Nineteen out of 24 currently recognized genera were sampled, representing 63 species. The variable mt23S-tRNA Val intergenic spacer could only be aligned within NVP-BKM120 purchase genera and could not be used to infer intergeneric relationships. The partial mt23S was also useful to delineate genera and was alignable at the family level but provided few informative characters. Analysis of mt23S

DNA sequences together with chloroplast-encoded psbA sequences resulted in a better resolved phylogeny. Hormophysa was the first genus to branch off within the Sargassaceae, followed by Myriodesma; then the three genera Caulocystis, Carpoglossum, and Scaberia in unresolved order; and then Acrocarpia. The other taxa studied here were divided over three major clades, but there was no branch support for the monophyly of two of these. The genera Bifurcaria, Cystoseira, Halidrys, and Sargassum appeared polyphyletic. The following taxonomic changes are proposed: Birinapant molecular weight a new genus Brassicophycus for Bifurcaria brassicaeformis (Kützing) E. S. Barton; reinstatement of the genus Sargassopsis for Sargassum decurrens (R. Brown ex Turner) C. Agardh; reinstatement of the genus Sirophysalis for Indo-Pacific Cystoseira trinodis (Forsskål) C. Agardh; reinstatement of the genus Polycladia for the western Indian Ocean species Cystoseira indica (Thivy et Doshi) Mairh,

Cystoseira myrica (S. G. Gmelin) C. Agardh, and Acystis heinii Schiffner; and reinstatement of the genus Stephanocystis for the North Pacific Cystoseira species and Halidrys dioica N. L. Gardner. The European Cystoseira species should be split into three genera, but no name changes are proposed yet, because diagnostic characters were found only for the clade including the type species. 上海皓元 Some evolutionary trends could be discerned from the mt23S + psbA phylogeny. “
“The present study describes a new dinoflagellate genus, Barrufeta N. Sampedro et S.

Fraga gen. nov., with one new species, B. bravensis Sampedro et S. Fraga sp. nov., isolated from the Costa Brava (NW Mediterranean Sea). The dinoflagellate was characterized at the genus and species levels by LM and EM; LSU and internal transcribed spacer (ITS) rDNA sequences; and HPLC analyses of the pigments, fatty acids, and possible presence of toxins of several cultured strains. The new Barrufeta species is oval shaped (22–35 μm long and 16–25 μm wide) and dorsoventrally flattened. It possesses numerous small chloroplasts that radiate from two large equatorially located pyrenoids and is a typical peridinin-containing dinoflagellate. The nucleus is in the anterior part of the epicone. The apical groove has a characteristic “Smurf-cap” shape that runs counterclockwise on the epicone and terminates on its right posterior part. B.

Nineteen out of 24 currently recognized genera were sampled, representing 63 species. The variable mt23S-tRNA Val intergenic spacer could only be aligned within ABT-263 molecular weight genera and could not be used to infer intergeneric relationships. The partial mt23S was also useful to delineate genera and was alignable at the family level but provided few informative characters. Analysis of mt23S

DNA sequences together with chloroplast-encoded psbA sequences resulted in a better resolved phylogeny. Hormophysa was the first genus to branch off within the Sargassaceae, followed by Myriodesma; then the three genera Caulocystis, Carpoglossum, and Scaberia in unresolved order; and then Acrocarpia. The other taxa studied here were divided over three major clades, but there was no branch support for the monophyly of two of these. The genera Bifurcaria, Cystoseira, Halidrys, and Sargassum appeared polyphyletic. The following taxonomic changes are proposed: selleck a new genus Brassicophycus for Bifurcaria brassicaeformis (Kützing) E. S. Barton; reinstatement of the genus Sargassopsis for Sargassum decurrens (R. Brown ex Turner) C. Agardh; reinstatement of the genus Sirophysalis for Indo-Pacific Cystoseira trinodis (Forsskål) C. Agardh; reinstatement of the genus Polycladia for the western Indian Ocean species Cystoseira indica (Thivy et Doshi) Mairh,

Cystoseira myrica (S. G. Gmelin) C. Agardh, and Acystis heinii Schiffner; and reinstatement of the genus Stephanocystis for the North Pacific Cystoseira species and Halidrys dioica N. L. Gardner. The European Cystoseira species should be split into three genera, but no name changes are proposed yet, because diagnostic characters were found only for the clade including the type species. medchemexpress Some evolutionary trends could be discerned from the mt23S + psbA phylogeny. “
“The present study describes a new dinoflagellate genus, Barrufeta N. Sampedro et S.

Fraga gen. nov., with one new species, B. bravensis Sampedro et S. Fraga sp. nov., isolated from the Costa Brava (NW Mediterranean Sea). The dinoflagellate was characterized at the genus and species levels by LM and EM; LSU and internal transcribed spacer (ITS) rDNA sequences; and HPLC analyses of the pigments, fatty acids, and possible presence of toxins of several cultured strains. The new Barrufeta species is oval shaped (22–35 μm long and 16–25 μm wide) and dorsoventrally flattened. It possesses numerous small chloroplasts that radiate from two large equatorially located pyrenoids and is a typical peridinin-containing dinoflagellate. The nucleus is in the anterior part of the epicone. The apical groove has a characteristic “Smurf-cap” shape that runs counterclockwise on the epicone and terminates on its right posterior part. B.

Nineteen out of 24 currently recognized genera were sampled, representing 63 species. The variable mt23S-tRNA Val intergenic spacer could only be aligned within SP600125 mw genera and could not be used to infer intergeneric relationships. The partial mt23S was also useful to delineate genera and was alignable at the family level but provided few informative characters. Analysis of mt23S

DNA sequences together with chloroplast-encoded psbA sequences resulted in a better resolved phylogeny. Hormophysa was the first genus to branch off within the Sargassaceae, followed by Myriodesma; then the three genera Caulocystis, Carpoglossum, and Scaberia in unresolved order; and then Acrocarpia. The other taxa studied here were divided over three major clades, but there was no branch support for the monophyly of two of these. The genera Bifurcaria, Cystoseira, Halidrys, and Sargassum appeared polyphyletic. The following taxonomic changes are proposed: Seliciclib manufacturer a new genus Brassicophycus for Bifurcaria brassicaeformis (Kützing) E. S. Barton; reinstatement of the genus Sargassopsis for Sargassum decurrens (R. Brown ex Turner) C. Agardh; reinstatement of the genus Sirophysalis for Indo-Pacific Cystoseira trinodis (Forsskål) C. Agardh; reinstatement of the genus Polycladia for the western Indian Ocean species Cystoseira indica (Thivy et Doshi) Mairh,

Cystoseira myrica (S. G. Gmelin) C. Agardh, and Acystis heinii Schiffner; and reinstatement of the genus Stephanocystis for the North Pacific Cystoseira species and Halidrys dioica N. L. Gardner. The European Cystoseira species should be split into three genera, but no name changes are proposed yet, because diagnostic characters were found only for the clade including the type species. MCE Some evolutionary trends could be discerned from the mt23S + psbA phylogeny. “
“The present study describes a new dinoflagellate genus, Barrufeta N. Sampedro et S.

Fraga gen. nov., with one new species, B. bravensis Sampedro et S. Fraga sp. nov., isolated from the Costa Brava (NW Mediterranean Sea). The dinoflagellate was characterized at the genus and species levels by LM and EM; LSU and internal transcribed spacer (ITS) rDNA sequences; and HPLC analyses of the pigments, fatty acids, and possible presence of toxins of several cultured strains. The new Barrufeta species is oval shaped (22–35 μm long and 16–25 μm wide) and dorsoventrally flattened. It possesses numerous small chloroplasts that radiate from two large equatorially located pyrenoids and is a typical peridinin-containing dinoflagellate. The nucleus is in the anterior part of the epicone. The apical groove has a characteristic “Smurf-cap” shape that runs counterclockwise on the epicone and terminates on its right posterior part. B.

This paper8 is still a mainstay of migraine literature and remains frequently cited (see Table 2). For the study concerned, they selected buy Venetoclax 30 “intelligent and cooperative” patients “free of apprehension and of preoccupation with pain, so that a minimal amount of local and general analgesia was required,” undergoing neurosurgical procedures. Several extra- and intracranial structures were studied by faradic stimulation, including the scalp, galea, fascia, muscles, arteries, veins, and sinuses in 150 observations in 30 subjects. The figures drawn from

all the experiments are instructive with respect to the areas where the (referred) pain was felt. An example is shown in Figure 2 in which stimulation of the middle meningeal artery resulted in temporal pain, Also, from other pain sensitive structures such as proximal cerebral arteries, larger intracranial, veins, and part of dura, there was a distinct

localization of the pain. Several conclusions were drawn. Extracranially, Selumetinib chemical structure most tissues are sensitive, the arteries in particular. Intracranially, the great venous sinuses and “venous tributaries from the surface of the brain,” as well as parts of the dura at the skull base, the dural arteries and the “cerebral arteries at the base of the brain,” are sensitive to pain. Structures not sensitive to pain include the skull, the brain parenchyma, most of the dura covering it, most of the pia-arachnoid, the ependymal lining of the ventricles, and the choroid plexuses. Of further importance was the observation that “stimulation of the pain-sensitive intracranial structures on or above the superior surface of the tentorium

cerebelli resulted in pain in various regions in front of a line drawn vertically from the ears across the top of the head,” the pathways running through 上海皓元医药股份有限公司 the trigeminal nerve. Stimulation on or below the inferior surface of the tentorium resulted in pain in various regions behind this line, the pathways running through the glossopharyngeal and vagus nerve, as well as the 3 upper cervical roots.8 In retrospect, we need to recognize that Ray and Wolff used localized short-lasting faradic stimulation, but both spatial and temporal summations are integral mechanisms of pain, particularly in persistent pain conditions.40-42 While focal and short-lasting stimulation of the dura mater or of a small blood vessel in the pia mater are not painful, it is likely that long lasting stimulation and/or stimulation of a large area of the dura mater or the pia may be painful. Supporting this possibility are clinical documentations of extreme pain during meningitis and subarachnoid hemorrhage.43 Lashley’s Description of Visual Auras (1941).

Fig. 4E shows an additive effect of the three antibodies used. Indeed, Luc-Jc1

HCVcc infection was inhibited by more than 90% after simultaneous blocking of three host cell factors at antibody concentrations that inhibited HCVcc infection between 15% and 60% when used individually. Taken together, these results suggest that CLDN1 mediates HCV entry in cooperation with CD81 and SR-BI. To investigate the role of CLDN1 in the entry process, we investigated the inhibitory capacity of anti-CLDN1 antibodies in kinetic studies.26, 29 To discriminate between virus binding and postbinding events, Luc-Jc1 HCVcc binding to Huh7.5.1 cells was performed for 1 hour at 4°C in the presence or absence of inhibitors before the temperature was shifted to Doxorubicin 37°C to initiate synchronous infection

(Fig. 5A). Fig. 5B shows that similarly to anti-CD81 and anti-SR-BI, rat anti-CLDN1 antibodies inhibited Luc-Jc1 HCVcc infection when added PD-0332991 purchase following binding of the virus to the target cell (Fig. 5B). To fine-map the entry step mediated by CLDN1, we added antibodies in side-by-side experiments every 20 minutes for up to 120 minutes after viral binding (Fig. 5C). The half-maximal times (t1/2) required for anti-CD81 and anti-CLDN1 antibodies to inhibit HCV entry were +30 and +33 minutes (Fig. 5C-E, Table 2), whereas the half-maximal time for heparin was −60 minutes and for concanamycin A was +60 minutes (Fig. 5C, Table 2). The time-course of anti-CLDN1 and anti-CD81 antibody–mediated inhibition was not significantly different, and both differed from those observed with heparin and concanamycin A (Table 2). Similar results were obtained in dimethyl sulfoxide–differentiated Huh7.5.127 cells (Fig. 5E). These data support a model where CLDN1 and CD81 exert their effects at a similar time in the viral internalization process. Using Flag-tagged CLDN1 transfected 293T cells, Evans et al.9 reported that anti-Flag inhibition of HCVpp infection

occurred at later time points compared with a CD81-specific antibody. These results differ from those obtained in this study that may be attributable to the experimental systems used in the two studies, including 293T/CLDN1 versus Huh7.5.1 cell lines, HCVpp versus HCVcc, MCE公司 the strain of HCV envelope glycoproteins H77 versus J6/JFH1, and the blocking antibodies (anti-CLDN1 versus anti-Flag antibodies). To further address this question, we studied the kinetics of anti-CLDN1 and anti-CD81 inhibition of HCVpp infection in 293T/CLDN1 cells. Inhibition of HCVpp infection of 293T/CLDN1 cells by anti-CLDN1 and anti-CD81 demonstrated similar kinetics (Fig. 5F) to those observed for HCVcc infection of Huh7.5.1 cells (Fig. 5D,E). Thus, the different kinetic results described by Evans et al.9 and us are most likely not related to the experimental model system but rather are related to the insertion of a Flag tag into CLDN1.

Alterations in the gut microbiome and increased gut permeability associated with ALD can result in increased LPS in the portal circulation. Rifaximin, a nonabsorbable antibiotic that alters the gut microbiota, is efficacious in the treatment of hepatic encephalopathy, and could have a role in ALD.[105] Inhibition of LPS-induced TLR4 signaling has been suggested as another target for novel therapies.[106] Endocannabinoids are involved in the pathogenesis of ALD through check details cannabinoid receptors 1 and 2 (CB1 and CB2).[107] Animals lacking cannabinoid receptors have differential responses to alcohol-induced liver

injury,[108, 109] suggesting the potential use of CB1 antagonists and CB2 agonists as therapeutic

agents. Although CB1 antagonists are limited by their neuropsychiatric side effects, peripherally Ferrostatin-1 mouse restricted agents may benefit patients with ALD.[107] Inflammasomes are intracellular multiprotein complexes that mediate the response to cellular danger signals activating and recruiting inflammatory cells. Inflammasome activation leads to activation of caspase-1, resulting in the release of IL-1β and IL-18.[110] Serum levels of IL-1β were found to be increased in patients with ALD as well as in animal models.[111, 112] Recent studies demonstrated mRNA expression of several inflammasomes in the liver thus suggesting that inflammasome activation is a component of the liver pathophysiology in ALD.[113] Alcohol consumption is a leading

cause of global morbidity and mortality, with much of its negative impact as a result of ALD. Despite some advances in our understanding of the pathogenesis and clinical characteristics of ALD, many questions remain. Standardized nomenclature and histologic classifications are lacking, and there have been no significant advances in therapy in the last 40 years. Recent translational work using human liver tissue has been informative in identifying some potential therapeutic targets for this disease. However, translation of these findings into novel therapies has been lacking. Additional detailed studies of 上海皓元 these potential targets in humans and animal models are urgently needed to improve outcomes in this patient population. Financial support: This work was supported, in part, by the National Institutes of Health, T32 DK07634 and UL1-TR000083. “
“Portal hypertension, a pathophysiological derangement of liver cirrhosis, is characterized by hyperdynamic circulation, angiogenesis and portosystemic collaterals. These may lead to lethal complication such as variceal bleeding. Caffeine has been noticed for the effects on liver inflammation, fibrogenesis, and vasoreactiveness. However, the relevant influences of caffeine in cirrhosis and portal hypertension have not been addressed.

[349] Alteration of PN management is also beneficial by keeping the glucose infusion rate below 15-16 mg/kg/minute as well as alternative lipid strategies.

Reduction of daily infusion of a soy-based lipid to 1 gm/kg/d has resulted in reversal of PNALD.[348] Use of lipid that is not soy-based (e.g., fish oil-based) at an infusion rate of 1 gm/kg/d has also resulted in reversal of cholestasis, but it may not reverse progression of fibrosis.[350, 351] 81. Prior to consideration of LT referral, strategies Selleckchem MK1775 should be initiated to prevent and reverse PNALD that include lipid-minimization, intravenous lipids that are not soy-based, enteral feeding, PN management, and prevention of infections. (1-B) 82. Referral for isolated LT for PNALD should be considered for children who have achieved enteral autonomy but have developed complications of cirrhosis (2-B); for those who continue to require PN, LT evaluation should take place at a center with an experienced multidisciplinary Selleckchem Ridaforolimus intestinal failure and intestinal transplant team (2-B). Cryptogenic cirrhosis leading to endstage liver disease is relatively rare in children. “Burnt out” nonalcoholic fatty liver disease needs to be considered,

particularly because of the associated risk of cardiovascular disease. In patients suspected of having “burnt out” nonalcoholic fatty liver disease, LT evaluation should include careful cardiovascular assessment, particularly impaired flow-mediated vasodilatation and increased carotid artery intimal medial thickness, both of which are markers of subclinical atherosclerosis.[352] Rare inborn errors of metabolism, such as bile acid synthetic defects, should be considered, as the diagnosis may inform subsequent pregnancies

and an available treatment medchemexpress may alter outcome. Factor VII deficiency is managed with fresh-frozen plasma, plasma-derived factor concentrates, or recombinant factor VIIa.[353, 354] Treatment is typically reserved for bleeding prevention prior to surgical procedures and spontaneous bleeding. Prophylaxis is reserved for newborns who are prone to early and severe gastrointestinal and central nervous system bleeding and others with a history of severe bleeding associated with surgery or menstruation. Affected patients can expect normal longevity if the condition is properly managed. LT is curative, but should be reserved for the most severely affected patients.[355, 356] Children undergoing transplantation will require factor replacement during the surgery and first 1-3 days after transplant surgery.[357] Purpura fulminans in the newborn period is the most dramatic and life-threatening presentation of protein C deficiency.[358, 359] Beyond the newborn period, clinical manifestations are heterogeneous but are associated with an increased risk of vascular thrombosis.

4% Sorafenib in vitro at 5 years, 5.1% at 10 years, and 9.8% at 15 years. Malignancies other than HCC occurred significantly when patients were of advanced age of ≤50 years, smoking index (package per day × year) was ≥ 20, and T2DM was present. T2DM caused a 1.70-fold enhancement in the development of malignancies other than HCC. Conclusion: T2DM causes an approximately 1.7-fold enhancement in the development of HCC and malignancies other than HCC in HCV-positive patients treated with IFN. In T2DM patients, maintaining a mean HbA1c level of <7.0% reduces the development of HCC. (HEPATOLOGY 2013) Hepatitis C virus (HCV) is one of

the more common causes of chronic liver disease worldwide. Chronic hepatitis C is an insidiously progressive form Rapamycin nmr of liver disease that relentlessly but silently progresses to cirrhosis in 20%-50% of cases over a period of 10-30 years.1,2 In addition, HCV is a major risk factor for hepatocellular carcinoma (HCC).3-7 On the other hand, the prevalence of patients with type 2 diabetes mellitus (T2DM) is increasing

in many nations, including Japan.8 Thus, the management of T2DM patients who are chronically infected with HCV is one of the most important issues confronted by physicians. Few studies have reported relationships between T2DM and total malignancies, including HCC in HCV patients. In addition, it is not clear whether the stringent control of T2DM is necessary for protecting the development of malignancies in HCV patients. This issue needs to be confirmed via long-term follow-up of a large cohort of patients at high risk of developing malignancy. With this background in mind, the present study was initiated to investigate the cumulative incidence and risk factors of malignancies, including HCC

after prolonged follow-up in HCV patients treated with interferon (IFN) monotherapy or combination therapy of IFN and ribavirin. The strengths of the current study are the large numbers of patients included and the long-term follow-up of patients. medchemexpress CH, chronic hepatitis; CI, confidence interval; HbA1c, hemoglobin A1c; HCC, hepatocellular carcinoma; HCV, hepatitis C virus; HR, hazard ratio; IFN, interferon; LC, liver cirrhosis; SVR, sustained virological response; T2DM, type 2 diabetes mellitus; TAI, total alcohol intake. The number of patients who were diagnosed with chronic HCV infection and treated for the first time with IFN monotherapy or combination therapy between September 1990 and March 2009 in the Department of Hepatology, Toranomon Hospital, Tokyo, Japan, was 7,205.

“
“Hepatocellular carcinoma (HCC) is a major complication of cirrhosis and has been increasing in incidence in recent years. Fatty liver disease is an increasingly common cause of chronic liver disease, and there have been several case reports

of HCC in patients with non-cirrhotic fatty liver disease. However, there is limited data from systematic studies with histological confirmation of the presence of both the HCC and the non-cirrhotic fatty liver disease. We studied the occurrence of fatty liver disease and the associated demographic, clinical, and pathological characteristics of a large cohort of patients with HCC in non-cirrhotic livers. Patients with intrahepatic cholangiocarcinoma Ixazomib solubility dmso (CC) occurring in non-cirrhotic livers and diagnosed during the same time period were used as the comparison group. Significant steatosis in the nontumor liver had a statistically significant association with HCC, being present in 54% (85/157) of HCC compared with 27% (32/120) of CC (P < 0.0001). Steatohepatitis was present in 15% (24/157) of HCC and 1% (2/120) of CC (P = 0.0014). Furthermore, HCC was more prevalent in cases with higher grades of steatosis. In addition, the

recently described intratumoral steatohepatitic morphology of HCC (SH-HCC) Selleck AZD9668 was also associated with significant steatosis in nontumor liver, with significant steatosis being present in 89% with SH-HCC compared with 50% without SH-HCC (P = 0.0162). Finally, SH-HCC was increasingly

more prevalent in patients with higher grades of nontumor steatosis. Taken together, these findings suggest a strong association between fatty liver disease and HCC in non-cirrhotic livers. “
“In prospective studies, drug rechallenge following drug-induced liver injury (DILI) is associated with up to 13% mortality,1 whereas retrospective case series report a 2% mortality rate across a broad range of drugs2 and a 51% mortality rate with halothane rechallenge.3 However, risk factors for severe liver injury with rechallenge are poorly characterized.1-4 Clinical outcomes following drug rechallenge appear to vary markedly by drug,2, 3, 5-7 suggesting that rechallenge risk may be related to drug-specific mechanisms of injury. Drug MCE公司 rechallenge is rarely deliberately performed due to potential fatalities.4 However, drug rechallenge may be considered in life-threatening disease, when no other treatments are available with informed consent and close follow-up. Because limited data on drug rechallenge are available, additional data are needed to enhance clinical decision making. The aim of this systematic analysis is to examine clinical outcomes and mechanisms of liver injury that may influence a drug’s potential for serious or fatal injury following rechallenge.

We have recently demonstrated that during lipotoxicity, hepatocytes release extracellular vesicles (EVs) enriched in miRNAs (Science Sig. Oct 2013). Our aim is to investigate if extracellular vesicles

released by hepatocytes during lipotoxicity may modulate hepatic HSC phenotype by delivering specific microRNAs. Methods. Human hepatoma cells (HepG2), and primary mouse hepatocytes were exposed to the saturated free fatty acid (FFA) palmitic acid for up to 24 hrs. EVs and EV-free supernatant were isolated from cell-free supernatants by ultracentrifuga-tion and quantitated by flow cytometry. HSC chemotaxis and chemokinesis were assessed by Boyden’s chamber and wound healing assay, respectively. HSC proliferation was assessed by BrDu-FITC staining and quantitation FK228 manufacturer of pro-fibrogenic transcripts was performed for cell activation. EVs internalization and delivery of miRNAs into HSC was addressed by immuno-fluorescence. Specific PPAR-γ-targeting miRNAs identified JQ1 research buy and quantified in EVs and HSCs by qPCR. Depletion of miRNAs from EVs was achieved by anti-miRNA and specific siRNA on maternal cells. A functional analysis of miRNA was assessed by miRNA mimics. Results. Hepatocyte-derived EVs released during

lipotoxicity are efficiently internalized by HSCs resulting in their activation, as shown by marked up-regulation of pro-fibrogenic genes, such as Collagen-I, α-SMA and TIMP-2, proliferation (EVs vs. EVs-free supernatant, p<0.04), chemo-taxis (EVs MCE公司 vs. EV-free supernatant, p<0.001) and chemokinesis (EVs vs. EVs-free supernatant, p<0.002), mainly after 16-24 hrs. These changes were associated with suppression of PPAR-γ expression in HSC. EVs internalization results in delivery of their miRNA content into HSCs. Lipotoxic hepatocyte-derived EVs miRNA content included various miRNAs that are known inhibitors of PPAR-γ expression with miR-128a being the most effective. Further loss- and gain-of-function studies identified miR-128a as a central modulator of the

effects of EVs on PPAR-γ inhibition and HSC activation. Conclusion. Our study demonstrates that EVs released by hepatocytes during lipotoxicity are critical signals that contribute to HSC activation in a process involving delivery of specific miRNAs and modulation of PPAR-γ expression. These results uncover a novel miRNA-regulated pathway committing HSC activation during lipotoxicity and have important implications for development of therapeutic strategies for patients with NAFLD. Disclosures: Akiko Eguchi – Grant/Research Support: Gilead The following people have nothing to disclose: Davide Povero, Nadia Panera, Anna Alisi, Valerio Nobili, Ariel E. Feldstein Background/Aims: Hepatic stellate cell (HSC) activation is required for fibrogenesis therefore understanding mechanisms governing HSC activation are important.