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Article ; Online: Research trends analysis of chronic hepatitis C versus nonalcoholic fatty liver disease

Eyal Klang / Shelly Soffer / Lee Alper / Orit Shimon / Yiftach Barash / Yana Davidov / Mariya Likhter / Oranit Cohen‐Ezra / Gil Ben Yakov / Ziv Ben‐Ari

Health Science Reports, Vol 5, Iss 6, Pp n/a-n/a (2022)

A literature review text‐mining analysis of publications

2022

Abstract: Abstract Background Hepatits C virus (HCV) rates have lowered due to direct‐acting antiviral treatment. Nonalcoholic steatohepatitis (NASH)/nonalcoholic fatty liver disease (NAFLD) is rising with no available therapy. We employed text‐mining to analyze ... ...

Abstract	Abstract Background Hepatits C virus (HCV) rates have lowered due to direct‐acting antiviral treatment. Nonalcoholic steatohepatitis (NASH)/nonalcoholic fatty liver disease (NAFLD) is rising with no available therapy. We employed text‐mining to analyze trends in HCV and NAFLD research from the past two decades. Materials and Methods We queried PubMed for all HCV and NASH/NAFLD entries published between 2000 and 2020. We compared the total number of publications on both etiologies. We performed subanalyses for different terms of interest and for geographic origin. Results Overall, 75,934 HCV‐related entries and 24,987 NASH/NAFLD‐related entries were published during the study period. Up to 2015, there was a linear upward slope in the number of annual HCV publications (154.9 publications/year, p < 0.001). In 2015, the yearly number of HCV publications started showing a downward slope (−242.2 publications/year, p < 0.001). The number of NASH/NAFLD publications showed a continuous upward slope during the study period. The NASH/NAFLD field lacks publications on screening and treatment methods. Conclusion Trends in publications varied between both etiologies. They reflect the success of antiviral treatment for HCV. The growing rates of NAFLD/NASH and the lack of a targeted cure explain the rise in related publications.
Keywords	chronic hepatitis C ; nonalcoholic fatty liver disease ; PubMed ; text mining ; Medicine ; R
Subject code	306
Language	English
Publishing date	2022-11-01T00:00:00Z
Publisher	Wiley
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Extracellular Vesicular Transmission of miR-423-5p from HepG2 Cells Inhibits the Differentiation of Hepatic Stellate Cells

Michal Safran / Rula Masoud / Maya Sultan / Irena Tachlytski / Chofit Chai Gadot / Ron Pery / Nora Balint-Lahat / Orit Pappo / Nahum Buzaglo / Ziv Ben-Ari

Cells, Vol 11, Iss 1715, p

2022 Volume 1715

Abstract: Liver fibrosis (LF) is a major cause of morbidity and mortality worldwide. Hepatic stellate cells (HSCs) are the primary source of extracellular matrix in the liver and their activation is a central event in LF development. Extracellular vesicles (EVs) ... ...

Abstract	Liver fibrosis (LF) is a major cause of morbidity and mortality worldwide. Hepatic stellate cells (HSCs) are the primary source of extracellular matrix in the liver and their activation is a central event in LF development. Extracellular vesicles (EVs) are intercellular communication agents, which play important roles in physiological processes in chronic liver diseases. The aim of this study was to examine the crosstalk between hepatocytes and HSCs mediated by hepatocyte-secreted EVs. EVs were purified from primary mouse hepatocytes, HepG2 cell lines, under normal or stressed conditions. The effect of EVs on primary HSCs (pHSCs) differentiation was evaluated by measuring of differentiation markers. In addition, their impact on the carbon tetrachloride (CCl4)-induced fibrosis mouse model was evaluated. The results demonstrated that HepG2-EVs regulate HSC differentiation and that under stress conditions, promoted pHSCs differentiation into the myofibroblast phenotype. The evaluation of miRNA sequences in the HepG2 secreted EVs demonstrated high levels of miR-423-5p. The examination of EV cargo following stress conditions identified a significant reduction of miR-423-5p in HepG2-EVs relative to HepG2-EVs under normal conditions. In addition, pHSCs transfected with miR-423-5p mimic and exhibit lower mRNA levels of alpha smooth muscle actin and Collagen type 1 alpha, and the mRNA expression level of genes targeted the family with sequence-similarity-3 (FAM3) and Monoacylglycerol lipase (Mgll). This study strengthened the hypothesis that EVs are involved in LF and that their cargo changes in stress conditions. In addition, miR-423-5p was shown to be involved in HSCs differentiation and hence, fibrosis development.
Keywords	liver fibrosis ; extracellular vesicles ; exosomes ; miRNA-423-5p ; hepatic stellate cells ; Biology (General) ; QH301-705.5
Subject code	610
Language	English
Publishing date	2022-05-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Both MAPK and STAT3 signal transduction pathways are necessary for IL-6-dependent hepatic stellate cells activation.

Polina Kagan / Maya Sultan / Irina Tachlytski / Michal Safran / Ziv Ben-Ari

PLoS ONE, Vol 12, Iss 5, p e

2017 Volume 0176173

Abstract: During liver injury, hepatic stellate cells (HSCs) can undergo activation and transform into alpha-smooth muscle actin (αSMA)-expressing contractile myofibroblast-like cells, leading to deposition of excessive scar matrix. We have recently demonstrated ... ...

Abstract	During liver injury, hepatic stellate cells (HSCs) can undergo activation and transform into alpha-smooth muscle actin (αSMA)-expressing contractile myofibroblast-like cells, leading to deposition of excessive scar matrix. We have recently demonstrated that depletion of adenosine deaminase acting on double-stranded RNA (ADAR1) from mouse hepatocytes leads to HSC activation and induction of inflammation and hepatic fibrosis that is mediated by interleukin 6 (IL-6). Our aim was to identify and characterize the molecular pathways involved in the direct, inflammation-independent activation of HSCs by IL-6.Primary HSCs were isolated from mouse livers. mRNA levels of αSMA and Col1a were analyzed using qRT-PCR. Protein levels of αSMA, MAPK, p-MAPK, p38, p-p38, STAT3 and p-STAT3 were assessed by Western Blot analysis. The effect of specific signal transduction pathway inhibitors (i.e., SB203580 (P-38 inhibitor), U0126 (MAPK inhibitor), S3I-201 (STAT3 inhibitor) and Ruxolitinib (Jak1/2 inhibitor)) was also studied.Primary HSCs treated with IL-6 demonstrated upregulation of αSMA and Col1a mRNA levels as well as increased αSMA protein levels. Moreover, the phenotypic transition of quiescent HSCs toward myofibroblast-like cells was noted upon administration of IL-6 and not in untreated samples. In addition, the phosphorylation levels of p38, MAPK and STAT3 increased 30 minutes after treatment, and was followed by a decline in the phosphorylation levels 2-4 hours post-treatment. However, addition of specific signal transduction pathway inhibitors curbed this effect, and resulted in αSMA and Col1a expression levels similar to those measured in untreated control samples.IL-6 can directly induce the transition of HSCs toward myofibroblast-like cells. The effect is mediated by the activation of both MAPK and JAK/STAT signaling pathways. Elimination of either MAPK or JAK/STAT signaling pathways inhibits HSC stimulation. These results might pave the road toward the development of potential therapeutic interventions for hepatic fibrosis.
Keywords	Medicine ; R ; Science ; Q
Subject code	630
Language	English
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Both MAPK and STAT3 signal transduction pathways are necessary for IL-6-dependent hepatic stellate cells activation.

Polina Kagan / Maya Sultan / Irina Tachlytski / Michal Safran / Ziv Ben-Ari

PLoS ONE, Vol 12, Iss 5, p e

2017 Volume 0176173

Abstract	During liver injury, hepatic stellate cells (HSCs) can undergo activation and transform into alpha-smooth muscle actin (αSMA)-expressing contractile myofibroblast-like cells, leading to deposition of excessive scar matrix. We have recently demonstrated that depletion of adenosine deaminase acting on double-stranded RNA (ADAR1) from mouse hepatocytes leads to HSC activation and induction of inflammation and hepatic fibrosis that is mediated by interleukin 6 (IL-6). Our aim was to identify and characterize the molecular pathways involved in the direct, inflammation-independent activation of HSCs by IL-6.Primary HSCs were isolated from mouse livers. mRNA levels of αSMA and Col1a were analyzed using qRT-PCR. Protein levels of αSMA, MAPK, p-MAPK, p38, p-p38, STAT3 and p-STAT3 were assessed by Western Blot analysis. The effect of specific signal transduction pathway inhibitors (i.e., SB203580 (P-38 inhibitor), U0126 (MAPK inhibitor), S3I-201 (STAT3 inhibitor) and Ruxolitinib (Jak1/2 inhibitor)) was also studied.Primary HSCs treated with IL-6 demonstrated upregulation of αSMA and Col1a mRNA levels as well as increased αSMA protein levels. Moreover, the phenotypic transition of quiescent HSCs toward myofibroblast-like cells was noted upon administration of IL-6 and not in untreated samples. In addition, the phosphorylation levels of p38, MAPK and STAT3 increased 30 minutes after treatment, and was followed by a decline in the phosphorylation levels 2-4 hours post-treatment. However, addition of specific signal transduction pathway inhibitors curbed this effect, and resulted in αSMA and Col1a expression levels similar to those measured in untreated control samples.IL-6 can directly induce the transition of HSCs toward myofibroblast-like cells. The effect is mediated by the activation of both MAPK and JAK/STAT signaling pathways. Elimination of either MAPK or JAK/STAT signaling pathways inhibits HSC stimulation. These results might pave the road toward the development of potential therapeutic interventions for hepatic ...
Keywords	Medicine ; R ; Science ; Q
Subject code	630
Language	English
Publishing date	2017-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Interleukin-1α and Interleukin-1β play a central role in the pathogenesis of fulminant hepatic failure in mice.

Maya Sultan / Ziv Ben-Ari / Rula Masoud / Orit Pappo / Dror Harats / Yehuda Kamari / Michal Safran

PLoS ONE, Vol 12, Iss 9, p e

2017 Volume 0184084

Abstract: Fulminant hepatitis failure (FHF) is marked by the sudden loss of hepatic function, with a severe life-threatening course in persons with no prior history of liver disease. Interleukin (IL)-1α and IL-1β are key inflammatory cytokines but little is known ... ...

Abstract	Fulminant hepatitis failure (FHF) is marked by the sudden loss of hepatic function, with a severe life-threatening course in persons with no prior history of liver disease. Interleukin (IL)-1α and IL-1β are key inflammatory cytokines but little is known about their role in the development of FHF. The aim of this study was to assess the involvement of IL-1α and IL-1β in the progression of LPS/GalN-induced FHF.WT, IL-1α or IL-1β deficient mice were injected with LPS/GalN. Blood and liver tissue were collected at different time points, FHF related pathways were examined.After FHF induction the survival of both IL-1α and IL-1β KO mice was longer than that of WT mice. Lower serum liver enzyme levels, demonstrated reduced hepatic injury in the IL-1α and IL-1βKO mice. Histologically detected liver injury and apoptotic hepatocytes were significantly reduced in the IL-1αand IL-1βKO mice compared to WT mice. Reduced hepatic IkB levels and upregulated NFκB activity in WT mice remained inhibited in IL-1α and IL-1β KO mice. Hepatic expression levels of TNFα and IL-6 were significantly increased in WT mice but not in IL-1α and IL-1β KO mice.IL-1α and IL-1β play a central role in the pathogenesis of LPS/GalN-induced FHF. These interleukins are associated with the activation of NFκB signaling, upregulation of the pro-inflammatory cytokines and liver damage and apoptosis. Since neither IL-1α nor IL-1β depletions completely rescued the phenotype, we believe that IL-1α and IL-1β have a similar and probably complementary role in FHF progression.
Keywords	Medicine ; R ; Science ; Q
Subject code	630
Language	English
Publishing date	2017-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Automated thermal imaging for the detection of fatty liver disease

Rafael Y. Brzezinski / Lapaz Levin-Kotler / Neta Rabin / Zehava Ovadia-Blechman / Yair Zimmer / Adi Sternfeld / Joanna Molad Finchelman / Razan Unis / Nir Lewis / Olga Tepper-Shaihov / Nili Naftali-Shani / Nora Balint-Lahat / Michal Safran / Ziv Ben-Ari / Ehud Grossman / Jonathan Leor / Oshrit Hoffer

Scientific Reports, Vol 10, Iss 1, Pp 1-

2020 Volume 11

Abstract: Abstract Non-alcoholic fatty liver disease (NAFLD) comprises a spectrum of progressive liver pathologies, ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), fibrosis and cirrhosis. A liver biopsy is currently required to stratify high- ...

Abstract	Abstract Non-alcoholic fatty liver disease (NAFLD) comprises a spectrum of progressive liver pathologies, ranging from simple steatosis to non-alcoholic steatohepatitis (NASH), fibrosis and cirrhosis. A liver biopsy is currently required to stratify high-risk patients, and predicting the degree of liver inflammation and fibrosis using non-invasive tests remains challenging. Here, we sought to develop a novel, cost-effective screening tool for NAFLD based on thermal imaging. We used a commercially available and non-invasive thermal camera and developed a new image processing algorithm to automatically predict disease status in a small animal model of fatty liver disease. To induce liver steatosis and inflammation, we fed C57/black female mice (8 weeks old) a methionine-choline deficient diet (MCD diet) for 6 weeks. We evaluated structural and functional liver changes by serial ultrasound studies, histopathological analysis, blood tests for liver enzymes and lipids, and measured liver inflammatory cell infiltration by flow cytometry. We developed an image processing algorithm that measures relative spatial thermal variation across the skin covering the liver. Thermal parameters including temperature variance, homogeneity levels and other textural features were fed as input to a t-SNE dimensionality reduction algorithm followed by k-means clustering. During weeks 3,4, and 5 of the experiment, our algorithm demonstrated a 100% detection rate and classified all mice correctly according to their disease status. Direct thermal imaging of the liver confirmed the presence of changes in surface thermography in diseased livers. We conclude that non-invasive thermal imaging combined with advanced image processing and machine learning-based analysis successfully correlates surface thermography with liver steatosis and inflammation in mice. Future development of this screening tool may improve our ability to study, diagnose and treat liver disease.
Keywords	Medicine ; R ; Science ; Q
Subject code	610
Language	English
Publishing date	2020-09-01T00:00:00Z
Publisher	Nature Publishing Group
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Bone marrow and nonbone marrow Toll like receptor 4 regulate acute hepatic injury induced by endotoxemia.

Edith Hochhauser / Orna Avlas / Reut Fallach / Larissa Bachmetov / Romy Zemel / Orit Pappo / Asher Shainberg / Ziv Ben Ari

PLoS ONE, Vol 8, Iss 8, p e

2013 Volume 73041

Abstract: BACKGROUND: Toll-like receptors (TLRs) are expressed in immune cells and hepatocytes. We examined whether hepatic Toll-like receptor 4 (TLR4) is involved in the acute hepatic injury caused by the administration of lipopolysaccharide (LPS) (septic shock ... ...

Abstract	BACKGROUND: Toll-like receptors (TLRs) are expressed in immune cells and hepatocytes. We examined whether hepatic Toll-like receptor 4 (TLR4) is involved in the acute hepatic injury caused by the administration of lipopolysaccharide (LPS) (septic shock model). METHODS: Wild type (WT), TLR4-deficient and chimera mice underwent myeloablative bone marrow transplantation to dissociate between TLR4 expression in the liver or in the immune-hematopoietic system. Mice were injected with LPS and sacrificed 4 hours later. RESULTS: Compared to TLR4 deficient mice, WT mice challenged with LPS displayed increased serum liver enzymes and hepatic cellular inflammatory infiltrate together with increased serum and hepatic levels of interleukin 1β (IL-1β), tumor necrosis factor α (TNFα) ,Up-regulation of hepatic mRNA encoding TLR4, IκB and c-jun expressions. TLR4 mutant mice transplanted with WT bone marrow were more protected than WT chimeric mice bearing TLR4 mutant hemopoietic cells from LPS, as seen by IL-1β and TNFα levels. We then used hepatocytes (Huh7) and macrophages from monocytic cell lines to detect TLR mRNA expression. Macrophages expressed a significantly higher level of TLR4 mRNA and TLR2 (more than 3000- and 8000-fold respectively) compared with the hepatocyte cell line. LPS administration induced TLR4 activation in a hepatocyte cell line in a dose dependent manner while TLR2 mRNA hardly changed. CONCLUSIONS: These results suggest that TLR4 activation of hepatocytes participate in the immediate response to LPS induced hepatic injury. However, in this response, the contribution of TLR4 on bone marrow derived cells is more significant than those of the hepatocytes. The absence of the TLR4 gene plays a pivotal role in reducing hepatic LPS induced injury.
Keywords	Medicine ; R ; Science ; Q
Subject code	616
Language	English
Publishing date	2013-01-01T00:00:00Z
Publisher	Public Library of Science (PLoS)
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Serum adipocyte fatty acid binding protein in liver transplant recipients and the metabolic syndrome

Hemda Schmilovitz-Weiss / Ido Laish / Zohar Levi / Yehudith Monsselise / Yael Harif / Marius Braun / Mona Boaz / Ziv Ben Ari

Annals of Hepatology, Vol 11, Iss 3, Pp 343-

2012 Volume 349

Abstract: Background. Liver transplantation is often associated with metabolic derangements. Adipocyte fatty-acid-binding protein 4 (AFABP4) integrates inflammatory and metabolic responses. It has also been associated with metabolic syndrome in animal models and ... ...

Abstract	Background. Liver transplantation is often associated with metabolic derangements. Adipocyte fatty-acid-binding protein 4 (AFABP4) integrates inflammatory and metabolic responses. It has also been associated with metabolic syndrome in animal models and clinical studies in the general population.Aim. To determine the role of AFABP4 in post-transplant metabolic syndrome.Material and methods. Consecutive patients followed for at least 6 months after liver transplantation were tested for insulin resistance by homeostasis model assessment (HOMA). Serum levels of AFABP4 were tested by an enzyme-linked immunosorbent assay.Results. The study group included 76 patients (64.5% male, mean age 56.3 ± 12.4 years). Hypertension was present in 56.5%, hyperlipidemia in 69.7%, diabetes mellitus in 23.6%. Half of the patients met at least 3 criteria for metabolic syndrome. Serum AFABP4 levels (p < 0.0001), HOMA index ≥ 2.5 vs. < 2.5 (p < 0.0002) and BMI ≥ 30 vs. < 30 (p < 0.0006) were significantly higher in patients with metabolic syndrome. Within the metabolic syndrome subgroup, AFABP4 levels significantly correlated with age, aspartate aminotransaminase level, waist circumference, and HOMA index. High AFABP4 significantly increased the odds of acquiring metabolic syndrome (OR 1.04, 95% CI 1.007-1.074, p = 0.017). On multiple logistic regression analysis, independent predictors of high AFABP4 were cryptogenic liver disease, steroid administration, high HOMA index, and a high degree of fatty infiltration.Conclusion. Prevalence of metabolic syndrome is significantly higher in liver transplant recipients than in the general population. AFABP4 may serve as a circulating biomarker in the clinical prediction/diagnosis of metabolic syndrome in patients post-liver transplantation.
Keywords	Post-transplant metabolic syndrome ; AFABP4 ; Prediction ; HOMA ; Fatty liver ; Specialties of internal medicine ; RC581-951
Subject code	610
Language	English
Publishing date	2012-05-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Secondary sclerosing cholangitis following major burn

Ziv Ben-Ari / David Levingston / Ella Weitzman / Yael Haviv-Yadid / Oranit Cohen-Ezra / Peretz Weiss / Eli Zuckerman / Yael Inbar / Michal Amitai / Uri Rimon / Maya Goder / Josef Haik

Annals of Hepatology, Vol 14, Iss 5, Pp 695-

2015 Volume 701

Abstract: Background and aims. Secondary sclerosing cholangitis in critically ill patients (SSC-CIP) is a relatively new previously unrecognized entity which may lead to severe biliary disease with rapid progression to cirrhosis. We present for the first time a ... ...

Abstract	Background and aims. Secondary sclerosing cholangitis in critically ill patients (SSC-CIP) is a relatively new previously unrecognized entity which may lead to severe biliary disease with rapid progression to cirrhosis. We present for the first time a case series of patients with rapidly progressive SSC-CIP requiring aggressive intensive care treatment following major burn injury.Results. SSC-CIP was diagnosed in 4 consecutive patients hospitalized due to major burn injuries at our Intensive Care Unit (ICU). SSC-CIP was diagnosed when ERCP (n = 1) or MRCP (n = 3) demonstrated irregular intrahepatic bile ducts with multiple strictures and dilatations and, when a liver biopsy (n = 3) demonstrated severe cholestasis and bile duct damage. All patients were males; none of whom had pre-existing liver disease. Ages: 18-56 y. All patients suffered from severe (grade 2-3) burn injuries with total burn surface area ranging from 35 to 95%. Mean length of ICU hospitalization was 129.2 ± 53.0 days. All patients required mechanical ventilation (with a mean PEEP of 8.4 ± 2.1 cm H2O) and the administration of catecholamines for hemodynamic stabilization. All patients demonstrated severe cholestasis. Blood cultures and cultures from drained liver abscesses grew hospital acquired multiple resistant bacteria. Liver cirrhosis developed within 12 months. One patient underwent orthotopic liver transplantation. Two patients (50%) died. In conclusion, SSC-CIP following major burn injury is a rapidly progressive disease with a poor outcome. Liver cirrhosis developed rapidly. Awareness of this grave complication is needed for prompt diagnosis and considerations of a liver transplantation.
Keywords	Liver transplantation ; SSC-CIP ; Cirrhosis ; Specialties of internal medicine ; RC581-951
Subject code	610
Language	English
Publishing date	2015-09-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Prevalence of Hepatitis E Virus Antibodies, Israel, 2009–2010

Orna Mor / Ravit Bassal / Michal Michaeli / Marina Wax / Daniela Ram / Oranit Cohen-Ezra / Dani Cohen / Ella Mendelson / Ziv Ben-Ari / Tamy Shohat

Emerging Infectious Diseases, Vol 21, Iss 4, Pp 692-

2015 Volume 694

Abstract: We investigated prevalence of hepatitis E virus in a sample of the population of Israel. The overall seroprevalence of antibodies to the virus was 10.6% (95% CI 8.4%–13.0%); age-adjusted prevalence was 7.6%. Seropositivity was associated with age, Arab ... ...

Abstract	We investigated prevalence of hepatitis E virus in a sample of the population of Israel. The overall seroprevalence of antibodies to the virus was 10.6% (95% CI 8.4%–13.0%); age-adjusted prevalence was 7.6%. Seropositivity was associated with age, Arab ethnicity, low socioeconomic status, and birth in Africa, Asia, or the former Soviet Union.
Keywords	Anti-HEV ; hepatitis E ; viruses ; antibodies ; IgG ; Israel ; Medicine ; R ; Infectious and parasitic diseases ; RC109-216
Language	English
Publishing date	2015-04-01T00:00:00Z
Publisher	Centers for Disease Control and Prevention
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