCC cell EMT. The above results support

the notion that Cryab does play an important role in the progression of HCC. Based on a combination of co-IP with subsequent MS or western blot-based identification learn more of binding partners, we demonstrated that Cryab physically complexes with 14-3-3ζ. Furthermore, our results showed that the forced expression of Cryab was accompanied by up-regulation of 14-3-3ζ protein, but not 14-3-3ζ mRNA, in HCC cells. In addition, the interference of 14-3-3ζ reverses the mesenchymal phenotype conferred by Cryab overexpression, suggesting that the Cryab can protect 14-3-3ζ protein from degradation. The correlation coefficient between the Cryab and 14-3-3ζ proteins reached 0.760 in HCC tissues, supporting the notion that the Cryab-14-3-3ζ complex functions as a cooperative unit in HCC cells. This notion was further supported by the observation that the patients with overexpression of both Cryab and 14-3-3ζ had the poorest prognosis. The 14-3-3 protein belongs to a family of conserved regulatory molecules expressed in all eukaryotic cells,29 and Verteporfin clinical trial Cryab is the most abundant sHsp in heart and muscle.30 Because both Cryab and 14-3-3ζ regulate many important proteins that are essential for homeostasis,31,

32 directly targeting Cryab or 14-3-3ζ may be a challenge. Here, we failed to detect the Cryab and 14-3-3ζ complex in normal liver cells L02 (unpubl. data), which indicates that this complex may not exist in normal cells, or may only exist in very small amounts. Thus, our findings may provide an alternative molecular target for HCC therapies by promoting the dissociation of the Cryab and 14-3-3ζ complex. By gene expression analysis, co-IP with MS, bioinformatics analysis, and step-by-step RNA interference, we demonstrated the Cryab overexpression-induced hyperactivity of the ERK signal by forming a complex with 14-3-3ζ. Specifically, this ERK signal hyperactivity was resistant to sorafenib. As one of the 14-3-3 proteins, 14-3-3ζ was first identified to be associated with Raf.

Now, most TIPS are created with polytetrafluoroethylene (PTFE)-co

Now, most TIPS are created with polytetrafluoroethylene (PTFE)-covered stent-grafts. Our study investigates the impact of distance from the HCJ on long-term patency of PTFE-covered TIPS. Methods PTFE-covered TIPS placed between 2002 and 2013 were retrospectively reviewed. selleck inhibitor Clinical and imaging data were collected from the electronic medical record and radiology imaging archive. Distance from HV end to the HCJ was recorded. Primary patency rates were calculated. Differences between groups based on distance

from HV end to HCJ were compared using Kaplan-Meier and Cox regression analyses. Results 300 PTFE-covered TIPS were included in the study. 201 were placed with a single stent-graft while 99 were extended at the HV end with additional BMS(N=70) or stent-grafts(N=29). No threshold distance between HV end of the TIPS and HCJ was found to impact long-term patency (p-values at thresholds of 0, 5,

10, 15, and 20 mm were 0.92, 0.79, 0.43, 0.36 and 0.24 respectively). Primary patency in TIPS placed with just a single stent-graft versus those using additional stents was 90% vs 82%, 83% vs 71%, 81% vs 60% 6 months, 1 and 2 years respectively (p = 0.03). In TIPS created with multiple stents, primary patency of those with BMS versus PTFE-covered extensions was 84% vs 78%, 73% vs 69%, and 69% vs 46% at 6 months, 1 and 2 years respectively (p = 0.28). Regression analysis demonstrated the length by which a TIPS was extended and

the final distance of the HV end to the Baf-A1 molecular weight HCJ were not predictors of patency failure (p>0.1 and p find more = 0.06 respectively). Conclusion If the HV end of PTFE-covered TIPS is within 2 cm of the HCJ, the primary patency is not determined by the actual distance from the HCJ nor is it improved by extending the TIPS to the HCJ. If extended, PTFE-covered extensions offer no patency benefit over BMS. The best patency rates occur with single PTFE-covered TIPS. Disclosures: The following people have nothing to disclose: Charles N. Weber, Gregory J. Nadolski, Michael C. Soulen Background and Aims: – Spontaneous bacterial peritonitis (SBP) is the commonest and life-threatening infection in liver cirrhosis. Identification of risk factors, choice and timing of antibiotic in relation to response can improve outcome.We investigated the role of serial ascitic tap for antibiotic response to predict the outcome. Patients and Methods: – Patients of decompensated cirrhosis diagnosed with spontaneous bacterial peritonitis (as per definition) were analyzed retrospectively. As per protocol, the patient underwent ascitic tap after 48hr in all cases and on 5th and 7th day depending upon the clinical parameters. Results:- Total 161 patient of decompensated cirrhosis, mean age 50.8yrs(±11.8SD, ) 82% male, with mean CTP =12.3±1.47 and median MELD = 22.7 (range=16-28) were analyzed.

, MD (Plenary Session) Grant/Research Support: BMS, VTI Speaking

, MD (Plenary Session) Grant/Research Support: BMS, VTI Speaking and Teaching: neuwave Reidy, Diane, MD (Transplant Surgery Workshop) Advisory Committees or Review Panels: Novartis, Pfizer Grant/Research Support: Novartis Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Reinus, John F., M. D. (Meet-the-Professor Luncheon) Nothing NVP-BEZ235 ic50 to disclose Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Reuben, Adrian, MBBS,

FRCP, FACG (AASLD Postgraduate Course, Early Morning Workshops) Nothing to disclose Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Reynaert, Hendrik, MD (Parallel Session) Advisory Committees or Review Panels: MSD, Gillead, Janssen, BMS Grant/Research Support: Roche Rinella, Mary E., MD (AASLD Postgraduate Course, Plenary Session, SIG Program) Advisory Committees or Review Panels: Gilead Roayaie, Sasan, MD (Transplant Surgery Workshop) Nothing to disclose Roberts, Lewis R., MD, PhD (AASLD Postgraduate Course)

Advisory Committees or Review Panels: Inova Grant/Research Support: Bristol Myers Squibb, Bayer, Nordion Speaking and Teaching: Nordion Content of the Opaganib presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Rodriguez-Torres, Maribel, MD (Meet-the-Professor Luncheon) Consulting: Hoffman La Roche, Abbott Labs, Pharmasset, Akros, Bristol-Myers Squibb, Merck, Vertex, Inhibitex, Genentech, Janssen R&D Ireland, Santaris Grant/Research Support: Anadys, Novartis, Hoffman-LaRoche, Glaxo Smith Kline, Inhibitex, Bristol-Myers Squibb, Vertex, Idera, Pharmasset, Sanofi-Aventis, Merck, Abbott, Pfizer, Human Genome Sciences, Gilead, Johnson & Johnson, Zymogenetics, AKROS, Scynexis,

Santaris, Boehringher, Idenix, Genentech, Beckman Coulter, almost Mochida Pharmaceutical Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Rosen, Hugo R., MD (Parallel Session) Nothing to disclose Rosenthal, Philip, MD (Early Morning Workshops) Advisory Committees or Review Panels: Ikaria, Gilead, Merck, General Electric Consulting: Roche Grant/Research Support: Roche, Bristol MyersSquibb, Gilead, Vertex Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Rossi, Simona, MD (Professional Development Workshop) Consulting: BMS Roy-Chowdhury, Jayanta, MD (Early Morning Workshops) Nothing to disclose Content of the presentation does not include discussion of off-label/investigative use of medicine(s), medical devices or procedure(s) Rudnick, David A., MD, PhD (Basic Research Workshop) Nothing to disclose Sanchez, Antonio J.