12, 15, 20, 25 Interestingly, the effect of the altered cytokine milieu generated by LPS-treated TK−/− Kupffer cells was more toxic to mouse hepatocytes in vitro compared to TK+/+ Kupffer Navitoclax solubility dmso cells. This may be due to higher TNF-α levels, the composition of cytokines, or the presence of an untested cytokine in the conditioned media. Moreover, it is possible that the kinetics of cytokine expression is as important as the composition of cytokines produced. TK−/− hepatocytes are protected compared to TK+/+ hepatocytes from TNF-α/ActD initiated cell death over the range of 0.5 to 5 ng/mL of TNF-α, which are similar to the serum TNF-α levels observed in the previously reported in vivo experiment.16

Whether the observed differences in hepatocyte viability are sufficient to explain the in vivo observations by Leonis et al.16 is not discernable by this assay. Hepatocytes plated ex vivo are without feedback mechanisms to Kupffer cells and other hepatic cell types and, thus, the magnitude of the effect of TNF-α ex vivo may not completely mimic what is observed in vivo. However, the results from the conditional deletion of Ron selectively in hepatocytes support the significance of our

http://www.selleckchem.com/products/idasanutlin-rg-7388.html ex vivo culture conditions and prior in vivo experiments. Previously, we demonstrated that the protected liver injury response to treatment with LPS/GalN in Ron TK−/− mice was associated with a 1- to 2-hour delay in the progression to death based on survival analyses.16 The lack of a more significant discrepancy in the time to mortality may be multifactorial and confounded by the sensitivity of the Ron TK−/− mice to LPS alone and by the severe necrosis and endothelial damage that is observed in the model. Despite the modest overall survival benefit of the TK−/− mice compared to controls, less liver injury was observed in the TK−/− mice as judged by liver histopathology, ALT levels, hepatocyte TUNEL staining, and the extent of hepatic apoptosis. Similar protected Glycogen branching enzyme phenotypes were observed in the Alb-Cre Ron TKfl/fl mice as the Ron

TK−/− mice compared to control mice. This is based on a reduction in liver histopathology and significantly decreased ALT levels and TUNEL staining in the Alb-Cre Ron TKfl/fl mice compared to controls. Interestingly, a 1- to 2-hour increase in survival time in the Alb-Cre Ron TKfl/fl mice was also observed compared to controls. Therefore, the data are consistent with a protected liver phenotype in the Alb-Cre Ron TKfl/fl mice compared to controls. Our data also show a significant decrease in survival of the LysCre mice and associated worsened liver phenotypes in these mice compared to Alb-Cre Ron TKfl/fl and wildtype mice and supports the premise that Ron functions in both cellular compartments in vivo. Our results show increased NF-κB activation in hepatocytes that lack Ron signaling.

12, 15, 20, 25 Interestingly, the effect of the altered cytokine milieu generated by LPS-treated TK−/− Kupffer cells was more toxic to mouse hepatocytes in vitro compared to TK+/+ Kupffer compound screening assay cells. This may be due to higher TNF-α levels, the composition of cytokines, or the presence of an untested cytokine in the conditioned media. Moreover, it is possible that the kinetics of cytokine expression is as important as the composition of cytokines produced. TK−/− hepatocytes are protected compared to TK+/+ hepatocytes from TNF-α/ActD initiated cell death over the range of 0.5 to 5 ng/mL of TNF-α, which are similar to the serum TNF-α levels observed in the previously reported in vivo experiment.16

Whether the observed differences in hepatocyte viability are sufficient to explain the in vivo observations by Leonis et al.16 is not discernable by this assay. Hepatocytes plated ex vivo are without feedback mechanisms to Kupffer cells and other hepatic cell types and, thus, the magnitude of the effect of TNF-α ex vivo may not completely mimic what is observed in vivo. However, the results from the conditional deletion of Ron selectively in hepatocytes support the significance of our

check details ex vivo culture conditions and prior in vivo experiments. Previously, we demonstrated that the protected liver injury response to treatment with LPS/GalN in Ron TK−/− mice was associated with a 1- to 2-hour delay in the progression to death based on survival analyses.16 The lack of a more significant discrepancy in the time to mortality may be multifactorial and confounded by the sensitivity of the Ron TK−/− mice to LPS alone and by the severe necrosis and endothelial damage that is observed in the model. Despite the modest overall survival benefit of the TK−/− mice compared to controls, less liver injury was observed in the TK−/− mice as judged by liver histopathology, ALT levels, hepatocyte TUNEL staining, and the extent of hepatic apoptosis. Similar protected Nintedanib (BIBF 1120) phenotypes were observed in the Alb-Cre Ron TKfl/fl mice as the Ron

TK−/− mice compared to control mice. This is based on a reduction in liver histopathology and significantly decreased ALT levels and TUNEL staining in the Alb-Cre Ron TKfl/fl mice compared to controls. Interestingly, a 1- to 2-hour increase in survival time in the Alb-Cre Ron TKfl/fl mice was also observed compared to controls. Therefore, the data are consistent with a protected liver phenotype in the Alb-Cre Ron TKfl/fl mice compared to controls. Our data also show a significant decrease in survival of the LysCre mice and associated worsened liver phenotypes in these mice compared to Alb-Cre Ron TKfl/fl and wildtype mice and supports the premise that Ron functions in both cellular compartments in vivo. Our results show increased NF-κB activation in hepatocytes that lack Ron signaling.

Partial liver grafts including split cadaveric liver grafts or living donor liver transplantation are established strategies to reduce mortality among those patients on the waiting list.1 However, some major risks are inherent to split cadaveric liver or living donor liver transplantation. In the latter strategy, a healthy donor must be subjected to major surgery. Typically, a hemi-hepatectomy is necessary. The

risk of mortality following such surgery is estimated at 0.2%-0.5% with a moderate but significant incidence of serious complications.2-5 Next, the recipient receiving a partial graft from a living donor or split cadaveric organ is subject to the risk of small-for-size (SFS) syndrome.6 PFT�� chemical structure It is estimated that at least 35% of the normal liver size (or 0.8% of liver/body ratio) should be implanted to minimize the risk of this syndrome. A revolutionary strategy would be transplantation of only a small part

of the liver (e.g., segments II and III) in a living donor, which can be performed laparoscopically7 and is associated with a low risk of complications similar to the range observed following living kidney donation. Such an operation would likewise be widely accepted and may alleviate the shortage of organs. A similar small graft could also be obtained from BTK inhibitor a cadaveric organ. To achieve this, however, the issue of SFS liver graft failure must be resolved. SFS syndrome is morphologically characterized by sinusoidal endothelial cell (SEC) injury and the rapid development of diffuse microsteatosis in hepatocytes. Presumably, due to the limited capacity of a small liver, the graft is unable to meet the functional demand in the recipient6 and fails to regenerate.8-10 Those findings are associated with increased portal flow and hypertension.11 We developed a model of partial liver transplantation in the mouse and showed that full preservation of the arterial supply

to the liver is essential.12 We also noted that mice receiving only 30% of the liver displayed histological changes of SFS syndrome with a poor survival rate. In contrast, the use of 50% of the total liver mass triggered a massive regenerative response resulting in a high animal survival after transplantation.10 Gefitinib In subsequent experiments, we demonstrated that SFS syndrome induces Kupffer cell activation with the release of tumor necrosis factor α (TNF-α). Blockade of this pathway by pentoxifylline (PTX) reduces injury and TNF-α production but increases the release of interleukin-6 (IL-6), and animal survival was dramatically improved.8 Concomitantly, we discovered in an in vivo model of major hepatectomy in mice that serotonin secreted by platelets mediates regeneration through its receptor subtypes 5-HT2A and 5-HT2B.13 Serotonin is a ligand for a large family of 5-hydroxytryptamine (5-HT) receptors with a major role in neurotransmission in the central nervous system.

(HEPATOLOGY 2012;56:1015–1024) Hepatocellular Buparlisib solubility dmso carcinoma (HCC) is one of the most common human cancers worldwide, particularly in Southeast Asia.1, 2 Considering the poor prognosis and high mortality of HCC, it is imperative to understand the molecular mechanisms that trigger the progression and development of HCC. Nevertheless, the exact molecular mechanisms involved in HCC are not completely

understood. Chronic infection of hepatitis B virus (HBV) is a major risk factor for HCC development.3 The HBV genome is a partial double-stranded DNA that contains four open reading frames encoding virus envelope, core protein, virus polymerase, and HBV X protein (HBx).4 Increasing evidence suggests that HBx plays an important role in hepatocarcinogenesis.3 Although HBx does not bind to DNA directly, as a multifunctional regulator, it modulates the transcription of a large number of cellular genes involved in cell survival and apoptosis by interacting with the components of signal pathways as well as the degradation

of various proteins by interacting with components of the ubiquitin (Ub)/proteasome system.5 For instance, it has been shown that HBx up-regulates the expression of several genes, such as c-jun and c-fos,6 TAM Receptor inhibitor and enhances the stability of ASC-2, c-Myc, and pituitary tumor transforming gene-1.7-9 In addition, HBx has been shown to promote the activation of several transcription factors, such as activator protein-1 (AP-1),10, 11 nuclear factor kappa light-chain enhancer of activated B cells (NF-κB),11, 12 androgen receptor (AR),13 and activating transcription factor/cyclic adenosine monophosphate–responsive element-binding transcription factor.14 Amplified in breast cancer 1 (AIB1/steroid receptor coactivator [SRC]-3/translocation-associated membrane protein-1/activator of thyroid hormone and retinoid receptor/CBP-interacting

protein/receptor-associated coactivator-3) is a member of the p160 family, which also includes SRC-1 (nuclear receptor coactivator-1) and SRC-2 (trancsiptional interacting factor 2/glucocorticoid receptor interacting protein 1).15 It has been reported that AIB1 is amplified and overexpressed in several human cancers, such as breast, mammary, prostate, stomach, colon, lung, and pancreatic cancers.15 AIB1 has been Isotretinoin shown to enhance the transactivation activity of some nuclear receptors, such as AR and estrogen receptor (ER), as well as a variety of transcription factors, such as AP-1 and NF-κB.15 Moreover, increasing evidence indicates that AIB1 is a bona fide oncogene that activates several signaling pathways, such as v-akt murine thymoma viral oncogene homolog (Akt), E2F1, NF-κB, HER2/neu, ERα, AR, and epidermal growth factor receptor, to promote cancer progression.15, 16 Recently, we reported that AIB1 protein is overexpressed in 68% of human HCC specimens and promotes HCC progression by enhancing cell proliferation and invasiveness.

Dorsal fin surface temperatures (Tdfin) were measured on wild, free-swimming dolphins using infrared thermography. Field and laboratory calibration studies were also undertaken to assess the efficacy of this non-invasive technology in the marine environment. The portability of infrared thermography permitted measurements of Tdfin across the entire range of environmental temperatures experienced by animals in this region. Results indicated a positive, linear relationship between Tdfin and Tw (r2= 0.978, P < 0.001). On average, Tdfin was 0.9°C warmer than Tw across seasons, despite the 22°C annual range in Tw. Changes in integumentary and vascular

insulation likely account for the stability of ΔTdfin − w and the protection of core temperature (Tcore) across seasons. The high thermal conductivity of water may also influence this ΔT. The use of infrared thermography is an effective, non-invasive LY2157299 research buy method of assessing dorsal fin skin surface temperatures (±1°C) across large numbers of wild, free-swimming dolphins throughout their thermally dynamic Akt inhibitor aquatic environment. “
“Activity budget data are essential for determining behavioral responses to physiological and ecological variables. Yet, few studies are available to investigate the robustness, accuracy, and biases

of the methods used to estimate activity budgets for cetaceans. In this study, we compare activity budgets of 55 adult female bottlenose dolphins in Shark Bay, Australia derived from two methods: surveys (n = 6,903) and focal follows (n = 1,185, totaling 2,721 h of observation). Activity budgets estimated from survey data differed in all behavioral states compared to focal

follow data. However, when controlling for temporal autocorrelation, only time spent socializing and time spent traveling remained disparate between the methods. To control for biases associated with assigning group-level behavior to Protein kinase N1 individuals, we also compared survey and focal follow activity budgets for lone females. Here we found differences between methods in time spent foraging and traveling regardless of whether we controlled for temporal autocorrelation, which suggests detection biases likely play a role in explaining differences in activity budget estimates between the two methodologies. Our results suggest that surveys are less representative of individual-level activity budgets, and thus, when individual-level knowledge about behavior is needed, focal follows are preferred. “
“Harbor seal (Phoca vitulina richardii) populations in the inland waters of Washington and British Columbia are at or near carrying capacity. Stranded pups often are collected and admitted to rehabilitation centers, and then released when they reach a weight of 22 kg and meet a variety of preestablished health and release conditions.

Louis, MO) containing 1 mg/mL of Mycobacterium tuberculosis strain H37RA, and was subsequently boosted every 2 weeks with 2OA-BSA in incomplete Freund’s adjuvant (Sigma-Aldrich). Additionally, mice received 100 ng of pertussis toxin selleck products (List Biological Laboratories, Campbell, CA) at the time of initial immunization with 2OA-BSA in Complete Freund’s Adjuvant. Peripheral blood samples from individual mice were obtained from the tail vein prior to the initiation of treatment with mAbs (baseline) and then at 2-week intervals. Sera was collected prior to mAb treatment, 1 week afterward, and thereafter every 4 weeks, and stored at −70°C until

use. Animals were sacrificed at 15 weeks of age. Serum titers of anti–PDC-E2 autoantibodies were measured by way of enzyme-linked immunosorbent assay using our well-standardized recombinant autoantigens.32 Peripheral blood mononuclear cells were isolated from heparinized murine blood using Accupaque (Accurate Chemical & Scientific Company, Westbury, CT) to assess levels of B cells. Cells were preincubated with anti-mouse FcR blocking reagent and then incubated at 4°C with a predetermined optimum concentration of antigen-presenting cell (APC)-conjugated anti–T cell receptor β (BioLegend), phycoerythrin-conjugated anti-mouse IgM

(Caltag), and fluorescein isothiocyanate–conjugated anti-CD19 selleck chemicals (BioLegend); B cell frequency was then determined by way of flow cytometry. The liver and spleens were collected from mice immediately following sacrifice, and single-cell mononuclear cell suspensions

were prepared for multicolor flow analysis as described.23 Immediately after sacrifice, liver and spleen tissues were harvested and fixed in 10% buffered formalin, embedded in paraffin, and cut into 4-μm sections for routine hematoxylin (DakoCytomation, Carpinteria, BCKDHA CA) and eosin (American Master Tech Scientific, Lodi, CA) staining. Evaluation under light microscopy and scoring of liver inflammation was performed on coded hematoxylin and eosin–stained sections of liver using a set of three indices by a blinded pathologist (K. T.); indices included degrees of portal inflammation, parenchymal inflammation, and bile duct damage.33 Phenotypic analysis of bile duct damage was performed as described.34 Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and alkaline phosphate (ALP) levels were measured using the Roche Diagnostics COBAS INTEGRA 400 Plus (Indianapolis, IN). Serum levels of the proinflammatory cytokines interleukin (IL)-6, IL-10, monocyte chemotactic protein-1 (MCP-1), interferon-γ (IFN-γ), tumor necrosis factor α, and IL-12p70 were quantified using the BD Cytometric Bead Array Mouse Inflammatory Kit (BD Biosciences) as described.35 The serum samples were loaded onto the plate neat.

Patients with CHD are susceptible to ischemic hepatitis because right heart failure elevates hepatic sinusoidal pressure and reduces portal inflow. This results in increased sensitivity Gefitinib mouse to any decrease in hepatic artery flow, resulting from a decrease in cardiac output (e.g., caused by concurrent arrhythmias or hypotension). For example, left ventricular outflow tract obstruction/coarctation of the aorta is associated with hypoperfusion and, in some clinical situations, may lead to

hepatic ischemia.6 Chronic hepatic ischemia may also lead to hepatic fibrosis.7 Hepatic disease caused by acute cardiac dysfunction results from a combination of low-output cardiac failure and passive congestion. Often, the clinical presentation may be indistinguishable from primary liver disease. For example, a marked elevation in transaminase levels characteristic of ischemic hepatitis may also be observed in patients presenting with drug-induced or acute viral hepatitis. However, a rapid reduction in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels in the setting of an acute decrease in cardiac output/systemic hypotension suggests hepatic ischemia. Acute cardiac dysfunction is more likely to be associated with jaundice and encephalopathy, as compared to chronic or acute on chronic cardiac dysfunction.7 In acute cardiac dysfunction (e.g., ischemic hepatitis), elevations in

the thousands of aminotransferase levels within 24 hours and

Erlotinib molecular weight increases in bilirubin Resveratrol and prothrombin time can be observed. A lag in the rise of serum bilirubin may be observed, and the elevation in bilirubin may take a longer time to resolve, as compared to aminotransferase levels. ALT levels are correlated highly with right atrial pressure, free hepatic venous pressure (FHVP), and wedge hepatic venous pressure (WHVP), but not the hepatic venous pressure gradient (HVPG) or cardiac index. Total bilirubin correlates better with HVPG. However, in persons with chronic cardiac dysfunction, a correlation of biochemical parameters with hepatic pressures is not present. Elevation of transaminases after cardiac surgery occurs more frequently than previously reported, particularly in the setting of right-sided heart failure. Extreme elevations of ALT, AST, and lactate dehydrogenase correlate negatively with postoperative survival.8 In a single-center study that predominantly examined cases of ischemic cardiomyopathy, hepatic centrilobular necrosis, inflammation, and hemorrhage were more common in the acute group. In contrast, centrilobular and periportal fibrosis were more frequent in patients with chronic cardiac dysfunction.7 The Fontan procedure, initially described in patients with tricuspid atresia, is the most common procedure in patients with single-ventricle physiology or when biventricular repair is not feasible (e.g., double-inlet left ventricle and hypoplastic left heart).

We grouped 65 genes

in risk scores in the context of the GO to summarize biological characteristics of risk score. Not surprisingly, genes involved in signaling transduction are enriched in those whose expression is positively associated with poor prognosis (high risk genes, Supporting Table 2), whereas genes associated with normal this website metabolic functions of liver are enriched in low risk genes (Supporting Table 3). In addition, we used gene expression data from the MSH cohort, for whom many biological characteristics are available.11 Ninety-one patients from the MSH cohort were stratified according to risk score by applying the coefficient and threshold values (8.36) derived from the NCI cohort. All three signaling events (phosphorylation) examined in the previous study with the MSH cohort were significantly associated with the risk score (Supporting Table 4). We found that a high risk score was significantly associated with enriched phosphorylation of AKT (P = 0.003, χ2 test), IGFR1 (P = 2.2 × 10−4, χ2 test), and RPS6 (P = 3.6 × 10−5, χ2 test). Mutation of TP53 is not associated with the risk score (P = 0.93), whereas a high frequency of mutations of CTNNB1 (beta-catenin) was significantly associated with Ku-0059436 concentration a low risk score (23/27 mutations, P = 0.05, χ2 test). To validate the association

between risk score and CTNNB1 mutations in HCC, patients in the INSERM cohort Sitaxentan (n = 57) were stratified by risk score using same 8.36 cutoff threshold.9 Of 17 HCC tumors with CTNNB1 mutations, 16 were in the low-risk group, and this association was statistically significant (Supporting Table 5; P = 0.015, χ2 test). By applying multistep exploration and validation strategy (Supporting Fig. 6), we identified and validated

a risk score based on expression patterns of 65 genes that can easily quantify the likelihood of OS in HCC patients who have undergone surgical resection as the primary treatment. Several lines of evidence strongly support that the risk score is an independent and significant predictor of prognosis. First, the risk score was the significant predictive factor for OS in the combined validation cohort in multivariate analysis (Table 3). Second, the risk score can identify high-risk patients in both early stage HCC (BCLC stage A) and those with intermediate or advanced stage (BCLC stage B and C) (Fig. 4). The strength and independence of the risk score over the current staging systems remained significant even when the AJCC staging system was applied (Supporting Fig. 3). Third, the risk score identified a poor prognosis patients without vasculature invasion, who are typically considered as good prognosis patients (Supporting Fig. 5). Fourth, the risk score was the most significant predictor of 3-year survival of patients in ROC analysis (Fig. 3).

Results are expressed in percentage. K2 test was used for comparison in between groups. Results: We recruited 242 PW, and 45 Carfilzomib purchase HP who met the selection criteria for the study. PW were aged 18 to 44 years with a mean age of 26.18 ± 5.39 years. HP comprised 10 MD; 24 state nurses; 3nurses

and 8 assistant nurses. Concerning the PW: 16% were tested positive to HBs Ag; Among those who were negative to HBs Ag, 50% had already come into contact with the virus B, as thy were positive to HBc antibody. We did not search for virus B DNA. 91% of PW had never done a screening, and 97% were not vaccinated against VHB. Only 7% of PW knew they was possible mother to child transmission of VHB.44% did not know that vaccine against VHB was included in the expanded program of immunization. Concerning the HP: 57% of the nurses, did not consider that screening, for VHB was necessary in PW, 70% denied to have given any health education on VHB to pregnant women and did not know what measures to take to prevent mother to child transmission of VHB. Conclusion: Mother- to- child transmission of HBV in Cameroon seems to be multi factorial. They are high prevalence, poor knowledge aptitude and practices of pregnant

women, non sufficient AZD4547 knowledge of health personnel. Key Word(s): 1. Hepatitis B; 2. Transmission; 3. Africa; Presenting Author: OLGANIKOLAEVNA KHOKHLOVA Additional Authors: ARAROMANOVNA REIZIS, LIDYAVASILIEVNA SEREBROVSKAYA, BORIS REIZIS Corresponding Author: OLGANIKOLAEVNA KHOKHLOVA Affiliations: The Central Institute

mafosfamide for Epidemiology, Federal Supervision Servise for Consumer Rights Protection and People,s Welfare; Dept. of Microbiology and Immunology Columbia University Medical Center Objective: Plasmacytoid dendritic cells (pDCs) are major producers of type I and type III interferons (IFN) in response to viral infections. The role of pDCs in the pathogenesis of hepatitis C virus (HCV) infection and in the therapeutic activity of IFN in HCV patients is poorly understood. Our goal was to assess the number and functional status of pDCs in children and adults with HCV and correlate it with disease progression and response to IFN therapy. Methods: We examined peripheral blood of 28 healthy controls and 133 patients (58 children and 75 adults) at different stages of HCV infection and during the course of therapy with recombinant IFNα. The pDC population was enumerated by flow cytometry, and in vitro IFN production in the whole blood in response to pDC-specific stimulus unmethylated CpG oligonucleotides was determined by ELISA. Results: The fraction and numbers of pDCs were significantly (P < 0.05) decreased in both children and adult HCV patients compared to age-matched healthy controls. The decrease was most pronounced in adult patients with advanced liver fibrosis (Metavir score 3-4).

Recently, it has been reported that serum and other body

fluids contain sufficiently KU-57788 supplier stable micro-RNA signatures. Thus, the profiles of circulating micro-RNAs have been explored in a variety of studies aiming at the identification of novel non-invasive biomarkers. The aim of the study is to develop a non-invasive diagnostic tool based on measuring the serum levels of different mi-RNAs in order to detect HCV-induced liver fibrosis at the early stages of the disease. Patients and methods: Subjects of the current study included 36 cases of chronic hepatitis C (CHC) with early stage of fibrosis, 35 cases of CHC with stage 4 of fibrosis admitted to department of hepato-gastroenterology, TBRI. 15 subjects were, also, included as normal controls. Laboratory investigation included urine and stool analysis, liver function test and prothrombin, serological markers for viral hepatitis and ultra-sonography were done for all cases of the study. Six main mi-RNAs (miRNA-138, miRNA-140, miRNA-143, miRNA-328, miRNA-325, and miRNA-349) were selected according to previous studies that demonstrated their noticeable expression pattern during the development of liver fibrosis. The six mi-RNAs were measured using real-time reverse transcription-polymerase chain reaction. Results: Circulating levels of miRNA-138, miRNA-140, miRNA-143, miRNA-328, miRNA-349, and miRNA-325 were significantly

increased (P< 0.01) in cases of both PI3K inhibition Racecadotril CHC with early stage of fibrosis and CHC with stage 4 of fibrosis compared to control group. Also, the circulating levels of the different mi-RNAs were significantly increased (p< 0.01) from cases of chronic CHC with early stage of fibrosis to cases of CHC with stage 4 of fibrosis. Conclusions: Our data suggest that circulating mi-RNAs could serve as novel biomarkers for the detection

and assessment of liver fibrosis. Disclosures: The following people have nothing to disclose: Maged T. EL-Ghannam, Eman G. El-Ahwany, Mona K. Zoheiry, Mona Nosseir, Suher K. Zada [Background/Aims] As hepatocellular carcinoma (HCC) occurs 8% per annum with liver cirrhosis (LC) patients, the diagnosis and therapies for LC are important. However, no significant serum markers predicting the prognosis of LC were reported. H1 -1 2 is one of the most promising glyco-biomarker candidate. In this study, we examined a utility of Wisteria floribunda agglu-tinin (WFA) reactive H1-12 as a useful glyco-biomarker through the strategy for glyco-biomarker development in hepatitis C virus (HCV) infected patients. [Methods] We enrolled total 21 8 HCV-infected patients from January 1 998 to April 2012 in our hospital. Overall chronic hepatitis (CH) is 47.2% (103/218) (F1/F2/F3/non-biopsy = 28/29/29/17) and liver cirrhosis (LC) is 52.8% (115/218) (F4/non-biopsy = 66/49), median age was 64 (21-87), male was 118 (54.0%). Among 115 patients with LC, Child A was 95 (82.6%) and Child B/C was 20 (17.4%). 52 HCC (54.