The digit recall task required participants to serially recall lists of digit strings that were set at their own maximum span and read by the examiner at the approximate rate of two per second. Participants performed the tracking and digit recall tasks separately

for a period of 2 min each prior to performing both tasks concurrently for a period of 2 min. A composite Autophagy Compound Library measure of dual-task performance (μ) was calculated according to the formula: μ = (1 − [(Pm + Pt)/2]) × 100 (Baddeley et al., 1997). Here, μ represents the combined change in dual-task performance relative to performance on the constituent tasks, where Pm is the proportional change in memory performance and Pt is the proportional change in tracking. Pm is calculated according to (ps − pd)/ps, where ps is the proportion of digit strings recalled correctly under single task conditions and pd is the proportion of digit strings recalled under dual task. Pt is calculated according to (ts − td)/ts, where ts is the number of boxes crossed under single-task conditions and td is the number of boxes selleck products crossed under dual-task conditions. Auditory and visual attentional capacities were measured with digit span and spatial

span respectively (see Lezak, Howieson, Bigler, & Tranel, 2012). The TMT (see Lezak et al., 2012) was used to measure divided attention; the elevator counting task from the Test of Everyday Attention (TEA-2; Robertson, Ward, Ridgeway, & Nimmo-Smith, 1994) measured sustained attention; the elevator task with distraction (TEA-3) was deployed to measure selective attention. The ability to maintain and shift mental set was assessed with the Odd-Man-Out test (OMO; Flowers & Roberston, 1985). The mean selleck chemical scores and standard deviations for the digit recall and tracking tasks achieved under single- and dual-task conditions

are displayed in Table 2. To ensure that any differences found between the groups reflect dual-task deficits per se and not inflated single-task differences, we followed Baddeley and colleagues (e.g., Cocchini, Logie, Della Sala, MacPherson, & Baddeley, 2002) and excluded data from participants who scored below 70% accuracy under single-digit recall conditions. Accordingly, data from four TLE patients (three left-sided and one right-sided) was excluded from further analyses. A 2 × 2 ANOVA of digit recall for the remaining participants, treating Group (TLE or control) as a between-subjects factor and condition (single or dual task) as a within-subjects factor did not reveal a main effect of group [F(1, 34) = 3.556, p > .068]. A main effect of condition was found [F(1, 34) = 5.880, p < .021] indicating that a higher proportion of digits were correctly recalled under single-task conditions. The interaction between group and condition did not approach significance [F(1, 34) = 0.501, p > .484].

Lake, MD 9:50 – 9:55 AM Discussion 9:55 – 10:15 AM Surviving and Thriving with Value and Excellence From an Administrative Perspective Jennifer

Milton, RN, MSN 10:15 – 10:20 AM Discussion 10:20 -10:30 AM Break Session II: Successes and Challenges in Sustaining Excellence in Private Health Care Systems 10:30 – 10:50 AM Perspectives From A Surgical Program Director William C. Chapman, MD 10:50 – 10:55 AM Discussion 10:55 – 11:15 AM Perspectives From A Medical Program Director-Private Sector James F. Trotter, MD 11:15 – 11:20 AM Discussion 11:20 – 11:40 Bcl-2 inhibitor AM Surviving and Thriving with Value and Excellence Karen Hess, RN, MS, MBA, ACNP 11:40 – 11:45 AM Discussion 11:45 AM – Noon Panel Discussion Meet-the-Professor Luncheon Saturday, November 2 12:15 -1:15 PM Refer to your luncheon ticket for meeting

room location. MTP-1 Use of Statins in Patients with Liver Disease Curtis K. Argo, MD and Naga P. Chalasani, MD MTP-2 Safe Prescribing in Liver Disease James H. Lewis, MD and Timothy J. Davern, MD MTP-3 Herbs and Natural Remedies in Patients with Liver Disease Victor J. Navarro, MD and Leonard B. Seeff, MD MTP-4 HCV: Treat Now or Wait Paul J. Pockros, MD and Christoph Sarrazin, MD MTP-5 HCV: Side Effects of New see more Antiviral Agents John F. Reinus, M.D. and Reem H. Ghalib, MD MTP-6 Hepatitis C Management in the Liver Transplant Candidate Catherine T. Frenette, MD and Marina Berenguer, MD MTP-7 The Hepatitis C Drug Pipeline Douglas T. Dieterich, MD and Raymond T. Chung, MD MTP-8 Optimal Management of Hepatic Encephalopathy Norman Gitlin, MD and Kevin D. Mullen, MD MTP-9 Viral Hepatitis and HIV Infection Norbert Brau, MD and Maribel Rodriguez-Torres, MD MTP-10 Viral Hepatitis in Patients Undergoing

Heart, Kidney and Bone Marrow Transplants Michael P. Curry, MD and Maya Gambarin-Gelwan, MD MTP-11 HCC: How to Screen Roniel Cabrera, MD and Jose Franco, MD MTP-12 NAFLD: Who to Biopsy Neeral L. Shah, MD and Nizar N. Zein, MD MTP-13 OLT: Improving Long-term Outcomes Francisco A. Durazo, MD and Jacqueline G. O’Leary, MD MTP-14 Endoscopy Issues in Patients with End-stage Liver Disease Vijay Shah, MD and Bruce A. Luxon, MD, PhD MTP-15 Alcoholic Hepatitis: selleck products What Should I do? Philippe Mathurin, MD, PhD and Timothy R. Morgan, MD Poster Session I Saturday, November 2 2: 00 – 7: 30 PM Hall E Refer to page 92A for Poster Presentations Exhibit Hall Opening and Reception Saturday, November 2 5: 00 – 7: 30 PM Hall D Transplant Surgery Workshop Saturday, November 2 3:30 – 7:00 PM Room 146A Management of Rare Liver Tumors COURSE DIRECTORS: Sasan Roayaie, MD Kenneth D. Chavin, MD, PhD 3.5 CME Credits The program will provide the audience with an evidence based review of the current diagnostic and treatment strategies for less commonly encountered liver tumors.

Disclosures: Eberhard L. Renner – Advisory Committees or Review Panels:

Vertex Canada, Novartis, Astellas Copanlisib clinical trial Canada, Rcohe Canada, Gambro; Grant/Research Support: Novartis Canada; Speaking and Teaching: Novartis, Astellas Canada, Roche Canada Florence Wong – Consulting: Gore Inc; Grant/Research Support: Grifols The following people have nothing to disclose: Angela C. Cheung, Rania N. Rabie, Max Marquez Objective: To determine the characteristics, publication rate, and availability of summary results for clinical trials of viral hepatitis registered on ClinicalTrials.gov (CT.gov), a registry of clinical trials mandated by the United States Congress. Background and Methods: Since October 2007, most phase 2–4 clinical trials of a drug or biological conducted in the United States are required to be registered on CT.gov and to submit summary results within a year after trial completion. In addition, many journals now require that clinical trials be registered in an approved registry prior to enrollment of the first subject.

A search of CT.gov on May 3, 201 3 identified 2,088 studies that listed hepatitis as a condition. Protocol descriptive data for this website these studies were downloaded and the studies were coded for analysis. PubMed was searched for publications to determine the publication rate for randomized clinical trials with completion dates in 2009–2010. Results: The 2,088 studies included 1,695 interventional trials, 307 of which were completed in 2009 or 2010. Of these, 193 were randomized, parallel group clinical trials and 1 04 were phase 2–4 trials of a drug or biologic for treatment of patients with hepatitis B or C. 58% of the 1 04 were sponsored by industry and 49% had a site in the United States. The primary outcome of the trial was change in viral level for 76%, 75% were studies of hepatitis C, the median sample size was 1 00 subjects, and 34% had a sample size of 200 or more. Journal publications with study results 3-mercaptopyruvate sulfurtransferase were found for 40 trials, 30 had summary results on CT.gov, and 55 (53%) were either published or had summary results on CT.gov. Results were more likely

to be available (publication or summary) for phase 3–4 studies (64% versus 31%, p=0.002), for studies sponsored by industry (62% versus 41 %, p=0.04), and for studies with a sample size of 200 or more (69% versus 45%, p=0.02). Availability was similar for trials with (53%) and without (53%) a site in the United States, for trials of hepatitis B (58%) or C (51%), and for trials completed in 2009 (60%) or 2010 (48%). Publication rates were similar (37% versus 41%), but industry sponsored trials were more likely to have summary results submitted to CTG (47% versus 5%, p<0.0001). Conclusions: Almost half of randomized clinical trials of therapy for hepatitis B or C completed in 2009–2010 did not have results available as either a journal publication or as results posted by CT.gov more than 2 years after trial completion.

Women with congenital FXIII deficiency suffer significant bleeding complications.

Menorrhagia and ovulation bleeding are common gynaecological problems and more prevalent than reported. Pregnancies in women with FXIII deficiency have a significant risk of miscarriage, placental abruption and PPH if not on prophylaxis treatment. “
“Prophylaxis was introduced for severe hemophilia more than 50 years ago in Sweden. Costs of treatment and the need for frequent infusions have delayed the acceptance of this very effective treatment. With primary prophylaxis, bleeding can be prevented and children can lead a normal life. Dosage and frequency of prophylaxis can be individualized to reduce cost and should make prophylaxis affordable for more

children. In the Western world, prophylaxis should be the standard Adriamycin supplier of care for all children RG-7388 datasheet with severe hemophilia A and B. When to begin prophylaxis in adults with hemophilic arthropathy is still under debate as it is considered less effective. “
“von Willebrand’s disease (VWD) patients undergoing major surgery are prophylactically treated to promote haemostasis. There is variability in perioperative clinical practice; however, most guidelines suggest replacing the deficient factor to a level of 1.0 IU mL−1 (or 100%). A review of the literature reveals a paucity of well constructed descriptive data quantifying the changes in coagulation that occur in response to surgical stress. The aim of this study was to quantify the changes in haemostatic variables occurring in response to elective orthopaedic surgery in normal individuals. Eligible subjects >18 years of age undergoing total hip or knee replacement were recruited. Blood samples were drawn at five time points: baseline, preoperatively, 30 min after surgical incision, 30 min postoperatively, postoperative day (POD) 1. Analyses included t-tests and repeated measures anova. Overall 30 patients, 21 women and 9 men, with a mean age of 65 were included in the final analysis. All von Willebrand factor (VWF) variables were seen to significantly decrease intraoperatively and increase

postoperatively. VWF multimers showed a statistically significant decrease in high molecular weight multimers Fossariinae intraoperatively and an increase postoperatively. On subgroup analysis, age, gender and anaesthesia type were significantly correlated with changes in VWF parameters. Data presented in the current study establish a physiological baseline for VWF parameters in the normal population and demonstrate mean VWF/factor VIII levels greater than 1.0 IU mL−1 intraoperatively. As such, current management in VWD patients does not appear to mimic the normal physiological response to surgery. “
“Our objective was to provide a synthesis of measurement properties for performance-based outcome measures used to evaluate physical function in children with haemophilia.

1%)achieved EVR, 67 ( 94.3% ) achieved ETVR. The rates of relapse were 17.9% on 24 week follow- up and 26.86% on 48 week follow-up. Univariate analysis showed that the rate of relapse was higher for age ≥50, gene type I,HCV RNA ≥ 1.0 × 10∧5copies/ml, HCV RNA in PBMC positive, liver fibrosis ≥S2 and leptin expression positive than for age <50, gene type non-I, HCV RNA<1.0 × 10∧5copies/ml, HCV RNA in PBMC negative, liver fibrosis

of transmission, RVR, EVR (χ2=0.19,0.46,0.16,0.06,P > 0.05, respectively). Multivariate logistic stepwise regression analysis BAY 57-1293 datasheet showed that gene type I, HCV RNA level and HCV RNA level in PBMC were independent factors for predicting

relapse[OR = 7.56(95%CI 1.418-40.311, OR = 7.553(95%CI 1.692-33.527, OR = 5.165(95%CI 1.102-24.210), P < 0.05, respectively]. Conclusion: Age, gene type, HCV RNA level, HCV RNA level in PBMC, liver fibrosis, leptin expression in liver were related with relapse. Gene type I, HCV RNA level and HCV RNA level in PBMC were independent factors for predicting relapse. Key Word(s): 1. Chronic hepatitis C; 2. Antiviral Erastin therapy; 3. relapse; 4. leptin; Presenting Author: CHING-CHUNG LIN Additional Authors: MING-JONG BAIR, CHIA-HSIEN WU, HUAN-LIN CHEN, I-TSUNG LIN, HORNG-YUAN WANG, SHOU-CHUAN SHIH Corresponding Author: CHING-CHUNG LIN Affiliations: Mackay Memorial Hospital Objective: The treatment efficacy of HCV genotype 1 is inferior to genotype 2 by peginterferon plus ribavirin, but it is unclear about the role of mixed-genotype 1 and 2. In recently, mixed genotype HCV infection could be detected, so a comprehensive and detailed investigation is worth to evaluate the clinical role. We compared the treatment outcome

of HCV genotype 1, genotype 2 and mixed-genotype 1 and 2 by peginterferon alfa-2b plus ribavirin in naïve chronic hepatitis C patients. Methods: In this retrospective case control study, total 150 patients (68 genotype 1, 55 genotype 2 and 27 mixed-genotype 1 and 2) were treated and received at least one dose medication, consisting peginterferon alfa-2b once weekly plus Paclitaxel supplier daily ribavirin (800 or 1000 mg, depending on body weight) for 24 weeks. The efficacy analysis was by intention to treat and endpoints including virological responses rate during the treatment and the influence of race. Results: Hepatitis C mixed-genotype 1 and 2 occupied about 20% of HCV treated patients in Taitung, Taiwan. There were no any differences in demographic and clinical characteristics among these 3 groups. There was significant difference in sustained virological response (SVR) rate between genotype 1 and genotype 2 (55.9% vs 83.6%; p = 0.001), and rapid virological response rate between genotype 1 and mixed-genotype 1 and 2 (64.7% vs 85.2%; p = 0.048).

Further, TLR4-deleted www.selleckchem.com/products/AZD0530.html hepatocytes are refractory to FC lipotoxicity. HMGB1 is an archetypical danger associated molecular pattern (DAMP) which may facilitates interactions between other DAMPs and pattern recognition receptors, such as TLRs. Cholesterol crystals have recently been identified in human NASH (Ioannou et al 2013), and are abundant

in livers from our metabolic syndrome mouse model. We tested whether conditioned media from lipotoxic hepatocytes and/or cholesterol crystals activates Kupffer cells via the NLRP3 inflammasome, which in this cell type is activated via TLR4. Materials and Methods: Primary murine hepatocytes from C57B6/J wild type (WT) mice were incubated with 40 μM LDL for 24 h to load with FC; conditioned media was collected and stored at −80°C. Primary (resting)

Kupffer cell cultures were prepared by selective centrifugation using Percoll gradients (50/25) and cultured in RPMI before addition of conditioned media. Highly purified cholesterol crystals were prepared in acetone, as reported (Duewell et al 2010). Pathways of inflammasome activation were determined by semiquantitative real time PC, by IL-1β secretion into media (ELISA), and use of the potent (Ki50∼10 nM) NLRP3-specific inhibitor, CRID3. Results: At 40 μM LDL, hepatocytes secreted HMGB1 into culture media and underwent liver injury (as LDH leakage) with cell death by apoptosis and necrosis. Addition of HMGB1-enriched culture medium from FC-loaded hepatocytes activated resting KCs, as assessed by nuclear translocation of NF-κB, release of IL-1β and TNF-α, Morin Hydrate and ultrastructural changes. To expose Kupffer cells directly to cholesterol NVP-BGJ398 clinical trial crystals, we coated culture vessels, using purified FC crystals solubilized in 1:100 acetone:ethanol solvent. Solvent was allowed to evaporate, leaving cholesterol crystals at 15, 20, and 60 mM concentrations per culture vessel. After 24 h culture on crystal-coated coverslips, Kupffer cells showed significant induction of NLRP3, caspase 1, ASC, IL-18 and IL-1β mRNA,

as well as a 50% increase in IL-1β secretion. KCs from Tlr4−/− mice were refractory to NLRP3 activation by cholesterol crystals. Even at 5 nM, the NLRP3 inhibitor CRID3 totally (100%) abrogated IL-1β secretion from Kupffer cells activated by cholesterol crystals directly. Conclusions: These highly novel findings reveal direct links (via HMGB1 and likely other DAMPs) between cholesterol lipotoxicity and engagement of Kupffer cell activation, in which cholesterol crystals may play an additional direct pathogenic role. Identification of TLR4 and the NLRP3 inflammasome, and particularly the impressive efficacy of CRID3 as an NLRP3 inhibitor, has implications for both the pathogenesis and treatment of NASH. 1. Ioannou GN, Haigh WG, Thorning D et al. Hepatic cholesterol crystals and crown-like structures distinguish NASH from simple steatosis.

“
“We investigated whether gene transfer of insulin-like growth factor I (IGF-I) to the hepatic tissue was able to improve liver histology and function in established liver cirrhosis. Rats with liver cirrhosis induced by carbon tetrachloride (CCl4) given orally for 8 weeks were injected through the hepatic artery with saline or with Simian virus 40 vectors encoding IGF-I (SVIGF-I), or luciferase (SVLuc). Animals were sacrificed 8 weeks after vector injection. In cirrhotic rats we observed that, whereas IGF-I was synthesized

by hepatocytes, IGF-I receptor was predominantly expressed by nonparenchymal cells, mainly in fibrous septa surrounding hepatic nodules. Rats treated with SVIGF-I showed increased hepatic levels of IGF-I, improved liver function Nutlin-3a tests, and reduced fibrosis in association PS-341 chemical structure with diminished α-smooth muscle actin expression, up-regulation of matrix metalloproteases (MMPs) and decreased expression of the tissue inhibitors of MMPs TIM-1 and TIM-2. SVIGF-I therapy induced down-regulation of the profibrogenic molecules transforming growth factor beta (TGFβ), amphiregulin, platelet-derived growth factor (PDGF), connective tissue growth factor (CTGF), and vascular endothelium growth factor (VEGF) and induction of the antifibrogenic and cytoprotective hepatocyte growth factor (HGF). Furthermore, SVIGF-I-treated animals showed decreased expression of Wilms tumor-1 (WT-1; a nuclear factor involved in

hepatocyte dedifferentiation) and up-regulation of hepatocyte nuclear factor 4 alpha (HNF4α) (which stimulates hepatocellular differentiation). The therapeutic potential of SVIGF-I was also tested in rats with thioacetamide-induced liver cirrhosis. Also in this model, SVIGF-I improved liver function and reduced Suplatast tosilate liver fibrosis in association with up-regulation of HGF and MMPs and down-regulation of tissue inhibitor of metalloproteinase 1 (TIMP-1). Conclusion: IGF-I gene transfer to cirrhotic livers

induces MMPs and hepatoprotective factors leading to reversion of fibrosis and improvement of liver function. IGF-I gene therapy may be a useful alternative therapy for patients with advanced cirrhosis without timely access to liver transplantation. (HEPATOLOGY 2010;51:912–921.) Liver transplantation is the only curative option for patients with advanced liver cirrhosis. This procedure can only be applied to a minority of patients due to the presence of surgical contraindications and organ scarcity. In fact, the waiting list in the USA includes ≈12,500 patients with a median time to transplantation of ≈300 days; more than 45% of the patients exceed 24 months on the waiting list, where the mortality reaches 130 per 1,000 patients/year.1 Insulin-like growth factor I (IGF-I) is a potent cytoprotective and anabolic hormone, synthesized mainly in the liver, which circulates bound to a set of binding proteins (IGFBPs) that regulate IGF-I biological activity.

The highest growth rate and DHA accumulation of this strain were obtained in 6.0% glucose, 1.0% yeast extract, 50% artificial seawater (ASW), and pH 7 at 28°C. In addition, carbon and nitrogen sources could be replaced by glycerol, ammonium acetate, sodium nitrate, or fertilizer N–P–K. Total lipid content reached 38.67% of dry cell

weight (DCW), in which DHA and eicosapentaenoic acid (EPA, C20:5n-3) contents accounted for 43.58% and 0.75% of the total fatty acid (TFA), respectively. In 5 and 10 L fermenters, the cell density, DCW, total lipid content, and maximum DHA yield were 46.50 × 106 cells · mL−1, 23.7 g · L−1, 38.56% of DCW, and 8.71 g · L−1 (in 5 L fermenter), respectively, and 49.71 × 106 cells · mL−1, 25.34 g · L−1, 46.23% of DCW, and 11.55 g · L−1 (in 10 L fermenter), respectively. Biomass of PQ6 strain possessed high contents of Na, I, and Fe (167.185, 278.3, and 43.69 mg · kg−1 IGF-1R inhibitor DCW, respectively). These

results serve as a foundation for the efficient production of PQ6 biomass that can be used as a food supplement for buy Cisplatin humans and aquaculture in the future. “
“There is increasing interest in naturally produced colorants, and microalgae represent a bio-technologically interesting source due to their wide range of colored pigments, including chlorophylls (green), carotenoids (red, orange and yellow), and phycobiliproteins (red and blue). However, the concentration of these pigments, under optimal growth conditions, is often too low to make microalgal-based pigment production economically feasible. In some Chlorophyta (green algae), specific process conditions such as oversaturating light intensities or a high salt concentration induce the overproduction of secondary carotenoids (β-carotene in Dunaliella salina (Dunal) Teodoresco and astaxanthin in Phospholipase D1 Haematococcus pluvialis (Flotow)). Overproduction of all other pigments (including

lutein, fucoxanthin, and phycocyanin) requires modification in gene expression or enzyme activity, most likely combined with the creation of storage space outside of the photosystems. The success of such modification strategies depends on an adequate understanding of the metabolic pathways and the functional roles of all the pigments involved. In this review, the distribution of commercially interesting pigments across the most common microalgal groups, the roles of these pigments in vivo and their biosynthesis routes are reviewed, and constraints and opportunities for overproduction of both primary and secondary pigments are presented. “
“Transcripts and enzyme activities of antioxidative enzymes were increased by hypersalinity (90‰) in a marine macroalga, Ulva fasciata Delile (Lu et al. 2006, Sung et al. 2009). This study examined the effects of polyamines (PAs) on the induction of hypersalinity tolerance through the modulation of expression of antioxidative defense enzymes. Incubation of U.

Despite the

better outcome of patients receiving prophylaxis, some will still develop structural joint damage. The new role of angiogenic mediators in the pathogenesis of joint disease remains to be fully elucidated. In future, better understanding of the cause of discrepancies check details between patients in outcome of arthropathy and the role of the blockade of chemokine and proangiogenic signalling could hasten the development of effective strategies. The authors received an honorarium from Grifols S.A. for their participation in the symposium and production of the article. The authors thank Content Ed Net for providing valuable editorial assistance in the preparation of the article; funding for this assistance Saracatinib molecular weight was provided by Grifols S.A. “
“Summary.  Most bleeding disorders encountered in clinical practice will be diagnosed, at least initially, by phenotypic assays. However, since the characterization of the genes that encode coagulation factors in the 1980s, significant progress has been made in translating this knowledge for diagnostic and therapeutic purposes. For the

haemophilias, in particular, molecular genetic testing to determine carrier status, prenatal diagnosis and prediction of the likelihood of inhibitor development has now become an established component of comprehensive clinical management. For von Willebrand’s disease (VWD), significant recent advances have allowed for PtdIns(3,4)P2 the establishment of genotype–phenotype correlations that have improved our understanding of the disease. The availability of high density single nucleotide polymorphism (SNP) maps will allow investigators to probe the genetic basis of

the general symptoms of bleeding and bruising using a comprehensive genome-wide approach. This article will review the state-of-the-art for molecular diagnostics for both haemophilia and VWD and will end with a discussion of plans for an international genome-wide association study (GWAS) designed to improve our understanding of blood coagulation. Von Willebrand’s disease is the most common inherited bleeding disorder known in humans, with prevalence estimates as high as 1% [2,3]. While an objective personal history of excessive mucocutaneous bleeding can usually be obtained from the patient, the documentation of a family history of the disease may not always be possible, and laboratory tests of haemostasis can be variable in their ability to reveal either a quantitative or qualitative defect of von Willebrand factor (VWF), making the diagnosis of VWD challenging in some situations. With these issues as background, this review will consider the role of molecular genetic analysis as a complementary diagnostic modality, particularly where existing clinical and laboratory approaches to diagnosis have failed to provide a definitive answer. The VWF gene was cloned in 1985 by four groups in the US and Europe [4–7].

To accomplish the GBD goal of estimating the burden of all diseases, it is first essential to improve primary data collection through establishment MK 1775 of nationally representative or population-based sampling sources and accessible databases (including

non-English and gray literature). For hepatitis C specifically, the burden of disease that is currently being estimated using the data presented in this study is hoped to further inform and empower advocates and policymakers to accelerate progress in global prevention and treatment of HCV infections. The fact that global anti-HCV prevalence is increasing requires a global response for renewed efforts in primary prevention, including vaccine development, as well as new approaches to secondary and tertiary prevention to reduce the burden of chronic liver disease and to improve survival of those who already have evidence of liver disease. We thank Don Ward and his team who abstracted the studies. We thank Erica Din, Craig Lammert, Gail Bang, and Melissa Creary for searching, abstracting, and organizing data. We thank Claire Preaud, Johan Lemarchand, Zaki Hanafiah, and Sandra Garnier for

providing support for the prevalence graphs and mapping, and Gretchen Stevens for technical insight in the use of DisMod III. Financial support was made possible through the Global Hepatitis 4��8C Prevention Cooperative. Agreement between the U.S. Centers for

Disease Control and Prevention and the World Nutlin3 Health Organization, the University of Washington’s Institute for Health Metrics and Evaluation and by an appointment to the Research Participation Program at the Centers for Disease Control and Prevention administered by the Oak Ridge Institute for Science and Education through an interagency agreement between the U.S. Department of Energy and CDC. K.M.H. Conducted data analysis and prepared the article; S.W. designed the study, supervised the study, and edited the article; J.G. Designed and led systematic search of articles and edited the article; A.F. Conducted data analysis and edited the article; all authors have read and approved the final article. “
“The term “translational research” is commonly used to describe efforts made toward bridging the gap between discoveries made at “the bench” to the patient’s “bedside” by moving basic discoveries into a candidate health application such as the production of a new treatment or diagnostic test, which is typically assessed in clinical trials. However, the benefits of therapies and diagnostic tests observed in those studies are often reduced once they are implemented in clinical practice.