Only the presence of moderate to severe MaS is associated with in

Only the presence of moderate to severe MaS is associated with inferior early allograft outcomes. The impact of severe

MaS on allograft survival appears greater than other donor factors, including the calculated DRI. “
“Background and Aim:  Saracatinib Fibrotic progression in non-alcoholic fatty liver disease (NAFLD) is associated with impaired hepatic function. The 13C-caffeine breath test (CBT) is a non-invasive, quantitative test of liver function. We sought to determine the utility of the CBT in detecting hepatic fibrosis in NAFLD. Methods:  The CBT was applied to 48 patients with NAFLD. CBT results were compared to clinical, biochemical and histological data. Twenty-four healthy subjects served as controls. Results:  Patients with

simple steatosis had similar CBT values (2.28 ± 0.71 Δ‰ per 100 mg caffeine) to controls (2.31 ± 0.85, P = 1.0). However, CBT was significantly reduced in patients with non-alcoholic steatohepatitis (1.59 ± 0.65, P = 0.005) and cirrhosis (1.00 ± 0.73, P < 0.001). CBT significantly correlated with Brunt's fibrosis score (r = −0.49, P < 0.001) but not with steatosis (P = 0.23) or inflammation (P = 0.08). CBT also correlated with international normalized ratio (r = −0.61, P < 0.001), albumin (r = 0.37, P = 0.009), aspartate aminotransferase/alanine aminotransferase (r = −0.34, P = 0.018) and platelets learn more (r = 0.31, P = 0.03). On multivariate analysis, age (odds ratio 1.12, 95% confidence interval 1.042–1.203, P = 0.002) and CBT (OR 0.264, 95% CI 0.084–0.822, P = 0.02) were independent predictors of significant fibrosis (F ≥ 2). CBT yielded an area under the receiver operating characteristic

curve of 0.86 for the diagnosis of cirrhosis. Conclusions:  The CBT reflects the extent of hepatic fibrosis in NAFLD and represents a non-invasive predictor MCE of fibrosis severity in this condition. “
“Incidence rates of hepatocellular carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC) have increased in the United States. Metabolic syndrome is recognized as a risk factor for HCC and a postulated one for ICC. The magnitude of risk, however, has not been investigated on a population level in the United States. We therefore examined the association between metabolic syndrome and the development of these cancers. All persons diagnosed with HCC and ICC between 1993 and 2005 were identified in the Surveillance, Epidemiology, and End Results (SEER)-Medicare database. For comparison, a 5% sample of individuals residing in the same regions as the SEER registries of the cases was selected. The prevalence of metabolic syndrome as defined by the U.S.

1 billion for comparative effectiveness research (CER)14 The ena

1 billion for comparative effectiveness research (CER).14 The enactment of this law was preceded by a report constructed by the Institute of Medicine (IOM), which defined the tenets of CER and developed a list of 100 priority topics for the National Insitutes of Health (NIH) to consider when funding research initiatives.15 The IOM defines CER as the generation and synthesis of evidence that compares the benefits and harms of alternative methods to prevent, diagnose, treat, and monitor a clinical condition or to improve BMS-907351 order the delivery

of care. Accordingly, the following six defining characteristics of CER were described. Consistent with the definition of effectiveness, CER is conducted in settings that are similar to those in which the intervention will be used in practice. An emphasis is placed on external validity, or the ability to generalize results to real-world decision making. CER measures outcomes, both benefits and harms, that are important to patients. This is familiar to clinicians because they routinely address risks

and benefits of an intervention in practice. Assessment of patient-reported outcomes is important for CER studies in which Trichostatin A order patient ratings of effectiveness or adverse events may differ from clinical measures. Methods used for CER range from nonexperimental studies (observational settings) to experiments (randomized and nonrandomized controlled trials) to synthesis of existing studies (systematic reviews and meta-analysis, technology assessments, and decision analysis). CER not only informs a specific clinical decision from the patient perspective but also directs a health policy decision from the population

perspective. Clinical questions refer to the health care of individual patients, including preventive, screening, diagnostic, therapeutic, monitoring, or rehabilitative interventions. Policy questions refer to the health and health care of populations through knowledge synthesis and transfer strategies, public health programs, or initiatives involving the organization, delivery, or payment for health services. 上海皓元医药股份有限公司 CER focuses on the individual rather than the average patient by analyzing results at the population and subgroup levels. Utilization of subgroup results and clinical prediction rules assists providers and patients in individualizing management decisions. Applying new knowledge in genomics, systems biology, and other biomedical sciences in subgroups of patients with demographic, ethnic, physiologic, and genetic characteristics introduces new possibilities of individualized and predictive medicine. CER compares at least two alternative interventions, each with the potential to be “best practice.” For many clinical decisions, “optimal usual care” reflecting current standards is an appropriate potential comparator, which may include the alternative of “watchful waiting. The process by which these 100 priority topics were selected and prioritized was exhaustive and iterative.

1 billion for comparative effectiveness research (CER)14 The ena

1 billion for comparative effectiveness research (CER).14 The enactment of this law was preceded by a report constructed by the Institute of Medicine (IOM), which defined the tenets of CER and developed a list of 100 priority topics for the National Insitutes of Health (NIH) to consider when funding research initiatives.15 The IOM defines CER as the generation and synthesis of evidence that compares the benefits and harms of alternative methods to prevent, diagnose, treat, and monitor a clinical condition or to improve Midostaurin chemical structure the delivery

of care. Accordingly, the following six defining characteristics of CER were described. Consistent with the definition of effectiveness, CER is conducted in settings that are similar to those in which the intervention will be used in practice. An emphasis is placed on external validity, or the ability to generalize results to real-world decision making. CER measures outcomes, both benefits and harms, that are important to patients. This is familiar to clinicians because they routinely address risks

and benefits of an intervention in practice. Assessment of patient-reported outcomes is important for CER studies in which Tamoxifen in vitro patient ratings of effectiveness or adverse events may differ from clinical measures. Methods used for CER range from nonexperimental studies (observational settings) to experiments (randomized and nonrandomized controlled trials) to synthesis of existing studies (systematic reviews and meta-analysis, technology assessments, and decision analysis). CER not only informs a specific clinical decision from the patient perspective but also directs a health policy decision from the population

perspective. Clinical questions refer to the health care of individual patients, including preventive, screening, diagnostic, therapeutic, monitoring, or rehabilitative interventions. Policy questions refer to the health and health care of populations through knowledge synthesis and transfer strategies, public health programs, or initiatives involving the organization, delivery, or payment for health services. medchemexpress CER focuses on the individual rather than the average patient by analyzing results at the population and subgroup levels. Utilization of subgroup results and clinical prediction rules assists providers and patients in individualizing management decisions. Applying new knowledge in genomics, systems biology, and other biomedical sciences in subgroups of patients with demographic, ethnic, physiologic, and genetic characteristics introduces new possibilities of individualized and predictive medicine. CER compares at least two alternative interventions, each with the potential to be “best practice.” For many clinical decisions, “optimal usual care” reflecting current standards is an appropriate potential comparator, which may include the alternative of “watchful waiting. The process by which these 100 priority topics were selected and prioritized was exhaustive and iterative.

Whether K+ channel blockade can modify the effect of LPS induced

Whether K+ channel blockade can modify the effect of LPS induced hypo-contractility remains unknown. We therefore hypothesized that the blockage of K+ channel antagonizes LPS effect on mouse jejunal excitability and contractility. Methods: In organ bath, Vorinostat research buy mouse jejunum segments were perfused in oxygenated Kreb’s solution at 37°C.

The spontaneous slow wave activity and muscle strip contractility were respectively recorded by using suction electrode and isometric force transducer. After equilibrated for 45 min, slow waves were recorded in condition of control, in presence of LPS (30 ug/ml, 30 min) and in addition of TEA, 4AP, E-4031, Cisapride and LNNA, respectively. Results: 1. LPS treatment resulted in significant attenuation of slow wave activity.

Compared Selleck LY294002 to control, the LPS induced the baseline downshift indicating hyperpolarization. The normalized amplitude of slow wave was decreased to 0.38 ± 0.08 (n = 5, P < 0.05); the frequency (CPM) was decreased from 42 ± 6.5 to 21 ± 3.6 (n = 5, P < 0.01). 2. K+ channel blockade partially reversed the effect of LPS on slow wave activity. The baseline was elevated upshift by 4AP (1 mM), E-4031 (2 uM), Cisapride (1 uM) and LNNA (200 uM), in presence of LPS, indicating a reversible depolarization against to LPS. In addition, E4031 increased the frequency to 35 ± 3.3 (n = 5, P < 0.05) and prolonged the duration to 2.25 ± 0.5 sec from 1.66 ± 0.3 sec in control (n = 5, P < 0.05); the initiation of firing superimposed onto plateau was remarkable. 3. E-4031 attenuated the LPS induced hypo-contractility. The muscle strip contraction respectively from control, LPS and E4031 (2 uM, in presence of LPS) was 0.45 ± 0.03, 0.28 ± 0.04 and 0.33 ± 0.08 (g.mm-2.s-1; n = 3; ANOVA: P < 0.05). Conclusion: The results of acute LPS treatment in this study demonstrate that blockade ERG-K reverses LPS attenuations in excitability and contractility and a potential new insight into an independent pathway during LPS endotoxemia. Key Word(s): 1. Lipopolysaccharide; 2. Dysmotility; 3. ERG-K; Presenting Author: WANG YAN Additional Authors:

SHIHAI TAO, ZOUBAI CANG, JIANG JIONG, CHENFEN RONG, JIA MIAO Corresponding Author: WANG YAN Affiliations: Second Hospital of Medical College, Xi’an Jiaotong University Objective: Ghrelin medchemexpress is an orexigenic peptide with prokinetic effects. However, the mechanism and effects of ghrelin in regulating of the small intestinal motility are not fully understood. Our study aimed to explore the effects and mechanism of ghrelin on interdigestive myoelectric complex (IMC) in rats, as well as the neural pathway of it on the central nervous system (CNS) and the enteric nervous system (ENS). Methods: 1). Two pairs of silver bipolar electrodes were chronically implanted in the duodenum and jejunum of rats for electromyography. Ghrelin (20 μg kg-1) was injected intravenously into rats during fasting.

Confocal fluorescence and immunoelectron microscopy (IEM) of tran

Confocal fluorescence and immunoelectron microscopy (IEM) of transiently GFP-MdRABE1 overexpressing interphase cells demonstrated that the GFP-MdRABE1 protein was localized Daporinad nmr to the endoplasmic reticulum, dictyosomes, exocytotic vesicles, the cell margin, the membranes of cell organelles, and in the isthmus zone around the nucleus. Although overexpression phenotyping of both N- and C-terminal green fluorescent protein (GFP) fusions failed to indicate

additional functional evidence of the MdRABE1 protein due to mortality of those transgenic cells, its expression profile, bioinformatics, and intracellular localization suggest a role in vesicle trafficking during morphogenesis. “
“Methionine (Met) residues of proteins can be oxidized by reactive oxygen species (ROS) with the formation of two epimers of methionine sulfoxide, S-MetSO and R-MetSO, which are reduced back to methionine by methionine sulfoxide reductase A (MSRA)

and B (MSRB), respectively. UfMSRA and UfMSRB were cloned from the marine macroalga Ulva fasciata Delile, and the role of retrograde signal in gene Selleck HM781-36B expression was studied. Transcripts of UfMSRA and UfMSRB were increased after light exposure with a peak at 1 h. Treatment of photosynthetic electron transport inhibitors, 3-(3,4-dichlorophenyl)-1,1-dimethylurea (DCMU), 2,5-dibromo-3-methyl-6-isopropyl-p-benzoquinone (DBMIB), or stigmatellin, promoted the light-activated increase in UfMSRA transcripts, and a PSI electron donor, 2,6-dichlorophenolindophenol (DCPIP), reversed their effects. Increase of UfMSRB transcript by light was inhibited by DCMU and DBMIB treatments, and their effects were not reversed by DCPIP. Stigmatellin treatment did not affect UfMSRB transcripts. Thus, a relatively oxidized state of electron transport downstream from the cytochrome b6f (cytb6 f ) complex is involved in the light up-regulation of UfMSRA gene expression, and a more reduced state of Qo of the cytb6 f complex is required for the light activation of gene VAV2 expression

of UfMSRB. “
“Species of Volvox sect. Volvox (Volvocaceae, Chlorophyceae) are unique because they have thick cytoplasmic bridges between somatic cells and spiny-walled zygotes. This section is taxonomically important because the genus Volvox is polyphyletic. However, taxonomic studies of species in Volvox sect. Volvox have not been carried out on cultured material. Here, we performed a taxonomic study of monoecious species of Volvox sect. Volvox based on the comparative morphology and molecular phylogeny of chloroplast genes and the internal transcribed spacer (ITS) regions of nuclear rDNA using various strains originating from Japan and two preserved strains from the USA. The strains were clearly divided into four species, V. globator L., V. barberi W. Shaw, V. kirkiorum sp. nov., and V. ferrisii sp. nov.

Various blood tests including liver function tests were normal A

Various blood tests including liver function tests were normal. At operation, he had a large defect in the right hemidiaphragm with herniation of multiple organs including the liver, right colon, distal stomach and proximal duodenum. After repositioning the organs in the abdomen, the defect in the right diaphragm was closed using surgical mesh. The right lobe of the liver (RL) was small and seemed cirrhotic while the left lobe (LL) was greatly enlarged (Figure 1). A follow-up CT scan confirmed the presence of atrophy-hypertrophy complex of the liver (Figure 2). The right lobe was small and was

recognized on only the most cranial CT sequences. The lateral segment of the left lobe (segment 3) was greatly enlarged, segment 4 was shown and the gallbladder (*) was in a retrohepatic position. The selleck kinase inhibitor portal vein (white arrow), hepatic artery (thin white arrow) and common hepatic duct (thick white arrow) were also in Pifithrin-�� price unusual positions because of clock-wise rotation of hilar structures. The radiological features described above are typical of right lobe atrophy associated with left lobe hypertrophy. This atrophy-hypertrophy complex of the liver is almost always due to biliary obstruction or to occlusion of the portal vein. Hilar or intrahepatic causes

of biliary obstruction include benign and malignant neoplasms and benign strictures including Caroli’s disease. Vascular causes include hilar or intrahepatic portal vein occlusion by neoplasms, cavernous transformation of the portal vein and congenital stenosis of the portal vein. Embolism into the right portal vein is also being used to enlarge the left lobe of the liver prior to surgical or other therapies for neoplasms Urease in the right lobe of the liver. In animal models, a compromised portal venous blood flow is a much stronger stimulus for atrophy-hypertrophy than biliary obstruction. In the patient described above, we have attributed the atrophy-hypertrophy complex to herniation of the liver causing distortion

of the right portal vein and a reduction in right portal blood flow. Contributed by “
“Hepatology recently published a study by Feuerstadt et al.,1 who reported a 3.3% effectiveness rate for hepatitis C treatment in an observational study; this is a stark contrast to the 56% to 63% efficacy rates reported for the same treatment regimen in the setting of randomized controlled trials (RCTs). Such comparisons have contributed to the growing awareness that real-world data derived from observational studies often vary widely from those data derived from the controlled settings of clinical trials. Contemporary methods for producing this type of real-world data can be performed with data from specialized registries or existing administrative and claims information and include a variety of designs, such as case-control, cohort, and cross-sectional studies, in which patients are not randomly assigned to treatment groups.

Various blood tests including liver function tests were normal A

Various blood tests including liver function tests were normal. At operation, he had a large defect in the right hemidiaphragm with herniation of multiple organs including the liver, right colon, distal stomach and proximal duodenum. After repositioning the organs in the abdomen, the defect in the right diaphragm was closed using surgical mesh. The right lobe of the liver (RL) was small and seemed cirrhotic while the left lobe (LL) was greatly enlarged (Figure 1). A follow-up CT scan confirmed the presence of atrophy-hypertrophy complex of the liver (Figure 2). The right lobe was small and was

recognized on only the most cranial CT sequences. The lateral segment of the left lobe (segment 3) was greatly enlarged, segment 4 was shown and the gallbladder (*) was in a retrohepatic position. The selleck products portal vein (white arrow), hepatic artery (thin white arrow) and common hepatic duct (thick white arrow) were also in selleck compound unusual positions because of clock-wise rotation of hilar structures. The radiological features described above are typical of right lobe atrophy associated with left lobe hypertrophy. This atrophy-hypertrophy complex of the liver is almost always due to biliary obstruction or to occlusion of the portal vein. Hilar or intrahepatic causes

of biliary obstruction include benign and malignant neoplasms and benign strictures including Caroli’s disease. Vascular causes include hilar or intrahepatic portal vein occlusion by neoplasms, cavernous transformation of the portal vein and congenital stenosis of the portal vein. Embolism into the right portal vein is also being used to enlarge the left lobe of the liver prior to surgical or other therapies for neoplasms Acesulfame Potassium in the right lobe of the liver. In animal models, a compromised portal venous blood flow is a much stronger stimulus for atrophy-hypertrophy than biliary obstruction. In the patient described above, we have attributed the atrophy-hypertrophy complex to herniation of the liver causing distortion

of the right portal vein and a reduction in right portal blood flow. Contributed by “
“Hepatology recently published a study by Feuerstadt et al.,1 who reported a 3.3% effectiveness rate for hepatitis C treatment in an observational study; this is a stark contrast to the 56% to 63% efficacy rates reported for the same treatment regimen in the setting of randomized controlled trials (RCTs). Such comparisons have contributed to the growing awareness that real-world data derived from observational studies often vary widely from those data derived from the controlled settings of clinical trials. Contemporary methods for producing this type of real-world data can be performed with data from specialized registries or existing administrative and claims information and include a variety of designs, such as case-control, cohort, and cross-sectional studies, in which patients are not randomly assigned to treatment groups.

The results of this study provide

an important insight in

The results of this study provide

an important insight into this issue. “
“Background and Aim:  The term “stress-related mucosal disease” (SRMD) represents conditions ranging from superficial mucosal damage to focal deep mucosal damage in the stomach, of which pathogenesis is deduced to be violent mucosal ischemia or excess oxidative stress, but not fully clarified yet. Under the hypothesis that mucosal cell apoptosis subsequent to endoplasmic reticulum (ER) stress might play a crucial role, we evaluated the efficacy and mechanism that novel acid pump antagonist (APA), revaprazan, alleviated water immersion restraint stress (WIRS) induced SRMD in rats. Methods:  In order to define whether WIRS-induced SRMD is associated with ER stress, we Selleck BMN673 checked the alteration in the expression of ER stress markers including GRP78, CHOP, XBP-1, BiP as well as apoptosis in WIRS-induced SRMD. The efficacy

of revaprazan on either alleviating ER stress or attenuating SRMD was compared with proton pump inhibitor (PPI) and gastroprotectant. Results:  Ten hours of WIRS induced a severe degree of SRMD, in which ER stress markers including CHOP, XBP1, and BiP were significantly overexpressed in the gastric tissues. However, these markers of ER stress were significantly decreased in the group pretreated with revaprazan compared to PPI or gastroprotectant, accompanied with a significant KU-57788 molecular weight reduction in apoptotic index. In addition to ER stress, revaprazan imposed anti-inflammatory benefit to limit SRMD based on significant levels of inflammatory cell apoptosis. Conclusion:  see more Endoplasmic reticulum stress accompanied with drastic apoptosis was implicated in the development of SRMD, but revaprazan could rescue the stomach from SRMD through alleviating ER stress in epithelial cells much better than either PPI or gastroprotectant. “
“See article in J. Gastroenterolol. Hepatol. 2011; 26: 1114–1122. Yoon et al.1 are to be congratulated on publishing the Korean experience of the clinical response to, and 1-year outcomes following, an initial

course of steroid therapy in ulcerative colitis (UC). While their data are not directly comparable to the series in the literature, due to variability in severity and referral patterns among studies, the results appear to be remarkably similar to what one sees in Western cohorts. In fact, the current data are highly reminiscent of one of the few studies mirroring their design.2 Following a cohort of 63 patients with UC treated with steroids between 1970 and 1993, Faubion et al. reported 1-year follow-up data. As one can appreciate, there are unlikely to be large, clinically-relevant differences in outcomes between these two cohorts (Table 1), especially when one applies a non-responder imputation to Yoon et al.’s1 data.

The results of this study provide

an important insight in

The results of this study provide

an important insight into this issue. “
“Background and Aim:  The term “stress-related mucosal disease” (SRMD) represents conditions ranging from superficial mucosal damage to focal deep mucosal damage in the stomach, of which pathogenesis is deduced to be violent mucosal ischemia or excess oxidative stress, but not fully clarified yet. Under the hypothesis that mucosal cell apoptosis subsequent to endoplasmic reticulum (ER) stress might play a crucial role, we evaluated the efficacy and mechanism that novel acid pump antagonist (APA), revaprazan, alleviated water immersion restraint stress (WIRS) induced SRMD in rats. Methods:  In order to define whether WIRS-induced SRMD is associated with ER stress, we Cell Cycle inhibitor checked the alteration in the expression of ER stress markers including GRP78, CHOP, XBP-1, BiP as well as apoptosis in WIRS-induced SRMD. The efficacy

of revaprazan on either alleviating ER stress or attenuating SRMD was compared with proton pump inhibitor (PPI) and gastroprotectant. Results:  Ten hours of WIRS induced a severe degree of SRMD, in which ER stress markers including CHOP, XBP1, and BiP were significantly overexpressed in the gastric tissues. However, these markers of ER stress were significantly decreased in the group pretreated with revaprazan compared to PPI or gastroprotectant, accompanied with a significant Panobinostat datasheet reduction in apoptotic index. In addition to ER stress, revaprazan imposed anti-inflammatory benefit to limit SRMD based on significant levels of inflammatory cell apoptosis. Conclusion:  Glutamate dehydrogenase Endoplasmic reticulum stress accompanied with drastic apoptosis was implicated in the development of SRMD, but revaprazan could rescue the stomach from SRMD through alleviating ER stress in epithelial cells much better than either PPI or gastroprotectant. “
“See article in J. Gastroenterolol. Hepatol. 2011; 26: 1114–1122. Yoon et al.1 are to be congratulated on publishing the Korean experience of the clinical response to, and 1-year outcomes following, an initial

course of steroid therapy in ulcerative colitis (UC). While their data are not directly comparable to the series in the literature, due to variability in severity and referral patterns among studies, the results appear to be remarkably similar to what one sees in Western cohorts. In fact, the current data are highly reminiscent of one of the few studies mirroring their design.2 Following a cohort of 63 patients with UC treated with steroids between 1970 and 1993, Faubion et al. reported 1-year follow-up data. As one can appreciate, there are unlikely to be large, clinically-relevant differences in outcomes between these two cohorts (Table 1), especially when one applies a non-responder imputation to Yoon et al.’s1 data.

pylori infection In addition, rebamipide scavenges free radicals

pylori infection. In addition, rebamipide scavenges free radicals, inhibits inflammatory cell responses, and reduces interleukin-8 production in response to H. pylori.[24-26] These effects might alter H. pylori status. The present systematic review Fer-1 in vivo and meta-analysis has several limitations

that need to be taken into account in interpreting the results. The most of these studies were performed in Japan, and similar publications examining other ethnic populations are limited. In addition, although most studies in the present analysis evaluated the supplementary effect of rebamipide on the PPI+amoxicillin dual therapy, it is rather outdated because the main stream of the recent H. pylori eradication regimens are based on the triple therapy. Due to the limited number of eligible studies, subgroup analysis was not performed. The highest quality study by Fujioka et al. showed no significant effect of rebamipide (odds ratio 0.86).[22] Further studies with large number of patients are warranted to clarify the efficacy of rebamipide-containing quadruple therapy. In conclusion, our analysis demonstrates that supplementation with rebamipide might be effective in increasing H. pylori eradication rates of PPI–amoxicillin dual therapy.


“Hepatitis B virus X (HBx) protein is implicated in hepatitis B virus (HBV)-associated liver carcinogenesis. However, it remains unclear whether HBx-expressing hepatic progenitor cells

(HPCs) are attributed to liver tumor formation. In this study, by using HBx selleck screening library transgenic mice and a 3,5-diethoxycarbonyl-1,4-dihydrocollidine Dimethyl sulfoxide (DDC)-induced liver injury model, the relationship between HBx expression and tumorigenicity of HPCs was analyzed. Compared with control mice, an elevated number of EpCAM+ cells with characteristics of HPCs was observed in HBx mice after 1 month and 4 months of DDC diet feeding. All HBx transgenic mice developed liver tumors characterized by histological features of both hepatocellular carcinoma (HCC) and cholangiocarcinoma after 7 months of DDC feeding. Notably, EpCAM+ HPCs isolated from premalignant HBx mice exposed to a DDC diet for 4 months formed subcutaneous mixed-lineage tumors (four out of six) in nonobese diabetic/severe-combined immunodeficient (NOD/SCID) mice, and none of the cells from wildtype (WT) induced tumor, indicating that HBx may induce malignant transformation of HPCs that contributes to tumorigenesis. We also found higher titers of circulating interleukin (IL)-6, activities of IL-6/STAT3, and Wnt/β-catenin signaling pathways in HBx transgenic mice, suggesting HBx may induce intrinsic changes in HPCs by way of the above signaling that enables HPCs with tumorigenicity potential. Finally, clinical evidence showed that high HBx expression in human HBV-related HCC was statistically associated with expansion of EpCAM+ or OV6+ tumor cells and aggressive clinicopathologic features.