The Doors and People Test is particularly well suited for studyin

The Doors and People Test is particularly well suited for studying material-specific long-term memory as contains separate assessments of visual and verbal four-choice recognition memory (Doors and Names subtests, respectively) as well as visual and verbal recall (Shapes and People subtests). The Rey Complex Figure Test provides measures of visual recall following delays of 3 min and 20 min; and the Logical memory subtests provide measures of immediate and delayed verbal recall, and immediate verbal

recognition. These standardized tests have also been used in many previous studies of amnesia, and, therefore, including them here provides a bridge with the literature.

According to the material-specific Pictilisib concentration hypothesis of long-term memory, a double dissociation Galunisertib is predicted, with OG’s right-sided lesion causing a disruption of visual memory and sparing of verbal memory, and SM’s left-sided lesion causing an impairment of verbal memory and sparing of visual memory. Furthermore, we predicted material-specific memory impairments to be evident for both patients in recognition and recall because both had suffered disruption of the perirhinal-mediodorsal thalamic pathway, which subserves recognition, and of the MTT that, as part of the hippocampus-anterior thalamus circuit, subserves recall (Aggleton & Brown, 1999, 2006). Two right-handed male patients (SM and OG) are reported. Patient OG is a right-handed, male of high average intelligence (see Table 2). He was aged 70 at the time of testing. OG enjoys

an active life-style that involves playing bridge a couple of times a week, walking up to 25 miles per week and caring for his grand-children. Prior to his stroke in 2000, he worked as an electrical engineer. The patient has a 30-year history of visual migraine and hypertension. Patient SM is a right-handed male of superior intelligence (see Table 2). He worked as a physician prior to suffering a stroke in 2006. He has now retired from clinical duties, but continues to teach and examine MCE medical students and junior doctors. SM has no premorbid medical history of significance. Both patients’ initials have been changed to preserve anonymity and fully informed written consent was obtained from all participants. The study was approved by North Staffordshire NHS research ethics committee. Because the patients varied in age and IQ, their performance on the tests of memory is compared to separate groups of healthy controls matched to each patient for gender, age, premorbid IQ (National Adult Reading Test, Nelson & Willison, 1991), and current levels of functioning (Wechsler Abbreviated Scale of Intelligence, Wechsler, 1999).

Although analysis of cost effectiveness has not been performed, E

Although analysis of cost effectiveness has not been performed, ERCP has drawbacks in terms of complications. Chromosome 7 contains genes for the epidermal growth factor, c-Met, and interleukin-6, which have been implicated with bile duct

carcinogenesis,25 so that cancers may develop later in these patients, and further study is needed. DeHaan et al.,26 in a study of paraffin-embedded cholangiocarcinoma from PSC patients, observed polysomy Pexidartinib solubility dmso not only in CCA but also in areas that had been interpreted as high-grade dysplasia (HGD).26 HGD of the bile ducts of PSC patients is the morphologic precursor to frank CCA. HGD has been observed to have a level of genetic abnormality by FISH that is similar to in situ and invasive carcinoma in other settings such as Barrett’s esophagus.27, 28 It is likely that the development of CCA in PSC patients is preceded by one or more foci of HGD. It may take months or years for areas of HGD in PSC patients to progress to CCA, and in some cases this progression may not occur. The finding of polysomy in HGD in PSC patients indicates that this genetic alteration is not absolutely specific for CCA in PSC patients. We believe that when polysomy is observed in patients with other

concerning findings (such as a dominant stricture), it has a high positive predictive value for the presence of CCA. However, when such additional clinical findings are not present, the positive predictive value of polysomy for CCA is significantly lower. Polysomy in PSC patients without additional concerning clinical findings should be interpreted more cautiously. Its occurrence in such patients may indicate that they are at higher risk of developing CCA but may not actually have frank CCA. Our results indicate that FISH testing should not be used

as a screening modality in unselected PSC patients undergoing ERCP. However, in patients with clinical or laboratory suspicion of CCA, such as weight loss, abdominal pain, dominant stricture, or high CA 19-9, these tests can be helpful. The analysis of our findings suggests the following guidelines: If a positive trisomy or tetrasomy are obtained without evidence of CCA on imaging, cross-sectional imaging should be repeated 3 months later. If other features such as dominant stricture, prominent 上海皓元 CA 19-9 elevation, or mass are present, cross-sectional imaging and ERCP should repeated at 3 months. These patients should thereafter be followed clinically as are other PSC patients with CA 19-9 levels and ultrasound at 6 months and then annually, as recently shown to be effective.9 The presence of FISH trisomy or tetrasomy does not indicate a high likelihood of CCA. If patients with positive polysomy are not found to have CCA at the initial examination, we would repeat the evaluation after 3 months. According to our Kaplan Meier analysis, patients with positive polysomy very rarely die within 3 months.

This paradox has made deciphering the context in which such behav

This paradox has made deciphering the context in which such behavior would be favored a popular, but contentious, field of inquiry. Indeed, the study of the evolution of eusociality has been plagued by disagreements: over how to describe the

attributes of social groups (Crespi & Yanega, 1995; Ibrutinib research buy Sherman et al., 1995); the level at which selection acts (Wilson, 1975; Foster, Wenseleers & Ratnieks, 2006); and the proper focus of fitness calculations (Taylor, Wild & Gardner, 2007). These arguments continue in the literature to this day (Nowak, Tarnita & Wilson, 2010; Abbot et al., 2011; Boomsma et al., 2011; Bourke, 2011). One challenge in evaluating alternative selective hypotheses for the evolution of eusociality is that eusociality is itself composed of multiple social traits, whose evolutionary history must be properly reconstructed in order to understand the conditions in which they evolved. Traditional models of social evolution posit that initial social groups PS-341 price formed due either to a loss of dispersal (the subsocial

route) or active group formation (the parasocial route). These groups presumably functioned as aggregations, with all individuals producing and caring for their own offspring (Oster & Wilson, 1978). Asymmetries in these behaviors evolved as secondary kin-selected adaptations (Hamilton, 1964), which were then amplified as concentration of reproduction into one or a few individuals released constraints on morphological adaptation to more and more specialized subsets of tasks (West-Eberhard, 1989; Gadagkar, 1997). Thus, to arrive at eusociality from a solitary ancestor required multiple MCE公司 successive evolutionary changes: first, a shift from solitary breeding to either loss of dispersal or group joining; second, a shift from independent to cooperative brood care; and third, a shift from equal reproductive

efforts to cessation of reproduction by some group members. Although this stepwise view follows a logical progression of social structures, the number of evolutionary transitions involved suggests that eusociality should be relatively difficult to evolve, as a multistep process would require adaptive benefits at every stage along the route, not just an adaptive end point. An alternative possibility that avoids this problem is that the evolution of eusociality may have occurred in a single evolutionary step: a shift in dispersal tendency or timing is accompanied by other eusocial traits as an automatic side effect (Michener, 1985; Linksvayer & Wade, 2005; Nowak et al., 2010).


to Ajap-1, Leda-1 localized to the basolateral co


to Ajap-1, Leda-1 localized to the basolateral compartment of the membrane as demonstrated by its location below ZO-1, a cytoplasmic protein that targets tight junctions separating the apical and basolateral compartments in polarized cells (Fig. 7A,C). Furthermore, Leda-1 specifically targeted adherens junctions in MDCK cells, as shown by colocalization with E-cadherin (Fig. 7B,D). These data suggest a role for Leda-1 in cell polarity and adhesion. As LSECs are a prime example of organ-specific Hydroxychloroquine molecular weight EC, this study sought to comprehensively analyze the molecular program underlying microenvironmentally controlled differentiation of LSEC in the liver. Multimodal microvascular gene expression profiling of freshly isolated LSEC versus LMEC and versus LSEC after short-term culture identified an LSEC-specific gene signature of 48 genes that is maintained by the hepatic microenvironment. Vice versa, induction of

a specific set of genes was also demonstrated in cultured LSEC, indicating that LSEC in culture rather undergo a process of transdifferentiation than of mere deterioration. Up-regulation of Esm1 and Cxcr4 in cultured LSEC, genes known to be expressed in lung and tumor EC (TEC),17, 18 in combination with acquisition of cobblestone morphology and reduction in endocytic capacity suggests that LSEC transdifferentiate in vitro toward a continuous MLN2238 EC phenotype. Interestingly,

these changes in culture are mirrored in vivo during sinusoidal capillarization in liver cirrhosis and in hepatocellular carcinoma (HCC), suggesting that related mechanisms could mediate LSEC transdifferentiation 上海皓元 in vivo and in vitro. This notion is further supported by overexpression of Ehd3 in LSEC, a member of the Ehd family of intracellular transport regulators.19 Colocalization of Ehd3 with Stabilin-1, but not Stabilin-2, implies a role for Ehd3 in trafficking of Stabilin-1-positive endosomes in LSEC. In addition, a strong decline in Ehd3 expression was found upon cultivation of LSEC. Interestingly, TEC isolated from rat HCC also showed strong down-regulation of Ehd3 protein as compared to normal LSEC,20 again indicating that the mechanisms that govern LSEC transdifferentiation in culture may also be responsible for pathogenic sinusoidal capillarization as in HCC. As the functional and molecular repertoire of LSEC differs in vivo and in vitro, current LSEC culture models do not allow to adequately study LSEC biology in culture. Experiments to improve LSEC culture,9, 10 however, were evaluated by a very limited set of LSEC markers, i.e., fenestrations and SE antigen/CD32b expression. Our study strongly broadens the knowledge of LSEC-specific genes and thereby allows for a much more sophisticated analysis as well as for further improvement of LSEC culture models.

We therefore conducted a large, pooled, post hoc analysis of pati

We therefore conducted a large, pooled, post hoc analysis of patients with HCV genotypes 1, 4, 5, or 6 from four trials of PEG-IFN alfa-2a and ribavirin therapy to better understand the association between p38 MAPK signaling pathway virologic response and pharmacodynamic effects as reflected by changes in hematologic parameters and body weight. HCV, hepatitis C virus; IFN, interferon; PEG-IFN, pegylated interferon; SVR, sustained virologic response. Patients with HCV genotypes 1, 4, 5, or 6 receiving 24 or 48 weeks of combination therapy with PEG-IFN alfa-2a (Pegasys; Roche, Nutley, NJ; 180 μg/week) and ribavirin (Copegus; Roche, Nutley, NJ; 1,000 or 1,200 mg/day) were pooled from

two registration trials1, 2 and two phase 4 trials.7, 8 The registration trials were randomized, multicenter, phase 3 studies in IFN-naïve patients with chronic hepatitis C; the first trial compared the efficacy of PEG-IFN alfa-2a and ribavirin therapy with IFN alfa-2b and ribavirin therapy for 48 weeks,1 and the second trial of PEG-IFN alfa-2a and ribavirin click here therapy compared different treatment duration and ribavirin dose combinations.2 The phase 4 studies were noncomparative, open-label studies of PEG-IFN alfa-2a

and ribavirin for 48 weeks in treatment-naïve patients with HCV genotype 1; the majority (>73%) of patients in the first study were African American patients,7 and the second study was conducted in Latino and non-Latino Caucasian patients ( Identifier NCT00087607).8 All studies included stopping rules for nonresponse except for the trial in African American patients.7 Patients

who received PEG-IFN monotherapy medchemexpress or IFN alfa-2b and ribavirin combination therapy (Rebetron) and patients with HCV/human immunodeficiency coinfection were excluded from the study. The objectives of this study were: (1) to explore the association between pharmacodynamic parameters and virologic response category (SVR, relapse, breakthrough, and nonresponders); (2) to explore the association between pharmacodynamic parameters and race/ethnicity (African American, Latino Caucasians, non-Latino Caucasians, and other races); and (3) to evaluate the effects of clinically significant hemoglobin decline (>3 g/dL versus ≤3 g/dL) on SVR. The pharmacodynamic effects of interest in this analysis were hematologic parameters (hemoglobin level, neutrophil count, and platelet count) and weight loss. Maximum decrease (baseline value for the hematologic test minus the lowest value for that test while on therapy) was used to assess the change in hematologic parameters. To better adjust for the impact of baseline difference, percentage of change from baseline was used to analyze racial/ethnic group differences and body weight changes. For patients without the specified hematologic test or body weight measurement during treatment, the corresponding maximum decrease was set as missing.

Similarly, a higher SVR rate was identified for TT and CC carrier

Similarly, a higher SVR rate was identified for TT and CC carriers with low versus high IP-10 (TT, 48% versus 20%; CC, 89% versus 79%). IL28B genotype and baseline IP-10 levels were additive but independent when predicting SVR in both AA and CA patients. Conclusion:

When IL28B genotype is combined with pretreatment serum IP-10 measurement, the predictive value for discrimination between SVR and nonresponse is significantly improved, especially in non-CC genotypes. This relationship warrants further click here investigation to elucidate the mechanisms of antiviral response and prospective validation. (Hepatology 2011;) Hepatitis C virus (HCV) is a single-stranded RNA virus that usually establishes persistent infection in its host. Neratinib research buy Among patients exposed to HCV, approximately 80% will develop chronic viral infection characterized by liver infiltration of HCV-specific and nonspecific T cells accompanied by proinflammatory cytokines resulting in damage to virus-infected, as well as bystander hepatocytes with resultant fibrosis formation. Approximately 30%-35% of patients will develop cirrhosis, and once a patient has cirrhosis, there is a 1%-4% annual rate of hepatocellular carcinoma development.1 Combined treatment with peginterferon (PEG-IFN) and ribavirin achieves sustained virological response (SVR) in 42%-52% of genotype 1 patients.2-4 Unfortunately, the remainder either fail to respond, or must discontinue treatment prematurely

due to adverse events. Response rates to PEG-IFN and ribavirin are associated with both viral and host factors. Pretreatment predictors of nonresponse include

genotype 1 infection, high viral load (>800,000 IU/mL), advanced fibrosis or cirrhosis, high body mass index, age >40 years, and African American race.2-4 Currently, on-treatment predictors of response to PEG-IFN and ribavirin include viral kinetics at weeks 4 and 12. Patients who do not attain an early virological response have only a 1%-3% chance of viral clearance, and therapy is usually halted.2, 5 Conversely, 87% of patients who achieve a rapid virological medchemexpress response (defined as HCV RNA undetectable at week 4 of therapy) achieve SVR.6 Although viral kinetics have proven useful, better predictors of SVR and nonresponse would be helpful to identify patients with the best chance of response before the initiation of combination antiviral therapy. The United States population has proven to be a more difficult group to treat than many others with lower SVR rates, perhaps due in part to higher body mass index and a greater racial variation. African Americans (AA) harbor predominantly genotype 1 virus and have notably lower overall response rates to PEG-IFN and ribavirin (≈26%-28%) compared with Caucasian Americans (CA).7-9 Determining why AA patients respond less well to antiviral therapy with PEG-IFN and ribavirin compared with CA patients was the focus of the Study of Viral Resistance to Antiviral Therapy of Chronic Hepatitis C (VIRAHEP-C).

Hepatic Vein Arrival Time (HVAT), ie the time an ultrasound con

Hepatic Vein Arrival Time (HVAT), i.e. the time an ultrasound contrast agent reaches the hepatic vein after intravenous injection, was found to be lower in cirrhotic patients. Transient elastography measures the speed of propagation of elastic waves through the liver, such that fibrotic livers generate higher liver stiffness measurements. Aim of this study was

to correlate liver stiffness with data obtained by Contrast-Enhanced UltraSound (CEUS) of the liver. Thirty consecutive patients affected by virus related chronic liver diseases were enrolled. After a standard B-Mode and Doppler examination, a bolus injection of 2.5 ml of Sonovue®

(Bracco Talazoparib order SpA, Milan, Italy) was injected intravenously Selleck Osimertinib followed by a saline flush. Using an ultrasound machine built-in contrast software, the intensity of a main hepatic vein was recorded from 20 seconds before (the basal enhancement trace) to 2 minutes after SonoVue® injection and we evaluated: the Hepatic Vein Arrival Time (HVAT), the Time To Peak (TTP) and the peak of contrast enhancement. Liver stiffness measurements were performed by FibroScan® (Echosens, Paris, France) by experienced operators. All patients were measured using the 3.5 MHz standard M probe. The final liver stiffness result was expressed in kPa and was the median value of 10 measurements. No side effects related both to SonoVue® injection and to FibroScan® examination were observed. Spearmann’s coefficient of rank correlation between HVAT and liver stiffness was observed to be −0,399 (95% Confidence interval −0,664 to −0,0453, p<0.05), thus confirming the hypothesis that

fibrotic livers showed lower HVATs and higher values of liver stiffness. 上海皓元医药股份有限公司 No significant correlation was observed among liver stiffness and TTP or the peak of contrast enhancement. When endoscopic signs of portal hypertension (such as oesophageal varices or hypertensive gastropathy) were assumed to be as the gold standard of liver cirrhosis, Receiver Operating Curves (ROC) analysis demonstrated liver stiffness to have the best accuracy in diagnosing liver cirrhosis with respect to HVAT (Area Under the ROC [AUROC]: 0.972 vs. 0.781). Combining liver stiffness ≤ 12.5 kPa and HVAT ≥ 18 seconds we reached 100% specificity for the diagnosis of liver cirrhosis. Earlier HVATs and higher values of liver stiffness can be observed during the progression of liver diseases.

Together with improvements of the killed bacteria formulation, th

Together with improvements of the killed bacteria formulation, this vaccine may show superior characteristics in future clinical trials. Hickey et al. [74] followed a different approach and tested transcutaneous vaccine delivery of a bacterial lysate formulated with a lipid mixture and CpG oligonucleotides as a further immune stimulants. This vaccine reduced H. pylori burdens in mice roughly by one to two orders of magnitude. It induced high levels of specific secretory IgA but comparatively little serum IgG, an interesting aspect given that Ig may be counter-protective.

In summary, vaccine development against H. pylori remains a focus of research. Progress is made but is incremental. There is need for a still better understanding of the protective Dorsomorphin mechanism and for improving efficacy. It will also be necessary to evaluate gain by protection versus the alleged danger of the same immune mechanism contributing to disease. Further clinical studies may help to avoid blurring this important issue by incongruent animal models. The authors thank Lesley A. Ogilvie, Bianca Bauer and Manuel Koch for helpful and insightful comments on the manuscript. This work was supported by a Grant of the Deutsche Forschungsgemeinschaft to TA and TFM in the framework of the Ruxolitinib purchase Sonderforschungsbereich 633 “Induktion und Modulation T-zellvermittelter Immunreaktionen im Gastrointestinaltrakt”. The authors declare no conflict of interest. “

Low Helicobacter pylori eradication rates are common in pediatric trials especially in developing countries. The aim of the study was to investigate the role of antibiotic resistance, drug dosage, and administration frequency on treatment outcome for children in Vietnam. Materials and Methods:  Antibiotics resistance of H. pylori was analyzed by the Etest in 222 pretreatment isolates from children 3–15 years of age who were originally recruited in a randomized trial with two treatment

regiments: lansoprazole with amoxicillin and either clarithromycin (LAC) or metronidazole (LAM) in two weight groups with once- or twice-daily administration. The study design was an observational study embedded in a randomized trial. Results:  The overall resistance to clarithromycin, metronidazole, and amoxicillin was 50.9%, 65.3%, and 0.5%, respectively. In LAC, eradication was linked to the strains being 上海皓元 susceptible to clarithromycin (78.2% vs 29.3%, p = .0001). Twice-daily dosage of proton-pump inhibitor (PPI) and clarithromycin was more effective for eradication than once-daily dosage for resistant strains (50.0% vs 14.7%, p = .004) and tended to be so also for sensitive strains (87.5% vs 65.2%, p = .051). Exact antibiotic dose per body weight resulted in more eradication for resistant strains (45.3% vs 8.0%, p = .006). These differences were less pronounced for the LAM regimen, with twice-daily PPI versus once daily for resistant strains resulting in 69.2% and 50.

However, familial, epidemiological, and twin studies have suggest

However, familial, epidemiological, and twin studies have suggested that inherited factors may also play a pivotal role in determining the susceptibility to developing NASH.11-14 Single nucleotide polymorphisms (SNPs) in genes Lumacaftor in vitro involved in inflammation, insulin signaling, oxidative

stress, and fibrogenesis have been associated with the severity of liver damage in NAFLD,15-18 but these factors explain only a small portion of fibrosis variability. Recently, genome-wide association studies have identified as a strong determinant of liver fat an SNP in adiponutrin/patatin-like phospholipase domain-containing 3 (PNPLA3), rs738409 C>G, which encodes the I148M protein variant.19-21 The I148M SNP influences liver fat without affecting the body mass, dyslipidemia, or insulin resistance. Adiponutrin expression in the liver and adipose tissue is increased by carbohydrate feeding and a Western-type diet.22-24 Furthermore, it has lipase activity against triglycerides and thus is likely involved in energy mobilization and storage in lipid droplets.25 It has been reported that the 148M PNPLA3 allele is a loss-of-function variant that predisposes patients to steatosis by decreasing triglyceride hydrolysis in hepatocytes.26 We recently showed that the rs738409 PNPLA3 SNP was strongly associated

with severe steatosis, NASH, and the progression of liver fibrosis in a large series of Italian and UK patients with NAFLD.27 However, even though genetic factors Ensartinib order likely play a stronger role in NASH development in children, no data are available concerning the role of the PNPLA3 genotype in this setting. The aim of this study was to evaluate whether the rs738409 PNPLA3 SNP, encoding the functional I148M protein

variant, is associated with a predisposition to NASH and progressive liver fibrosis in a large series of Italian pediatric patients with a histological diagnosis of NAFLD and may represent a noninvasive early marker of advanced disease. ALT, alanine aminotransferase; AST, aspartate aminotransferase; BMI, body mass index; CI, confidence interval; GGT, gamma-glutamyl transferase; HOMA-IR, homeostasis model assessment of insulin resistance; IGT, impaired glucose tolerance; NAFLD, nonalcoholic fatty liver disease; NASH, nonalcoholic steatohepatitis; NS, not significant; MCE公司 OR, odds ratio; PNPLA3, patatin-like phospholipase domain-containing 3; SD, standard deviation; SNP, single nucleotide polymorphism. This prospective study included 149 consecutive untreated children and adolescents (93 males and 56 females) with biopsy-proven NAFLD who were referred to Bambino Gesù Children’s Hospital between May 2006 and November 2009. All patients were tested for secondary causes of steatosis such as alcohol abuse (≥140 g/week), total parenteral nutrition, and the use of drugs known to precipitate steatosis (e.g., valproate, amiodarone, and prednisone).

,60 who observed in B-cell-specific TNF-α−/− mice a markedly redu

,60 who observed in B-cell-specific TNF-α−/− mice a markedly reduced promotion of the HPV16 SCC model and a modulation of B10 cell activity. Collectively, these studies suggest a significant tumor-promoting role for B cells

during carcinogenesis. Chronic liver injury, inflammatory pathway activation, and oxidative stress intersect within the context of the uniquely tolerant liver microenvironment, thus facilitating hepatic oncogenesis. This review emphasizes the dynamic juncture of inflammation and oncogenesis, highlighting the critical players and immunological therapeutic targets, and suggesting areas for further research. “
“Background and Aim:  The incidence of hepatocellular carcinoma (HCC) has increased in Australia in recent decades, a large and growing proportion of which occurs

among a population Palbociclib chronically infected with hepatitis B virus (HBV) or hepatitis C virus (HCV). However, risk factors for HCC among these high-risk groups require further characterization. Methods:  We conducted a population-based cohort study using HBV and HCV cases notified to the New South Wales Health Department between 2000 and 2007. These were linked to cause of death data, HIV/AIDS notifications, and hospital records. Proportional hazards regression was used to identify significant risk Selleck Decitabine factors for developing HCC. Results:  A total of 242 and 339 HCC cases were linked to HBV (n = 43 892) and HCV (n = 83 817) notifications, respectively. For both

HBV and HCV groups, being male and increasing age were significantly associated with risk of HCC. Increasing comorbidity score indicated high risk, while living outside urban areas was associated with lower risk. Hazard ratios for males were two to three times those of females. For both HBV and HCV groups, cirrhosis, alcoholic liver disease, and the interaction between the two were associated with significantly and considerably elevated risk. Conclusion:  This large population-based study confirms known risk factors for HCC. The association with older age highlights the potential impact of HBV and HCV screening of at-risk groups and early clinical assessment. Additional research is required to evaluate the impact of improving antiviral therapy on HCC risk. “
“Lipopolysaccharide (LPS)-induced 上海皓元 liver injury in D-galactosamine (D-Gal)-sensitized mice is a well-established animal model widely used in exploring the pathogenesis of fulminant hepatitis. Increasing evidence has indicated that reactive oxygen species (ROS)-induced oxidative injury may be involved in LPS/D-Gal-induced hepatitis. Catalase (CAT) is a major antioxidant enzyme while aminotriazole (ATZ) is commonly used as a CAT inhibitor. In the present study, the effects of ATZ on LPS/D-Gal-induced liver injury were investigated. Fuliminant liver injury was induced by intraperitoneal injection of LPS combined with D-Gal, ATZ was administrated 0.5 h prior to LPS/D-Gal challenge.