Various investigations for viral hepatitis, autoimmune disease and Wilson’s disease were unhelpful. An abdominal ultrasound study and computed tomography (CT) scan showed dilatation of intrahepatic ducts and splenomegaly. Magnetic resonance cholangiopancreatography (MRCP) showed cystic dilatation of the hilar bile duct Selleckchem Peptide 17 and moderate dilatation of intrahepatic ducts. The gallbladder (GB) and common bile duct (BD) were clearly shown and the gallbladder appeared to be linked to intrahepatic ducts (Figure 1). Endoscopic retrograde cholangiopancreatography

(ERCP) was also performed and showed contrast passing from the common bile duct into the cystic duct and gallbladder (Figure 2). The common hepatic duct was not outlined. Endoscopy revealed esophageal and gastric

varices while CT angiography showed a normal hepatic artery, portal vein and inferior vena cava. At laparotomy, the patient had features of cirrhosis. An operative cholangiogram was performed by injection of contrast into the gallbladder and only showed contrast in the common bile duct, similar to findings at ERCP. In the process of mobilizing the gallbladder, bile ducts in the gallbladder bed were shown to communicate with the gallbladder. The common hepatic duct could not be identified but dissection revealed a hilar pouch containing bile. Two hepaticojejunostomies were performed to drain bile from the gallbladder BMS-354825 in vitro bed and from the hilar pouch. Splenectomy was also performed. The anastomoses in the gallbladder bed were shown to be patent by passage of contrast through a stent. Liver function tests returned to normal after Ponatinib order 8 months. This may be the first report of biliary atresia diagnosed in an adult. In this case, he had an unusual variant characterized by absence of the common hepatic duct (type II). The diagnosis was delayed because of the development of anastomoses between branches of the right hepatic duct and the gallbladder. Despite this,

there was persistent cholestasis with the development of biliary cirrhosis and portal hypertension. The surgical procedure appears to have been helpful in the short-term but the longer-term outcome remains unclear. Contributed by “
“We read with great interest the excellent article by Ghouri and coworkers,1 who reviewed the current literature on the levels of gamma-glutamyltransferase (GGT) and alanine aminotransferase (ALT) as potential predictors of incident cardiovascular disease. The authors elegantly demonstrate that there may be a statistically significant association between higher GGT levels and incident cardiovascular disease events, although this association may be clinically questionable because it is confounded by age. In contrast, ALT levels are not significantly associated with cardiovascular risk.

Since accumulating evidence demonstrates that aberrant expression of microRNAs (miRNAs) contributes to tumor radiosensitivity,

we attempted to identify miRNAs associated with radioresistance of ESCC. Methods: In this study, we detected the radiosensitivity selleck products of six ESCC cell lines including TE1, ECA109, EC9706, KYSE30, KYSE150, and KYSE450 by colony formation assays. Then we used GeneChip miRNA array to perform a comparison of miRNAs expression in these ESCC cell lines. One miRNA candidate found to be down-regulated in radiation resistant cells was miRNA-381. Furthermore, we detected the effect of miRNA-381 on radiosensitivity, cellular proliferation and migration of ESCC by using pre-miR-381 or antisense

of miRNA-381 in vitro and in vivo. Results: The trend of radiosensitivity in these six cell lines was TE1>ECA109>EC9706>KYSE30>KYSE150>KYSE450. The expression of miRNA-381 in radiation sensitive ESCC cell lines was higher. Enforced expression of miRNA-381 increased radiosensitivity of radioresistant ESCC cells and promoted the formation of nonaggressive phenotype including decreased cellular proliferation and migration. In contrast, inhibition this website of miRNA-381 in radiosensitive ESCC cells promoted radiation resistance and development of an aggressive phenotype. In vivo assays extended the significance of these results, showing that miRNA-381 overe-xpression decreased tumor growth and resistance to radiation treatment in tumor xenografts. Conclusion: Together, our work reveals miRNA-381 TCL expression as a critical determinant of radiation resistance in esophageal cancer cells. Key

Word(s): 1. microRNA; 2. esophageal squamous cell carcinoma; 3. radioresistance; 4. aberrant expression Presenting Author: VISHNU BIRADAR Additional Authors: SONIA NAIK, NACHIKET DUBALE, SHITAL BIRADAR, VIJAYASHRI BHIDE, AMOL BAPAYE Corresponding Author: AMOL BAPAYE Affiliations: Deenanath Mangeshkar Hospital And Research Center, Deenanath Mangeshkar Hospital And Research Center, Deenanath Mangeshkar Hospital And Research Center, Deenanath Mangeshkar Hospital And Research Center, Deenanath Mangeshkar Hospital and Research Center Objective: Cow’s milk protein allergy (CMPA) is a leading cause of food allergy in infants and children up to 5 years of age. We aimed this study to know the clinical profile of CMPA in western India and need of special formula for management. Methods: Design: Retrospective Duration: Jan 2011 to May 2014 Diagnosis of CMPA was based on 1. Relevant clinical history 2.

[12-14] The acquired flora in such artificially colonized animal models remains stable over a long period. Further, the animals naturally pass their flora to their progeny.[15] However, these models have a relatively limited bacterial diversity than the flora in human gut. In this model, mouse or human fecal material is used to colonize the gut of GF animals. The flora in such animals also show long-term stability and are passed on to offsprings. These models are also useful in studying the alterations in gut flora and intestinal ecosystem

during physiological and pharmacological interventions, PARP inhibitor such as antibiotic administration,[16] circumventing the ethical issues associated with similar studies in humans. Another advantage of such models relates to avoidance

of confounding by variations in human diet, lifestyle patterns, and host genetics. Although these models more closely resemble http://www.selleckchem.com/products/azd9291.html the human situation than the mono- or bi- and poly-associated models, these may still not fully replicate the human situation. For instance, feces from humans and human flora-associated animals differ significantly in concentration of short-chain fatty acids, despite being similar in several other characteristics.[17] Liver has a dual blood supply with nearly 70% of its blood coming from intestines through the portal circulation and the remaining through the hepatic Thiamet G artery. Although the intestinal mucosa acts as an effective barrier against translocation of microbes and microbial

products from the gut to the circulation, small quantities of these do enter the portal venous blood. Liver, being strategically located between highly contaminated bowel and sterile systemic circulation, works as a filter. Immune cells in hepatic sinusoids effectively remove bacteria and bacterial products from the portal blood,[18] protecting the systemic circulation from endotoxemia. Liver is also rich in a variety of innate immune cells, namely natural killer cells (NK cells), NK T cells, Kupffer cells, and hepatic stellate cells. These cells serve to maintain a sensitive balance between protective immune response against exogenous antigens and immune tolerance; the latter is particularly important because excessive activation of hepatic immune cells in response to exogenous antigens may induce inflammation, autoimmune phenomena, fibrosis, or carcinogenesis in the liver. Alterations in nature and number of bacterial species in the gut microflora or their increased translocation may also disturb this fine balance and lead to liver injury, particularly when “liver tolerance” to bacterial products has been breached.

9% in the general population,3 to 17% in HIV-infected

individuals.4 Most african countries in the study by Rein et al. are areas of high endemicity for HIV.5 Prevalence of HIV infection in a population is of importance when addressing prevalence, and relevance, of HBV infection. Patients infected with HIV are known to have higher rates of occult hepatitis B.6 This means that individuals will be negative for HBsAg, with positive anticore antibody and detectable HBV viral load. The consequences of occult hepatitis B are still under investigation. However, occult hepatitis B has been reported to reactivate in patients with HIV.7 Moreover, the effects and protection of vaccination against HBV in this population are unknown. Any study attempting to address prevalence of HBsAg in individuals from African Dinaciclib solubility dmso countries should take into account the presence of HIV infection, in order to better evaluate the significance of the findings. I applaud the initiative of Rein et al. to try to achieve a much-needed clarification on the prevalence of HBsAg in refugees entering the United States. However, well-conducted prospective or cross-sectional studies with larger samples for each country are needed. Y-27632 chemical structure Jose Daniel Debes M.D.*, * Internal Medicine, University of Minnesota, Minneapolis, MN. “
“The liver constantly encounters food-derived antigens and bacterial components such as lipopolysaccharide translocated from the gut into the portal

vein. Bacterial components stimulate Toll-like Ribonucleotide reductase receptors (TLR), which are expressed on Kupffer cells, biliary

epithelial cells, hepatocytes, hepatic stellate cells, endothelial cells and dendritic cells and recognize specific pathogen-associated molecular patterns. The signaling of TLR to its main ligand triggers inflammation. Usually, in order to protect against hyperactivation of the immune system and to prevent organ failure by persistent inflammation, TLR tolerance to repeated stimuli is induced. In chronic liver diseases, a breakdown in TLR tolerance occurs. Furthermore, Kupffer cells, hepatic stellate cells and natural killer T cells are key components of innate immunity. Decreased numbers and impaired ability of these cells lead to failures in immune tolerance, resulting in persistent inflammation. Recently, the activation of inflammasome was revealed to control the secretion of pro-inflammatory cytokines such as interleukin-1β in response to bacterial pathogens. Innate immunity seems to be an important contributor to the pathogenesis of fatty liver disease and autoimmune liver disease. Recently, probiotics were reported to affect various liver diseases via shifts in gut microbiota and the stability of intestinal permeability. However, many unresolved questions remain. Further analysis will be needed to gain a more comprehensive understanding of the association of innate immunity with the pathogenesis of various liver diseases. THE LIVER, THE largest organ in the body, weight 1200–1500 g and has a double blood supply.

Caution is requires, as HBV genotype Bj and the 1896 mutation have been identified as independent risk factors for fulminant hepatitis.[60] HBV genotype Ba is a recombinant gene arrangement resembling in part HBV genotype C from the core promoter through to the core. HBV genotype Ba reportedly has a relatively KPT-330 clinical trial high HCC risk, though the characteristics differ significantly between subtypes. HBV genotype C has a high HCC risk (higher even than HBV genotype Ba) and poor prognosis.[61] HBV genotype C is resistant to conventional IFN treatment. HBV genotype D is normally found in Western countries. There are several localized pockets of infection and a number of subtypes in existence. R428 in vivo The most common

form is HBV genotype D1, which has been studied extensively and found to include a specific genetic mutation linked to disease phenotype.[62] Reports from Europe suggest

that HBV genotype D is more resistant to IFN treatment than HBV genotype A, with a poor overall prognosis.[63] Recommendations HBV genotype A has been linked to horizontal infection among young people in Japan, who often become carriers following the acute hepatitis phase. Among HBV genotype B, subtype Bj is found only in Japan. Most cases remain asymptomatic carriers indefinitely, with negligible risk of HCC. However infection with pre-core mutations can lead to fulminant hepatitis. HBV genotype C has a high HCC risk and is resistant to conventional IFN treatment. The prognosis is poor. HBV DNA quantification is for assessment of liver disease, evaluation of therapeutic effects, and diagnosis of breakthrough hepatitis via HBV mutation. It is also linked to prognosis, since high HBV DNA levels indicates a high risk of cancer.[34] Conventional techniques for measuring HBV DNA levels in the past included the Amplicor HBV Monitor test (Roche Diagnostics Systems, Branchburg, NJ, USA) and the HBV DNA TMA-HPA test (transcription-mediated amplification-hybridization Y-27632 mouse protection

assay, Chugai Diagnostics Science, Tokyo). Real-time detection PCR testing has become more popular in recent years, as it offers greater sensitivity and a wider measurement range. Real-time detection PCR installs primers and a probe on the well conserved S domain sequences on the HBV genome. The HBV probe is a short oligonucleotide for 5′-end fluorescence labeling and 3′-end quencher labeling. Real-time PCR HBV DNA quantification offers both high sensitivity and a broad dynamic range for detecting the quantity of PCR products based on PCR cycles once the fluorescence intensity reaches a given level. In addition to evaluation of antiviral therapeutic effects, improved sensitivity allows detection of viral breakthroughs, detection of HBV in HBeAg negative cases and latent HBV infections, as well as early prediction of exacerbation of hepatitis and HBV reactivation.

1, p = 0.012). The mean score of the Boston Bowel Preparation Scale was similar between the two groups but there was a trend towards higher percentage of satisfactory

overall grading of bowel preparation in the split-dose group (96.9% vs. 91.4%, p = 0.056). Patients in the split-dose group were more likely to be able to complete their bowel preparation (98.4% vs. 94.2%, p = 0.07). Patients in whole-dose group were more likely to experience nausea (35.3% vs. 23.3%, p = 0.031). Although there was no significant difference in overall comfort during bowel preparation between the two groups, patients in the whole-dose group were more likely to refuse the same regime (13.7% vs. 6.2%, p = 0.042) and to want to try another regime (78.4% vs. 55.8%, p < 0.001). Conclusion: We conclude that split-dosing PEG-ELS PLX4032 group has better polyps detection rate and less side effects compared to whole-dose PEG-ELS group. Key Word(s): 1. Bowel preparation; 2. PEG-ELS; 3. Split-dosing; 4. RCT; Presenting Author: ZHEN LI Additional Authors: XIU-LI ZUO, YAN-QING LI Corresponding Author: ZHEN LI Affiliations: Shandong University, Qilu Hospital Objective: Gastric intestinal metaplasia (GIM) is a well-known premalignant lesion Dabrafenib supplier for intestinal type gastric cancer. However, present guidelines such as the updated Sydney System require multiple biopsies whereas reveal an unsatisfactory yield considering the

detection and surveillance of these lesions because of their inconspicuous endoscopic appearance. This study primarily aims at comparing the diagnostic yield of GIM by confocal laser endomicroscopy (CLE) and standard endoscopy in a high risk population. The second objective is to determine if CLE can reduce the biopsy number needed per patient for the detection of GIM in this patient specific population. Methods: Consecutive patients that were scheduled for upper CLE examinations were prospectively recruited. Enrolled subjects were randomized at a 1:1 ratio into group A (Standard white-light endoscopy)

or group B (CLE) by using computer-generated random numbers. In group A, patients received standard white-light endoscopic examination. Random biopsies Idoxuridine following the updated Sydney System (distal antrum + mid corpus + angle; greater/lesser curvature) were performed in addition to targeted biopsies of the endoscopic suspicious lesions. For patients in group B, CLE examinations were performed at endoscopic suspicious lesions and the aforementioned 5 standard areas. Biopsies were taken only in the presence of in vivo mucosal abnormalities including GIM and gastric neoplasia as determined by previously published CLE diagnostic criteria. Results: A total of 168 patients were finally analyzed in this study (85 in group A and 83 in group B). On a per-biopsy analysis, Endomicroscopy targeted biopsies significantly increased the diagnostic yield of GIM as compared to WLE and standard biopsies from 15.

peruvianum is a heterotypic synonym of A. ostenfeldii and this taxon name should be discontinued. Many of the global harmful algal blooms (HABs) are caused by the genus Alexandrium.

A number of species belonging to this genus produce neurotoxic paralytic shellfish poisoning (PSP) toxins (Anderson et al. 2012) that can severely affect human health and marine biota (Wang 2008). PSP toxins account for the majority of harmful events caused by Alexandrium, however other toxin families, such as spirolides, goniodomins, and gymnodimines (Cembella et al. 2000, Hsia et al. 2006, Van Wagoner et al. 2011) have been detected in some species of the genus and may sometimes occur together in one species or Lapatinib concentration strain (Tomas et al. 2012). Alexandrium species are often globally distributed, occurring in a variety of habitats and spanning all geographic zones (Taylor et al. 1995, Lilly et al. 2007, McCauley et al. 2009). The successful colonization and persistence of Alexandrium in diverse environments have been attributed to advantageous ecophysiological adaptations that many members of the genus possess (Anderson

et al. 2012). Within the genus, Balech (1995) classified species that were morphologically distinct, but clearly related, selleck screening library into groups. Molecular trees, showing that the species of the respective groups typically cluster together, generally support such relationships (Scholin et al. 1994, John et al. 2003, Leaw et al. 2005, Orr et al. 2011). However, morphological delineations within the complexes are not always confirmed by molecular

data (Hansen et al. 2003, Lilly et al. 2005, 2007, Penna et al. 2005) suggesting that original taxonomic distinction of the species in the complexes may not reflect evolutionary relationships. One of the groups defined by Balech is the A. ostenfeldii group (Balech 1995), a globally distributed complex Dynein of species known to produce several different potent phycotoxins: PSTs, spirolides, and gymnodimines (Hansen et al. 1992, Cembella et al. 2000, Van Wagoner et al. 2011). Based on their similar morphology, Balech (1995) considered three formally described species, A. ostenfeldii (Paulsen) Balech and Tangen (Paulsen 1904, Balech and Tangen 1985), A. peruvianum (Balech and B.R. Mendiola) Balech and Tangen (Balech and de Mendiola 1977, Balech and Tangen 1985) and Gonyaulax dimorpha Biecheler (Biecheler 1952) to be closely related. All are characterized by large globe shaped cells covered by thin walled thecae that easily collapse. Most importantly, they share a narrow, conspicuously asymmetrical first apical plate exhibiting a definite large ventral pore with varying dimensions. Alexandrium ostenfeldii and A. peruvianum are formally delineated by differences in cell shape and features of the first apical (1′), sulcal anterior (s.a.

Up to 30 %of GenBank HBV genome sequences are recombinations between genotypes (1), a fact that could influence clinical outcomes and antiviral treatment response in chronic HBV (CHB) patients. Our aim was to study the evolution of the HBV genotypic pattern in the absence and presence of lamivudine (LAM) and identify possible genotypic recombinations. METHODS Thirty sequential serum samples from 10 CHB patients failing LAM were included: baseline (BA), after a treatment-free period (TF), and after LAM. In each sample, 2 HBV genome fragments were analyzed by ultra-deep pyrosequenc-ing (GS-FLX, Roche): nucleotides (nt) 1596-1912 (overlapping the X and pre-core [PC] regions) and nt 615-969

(overlapping the polymerase [P] and surface [S] regions). In variants

at frequencies >0.25%, HBV genotype was determined by phylogenesis using an in-house bioinformatics algorithm. RESULTS We obtained 379 438 sequences in the X-PC region and 864 944 BMS-777607 mouse in P-S. Genotype mixtures differed between the two regions (Table), and both regions showed genotype mixture variations over time (BA-TF-LAM), CONCLUSIONS Discrepancies between genotype HM781-36B mouse mixtures in the P-S and X-PC regions suggest inter-genotypic recombination that questions the current classification of HBV genotypes. Changes over time in genotype mixtures evidence the complex dynamics of the HBV quasi-species to adapt to new situations, as was shown by dominant selection of genotype A polymerase after LAM. (1)Weifeng Shi, Virology 2012;427:51-59 Funding: FIS-PI12/1893 (Insti-tuto de Salud Carlos III, European Regional Development Fund) ID: Patient. S-P region (nucleotides [nt] 615-969). X-PC region {nt 1596-1912], in this region genotypes D and E are too similar to be distinguished Tolmetin therefore are classified as D/E. BA: Basal sample; UT: Sample after 1-2 years without treatment,

LAM: Sample after 1-4 years treatment with Lamivudine. *Patient 9-UT: viral load level did not allow ultra-deep pyrosequencing analysis. Disclosures: Rafael Esteban – Speaking and Teaching: MSD, BMS, Novartis, Gilead, Glaxo, MSD, BMS, Novartis, Gilead, Glaxo, Janssen Maria Buti – Advisory Committees or Review Panels: Gilead, Janssen, Vertex, MSD; Grant/Research Support: Gilead, Janssen; Speaking and Teaching: Gil-ead, Janssen, Vertex, Novartis The following people have nothing to disclose: Andrea Caballero, Josep Gregori, Maria Homs, David Tabernero, Maria Blasi, Rosario Casillas, Josep Quer, Leonardo Nieto, Henar Valbuena, Francisco Rodriguez-Frias Background and aim: In HBV infection, interferon and other antiviral drugs can control HBV replication. However it is still difficult to eradicate HBV completely because covalently closed circular DNA (cccDNA) stably remains in the nucleus of hepato-cytes as mini-chromosomes. cccDNA works as a template for transcription for viral mRNAs after removal of nucleoside analogues and viral replication and worsening of hepatitis often occurs.

Compared to healthy controls

or primary biliary cirrhosis patients, PBMCs from PSC patients manifested significantly higher frequencies of Th17 and Th1/Th17 cells after pathogen stimulation. The highest frequencies of Th17 cells were detected after stimulation with Candida albicans, a pathogen that has been linked to disease progression. Immunohistochemically, IL-17A-expressing lymphocytes were detected within the periductal areas of PSC patients. Th17 induction was also noted after stimulation of Toll-like receptor 5 or 7, but not of other pattern recognition selleck chemical receptors tested, pointing to signaling pathways potentially involved in Th17 induction in PSC. Conclusion: We demonstrate an increased Th17 response to microbial stimulation in patients with

PSC. These data should prompt further studies investigating the link between pathogen responses, Torin 1 in vivo inflammation, and fibrosis in patients with PSC. (Hepatology 2013;53:1084–1093) Primary sclerosing cholangitis (PSC) is a chronic liver disease characterized by inflammation and fibrosis of the intrahepatic and/or extrahepatic bile ducts, finally leading to liver cirrhosis and end-stage liver disease.[1] To date, there is no medical treatment with a proven benefit on the progressive course of the disease. A key characteristic of PSC is the association with inflammatory bowel disease (IBD), mostly an ulcerative colitis-like disease, in approximately two thirds of the cases. A dysregulated response to pathogen stimulation may contribute to the immune activation in PSC, as has been postulated for the associated IBD.[2, 3] From the clinical point of view, it is Resveratrol well known that dominant biliary strictures in patients with PSC are associated with bacterial cholangitis, and that bacterial and, especially, fungal cholangitis may accelerate the progression of PSC.[4, 5] A higher rate of positive bacterial cultures could be obtained from bile of explanted livers from PSC patients, as compared to patients with primary biliary

cirrhosis (PBC).[6] In addition, treatment with the antibiotic, metronidazole, resulted in some beneficial effects on liver histology, as compared to treatment with ursodeoxycholic acid (UDCA) alone.[7] T helper (Th)17 cells, which are characterized by the signature cytokine, interleukin (IL)-17A, play an important role in the defense against extracellular bacteria and fungi,[8, 9] particularly at epithelial and mucosal surfaces.[10] Interestingly, functional as well as genetic evidence suggests a role of Th17 cells for the pathogenesis of IBD.[11] Th17 cells have also been implicated in the pathogenesis of several human autoimmune diseases, such as lupus erythematodes, multiple sclerosis, psoriasis, and rheumatoid arthritis.

Moreover, tumors developed from HBx mice exhibited phenotypes of mixed HCC and cholangiocarcinoma (CC) within the same liver. The HCC-like tumors exhibited features of hepatocellular morphologies, whereas CC-like tumors strongly resembled the “cholangiolocellular” subtype described in humans that exhibits poorly differentiated characteristics (Fig. 3B). Staining of tumor Metformin cell line sections with AFP and

CK19 confirmed that the tumors are composed of hepatocytes and cholangiocytes (Fig. 3C). Furthermore, we detected EpCAM+ tumor cells in both HCC and CC tumor tissues (Fig. 3D). The complete penetrance of both tumor types subsequent to HPC expansion suggested that tumors may derive from stem/progenitor cells and supported our hypothesis that HPCs are involved in HBx-induced tumorigenesis. As shown in Fig. 3A, consistent DDC treatment induced bilineage tumors in HBx-expressed livers. The results raised a question if tumors are derived from transformed HPCs. To identify if the bilineage tumor derived from HBx-induced HPCs, we isolated EpCAM+CD45− HPCs from HBx transgenic mice and WT control mice after 1, 2, 3, or 4 months of DCC treatment, respectively. One × 106 cells were then injected subcutaneously into NOD/SCID mice (n = 6). Eight weeks later, EpCAM+CD45− HPCs derived from all WT mice and 1, 2, or 3-month

DDC-treated HBx mice did not produce any tumors, whereas EpCAM+CD45−HPCs Baricitinib CHIR-99021 clinical trial from 4-month DDC-treated HBx mice formed tumor in four out of six mice (Fig. 4A,B). H&E staining and immunohistochemical analysis of AFP and CK19 revealed that these tumors contained mixed cell characteristics (Fig. 4C-E). EpCAM+ cells were also detected in these tumors (Fig. 4F). Therefore, these results demonstrate that chronic injury induced by DDC in the long term (at least 4 months) gradually enhanced the effect of HBx on HPCs and increased

their tumorigenicity potential. Our results have shown that HBx induced expansion of HPCs with increased expression of stemness genes and oncogenes (Fig. 2B). Importantly, HPCs isolated from premalignant HBx mice induced a subcutaneous tumor xenograft (Fig. 4A,B). The question is, what is the mechanism underlying HBx-promoted expansion and transformation of HPCs? To answer the question we analyzed the liver injury, inflammatory response, and signaling pathways during the process of HPC’s response to DCC. To determine if it was because of HBx exacerbated DDC-induced liver injury, we detected the serum alanine aminotransferase (ALT) level and found there was no difference between WT and HBx groups at any timepoint (Fig. 5A), concluding that the degree of liver damage is not associated with HPC proliferation.