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Article: Positive Effect of Manipulated Virtual Kinematic Intervention in Individuals with Traumatic Stiff Shoulder: A Pilot Study.

Schwartz, Isabella / Safran, Ori / Karniel, Naama / Abel, Michal / Berko, Adina / Seyres, Martin / Tsoar, Tamir / Portnoy, Sigal

Journal of clinical medicine

2022 Volume 11, Issue 13

Abstract: Virtual reality enables the manipulation of a patient's perception, providing additional motivation to real-time biofeedback exercises. We aimed to test the effect of manipulated virtual kinematic intervention on measures of active and passive range of ... ...

Abstract	Virtual reality enables the manipulation of a patient's perception, providing additional motivation to real-time biofeedback exercises. We aimed to test the effect of manipulated virtual kinematic intervention on measures of active and passive range of motion (ROM), pain, and disability level in individuals with traumatic stiff shoulder. In a double-blinded study, patients with stiff shoulder following proximal humerus fracture and non-operative treatment were randomly divided into a non-manipulated feedback group (NM-group;
Language	English
Publishing date	2022-07-05
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662592-1
ISSN	2077-0383
ISSN	2077-0383
DOI	10.3390/jcm11133919
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Article ; Online: Positive Effect of Manipulated Virtual Kinematic Intervention in Individuals with Traumatic Stiff Shoulder

Isabella Schwartz / Ori Safran / Naama Karniel / Michal Abel / Adina Berko / Martin Seyres / Tamir Tsoar / Sigal Portnoy

Journal of Clinical Medicine, Vol 11, Iss 13, p

A Pilot Study

2022 Volume 3919

Abstract: Virtual reality enables the manipulation of a patient’s perception, providing additional motivation to real-time biofeedback exercises. We aimed to test the effect of manipulated virtual kinematic intervention on measures of active and passive range of ... ...

Abstract	Virtual reality enables the manipulation of a patient’s perception, providing additional motivation to real-time biofeedback exercises. We aimed to test the effect of manipulated virtual kinematic intervention on measures of active and passive range of motion (ROM), pain, and disability level in individuals with traumatic stiff shoulder. In a double-blinded study, patients with stiff shoulder following proximal humerus fracture and non-operative treatment were randomly divided into a non-manipulated feedback group (NM-group; n = 6) and a manipulated feedback group (M-group; n = 7). The shoulder ROM, pain, and disabilities of the arm, shoulder and hand (DASH) scores were tested at baseline and after 6 sessions, during which the subjects performed shoulder flexion and abduction in front of a graphic visualization of the shoulder angle. The biofeedback provided to the NM-group was the actual shoulder angle while the feedback provided to the M-group was manipulated so that 10° were constantly subtracted from the actual angle detected by the motion capture system. The M-group showed greater improvement in the active flexion ROM ( p = 0.046) and DASH scores ( p = 0.022). While both groups improved following the real-time virtual feedback intervention, the manipulated intervention provided to the M-group was more beneficial in individuals with traumatic stiff shoulder and should be further tested in other populations with orthopedic injuries.
Keywords	virtual reality ; biofeedback ; shoulder pain ; range of motion ; motion capture ; Medicine ; R
Subject code	796
Language	English
Publishing date	2022-07-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
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Article ; Online: Extracellular Vesicular Transmission of miR-423-5p from HepG2 Cells Inhibits the Differentiation of Hepatic Stellate Cells.

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

Cells

2022 Volume 11, Issue 10

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.
MeSH term(s)	Animals ; Humans ; Mice ; Extracellular Vesicles/metabolism ; Hep G2 Cells ; Hepatic Stellate Cells/metabolism ; Liver Cirrhosis/metabolism ; MicroRNAs/genetics ; MicroRNAs/metabolism ; RNA, Messenger/metabolism
Chemical Substances	MicroRNAs ; RNA, Messenger ; MIRN423 microRNA, human
Language	English
Publishing date	2022-05-23
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells11101715
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Article ; Online: Oncogenic viruses and hepatocellular carcinoma.

Ben Ari, Ziv / Weitzman, Ella / Safran, Michal

Clinics in liver disease

2015 Volume 19, Issue 2, Page(s) 341–360

Abstract: About 80% of hepatocellular carcinoma (HCC) is caused by hepatitis B virus (HBV) and/or hepatitis C virus (HCV) infections especially in the setting of established cirrhosis or advanced fibrosis, making HCC prevention a major goal of antiviral therapy. ... ...

Abstract	About 80% of hepatocellular carcinoma (HCC) is caused by hepatitis B virus (HBV) and/or hepatitis C virus (HCV) infections especially in the setting of established cirrhosis or advanced fibrosis, making HCC prevention a major goal of antiviral therapy. HCC tumors are highly complex and heterogeneous resulting from the aberrant function of multiple molecular pathways. The roles of HCV or HBV in promoting HCC development are still either directly or indirectly are still speculative, but the evidence for both effects is compelling. In patients with chronic hepatitis viral infection, cirrhosis is not a prerequisite for tumorigenesis.
MeSH term(s)	Animals ; Antiviral Agents/therapeutic use ; Carcinoma, Hepatocellular/prevention & control ; Carcinoma, Hepatocellular/virology ; DNA, Viral ; Hepacivirus/genetics ; Hepacivirus/physiology ; Hepatitis B virus/genetics ; Hepatitis B virus/physiology ; Hepatitis B, Chronic/complications ; Hepatitis B, Chronic/drug therapy ; Hepatitis C, Chronic/complications ; Hepatitis C, Chronic/drug therapy ; Humans ; Liver Cirrhosis/complications ; Liver Cirrhosis/virology ; Liver Neoplasms/prevention & control ; Liver Neoplasms/virology ; Oncogenic Viruses ; Virus Integration
Chemical Substances	Antiviral Agents ; DNA, Viral
Language	English
Publishing date	2015-05
Publishing country	United States
Document type	Journal Article ; Review
ZDB-ID	1472315-3
ISSN	1557-8224 ; 1089-3261
ISSN (online)	1557-8224
ISSN	1089-3261
DOI	10.1016/j.cld.2015.01.006
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Article ; Online: Hepatitis B virus downregulates vitamin D receptor levels in hepatoma cell lines, thereby preventing vitamin D-dependent inhibition of viral transcription and production.

Gotlieb, Neta / Tachlytski, Irena / Lapidot, Yelena / Sultan, Maya / Safran, Michal / Ben-Ari, Ziv

Molecular medicine (Cambridge, Mass.)

2018 Volume 24, Issue 1, Page(s) 53

Abstract: Background: Vitamin D is a key immune-modulator that plays a role in the innate and adaptive immune systems. Certain pathogens impair the immune defense by downregulating the vitamin D receptor (VDR) pathway. Low serum levels of vitamin D are associated ...

Abstract	Background: Vitamin D is a key immune-modulator that plays a role in the innate and adaptive immune systems. Certain pathogens impair the immune defense by downregulating the vitamin D receptor (VDR) pathway. Low serum levels of vitamin D are associated with increased hepatitis B virus (HBV) replication. Our study aimed to assess the in-vitro relationship between HBV production and Vitamin D signaling pathway and to explore the associated mechanism(s). Methods: HBV transcription and replication was evaluated by qRT-PCR of the HBV-RNA and covalently closed circular DNA (cccDNA). Furthermore, we have transfected the 1.3 X HBV-Luc plasmid to the cells and measured the Luciferase activity using Luminometer. Vitamin D signaling pathway activation was evaluated by measuring the expression levels of VDR, CYP24A1, Tumor necrosis factor α (TNFα) and cathelicidin (CAMP) by qRT-PCR. All assays were performed on HepG2.2.15, HepG2, and HepAD38 cells treated with or without Vitamin D active metabolite: calcitriol. Results: Calcitriol did not suppress HBV transcription, cccDNA expression or HBV RNA levels in HepG2.2.15 cells. However, VDR transcript levels in HepG2.215 cells were significantly lower compared to HepG2 cells. Similar results were obtained in HepAD38 cell where VDR expression was down-regulated when HBV transcript level was up-regulated. In addition, calcitriol induced VDR-associated signaling, resulting in upregulation of CYP24A1, TNFα and CAMP expression level in HepG2 cells but not in the HepG2.2.15 cells. Conclusions: These findings indicate that VDR expression is downregulated in HBV-transfected cells, thereby preventing vitamin D from inhibiting transcription and translation of HBV in vitro. HBV might use this mechanism to avoid the immunological defense system by affecting both TNFα and CAMP signaling pathways.
MeSH term(s)	Antimicrobial Cationic Peptides/genetics ; Calcitriol/pharmacology ; Carcinoma, Hepatocellular/genetics ; Carcinoma, Hepatocellular/metabolism ; Cell Line, Tumor ; Down-Regulation ; Hepatitis B virus/drug effects ; Hepatitis B virus/physiology ; Humans ; Liver Neoplasms/genetics ; Liver Neoplasms/metabolism ; RNA, Viral ; Receptors, Calcitriol/genetics ; Receptors, Calcitriol/metabolism ; Tumor Necrosis Factor-alpha/genetics ; Virus Replication/drug effects
Chemical Substances	Antimicrobial Cationic Peptides ; RNA, Viral ; Receptors, Calcitriol ; Tumor Necrosis Factor-alpha ; VDR protein, human ; ropocamptide (3DD771JO2H) ; Calcitriol (FXC9231JVH)
Language	English
Publishing date	2018-10-16
Publishing country	England
Document type	Journal Article
ZDB-ID	1283676-x
ISSN	1528-3658 ; 1076-1551
ISSN (online)	1528-3658
ISSN	1076-1551
DOI	10.1186/s10020-018-0055-0
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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) 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.

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

PloS one

2017 Volume 12, Issue 5, Page(s) e0176173

Abstract: Background: 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 ... ...

Abstract	Background: 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. Methods: 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. Results: 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. Conclusion: 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.
MeSH term(s)	Animals ; Hepatic Stellate Cells/metabolism ; Interleukin-6/metabolism ; Mice ; Mice, Inbred ICR ; Mitogen-Activated Protein Kinases/metabolism ; STAT3 Transcription Factor/metabolism ; Signal Transduction
Chemical Substances	Interleukin-6 ; STAT3 Transcription Factor ; Stat3 protein, mouse ; Mitogen-Activated Protein Kinases (EC 2.7.11.24)
Language	English
Publishing date	2017
Publishing country	United States
Document type	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0176173
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Article: Alterations in the Gut Microbiome in the Progression of Cirrhosis to Hepatocellular Carcinoma.

Lapidot, Yelena / Amir, Amnon / Nosenko, Rita / Uzan-Yulzari, Atara / Veitsman, Ella / Cohen-Ezra, Oranit / Davidov, Yana / Weiss, Peretz / Bradichevski, Tanya / Segev, Shlomo / Koren, Omry / Safran, Michal / Ben-Ari, Ziv

mSystems

2020 Volume 5, Issue 3

Abstract: Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related mortality worldwide. While cirrhosis is the main risk factor for HCC, the factors influencing progression from cirrhosis to HCC remain largely unknown. Gut microbiota plays a ... ...

Abstract	Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related mortality worldwide. While cirrhosis is the main risk factor for HCC, the factors influencing progression from cirrhosis to HCC remain largely unknown. Gut microbiota plays a key role in liver diseases; however, its association with HCC remains elusive. This study aimed to elucidate microbial differences between patients with HCC-associated cirrhosis (HCC-cirrhosis) and cirrhotic patients without HCC and healthy volunteers and to explore the associations between diet, lifestyle, and the microbiome of these patients. Fecal samples and food frequency questionnaires were collected from 95 individuals (30 HCC-cirrhosis patients, 38 cirrhotic patients without HCC, and 27 age- and body mass index [BMI]-matched healthy volunteers). 16S rRNA gene sequencing was performed. Bacterial richness in cirrhosis and HCC-cirrhosis patients was significantly lower than in healthy controls. The HCC-cirrhosis group was successfully classified with an area under the curve (AUC) value of 0.9 based on the dysbiotic fecal microbial signature. The HCC-cirrhosis group had a significant overrepresentation of
Language	English
Publishing date	2020-06-16
Publishing country	United States
Document type	Journal Article
ISSN	2379-5077
ISSN	2379-5077
DOI	10.1128/mSystems.00153-20
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Article ; Online: The impact of bariatric surgery on nonalcoholic fatty liver disease as measured using non-invasive tests.

Netanel, Carmit / Goitein, David / Rubin, Moshe / Kleinbaum, Yeruham / Katsherginsky, Sima / Hermon, Hila / Tsaraf, Keren / Tachlytski, Irina / Herman, Amir / Safran, Michal / Ben-Ari, Ziv

American journal of surgery

2020 Volume 222, Issue 1, Page(s) 214–219

Abstract: Background: Nonalcoholic fatty liver disease (NAFLD) is common in bariatric surgery candidates. We evaluated the effect of sleeve gastrectomy (SG) on NAFLD using validated non-invasive measures.: Methods: Patients with morbid obesity and NAFLD, ... ...

Abstract	Background: Nonalcoholic fatty liver disease (NAFLD) is common in bariatric surgery candidates. We evaluated the effect of sleeve gastrectomy (SG) on NAFLD using validated non-invasive measures. Methods: Patients with morbid obesity and NAFLD, planned for SG, were evaluated before and after surgery. Data collected included anthropometrics, biochemistry, adiponectin, SteatoTest™, NashTest™, FibroTest™, OWLiver® test and real-time ShearWave™ elastography (SWE). Results: Twenty-six subjects were included in the study, mean age 44.1 ± 4.8 years, 69.2% males. One year following SG, body mass index decreased significantly from 41.7 ± 4.8 kg/m Conclusion: Steatosis and steatohepatitis are significantly improved by SG as measured by non-invasive measures.
MeSH term(s)	Adult ; Aged ; Bariatric Surgery ; Elasticity Imaging Techniques ; Feasibility Studies ; Female ; Humans ; Liver/diagnostic imaging ; Liver Cirrhosis/blood ; Liver Cirrhosis/diagnosis ; Liver Cirrhosis/etiology ; Liver Cirrhosis/surgery ; Liver Function Tests ; Male ; Middle Aged ; Non-alcoholic Fatty Liver Disease/blood ; Non-alcoholic Fatty Liver Disease/diagnosis ; Non-alcoholic Fatty Liver Disease/etiology ; Non-alcoholic Fatty Liver Disease/surgery ; Obesity, Morbid/complications ; Obesity, Morbid/surgery ; Prospective Studies ; Severity of Illness Index ; Treatment Outcome ; Weight Loss ; Young Adult
Language	English
Publishing date	2020-11-25
Publishing country	United States
Document type	Journal Article ; Observational Study
ZDB-ID	2953-1
ISSN	1879-1883 ; 0002-9610
ISSN (online)	1879-1883
ISSN	0002-9610
DOI	10.1016/j.amjsurg.2020.11.045
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Article ; Online: GeneHancer: genome-wide integration of enhancers and target genes in GeneCards.

Fishilevich, Simon / Nudel, Ron / Rappaport, Noa / Hadar, Rotem / Plaschkes, Inbar / Iny Stein, Tsippi / Rosen, Naomi / Kohn, Asher / Twik, Michal / Safran, Marilyn / Lancet, Doron / Cohen, Dana

Database : the journal of biological databases and curation

2017 Volume 2017

Language	English
Publishing date	2017--01
Publishing country	England
Document type	Journal Article
ZDB-ID	2496706-3
ISSN	1758-0463 ; 1758-0463
ISSN (online)	1758-0463
ISSN	1758-0463
DOI	10.1093/database/bax028
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