Taxonomic analysis of H. bilis strains isolated from dogs and cats showed two different genomic groups to be present with a suggested independent evolution that the authors VX-809 clinical trial proposed might be referred as two genomospecies: H. bilis sensu stricto and Helicobacter sp. ‘FL56’ [39]. Induction of differential gene expression profiles in the intestinal mucosa due to H. bilis colonization was studied using microarray analysis in defined-flora mice experimentally colonized with H. bilis (ATCC 51630). Up- or downregulation of genes involved in different functions was suggested

to potentially predispose the host to the development of typhlocolitis [40]. Chaouche-Drider et al. conducted in vitro coculture studies using a murine cell line (m-ICcl2) and H. hepaticus, H. bilis or H. muridarum and showed that each of these species induced increased gene expression of CxclI and Cxcl2, with H. bilis and H. muridarum stimulating check details the highest mRNA levels. Further investigation in HEK293 and AGS cells lines, neither of which expresses functional TLR2 or TLR4, showed that live H. muridarum had a dramatic effect on NF-KB reporter activity in HEK293 cells. The possibility that H. muridarum may confound studies in colitis mouse models was raised [41]. Finally, based on identification of 104 candidate structured RNAs from genome and metagenome sequences of bacteria and archaea,

a newly identified cis-regulatory RNA was reported to be implicated in Helicobacter gastric infection [42]. The authors suggest that biochemical and genetic investigations are required to validate the biologic functions of the identified structured RNAs. In vitro and in vivo experiments have demonstrated the

bacteriostatic and bactericidal effects of green tea against H. felis and H. pylori, as well as its ability to prevent gastric mucosal inflammation in mice when consumed prior to Helicobacter exposure [43]. Another study that evaluated the effect of dietary L-glutamine supplementation on the intestinal microbiota and mortality of postweaned rabbits reported a reduced frequency of PCR-RFLP detection of intestinal bacterial species including Helicobacter selleck inhibitor sp. as well as reduced mortality because of epizootic rabbit enteropathy [44]. Based on the International Council for Laboratory Animal Science Animal Quality Network Program, the “Performance Evaluation Program” was designed to assist animal diagnostic laboratories in assessing their monitoring methods. The results of the first trial in the developmental phase of this program showed the successful assessment of pathogens including Helicobacter spp. [45]. A novel immunoblot analysis was developed to monitor H. bilis, H. hepaticus, and Helicobacter ganmani infections in laboratory rodents, showing promising results after its comparison with PCR-DGGE [46]. Fukuda et al. [47] reported the development of a novel antigen capture ELISA assay for the detection of H. hepaticus using a monoclonal antibody HRII-51, which showed 87.

Conclusion:  Our results indicate that a special group of miRNAs may play an important role in human fetal liver development, while their

roles in the adult livers are limited. “
“Nonalcoholic steatohepatitis (NASH) is a serious liver disease associated with obesity. Characterized by metabolic syndrome, hepatic steatosis, and liver inflammation, NASH is believed to be under the influence of the gut microflora. Here, the composition of gut bacterial communities of NASH, obese, and healthy children was determined by 16S ribosomal RNA pyrosequencing. In addition, ZVADFMK peripheral blood ethanol was analyzed to monitor endogenous ethanol production of patients and healthy controls. UniFrac-based principle coordinates analysis indicated that most of the microbiome samples clustered by disease status. Each group was associated with a unique pattern of enterotypes. Differences were abundant at phylum, family, and genus levels between healthy subjects and obese patients (with or without NASH), and relatively fewer differences were observed between obese and the NASH microbiomes. Among those taxa with greater than 1% representation

in any of the disease groups, Proteobacteria, Enterobacteriaceae, and Escherichia were the only phylum, family and genus types exhibiting significant difference between obese and NASH microbiomes. Similar blood-ethanol concentrations were observed PD0325901 between healthy subjects and obese non-NASH patients, but NASH patients exhibited significantly elevated blood ethanol levels. Conclusions: The increased abundance of alcohol-producing bacteria in NASH microbiomes, elevated blood-ethanol concentration in NASH patients, and the well-established role of alcohol learn more metabolism in oxidative stress and, consequently, liver inflammation suggest a role for alcohol-producing microbiota in the pathogenesis of NASH. We postulate that the distinct composition of the gut microbiome among NASH, obese, and healthy controls could offer a target for intervention or a marker for disease. (HEPATOLOGY 2013) Nonalcoholic fatty

liver disease (NAFLD), the hepatic manifestation of metabolic syndrome, is the most common cause of elevated liver enzymes in the United States.1 NAFLD with inflammation and fibrosis is known as nonalcoholic steatohepatitis (NASH) because it resembles alcoholic liver disease (ALD) without a history of alcohol ingestion.2 The incidence of NASH has been increasing over the past 20 years.3 In the United States, the current prevalence of NAFLD and NASH could be as high as 46% and 12%, respectively.4 Without an effective available treatment, the prognosis of NASH is not optimistic. NASH is responsible for approximately 10% of liver transplants in the United States and is projected to become the most common indication for liver transplantation in the near future.

Conclusion:  Our results indicate that a special group of miRNAs may play an important role in human fetal liver development, while their

roles in the adult livers are limited. “
“Nonalcoholic steatohepatitis (NASH) is a serious liver disease associated with obesity. Characterized by metabolic syndrome, hepatic steatosis, and liver inflammation, NASH is believed to be under the influence of the gut microflora. Here, the composition of gut bacterial communities of NASH, obese, and healthy children was determined by 16S ribosomal RNA pyrosequencing. In addition, LBH589 ic50 peripheral blood ethanol was analyzed to monitor endogenous ethanol production of patients and healthy controls. UniFrac-based principle coordinates analysis indicated that most of the microbiome samples clustered by disease status. Each group was associated with a unique pattern of enterotypes. Differences were abundant at phylum, family, and genus levels between healthy subjects and obese patients (with or without NASH), and relatively fewer differences were observed between obese and the NASH microbiomes. Among those taxa with greater than 1% representation

in any of the disease groups, Proteobacteria, Enterobacteriaceae, and Escherichia were the only phylum, family and genus types exhibiting significant difference between obese and NASH microbiomes. Similar blood-ethanol concentrations were observed find more between healthy subjects and obese non-NASH patients, but NASH patients exhibited significantly elevated blood ethanol levels. Conclusions: The increased abundance of alcohol-producing bacteria in NASH microbiomes, elevated blood-ethanol concentration in NASH patients, and the well-established role of alcohol see more metabolism in oxidative stress and, consequently, liver inflammation suggest a role for alcohol-producing microbiota in the pathogenesis of NASH. We postulate that the distinct composition of the gut microbiome among NASH, obese, and healthy controls could offer a target for intervention or a marker for disease. (HEPATOLOGY 2013) Nonalcoholic fatty

liver disease (NAFLD), the hepatic manifestation of metabolic syndrome, is the most common cause of elevated liver enzymes in the United States.1 NAFLD with inflammation and fibrosis is known as nonalcoholic steatohepatitis (NASH) because it resembles alcoholic liver disease (ALD) without a history of alcohol ingestion.2 The incidence of NASH has been increasing over the past 20 years.3 In the United States, the current prevalence of NAFLD and NASH could be as high as 46% and 12%, respectively.4 Without an effective available treatment, the prognosis of NASH is not optimistic. NASH is responsible for approximately 10% of liver transplants in the United States and is projected to become the most common indication for liver transplantation in the near future.

As shown in Fig. 5A, TZM cells cocultured with HIV-infected HSCs showed a significant increase in luciferase activity versus coculture with mock-infected HSCs. To further confirm this finding, HSCs were

infected with the HIV-GFP–expressing constructs, washed, trypsinized, and subsequently cultured with MT4 lymphocytes (Fig. 5B). Over time, MT4 cells became infected with HIV, which was blocked by AZT. Selleckchem Z-VAD-FMK These results indicate that HSCs are able to capture HIV and transfer viable virus to surrounding lymphocytes. Given that most of the viral particles released in culture supernatants were defective and unable to infect cells, this phenomena appears to require cell–cell contact and potentially occurs through a virological synapse, as demonstrated for other cells,20 and thus requires further investigation. HIV/HCV coinfection is associated with rapid fibrosis progression and increased necro-inflammatory activity on biopsy compared with HCV monoinfected patients.4 Therefore, we hypothesized that direct effects of HIV on HSCs may contribute to these clinical observations. Because HSC expression of collagen I is critical to fibrosis, we examined whether HIV infection of HSCs results in increased expression H 89 mouse of collagen I. As shown in Fig. 6A, a greater than two-fold increase in collagen I expression

by HSCs was observed 48 hours after HIV infection. Chronic inflammation is important for activation of HSCs and fibrogenesis. Because MCP-1 is a potent chemoattractant for

monocytes and lymphocytes, is up-regulated during chronic hepatitis, and correlates with the number of cells infiltrating the portal tract,21 we examined whether HIV stimulates the HSC secretion of MCP-1. An average 80-fold increase in MCP-1 secretion was observed 48 hours after HIV infection (Fig. 6B). Therefore, HIV may have both profibrogenic and proinflammatory effects on HSCs. HIV/HCV-coinfected patients have accelerated fibrosis progression rates compared with HCV-monoinfected patients with the development of cirrhosis 12-16 years earlier.4, 22 Moreover, HIV/HCV-coinfected patients with ongoing HIV viremia have faster rates of HCV-related click here fibrosis progression,7 suggesting an accelerating effect of HIV on fibrosis progression. When HIV is successfully suppressed with HAART, fibrosis progression rates and necro-inflammatory activity are reduced, closely resembling HCV-monoinfected patients. These observations reinforce the role of HIV in promoting inflammation and fibrosis in HIV/HCV-coinfected livers. The molecular mechanisms by which HIV accelerates fibrosis are not clearly understood, and direct HIV infection of activated HSCs, the main fibrogenic cell in the liver, has not been reported. In the present study, we provide some insight into potential molecular mechanisms by which HIV, through its effects on activated HSCs, can accentuate liver injury in chronic liver diseases.

As shown in Fig. 5A, TZM cells cocultured with HIV-infected HSCs showed a significant increase in luciferase activity versus coculture with mock-infected HSCs. To further confirm this finding, HSCs were

infected with the HIV-GFP–expressing constructs, washed, trypsinized, and subsequently cultured with MT4 lymphocytes (Fig. 5B). Over time, MT4 cells became infected with HIV, which was blocked by AZT. Roxadustat cell line These results indicate that HSCs are able to capture HIV and transfer viable virus to surrounding lymphocytes. Given that most of the viral particles released in culture supernatants were defective and unable to infect cells, this phenomena appears to require cell–cell contact and potentially occurs through a virological synapse, as demonstrated for other cells,20 and thus requires further investigation. HIV/HCV coinfection is associated with rapid fibrosis progression and increased necro-inflammatory activity on biopsy compared with HCV monoinfected patients.4 Therefore, we hypothesized that direct effects of HIV on HSCs may contribute to these clinical observations. Because HSC expression of collagen I is critical to fibrosis, we examined whether HIV infection of HSCs results in increased expression BMS-907351 manufacturer of collagen I. As shown in Fig. 6A, a greater than two-fold increase in collagen I expression

by HSCs was observed 48 hours after HIV infection. Chronic inflammation is important for activation of HSCs and fibrogenesis. Because MCP-1 is a potent chemoattractant for

monocytes and lymphocytes, is up-regulated during chronic hepatitis, and correlates with the number of cells infiltrating the portal tract,21 we examined whether HIV stimulates the HSC secretion of MCP-1. An average 80-fold increase in MCP-1 secretion was observed 48 hours after HIV infection (Fig. 6B). Therefore, HIV may have both profibrogenic and proinflammatory effects on HSCs. HIV/HCV-coinfected patients have accelerated fibrosis progression rates compared with HCV-monoinfected patients with the development of cirrhosis 12-16 years earlier.4, 22 Moreover, HIV/HCV-coinfected patients with ongoing HIV viremia have faster rates of HCV-related this website fibrosis progression,7 suggesting an accelerating effect of HIV on fibrosis progression. When HIV is successfully suppressed with HAART, fibrosis progression rates and necro-inflammatory activity are reduced, closely resembling HCV-monoinfected patients. These observations reinforce the role of HIV in promoting inflammation and fibrosis in HIV/HCV-coinfected livers. The molecular mechanisms by which HIV accelerates fibrosis are not clearly understood, and direct HIV infection of activated HSCs, the main fibrogenic cell in the liver, has not been reported. In the present study, we provide some insight into potential molecular mechanisms by which HIV, through its effects on activated HSCs, can accentuate liver injury in chronic liver diseases.

Hepatocellular (HC) type (74.2%) was the most common, followed by cholestatic (CS) type (19.2%) and mixed

type (6.6%). Compared with group CS/MIXED, the patients in group HC had higher serum levels of ALT and CHE (P < 0.05), but lower serum levels of GGT, ALP, TBIL, DBIL and TBA (P < 0.05). The type of DILD and level of TBA were important factors determing the prognosis. The patients with hepatocelluar type liver injury and higher TBA level were more likely to become chronic DILD. Conclusion: Hepatocelluar type is most common clinical type of DILD. Herbal medicine was most common cause of DILD. Cholestataic or mixed type liver injuries or higher TBA are associated with development of chronicity. Key Word(s): 1. DILD; 2. Clinical feature; 3. Chronic DILD; Presenting Author: BOWAN LAN Corresponding Author: BOWAN LAN Affiliations: The First Affiliated Hospital of Harbin Medical see more University Objective: To investigate the mechanism that the Bone marrow stromal stem cells (BMSCs) can secrete adrenomedullin (AM) to treat liver fibrosis. Methods: Bone marrow stromal stem cells (BMSCs) were isolated check details and harvested from Bone marrow in SD rats, weighing from 110 to 120 g, by their adherence capacity and cells were then amplified. The cells phenotype were analyzed by flow cytometry assay. CFSCs were generously gifted directly

by the Department of Neurobiology, Harbin Medical University. The secretion of AM in the supernatants of different culture passages of BMSCs were determined by ELISA analysis. We selected the culture supernatants of the third passage of BMSCs with relatively large number of AM as the experimental target. CFSCs were the control group. The co-culture system were set up with BMSCs + CFSCs and BMSCs + CFSCs +CGRP8–37, an AM/CGRP receptor antagonist, as experimental group. Activated HSCs (CFSCs) express a-smooth muscle actin

(a-SMA) and produce an excess of collagen protein type I (Collagen-I). The a-SMA was the essential mark of CFSCs and Collagen-I was the essential component of hepatic cell extracellular matrix when hepatic fibrosis and hepatic cirrhosis. Fluorescence selleckchem immunocytochemistry analysis and Western-blot analysis were used to test the expression of a-SMA and Collagen-I. p47-phox were assessed by Western blot to analyze the expression of inflammation. Results: AM was a paracrine factor of BMSCs. In the supernatants of different culture passages of BMSCs, the expression of AM continued to be at significantly higher levels in P1-P6. In the co-culture system of BMSCs + CFSCs, α-SMA, Collagen-I and p47-phox had significantly lower expression levels compared with Control. This effect was significantly blocked by CGRP8–37, an AM/CGRP receptor antagonist, and the therapeutic effect of BMSCs was significantly reduced. Conclusion: AM was a paracrine factor of BMSCs.

45,55,56 The combination of pANCA+ and ASCA- test may occasionally be helpful in differentiating UC from CD, with improved specificity to 94.3% but lower sensitivity of only 51.3%. In the pediatric population an improved sensitivity of up to 70% was observed.45 The extent of the disease of UC in the Asia Pacific region is similar to that in the West. The extent of disease should be described as proctitis, left sided colitis DAPT ic50 and extensive colitis (Montreal classification—E1, E2, E3). Level of agreement: a-94%, b-6%, c-0%, d-0%, e-0% Quality of evidence: II-2 Classification of recommendation: B Studies from the Asia-Pacific region included

those from South Korea, Japan, Thailand, China, Hong Kong, Singapore and Malaysia attest to fairly similar disease presentation in terms of extent.57–63 Western data from Olmsted county(USA), Norwegian, New Zealand and Australian populations were in keeping with the presentation noted in Asia-Pacific.55,64–66 For purposes of future data collection, the group agreed that the extent of disease should follow the Montreal classification for uniformity. Colonoscopy with ileoscopy and biopsies is preferred over barium enema in the evaluation of extent and severity of UC Level of agreement: Luminespib a-88%, b-6%, c-6%, d-0%,

e-0% Quality of evidence: II-3 Classification of recommendation: B Many studies showed the utility of biopsies to distinguish UC from other colitides.7,67–69 They also show the superiority of colonoscopy and biopsies selleck kinase inhibitor in determining extent and severity.19,68,69 The group agrees with the ASGE 2006 guidelines that colonoscopy and ileoscopy with biopsies are required to evaluate IBD and are useful to differentiate UC from CD. It is important to perform abdominal X-ray (AXR) to exclude toxic megacolon in severe UC Level of agreement:

a-94%, b-6%, c-0%, d-0%, e-0% Quality of evidence: II-3 Classification of recommendation: B There was good agreement that AXR should be done to exclude the complications of toxic megacolon in severe attacks of UC.70,71 The group recognises that serial AXRs are also important in the management of acute severe attacks. Computerized tomographic (CT) scan of the abdomen may also play a role in excluding toxic megacolon. The assessment of UC severity is based on a combination of clinical features (fever, number of liquid stools, bleeding, abdominal pain), vital signs, functional status and objective assessment (laboratory endoscopic features). Level of agreement: a-47%, b-47%, c-6%, d-0%, e-0% Quality of evidence: III Classification of recommendation: C Many activity indexes have been formulated to standardize methods for assessing the activity of disease. These indexes may employ clinical characteristics alone, or with laboratory and/or endoscopic information. Except for a few, many of these indexes have not been validated.

45,55,56 The combination of pANCA+ and ASCA- test may occasionally be helpful in differentiating UC from CD, with improved specificity to 94.3% but lower sensitivity of only 51.3%. In the pediatric population an improved sensitivity of up to 70% was observed.45 The extent of the disease of UC in the Asia Pacific region is similar to that in the West. The extent of disease should be described as proctitis, left sided colitis Selleckchem Pictilisib and extensive colitis (Montreal classification—E1, E2, E3). Level of agreement: a-94%, b-6%, c-0%, d-0%, e-0% Quality of evidence: II-2 Classification of recommendation: B Studies from the Asia-Pacific region included

those from South Korea, Japan, Thailand, China, Hong Kong, Singapore and Malaysia attest to fairly similar disease presentation in terms of extent.57–63 Western data from Olmsted county(USA), Norwegian, New Zealand and Australian populations were in keeping with the presentation noted in Asia-Pacific.55,64–66 For purposes of future data collection, the group agreed that the extent of disease should follow the Montreal classification for uniformity. Colonoscopy with ileoscopy and biopsies is preferred over barium enema in the evaluation of extent and severity of UC Level of agreement: Galunisertib datasheet a-88%, b-6%, c-6%, d-0%,

e-0% Quality of evidence: II-3 Classification of recommendation: B Many studies showed the utility of biopsies to distinguish UC from other colitides.7,67–69 They also show the superiority of colonoscopy and biopsies selleck kinase inhibitor in determining extent and severity.19,68,69 The group agrees with the ASGE 2006 guidelines that colonoscopy and ileoscopy with biopsies are required to evaluate IBD and are useful to differentiate UC from CD. It is important to perform abdominal X-ray (AXR) to exclude toxic megacolon in severe UC Level of agreement:

a-94%, b-6%, c-0%, d-0%, e-0% Quality of evidence: II-3 Classification of recommendation: B There was good agreement that AXR should be done to exclude the complications of toxic megacolon in severe attacks of UC.70,71 The group recognises that serial AXRs are also important in the management of acute severe attacks. Computerized tomographic (CT) scan of the abdomen may also play a role in excluding toxic megacolon. The assessment of UC severity is based on a combination of clinical features (fever, number of liquid stools, bleeding, abdominal pain), vital signs, functional status and objective assessment (laboratory endoscopic features). Level of agreement: a-47%, b-47%, c-6%, d-0%, e-0% Quality of evidence: III Classification of recommendation: C Many activity indexes have been formulated to standardize methods for assessing the activity of disease. These indexes may employ clinical characteristics alone, or with laboratory and/or endoscopic information. Except for a few, many of these indexes have not been validated.

M-CSF-Mφ and IL-34-Mφ also express the hepatic stellate cell (HSC) activators, platelet-derived growth factor, transforming growth factor beta, and galectin-3. IL-34-Mφ and M-CSF-Mφ induce type I collagen synthesis by HSCs, the main

collagen-producing cells in liver fibrosis. IL-13, whose expression correlates with the fibrosis stage in HCV-infected patients, decreases the expression of the collagenase, matrix metalloproteinase 1, by IL-34-Mφ and M-CSF-Mφ, thereby enhancing collagen synthesis. By inhibiting the production of interferon-gamma (IFN-γ) by activated natural killer cells, IL-34-Mφ and M-CSF-Mφ prevent the IFN-γ-induced killing of HSCs. Conclusion: These results identify M-CSF and IL-34 as potent profibrotic factors in HCV liver fibrosis. (Hepatology 2014;60:1878–1889) “
“Over the last decade, GSI-IX in vitro a wealth of data has emerged illustrating both the rather benign clinical course of nonalcoholic fatty liver disease (NAFLD) in many individuals, and the unfavorable prognosis of this condition in others. Several studies on long-term mortality of patients suffering from NAFLD confirmed by imaging and/or liver biopsy have been reported. Studies with an average follow-up of at

least 5 Palbociclib solubility dmso years are summarized in Table 1.1–10 Compared to the general population of same age and gender, NAFLD is associated with a significantly higher overall mortality1, 2, 4 and liver-related mortality.1, 2 The long-term prognosis of patients with NAFLD, however, find more varies across the disease stage. Although the terms simple steatosis and nonalcoholic steatohepatitis (NASH) are often used in studies on long-term prognosis

to classify patient risk, differing definitions have been used across the studies. Despite that, however, some conclusions can be derived from pooling data from these studies together (Table 1). Within the first 15 years of follow-up, the prevalence of cirrhosis development is significantly higher in patients with NASH as compared to patients with simple steatosis (10.8% versus 0.7%, respectively, x2 = 23.3, P < 0.001). Consequently, the liver-related mortality is also significantly higher in patients with NASH as compared to simple steatosis (7.3% versus 0.9%, respectively, x2 = 16.7, P < 0.001). The overall mortality between these two groups, however, is not significantly different, although there is a trend toward a higher overall mortality in the NASH group (40.5% versus 32.5%, respectively, x2= 3.61, P < 0.1). NAFLD, nonalcoholic fatty liver disease; NASH, nonalcoholic steatohepatitis.

M-CSF-Mφ and IL-34-Mφ also express the hepatic stellate cell (HSC) activators, platelet-derived growth factor, transforming growth factor beta, and galectin-3. IL-34-Mφ and M-CSF-Mφ induce type I collagen synthesis by HSCs, the main

collagen-producing cells in liver fibrosis. IL-13, whose expression correlates with the fibrosis stage in HCV-infected patients, decreases the expression of the collagenase, matrix metalloproteinase 1, by IL-34-Mφ and M-CSF-Mφ, thereby enhancing collagen synthesis. By inhibiting the production of interferon-gamma (IFN-γ) by activated natural killer cells, IL-34-Mφ and M-CSF-Mφ prevent the IFN-γ-induced killing of HSCs. Conclusion: These results identify M-CSF and IL-34 as potent profibrotic factors in HCV liver fibrosis. (Hepatology 2014;60:1878–1889) “
“Over the last decade, buy SCH727965 a wealth of data has emerged illustrating both the rather benign clinical course of nonalcoholic fatty liver disease (NAFLD) in many individuals, and the unfavorable prognosis of this condition in others. Several studies on long-term mortality of patients suffering from NAFLD confirmed by imaging and/or liver biopsy have been reported. Studies with an average follow-up of at

least 5 p38 MAPK activity years are summarized in Table 1.1–10 Compared to the general population of same age and gender, NAFLD is associated with a significantly higher overall mortality1, 2, 4 and liver-related mortality.1, 2 The long-term prognosis of patients with NAFLD, however, this website varies across the disease stage. Although the terms simple steatosis and nonalcoholic steatohepatitis (NASH) are often used in studies on long-term prognosis

to classify patient risk, differing definitions have been used across the studies. Despite that, however, some conclusions can be derived from pooling data from these studies together (Table 1). Within the first 15 years of follow-up, the prevalence of cirrhosis development is significantly higher in patients with NASH as compared to patients with simple steatosis (10.8% versus 0.7%, respectively, x2 = 23.3, P < 0.001). Consequently, the liver-related mortality is also significantly higher in patients with NASH as compared to simple steatosis (7.3% versus 0.9%, respectively, x2 = 16.7, P < 0.001). The overall mortality between these two groups, however, is not significantly different, although there is a trend toward a higher overall mortality in the NASH group (40.5% versus 32.5%, respectively, x2= 3.61, P < 0.1). NAFLD, nonalcoholic fatty liver disease; NASH, nonalcoholic steatohepatitis.