Programs that can provide HCV patients with information and skills, and improve clinical outcomes, are crucial for optimizing the Rapamycin health

benefits of antiviral treatment (PLoS ONE 2014; 9(5): e97317). The HCV Self-Management Program is a 6-week program that has been shown to significantly increase HCV knowledge, self-efficacy, and quality of life measures in both short term and 1-year time points (J Viral Hepat 2011;18:358, Health Educ Behav 2013; 40:730). The objectives of this study were to examine the costs for an organization to deliver the intervention, and then analyze the incremental cost-effectiveness of the HCV Self-Management Program. Methods: Effectiveness data in terms of QALYs were derived from the previously published prospective, randomized, controlled trial (RCT; n = 134). Healthcare utilization was abstracted from medical records for the 12 months before and after

study http://www.selleckchem.com/products/yap-tead-inhibitor-1-peptide-17.html enrollment. Intervention costs were tracked from the healthcare organization perspective and combined with healthcare costs. The incremental benefit of HCV self-management was compared to receiving HCV information only. Sensitivity analyses were used to examine assumptions. Results: The estimated intervention cost including organizational overhead was $1,777 per 6-week workshop, or $232/person. Healthcare costs were $815 lower/person for self-management participants, resulting in a total cost savings of $583/person. Self-management participants had an average net gain of 0.037 QALYs after 1 year. When removing inpatient substance-use

treatment days (accounted for most of the savings) from analyses, healthcare costs were very similar, producing an incremental cost-effectiveness others ratio of $5,081/ QALY. Sensitivity analyses showed that the results and conclusions did not change much when assumptions were varied. Conclusions: When compared to information-only, the HCV Self-Management Program led to more QALYs and cost savings in the RCT. Independent of healthcare costs, the intervention is low-cost, improves quality of life, and educates HCV-infected individuals about antiviral treatment and avoiding viral transmission. Low-cost interventions that can enhance the outcomes derived from expensive antiviral treatments should be studied further. Disclosures: Erik J. Groessl – Stock Shareholder: Bristol Myers Squibb Samuel B. Ho – Consulting: Genentech; Grant/Research Support: Roche The following people have nothing to disclose: Marisa Sklar, Ted Ganiats Background All-oral treatments for hepatitis C virus (HCV) are effective at curing HCV infection, but are associated with high costs. No firm guidelines exist on when to initiate treatment. Previously, treatment guidelines recommended that a patient’s treatment urgency be determined by histologic evaluation of the patient’s liver for fibrosis levels, and interferon-based therapy was recommended for patients with moderate or worse fibrosis (Metavir stage F2 or higher).

2. Aralia Chinesis L simultaneously suppress the proliferation of collagen fibers in the liver tissue in order to reduce the degree of liver fibrosis in rats. and at the same time with the suppression of protein expression of a-SMA. Key Word(s): 1. Aralia Chinesis L; 2. Hepatic fibrosis; 3. cytokines; 4. Apoptosis; Presenting Author: GANG ZHAO check details Additional Authors: LEI DONG, HONG LI, HAITAO SHI, XIAOLAN LU Corresponding Author: GANG ZHAO Affiliations: Xi′an Jiaotong University; [email protected] Objective: To observe the expression of fatty acid synthase (FASN) in alcohol-induced liver injury in mice, and investigate the possible mechanism of

EGFR in the process. Methods: Primary mice hepatocytes were cultured conventionally.

Four groups included normal group (saline group), ethanol group, ethanol plus EGFR tyrosine kinase inhibitor (Gefitinib) group and Gefitinib alone group were set up randomly. Total RNA and protein from liver cells were extracted, and real time-PCR and western-blot were applied to measure the gene and protein expression of FASN, Sterol regulatory element binding proteins (SREBP-1c) and EGFR. Results: Normal liver cells only slightly expression of FASN. After treated with Gefitinib, FASN expression in liver cells was no significant difference between normal liver cells. After treated with ethanol, FASN, SREBP-1c and EGFR expression both in gene and protein levels selleck chemicals were significantly increased in liver triclocarban cells. In ethanol plus Gefitinib group, expression levels of FASN and SREBP-1c were significantly lower, EGFR mRNA expression was still in the high value, while its protein expression was significantly decreased.

Conclusion: FASN slightly expresses in normal liver cells, but has a high abundance expression in alcohol-induced liver injury, maybe EGFR signaling pathway plays an important role during the process. Key Word(s): 1. EGFR; 2. Liver injury; 3. Fatty acid synthase; 4. TKI; Presenting Author: JOHNC HSIANG Additional Authors: WAYNE BAI, ARLO UPTON, ED GANE, STEPHEN GERRED Corresponding Author: JOHNC HSIANG Affiliations: Middlemore Hospital Objective: Local guidelines recommend six monthly hepatic ultrasound (US) and alpha –fetoprotein (AFP) testing for patients with a high risk of developing hepatocellular carcinomna (HCC). To assess the adherence to HCC surveillance guidelines at our institution. Methods: Patients with a high risk of HCC between 2007 and 2011 were identified from our clinic database. A retrospective review of electronic records was undertaken to record clinic attendance and adherence to six monthly AFP and US surveillance. Results: A total of 460 patients were identified. Cirrhosis was present in 409, severe hepatic fibrosis in 38, chronic hepatitis B and a family history of HCC in 13.

It has been proved that the transcription of MnSOD is regulated by STAT319, 29 depending on the JAK2/STAT3 protein complex

that is formed by the interaction of Hes proteins with STAT3.30 We found that Hes5 was the major downstream effector of Notch signaling in hepatocytes during I/R injury. Thus, disruption of Notch signaling resulted in decreased Hes5-STAT3 complex, and overexpressing constitutively active STAT3 or Hes5 rescued MnSOD expression, leading to reduced ROS levels and hepatocyte apoptosis subjected to I/R in the absence of Notch signaling. In summary, the data presented in this study learn more establish a signal axis by which canonical Notch signaling regulates hepatic I/R injury: the activated Notch receptors up-regulate Hes5 through transcription factor RBP-J, and Hes5 facilitates STAT3 activation through the formation of a Hes5-JAK2/STAT3 complex,30 which in turn activates the transcription of MnSOD gene to scavenge ROS and restricts I/R injury (Supporting Fig. 12, left). The JAK/STAT pathway mediates cytokine signaling and participates

in the initiation, propagation, and resolution of inflammation.32 The basic selleckchem players in this pathway include four JAK kinases and seven STAT members, with other modifiers such as SOCSs. The JAK2/STAT3-SOCS3 module mediates proinflammation or anti-inflammation signaling, depending on cell types and other environmental cues, and is involved in both hepatic and myocardial I/R injury.33, 34 We have shown recently that Notch signaling down-regulates JAK2/STAT3 signaling through the up-regulation of SOCS3 in macrophages.23 This signal could be enhanced through the auto-amplification of Notch signaling by TLR-induced and RBP-J–dependent induction of Notch ligands,35 likely to result in down-regulation of MnSOD and increased ROS levels, to facilitate the destruction of ingested pathogens in macrophages G protein-coupled receptor kinase (Supporting Fig. 12, right). In tissue parenchymal cells such as hepatocytes, as shown in the current study, I/R also up-regulates

Notch signal activation, but it assists JAK2/STAT3 signaling without the activation of SOCS3 expression, resulting in the up-regulation of MnSOD and increased scavenging of ROS, restricting the extent of tissue damage. Therefore, it appears that, as one of the early response signals, the Notch pathway plays differential roles through JAK2/STAT3-MnSOD in macrophages and hepatocytes—namely, increasing ROS in macrophages to destroy pathogens but reducing ROS in hepatocytes to protect cells. This scenario might also be an explanation of the contradictory observations about the roles of Notch signaling in myocardial and brain I/R injuries.12, 14 However, mechanisms such as epigenetic elements by which Notch signal differentially regulates SOCS3 expression between macrophages and hepatocytes should be determined by further studies. We thank Klaus Rajewski for Mx-Cre transgenic mice, J. C. Zúñiga-Pflücke for OP9 derivatives, and Yongzhan Nie for plasmids expressing STAT3 mutants.

1-4 These coated invaginations are believed to be liberated from the

PM by the combined efforts of lipid-modifying enzymes,5, 6 the actin-myosin cytoskeleton,7, 8 and the large guanosine triphosphate (GTP)ase dynamin.9-12 It is unclear how the location, interaction, and function of dynamin and other proteins are regulated. Further, whether these endocytic proteins assemble randomly along the PM or at discrete, predefined membrane areas similar to what occurs in the synapse is undefined. To better understand how the endocytic machinery in hepatocytes is spatially organized and temporally regulated, RG7422 manufacturer we utilized confocal microscopy to observe these processes directly in living cultured epithelial cells expressing dynamin 2 (Dyn2) coupled to green fluorescent protein (GFP). Dynamin is a large GTPase that has been implicated in the final stages of clathrin-mediated endocytosis.9-12 In defined in vitro systems,

recombinant Enzalutamide concentration dynamin alone can sever or deform lipid tubules, indicating that this enzyme has mechanochemical properties that could pinch forming vesicle buds from donor membrane compartments in cells. Because dynamin is considered a major component of the clathrin-coated pit-generating machinery, we predicted that recording the distribution of the labeled enzyme in cells over time would provide useful information about the function and distribution of the endocytic machinery in hepatocytes. The dynamins encompass a broad family of at least three distinct conventional gene products encoding multiple splice forms, which exhibit tissue-specific expression and reside at different cytoplasmic locations. In this study Lck we tagged and expressed the Dyn2(aa) form, found predominantly in epithelial cells, in a nontransformed hepatocyte cell line derived from rat (Clone 9). Our findings were confirmed in primary rat hepatocytes isolated in culture. As for most epithelial cells, these cell

lines do not express Dyn1 or Dyn3, which are found in brain, lung, testis, and heart.13 We report here that hepatocytes expressing Dyn2(aa)-GFP display a distribution identical to untransfected cells stained with a Dyn2 antibody. Both tagged and endogenous Dyn2 localize to a punctate “lawn” of vesicular structures along the basal PM. Interestingly, interspersed among individual Dyn2 spots are large tubulovesicular structures that sequester the transferrin receptor 1 (TfR1) and stain positive for the endocytic coat proteins clathrin and AP2. Most remarkable is the highly dynamic nature of these Dyn2, clathrin, and AP2 structures. Time-lapse movies of transfected cells revealed that these endocytic regions generate large numbers of discrete endosomal vesicles. These findings suggest that the clathrin-based endocytic machinery maintains a dorsal/ventral distribution even in “nonpolarized” cells.

Conclusions: The DSS-induced mouse colitis may promote hepatic inflammation and fibrosis in mice treated by CCl4. Disclosures: The following people have nothing to disclose: Xiaolan Zhang, Yufeng Liu, Libo Zheng, Guochao Niu, Hong Zhang, Jinbo Guo, Guozun Zhang, Huicong Sun “
“Clinical trials and animal models suggest that infusion of Venetoclax bone marrow cells (BMCs) is effective therapy for liver fibrosis,

but the underlying mechanisms are obscure, especially those associated with early effects of BMCs. Here, we analyzed the early impact of BMC infusion and identified the subsets of BMCs showing antifibrotic effects in mice with carbon tetrachloride–induced liver selleck products fibrosis. An interaction between BMCs and activated hepatic stellate cells (HSCs) was investigated using an in vitro coculturing system. Within 24 hours, infused BMCs were in close contact with activated HSCs, which was associated with reduced liver fibrosis, enhanced hepatic expression of interleukin (IL)-10, and expanded regulatory T cells

but decreased macrophage infiltration in the liver at 24 hours after BMC infusion. In contrast, IL-10–deficient (IL-10−/−) BMCs failed to reproduce these effects in fibrotic livers. Intriguingly, in isolated cells, CD11b+Gr1highF4/80− and CD11b+Gr1+F4/80+ BMCs expressed more IL-10 after coculturing with activated HSCs, leading to suppressed expression of collagen and α-smooth Etofibrate muscle actin in HSCs. Moreover, these effects were either enhanced or abrogated, respectively, when BMCs were cocultured with IL-6−/− and retinaldehyde dehydrogenase 1−/− HSCs. Similar to murine data, human BMCs expressed

more IL-10 after coculturing with human HSC lines (LX-2 or hTERT), and serum IL-10 levels were significantly elevated in patients with liver cirrhosis after autologous BMC infusion. Conclusion: Activated HSCs increase IL-10 expression in BMCs (CD11b+Gr1highF4/80− and CD11b+Gr1+F4/80+ cells), which in turn ameliorates liver fibrosis. Our findings could enhance the design of BMC therapy for liver fibrosis. (HEPATOLOGY 2012;56:1902–1912) For the past decade, clinical trials and experimental studies have suggested that infusion therapy of whole bone marrow cells (BMCs) has beneficial effects toward liver regeneration, injury, and fibrosis/cirrhosis by stimulating the proliferation of hepatocytes, increasing progenitor cells, and enhancing matrix degradation.1-3 However, the underlying mechanisms are unknown, in part because whole BMCs contain a wide range of cell types, including several types of stem and precursor cells of monocytic and granulocytic lineages.4 Events associated with hepatic fibrosis are well characterized, notably the excessive production of extracellular matrix (ECM) by activated hepatic stellate cells (HSCs).

In the earliest reports in the 1990s, large deletions, nonsense mutations and inversions were defined

as high-risk mutations, as the highest percentages of inhibitor patients were observed in these subgroups [8, 9]. The risk is not, however, consistent among patients with these mutations as has been observed in family studies in which high rates of discordance have MK1775 been found between siblings with the same mutation [10, 11]. In a recent meta-analysis by Gouw et al., the inhibitor risks in patients with large deletions and nonsense mutations were higher than in patients with intron 22 inversions (pooled OR = 3.6, 95% confidence interval [95% CI], 2.3–5.7 and OR = 1.4, 95% CI, 1.1–1.8, respectively) confirming the relatively high risk for inhibitors associated with these mutation types [12]. However, a high frequency of inhibitors has also been reported

for other mutations. The current view is that, besides these null mutations, small deletions/insertions outside A-runs, splice-site mutation at conserved nucleotides at position 1/2, and certain missense mutations, e.g. Arg593>Cys, Tyr2105>Cys, Arg2150>His, Arg2163>His, selleck inhibitor Trp2229>Cys and Pro2300>Leu, will also confer a relatively high inhibitor risk [13]. The question can also be raised as to whether a cross-reactive material-negative mutation with no circulating antigen, such as the intron 22 inversion, which only causes inhibitors in 20% of patients, really should be classified as a high-risk mutation or rather a protective mutation instead. Further light on this was recently provided by Pandey et al. who described that endogenous FVIII synthesis from Casein kinase 1 the inverted F8 locus may modulate the immune response [14]. They actually found that the levels of F8 mRNA and intracellular FVIII in subjects with intron 22 inversions were similar to those of healthy subjects. They therefore suggested that most patients with intron 22 inversions were, in fact,

tolerized against FVIII, which could explain the inhibitor rate of only 20%. The importance of the HLA class II molecules is easily appreciated when considering that these molecules will determine the peptides to be presented to the T-helper cells [15]. If only peptides with sequences previously recognized by the immune system and not able to elicit an immune response are presented, then an immune reaction against the infused factor will not occur (Fig. 2). However, if this is not the case and immunogenic peptides with foreign sequences are presented, then the reaction can take place. Whether the final outcome of this will be inhibitory antibodies produced by the plasma cells or not will then depend on the levels of a variety of immune-regulatory elements. Perhaps due to the heterogeneity of the HLA system and the repertoire of peptides that can be bound, consistent associations with inhibitor development have not been observed across studies.

These inductive effects were restricted to c-kit+ endoderm-enriched EB-derived populations, suggesting that Hex functions at the level of hepatic specification of endoderm in this model. Microarray analysis revealed that Hex regulated the expression of a broad spectrum of hepatocyte-related

genes, including fibrinogens, apolipoproteins, and cytochromes. When added to the endoderm-induced EBs, bone morphogenetic protein 4 acted synergistically with Hex in the induction of expression of Alb, Afp, carbamoyl phosphate synthetase, transcription factor 1, and CCAAT/enhancer binding protein α. These findings indicate that Hex plays a pivotal role during induction of liver development from endoderm in this in vitro model and suggest that this strategy may provide important insight into the generation of functional hepatocytes from ESCs. (HEPATOLOGY 2010.) In the Wnt inhibitor mouse embryo, the liver is first detected as an outgrowth bud of proliferating endodermal cells in the ventral foregut on day

8 of gestation.1–3 The liver develops in close proximity to the cardiac mesoderm, which produces fibroblast growth factor 1 and 2, which in turn are required for the outgrowth of the ventral foregut endoderm2, GSK126 clinical trial 4 and the induction of several liver-specific genes, including albumin (Alb) and α-fetoprotein (Afp).5 In addition to fibroblast growth factors, bone morphogenetic protein 4 (BMP-4) expressed in the septum transversum mesenchyme6 has been shown to be essential for early liver development.

In the absence of BMP-4, the foregut endoderm does not thicken, and consequently a distinct Rebamipide liver bud does not form. In spite of the lack of liver bud formation in BMP-4–null embryos, Alb expression is induced, suggesting that this factor may play a role in the proper movement of hepatoblasts into the developing liver. Beyond the induction stage, numerous other transcription factors are required for endoderm patterning and organ development. Among these, the hematopoietically expressed homeobox gene Hex (also known as Prh)7–9 is of particular interest, because it has been shown to play a pivotal role in hepatic development. Hex is expressed at multiple sites in the developing embryo, including the yolk sac and the region of gut endoderm that gives rise to the liver and thyroid bud.10–12 Analysis of Hex-null embryos demonstrated that formation of the liver bud initiates in the absence of a functional protein and that expression of liver-specific genes including Alb, Afp, and Ttr is up-regulated in this endodermal population.13, 14 Whereas the early stages of morphogenesis to a columnar structure can be detected in these mutant embryos, development beyond day 9.

Furthermore, iPSC-derived hepatocytes produced and secreted the plasma proteins, fibrinogen, fibronectin, transthyretin, and alpha-fetoprotein, an essential feature for functional HE. Additionally iPSC-derived HE supported both CYP1A2 and CYP3A4 metabolism, which is essential for drug and toxicology testing. Conclusion: This work is first to demonstrate the efficient generation of hepatic endodermal lineage from human iPSCs that exhibits key attributes of

hepatocytes, and the DMXAA potential application of iPSC-derived HE in studying human liver biology. In particular, iPSCs from individuals representing highly polymorphic variants in metabolic genes and different ethnic groups will provide pharmaceutical development and toxicology studies a unique opportunity to revolutionize predictive drug toxicology assays and allow the creation of in vitro hepatic disease models. (HEPATOLOGY 2009.) Human induced pluripotent stem cells (iPSCs) are reprogrammed mature somatic fibroblasts which represent a pluripotent cell population able to generate all primary cell types in vitro.1–3 The ability to derive iPSCs from an indefinite range of genotypes makes them an attractive resource on which to model liver function reflecting the complexity of polygenic influences on metabolism in vitro. Another BIBW2992 in vivo facet of iPSC technology

is the ability to study the impact of gene polymorphisms in a native chromatin setting and model gene interactions with precision. Therefore iPSC-derived models hold great potential to develop a detailed understanding of human liver disease and metabolism including drug toxicity (for a review, see Dalgetty et al.4). Any methods which might streamline and standardize the process of drug and toxicology testing, which currently relies on primary human hepatocytes (PHHs), would represent a significant development. Therefore, an iPSC resource representative of polymorphic Mannose-binding protein-associated serine protease variants and ethnic groups, unhindered by quality and supply, would revolutionize predictive drug toxicology assays and

have an effect on drug attrition. Presently, PHHs are the gold standard cell type used in predictive drug toxicology. Unfortunately, PHHs are a scarce, heterogeneous, and expensive resource which function only short-term in vitro. The generation of hepatic endoderm (HE) from iPSCs has the potential to fulfill the major challenge to acquire the reliable and clonal source of functional human hepatocyte cells for biotechnology purposes. To date, efficient models of deriving HE from iPSCs have not been described or developed. Capitalizing on our recent investigations that human embryonic stem cells (hESCs) can be stimulated to form HE,5 we have developed a parallel methodology for iPSCs; here, we describe the generation of functional HE from multiple human iPSC lines that can potentially model human drug metabolism.

[3] Interestingly, Cbs−/− mice exhibit severe liver injury, steatosis, and fibrosis.[32] In a similar manner, we also investigated the role of PLIN2 on a background of high SAMe. For these studies we generated a novel, double Gnmt−/−/Plin2−/− knockout mouse model that is characterized by high hepatic SAMe and low PE content, much like Gnmt−/− mice, that in contrast did not develop fatty liver. Consistent with previous findings,[12, 13] knockout of Plin2 in GNMT-depleted livers decreased lipogenesis and increased TG secretion. Plin2 ablation increased Hydroxychloroquine cell line gluconeogenesis, indicating that crosstalk exists between lipid synthesis and sequestration

and glucose metabolism. Since PE methylation has been shown to promote LD formation,[26] these results Panobinostat chemical structure support a model where increased

PEMT activity induces both TG synthesis and its accumulation into newly formed LD. Collectively, these observations, taken in light of previous findings,[5, 6] demonstrate that SAMe regulates liver lipid homeostasis through a concerted series of homeostatic actions that include: activation of lipogenesis and inhibition of TG secretion at low SAMe, and activation of TG synthesis via PEMT at high SAMe. This cascade of events goes a long way towards explaining why a chronic imbalance in hepatic SAMe synthesis,[4] or catabolism,[8] is capable of inducing NAFLD. We thank Virginia Gutiérrez de Juan and Begoña Rodríguez-Iruretagoyena for technical Dichloromethane dehalogenase support and Azucena Castro for discussion; and human and technical support from Unidad de formación e investigación UFI11/20, University of Basque Country. Additional Supporting Information may be found in the online version of this article. “
“An 83-year-old man with hepatocellular carcinoma was found to have a low-echoic and low-density tumor measuring 7.2 cm × 5.6 cm. Caroli’s disease was absent. Clinical diagnosis was intrahepatic cholangiocarcinoma. Three cores of liver biopsy were obtained from the tumor. Histologically, it consisted of

liver cysts, ductal plate malformations, peribiliary glands, hepatocytes, portal tracts and mesenchymal tissue. Apparent features of cirrhosis were not found. The liver cysts were lined by a layer of cuboidal cells with multiple papillary protrusions. The ductal plate malformations resembled fetal ductal plates. The peribiliary glands were seromucous glands. Immunohistochemically, these abnormal ductal structures showed positive reaction to biliary type cytokeratins, namely, cytokeratin (CK)7, CK8, CK18 and CK19. Mucin gene expression showed that these biliary structures are positive for fetal antigen MUC1. MUC6 is also positive in them. Aberrant expression of CD10 was observed in these biliary structures. MUC2, MUC5AC and CDX2 were negative.

To increase knowledge and awareness about hepatitis B and hepatitis C in at-risk populations and the general population, the committee recommends: The CDC should work with key stakeholders to develop, coordinate, and evaluate innovative and effective outreach and education programs to target at-risk populations and to increase awareness in the general population about hepatitis B and hepatitis C. The programs should Crizotinib cell line be linguistically and culturally appropriate and should integrate viral hepatitis and liver-health education into other health programs that serve at-risk populations. They should: (1) Promote better understanding of

HBV and HCV infections, transmission, prevention, and treatment in the at-risk and general populations. The longstanding availability of effective hepatitis B vaccines makes the elimination of new HBV infections possible, particularly in children. As noted above, about

1,000 newborns are infected by their HBV-positive mothers at birth each year in the U.S. That number has not declined in the last decade. To prevent transmission selleck inhibitor of HBV from mothers to newborns, the Advisory Committee on Immunization Practices recommends that infants born to mothers who are positive for hepatitis B surface antigen receive hepatitis B immune globulin and a first dose of the hepatitis B vaccine within 12 hours of birth. To improve adherence to that guideline, the committee recommends: All infants weighing at least 2,000 g and born to hepatitis B surface antigen–positive women should receive single-antigen hepatitis B vaccine and hepatitis B immune globulin in the delivery room as soon as they are stable and washed. The Advisory Committee on Immunization Practices recommends administration of the hepatitis B vaccine series to unvaccinated children under 19 years old. School-entry mandates have been shown to increase

hepatitis B vaccination rates and to reduce disparities in vaccination rates. Overall, hepatitis B vaccination rates in school-age children are high, but coverage click here varies among states. Additionally, there are racial and ethnic disparities in childhood vaccination rates—Asian and Pacific Islander, Hispanic, and African American children have lower vaccination rates than non-Hispanic white children. Regarding vaccination of children, the committee recommends: All states should mandate that the hepatitis B vaccine series be completed or in progress as a requirement for school attendance. Hepatitis B vaccination for adults is directed at high-risk groups—people at risk for HBV infection from infected sex partners, from IDU, from occupational exposure to infected blood or body fluids, and from travel to regions that have high or intermediate HBV endemicity. Only about half the adults at high risk for HBV infection receive the vaccine.