Almost the entire Pacific coast of the Tohoku region suffered catastrophic damage from the great earthquake and the tsunami in particular. Indeed, almost 20 000 people, both young and old, perished. It was the greatest tragedy for Japan since the Second World War. The response to international aid for this disaster, as at the time of the Great Hanshin-Awaji Earthquake, was exceedingly quick and large-scale, for which we are sincerely appreciative. It is already a year since the disaster, when normally the hammering

sounds of reconstruction would be reverberating loudly. But there was an additional disaster, one that might be described as man-made. It was of course the Fukushima nuclear power plant accident, a global-scale major accident on a level with Chernobyl. The radioactive contamination from this accident affected LEE011 the international community as well as Japan. For several ten years to come it may continue to adversely affect the health of men and Doxorubicin chemical structure women. Although embarrassed by this catastrophe, the Japanese government has been unable to work out effective countermeasures, which has been aggravating the situation. The radioactive contamination problem on top of the damage from the earthquake and tsunami requires constructive actions from us in the medical profession. We have been going to the disaster site as volunteers

and giving help to many. We have learned firsthand the importance of disaster medicine. Stress-related ulcers, intestinal infections and other gastroenterological disorders also occur frequently and many specialist gastroenterologists have been out to hospitals in the Tohoku area. However, damage to health from exposure to radiation, although experienced in the Hiroshima and Nagasaki atomic bombs, is an unknown area for us and is an important one for future research. Creative research in the field of gastroenterology may also be called for. We shall also have to consider covering the topic of disaster

and radiation medicine in gastroenterology in the next Symposium. Under such circumstances, we were forced to cancel the 14th Taishotoyama International Symposium on Gastroenterology and hope you understand. However, many excellent research outcomes had been submitted for that Symposium and, although it could not be held, we thought that these should be published as papers. To date medchemexpress the findings in these symposia have been released in international journals, and therefore this time too we decided to include them in the Journal of Gastroenterology and Hepatology. Fortunately there was general agreement to this and 19 papers were received. Following their peer review, these have finally been published. For this we are grateful for the assistance of the peer reviewers and numerous medical scientists. The cover shows the beautiful Rainbow Bridge over Tokyo Bay, representing the Bridge of Friendship. It could also be a symbol of the current reconstruction work following the major disaster.

Other reasons for head CT scans, such as stroke evaluations, probably also

contribute to testing. In data from the NHAMCS for 2009, CT scans of the head accounted for 7.1% (SE 0.3) of all ED imaging tests ordered, which extrapolates SRT1720 purchase to 9,669,000 (SE 678,000) ED visits in which a head CT was ordered. Information on magnetic resonance imaging scans is not available. The response rate to the 2004 AMPP survey was 64.9% (77,879 households), with information obtained on 162,756 people 12 years of age or older. Of these, 30,721 reported that they experienced severe headache in the year preceding the survey. Of those who returned usable data, 18,968 met ICHD-II diagnostic criteria for migraine, for an unadjusted 1-year period prevalence of 11.7%.[6] With the highest prevalence observed among those ages 18-59, 17.1% of women and 5.6% of men met diagnostic criteria for migraine. Migraine was more common among whites than blacks and among those with lower income levels. find more Over half (53.7%) of migraineurs endorsed severe impairment or need for bed rest during their attacks, and 22.0% obtained scores indicative of moderate or severe migraine-related disability on the Migraine Disability Assessment

Questionnaire (MIDAS).[13] Thirty-two percent of migraineurs who had never used a preventive medication were current candidates for pharmacological prophylaxis based on expert-defined consensus 上海皓元 criteria. The 1-year period prevalence of probable migraine (meeting all but 1 criterion for a diagnosis of migraine) was 4.5% overall (5.1% in women and 3.9% in men).[14] The overall prevalence of chronic migraine (CM), defined as meeting criteria for migraine and having an average of 15 or more days of headache per month over the preceding 3 months, was 0.91% (1.29% of females and 0.48% of males). CM comprised 7.7% of total migraine cases and was inversely related to household income. In both sexes, the prevalence of CM was highest between ages 18 and 49 (as high as 1.9% for women ages 40-49).[15] CM was associated with significantly

greater headache-related disability than episodic migraine (38.0% vs 9.5% endorsing severe disability on the MIDAS),[11] as well as rates of significant depression or anxiety that were more than double those of individuals with episodic migraine.[16] With 1% of migraineurs reporting 4 or more visits during the year, 7.3% of migraineurs in the AMPP reported an ED visit for headache during 2004. That 1%, however, accounted for 51% (95% CI 49-53%) of all ED visits.[17] This report summarizes the best available data on migraine prevalence, impact, and treatment in the US using data from recent large-scale surveillance studies. These large, ongoing, government-funded population surveys used different sampling frames and methods to identify migraine and severe headaches.

There is accumulating evidence for a role of H. pylori infection also in colorectal carcinogenesis. Seropositive individuals are at higher risk for the development of colorectal adenomas and consequently adenocarcinomas of this anatomical region. This phenomenon can partly be attributed to the increase of serum gastrin as response to atrophic changes of the gastric mucosa.

BAY 57-1293 supplier In 2012, the infection with Helicobacter pylori remains one of the most challenging infectious diseases of the world, causing high morbidity and mortality. The major burden in global health care is still given by H. pylori representing the main risk factor for gastric cancer (GC), the second leading cause of cancer-related death. During the past years, the progress in the clinical management of GC has been modest. Innovations are limited to modifications of the existing chemotherapy regimens in either palliative or perioperative settings. Furthermore, Ferroptosis inhibitor new data have been gained concerning the endoscopic treatment

of early GC. This review summarizes recent clinical- and research-related advances in the field of H. pylori and GC that have been published between April 2011 and April 2012, including also recent insights concerning the association between H. pylori infection and colorectal neoplasias. H. pylori infection leads in all infected individuals to a chronic active gastritis, MCE which can proceed, via the so-called Correa cascade, to gastric mucosal atrophy and intestinal metaplasia (IM), and finally to the development of GC. Thus, atrophy and IM are considered as precancerous conditions, and H. pylori eradication therapy is considered as preventive for GC [1]. Several studies have proven that eradication therapy also improves, or at least prevents, progression of gastric atrophy and IM; however, some did not show a benefit [2-5].

A recent study therefore evaluated the gastric mucosa of patients that underwent eradication therapy in a long-term follow-up [6]. A total of 118 patients have been monitored after successful eradication therapy, for a mean of 8.6 years. After eradication therapy, atrophy scores significantly decreased both in the antrum and corpus. The score for IM significantly decreased in the corpus of the stomach, but not in the antrum. In this study, 21 patients with unsuccessful eradication therapy were also monitored for a mean of 7.2 years. In this group, no difference in the scores was observed. The significant improvements in gastric atrophy and IM that were observed after H. pylori eradication may result in a decreased risk for GC development. Early detection of GC represents the current best option to reduce its morbidity and mortality. The combination of the detection of serum anti-H.

We evaluated whether the prototype holder was adequate to complete an entire BAESD procedure. Results: A total of 34 lesions required BAESD for resection, including 4 lesions in the cecum, 15 in the ascending colon, 13 in the transverse colon, and 2 in the sigmoid

colon. The prototype holder was used in all of the BAESD procedures Selleck GSK126 (34/34) without relief by an assistant. The mean duration of the BAESDs was 120 ± 108 minutes. Conclusion: The prototype holder can take the place of an assistant during BAESD procedures eliminating Key Word(s): 1. ESD; 2. BAESD; 3. balloon-assisted endoscopic submucosal dissection; 4. overtube; 5. holder Presenting Author: SU JIN click here HONG Additional

Authors: MYUNG SOO KANG, DAE YONG KIM, JAE PIL HAN, MOON HAN CHOI, HEE KYUNG KIM, BONG MIN KO, MOON SUNG LEE Corresponding Author: SU JIN HONG Affiliations: Soonchunhyang University College of Medicine, Soonchunhyang University College of Medicine, Soonchunhyang University College of Medicine, Soonchunhyang University College of Medicine, Soonchunhyang University College of Medicine, Soonchunhyang University College of Medicine, Soonchunhyang University College of Medicine Objective: In order to know the long-term outcome after ESD in EGC, we analyzed the results and the clinical outcomes after ESD of

EGC according to the pathologic extent. Methods: The ESDs were performed in 309 EGCs of 280 patients. Among them, 228 patients, who had ESD for EGC were classified by pathological severity based on absolute indication (AI), expanded indication (EI) or beyond expanded indication (BEI). Results: The complete resection rates were 96.4% in AI-group, 78.7% in EI-group, and 41.2% in BEI-group (P = 0.000). The en bloc resection rates were 97.6% in AI-group, 87.4% in EI-group, and 86.3% in BEI-group (P = 0.023). The 5-year tumor recurrence rates were 1.8% in the AI-group, 1.5% in the EI-group and 15.4% in the 上海皓元 BEI-group (P = 0.000). The 5-year disease-specific survival rates were 100% in the AI-group, 100% in the EI-group, and 97.4% in the BEI-group (P = 0.088). The 5-year disease-free survival rates were 98.2% in the AI-group, 98.5% in the EI-group, and 84.6% in the BEI-group (P = 0.000). Conclusion: ESD was effective and safe in the AI or EI-group but a comparatively high rate of recurrence resulted from performance of ESD in the BEI-group. ESD may be useful in EGC patients at high-risk for surgery. Key Word(s): 1. early gastric cancer; 2. endoscopic submucosal dissection; 3. expanded indication; 4. long-term; 5.

4C), IFN-β protein levels remained below 4 pg/mL, and IFN-α protein was undetectable (Fig. 4D). In contrast, IL-28 and IL-29 peaked to significantly higher mRNA levels within 24-48 hours and protein levels reached up to 250 pg/mL 72 hours after HCV infection (Fig. 4C-D). Variations in ISG and IFN responses among donors did not correlate with HCV RNA levels in PHH cultures (Fig. 4E,F and Supporting Fig. 1) nor with IL28B SNPs (Supporting Fig. 2). Overall, our results demonstrate that transfection of PHH with double-stranded RNA (dsRNA) and infection with HCV reproduced the ISG and IFN expression

profile that we observed in the liver during acute HCV infection. To study the functional relevance of the strong type III IFN response during HCV infection, we examined its effect on HCV replication using Huh7-Lunet cells with a subgenomic HCV ABT-263 cell line luciferase replicon as a readout.23 Recombinant type I (500 pg/mL) and type III IFNs (100 ng/mL) inhibited HCV replication by more than 90%, and this inhibition was almost completely abrogated by cytokine-specific neutralizing Abs (Fig. 5A). IL-29, IL-28A, and IL-28B showed 50% inhibition of HCV replication at 200-500 pg/mL (Fig. 5B), which is the maximum amount of type III IFNs that PHH produced 72 hours postinfection

(Figs. 4D and 6). Because 50% antiviral activity can also be mediated by very low concentrations of type I IFNs below the ELISA detection limit, we used an indirect method to further evaluate the relative effect of type I and III IFNs on HCV replication. Supernatants from PHH cultures harvested 72 hours post-HCV infection reduced PARP inhibitor HCV replication by 50% (Fig. 5C). Whereas neutralization of the supernatant with Abs against either type I (IFN-α and IFN-β) medchemexpress or III IFNs (IL-28A, IL-28B, and IL-29) significantly increased HCV replication, neutralization of type III IFNs had a greater effect than neutralization of type I IFNs (P = 0.0244). This result suggests that type III IFNs contribute significantly to antiviral activity during

HCV infection. Experiments with hepatoma cell lines and TLR-stimulated macrophages suggest that type III IFNs are ISGs themselves and can be induced in a type I IFN-mediated manner.8, 24 To evaluate whether this holds true for HCV-infected PHH, we infected PHH with HCV in the presence or absence of neutralizing Abs against IFN-α and IFN-β. Whereas IL-28 secretion decreased in the presence of neutralizing Abs against type I IFNs (P = 0.0078), IL-29 production was not affected in the majority of cultures (P = not significant; Fig. 6). Thus, IL-29 can be induced independently from type I IFN signaling in HCV-infected hepatocytes. pDCs were recently shown to contribute to the induction of IFN-α and ISGs when cocultured with HCV-replicating hepatoma cells.7 We therefore asked whether this result extended to pDCs cocultured with HCV-infected PHH and to the production of type III IFNs. Less than 0.

However,

because most studies have relied on population surveys, liver histology was not evaluated, and the possible effects of coffee/caffeine on liver fibrosis had to be indirectly assessed. The distinction between anti-fibrogenic effects and protection against decompensation is important in understanding the underlying beneficial mechanism. With complete liver biopsy data on all 177 patients, across the spectrum of liver fibrosis, the data from this study suggest that the beneficial effect of caffeine is mediated through reduced rate of progression of fibrosis. However, the lack of association between caffeine intake and hepatic inflammation suggests that, rather than reducing fibrosis by minimizing ongoing inflammation, the protective effect of caffeine may be mediated through a direct anti-fibrogenic mechanism Recent in vitro data suggest possible mechanisms by which coffee or caffeine may affect liver disease and specifically Raf inhibitor hepatic fibrogenesis. Studies in mice and rats as well as human hepatoma cell lines have shown that coffee and some of its major components (caffeine, cafestol, and kahweol) alter

expression and see more activity of enzymes involved in xenobiotic metabolisms.25–28 Inhibition of phase I enzymes and up-regulation of phase II enzymes such as glutathione-S-transferase have been reported, both of which would favor reduced accumulation of toxic metabolites within hepatocytes.27 Pretreatment with cafestol and kahweol protected mice from carbon tetrachloride hepatotoxicity by inhibiting cytochrome CYP 2E1, the enzyme responsible for carbon tetrachloride bioactivation.29 With respect to caffeine specifically, Gressner and colleagues30 recently reported that caffeine inhibits expression of connective tissue growth factor (CTGF) by interfering with transforming growth factor beta (TGFβ) signaling through the SMAD pathway.30 Caffeine was also found to up-regulate peroxisome proliferator-activated receptor gamma (PPARγ) levels, which further reduce CTGF medchemexpress expression. Although these results from primary cell culture

clearly need in vivo confirmation, inhibition of the transforming growth factor beta pathway is an attractive explanation for anti-fibrogenic effects attributed to caffeine. It is important to consider potential confounding factors when interpreting the data from this study. The study was cross-sectional in nature, and caffeine consumption was estimated at the time of liver biopsy, despite the fact that any protective effect would likely occur over many years. Patients consuming the greatest amount of caffeine had less fibrosis on biopsy. Although it is tempting to conclude that caffeine has a protective effect on fibrogenesis, other explanations are also possible. Patients with more advanced liver fibrosis may have reduced their caffeine intake because of a presumption that caffeine may not be good for their health.

35 These controversies notwithstanding, Ronis et al. recently demonstrated that a significant proportion of alcohol-mediated liver injury occurs independently of alcohol metabolism. 36 Our results, showing that KO mice develop severe steatosis despite a significant block in hepatic

ethanol metabolism, are consistent with their study. A remarkable feature of the adult liver is the zonation of metabolic function across the liver acinus. 37 β-catenin is a key player in establishing hepatic metabolic zonation and is a regulator of the perivenous program of gene expression. 17, 18, 24 Whether alcohol metabolism is zonated is somewhat controversial, and two opposing views of alcohol metabolism have been proposed. Studies with microquantitative techniques or immunohistochemistry suggested that ADH activity was maximal in the selleck chemical perivenous area. 38, 39 Microquantitative techniques for ADH check details and ALDH from the human liver similarly showed an increasing periportal to perivenous gradient, although there were gender- and age-related differences. 40 On the other hand, Kashiwagi et al. reported no zonal differences in ADH-dependent ethanol metabolism in hemoglobin-free perfused rat liver. 41 The effect of the hepatic zonal architecture on ethanol metabolism is highlighted by the fact that Cyp2E1

is strongly perivenous in its distribution. 12, 15 Our results suggest a modest increase in perivenous ADH1 staining in WT mice, which is absent in KO livers. Furthermore, in contrast to WT mice, we found that EtOH KO mice exhibited a nonuniform pattern MCE of cytoplasmic ADH staining and vacuoles within hepatocytes where there was intense, localized ADH staining. The functional significance of these findings is currently under investigation, but may represent defective protein trafficking within KO hepatocytes, as previously reported for specific proteins in cells depleted of β-catenin/E-cadherin–based adherens junctions, or stress-induced autophagy. 42, 43 We could not detect binding of TCF4,

the transcriptional coactivator of β-catenin, at the ADH1A and CYP2E1 promoters. Though these negative results may imply that these genes are not direct transcriptional targets of β-catenin, it is possible that β-catenin/TCF4 bind to enhancers located outside these approximately 5-kb (kilobase) regions spanning the transcription start sites that were targeted by us. Hatzis et al. showed that TCF4-binding sites could be located at large distances (>100 kb) and could be far upstream, intronic, or downstream of transcription start sites of target genes. 44 Similarly, there are five β-catenin responsive elements located 400 kb upstream from its target gene, MYC, and align with the MYC promoter through long-range chromatin loops. 45 Thus, further studies will be needed to determine whether β-catenin directly or indirectly regulates ethanol-metabolizing genes in the liver.

001). Functionally, the suppression of Rap1b expression was sufficient to decrease cell motility by inhibiting expression of p38 MAPK rather than VEGF or p42/44 ERK in vitro and in vivo. Moreover, there was a significantly positive correlation between Rap1b and

p38 MAPK expression in ESCC tissues. Conclusion: Our results suggest that the Rap1b/p38 MAPK pathway is associated with survival, tumor progression, and metastasis of ESCC patients. Key Word(s): 1. Rap1b; 2. esophageal squamous cell carcinoma; 3. invasion; 4. P38 MAPK Presenting Author: MINGXIN ZHANG Additional Authors: MINGXIN ZHANG, PENGJIANG ZHANG, QI YANG, QINSHENG WEN, JINGJIE WANG Corresponding Author: MINGXIN ZHANG Affiliations: Tangdu Hospital Fourth Military Medical University, Tangdu Hospital Fourth Military Medical University, NU7441 mw Tangdu Hospital Fourth Military Medical University, Tangdu Hospital Fourth Military Medical University, Tangdu Hospital Fourth Military Medical University Objective: Cancer related inflammation (CRI) is abnormal signal pathway in cancer cell induced by inflammation and plays important role in esophageal squamous cell carcinoma (ESCC). Our previous study found that miR-302b down-regulated Luminespib in vivo in ESCC, but the exact role of miR-302b in the regulation of CRI and its molecular mechanism in ESCC is still unclear. Methods: First,

we examined the expression of miR-302b by quantitative RT-PCR in ESCC patient specimens compared to paired

esophagitis tissues and normal esophageal tissues (NET). Then, to determine the possible correlation between miR-302b and CRI signal pathway, ESCC cell lines (EC9706, Eca109, TE1, TE10, TE11, and OE33) were treated with by various inflammation stimulation factors (LPS, IL-6, IFN-γ, and TGF-β). Expression of miR-302b was detected by quantitative medchemexpress RT-PCR and gene profiles were tested by gene microarray. Finally, immunohistochemical staining and western blotting analysis of ESCC specimens were carried out to reveal correlation between miR-302b and miR-302b potential targeted CRI related gene (ERBB4, TGFBR2, CXCR4, and IRF2) expression. Results: Expression of miR-302b showed a trend to decrease form NET to ESCC tissues. After inflammation stimulation, miR-302b decreased. Gene profiles revealed an inflammatory gene signature with upregulation of numerous cancer-related inflammation genes including some miR-302b potential targeted CRI related genes (ERBB4, TGFBR2, CXCR4, and IRF2). Moreover, there was a significantly negative correlation between miR-302b and CRI related genes (ERBB4, TGFBR2, CXCR4, and IRF2) expression in ESCC tissues. Conclusion: Our results suggest that miR-302b plays important role in the CRI of ESCC possibly by regulation expression of CRI related genes (ERBB4, TGFBR2, CXCR4, and IRF2). Key Word(s): 1. miR-302b; 2. esophageal squamous cell carcinoma; 3.

001). Functionally, the suppression of Rap1b expression was sufficient to decrease cell motility by inhibiting expression of p38 MAPK rather than VEGF or p42/44 ERK in vitro and in vivo. Moreover, there was a significantly positive correlation between Rap1b and

p38 MAPK expression in ESCC tissues. Conclusion: Our results suggest that the Rap1b/p38 MAPK pathway is associated with survival, tumor progression, and metastasis of ESCC patients. Key Word(s): 1. Rap1b; 2. esophageal squamous cell carcinoma; 3. invasion; 4. P38 MAPK Presenting Author: MINGXIN ZHANG Additional Authors: MINGXIN ZHANG, PENGJIANG ZHANG, QI YANG, QINSHENG WEN, JINGJIE WANG Corresponding Author: MINGXIN ZHANG Affiliations: Tangdu Hospital Fourth Military Medical University, Tangdu Hospital Fourth Military Medical University, selleck Tangdu Hospital Fourth Military Medical University, Tangdu Hospital Fourth Military Medical University, Tangdu Hospital Fourth Military Medical University Objective: Cancer related inflammation (CRI) is abnormal signal pathway in cancer cell induced by inflammation and plays important role in esophageal squamous cell carcinoma (ESCC). Our previous study found that miR-302b down-regulated this website in ESCC, but the exact role of miR-302b in the regulation of CRI and its molecular mechanism in ESCC is still unclear. Methods: First,

we examined the expression of miR-302b by quantitative RT-PCR in ESCC patient specimens compared to paired

esophagitis tissues and normal esophageal tissues (NET). Then, to determine the possible correlation between miR-302b and CRI signal pathway, ESCC cell lines (EC9706, Eca109, TE1, TE10, TE11, and OE33) were treated with by various inflammation stimulation factors (LPS, IL-6, IFN-γ, and TGF-β). Expression of miR-302b was detected by quantitative medchemexpress RT-PCR and gene profiles were tested by gene microarray. Finally, immunohistochemical staining and western blotting analysis of ESCC specimens were carried out to reveal correlation between miR-302b and miR-302b potential targeted CRI related gene (ERBB4, TGFBR2, CXCR4, and IRF2) expression. Results: Expression of miR-302b showed a trend to decrease form NET to ESCC tissues. After inflammation stimulation, miR-302b decreased. Gene profiles revealed an inflammatory gene signature with upregulation of numerous cancer-related inflammation genes including some miR-302b potential targeted CRI related genes (ERBB4, TGFBR2, CXCR4, and IRF2). Moreover, there was a significantly negative correlation between miR-302b and CRI related genes (ERBB4, TGFBR2, CXCR4, and IRF2) expression in ESCC tissues. Conclusion: Our results suggest that miR-302b plays important role in the CRI of ESCC possibly by regulation expression of CRI related genes (ERBB4, TGFBR2, CXCR4, and IRF2). Key Word(s): 1. miR-302b; 2. esophageal squamous cell carcinoma; 3.

Kidney failure was defined as an increase of serum creatinine > 2 mg/dl or requirement of renal replacement therapy. Factors

considered for univariate analysis for Predisposition included patient demographics, severity and etiology of underlying liver disease, baseline biochemical parameters, presence of ascites,comorbidities including chronic kidney disease; for Injury- diuretic use, nephrotoxicity, bacterial infections, variceal bleed; for Response-components of systemic inflammatory response syndrome and for Organ failure-extrarenal organ failures i.e. cerebral, circulatory and respiratory defined according to CLIF-SOFA score. Results: Of 1365 patients with ACLF (age 44 ±12.9 years, 83% males) with MELD PD98059 order score of 32.6 ± 9.4, 29% developed kidney

failure. Factors significant (p,OR, 95% CI) on multivariate analysis for P component were high baseline MELD (&30) (<0.001, 1.72, 1.34-2.2) and low serum sodium (<130mEq/l) (0.002, 1.4, 1.14-1.9); for I component, bacterial infections (0.02, 1.4, 1.04-1.96); for R component, leucocytosis (0.03, 1.3, 1.021.71); for O component, circulatory failure (<0.0001, 4.6, 3.2-6.7) and cerebral failure (<0.001,2.7, 2.1-3.6). The combination of these four components into a single-value predictor of kidney failure in the combined PIRO model identified circulatory failure (OR 5.8, 95% CI 3.1-11.1) and cerebral failure (OR 2.1, 95% CI 1.2-3.7) as the most significant predictors. Amongst all organ failures, presence of circulatory failure at baseline was

the most http://www.selleckchem.com/products/kpt-330.html significant predictor of mortality 上海皓元 (OR 1.8, 95% CI 1.1-3.3). Conclusions: The PIRO model could be a novel approach to identify and stratify ACLF patients at risk of kidney failure. Kidney failure is commonly associated with presence of extra-renal organ failures at baseline amongst which circulatory failure predicts mortality independent of both renal and other organ failures. Disclosures: George K. Lau – Consulting: Roche, Novartis, Roche, Novartis, Roche, Novartis, Roche, Novartis Qin Ning – Advisory Committees or Review Panels: ROCHE, NOVARTIS, BMS, MSD, GSK; Consulting: ROCHE, NOVARTIS, BMS, MSD, GSK; Grant/Research Support: ROCHE, NOVARTIS, BMS; Speaking and Teaching: ROCHE, NOVAR-TIS, BMS, MSD, GSK Diana A. Payawal – Advisory Committees or Review Panels: United Laboratories; Consulting: Takeda Pharmaceutical; Speaking and Teaching: Fatima Medical University Hospital Soek Siam Tan – Advisory Committees or Review Panels: Abbvie Osamu Yokosuka – Grant/Research Support: Chugai, Taiho, Bristol Myers The following people have nothing to disclose: Rakhi Maiwall, Shiv K. Sarin, Chandan K. Kedarisetty, Richard Moreau, Suman Kumar, Zaigham Abbas, Deepak N.