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Artikel ; Online: Gene expression dynamics following mithramycin treatment: A possible model for post-chemotherapy cognitive impairment.

Asor, Eyal / Ben-Shachar, Dorit

Clinical and experimental pharmacology & physiology

2018 Band 45, Heft 10, Seite(n) 1028–1037

Abstract: Chemotherapy-induced cognitive changes is a major burden on a substantial number of cancer survivors. The mechanism of this sequel is unknown. In this study, we followed long-term effects of early in life mithramycin (MTR) treatment on behaviour and on ... ...

Abstract	Chemotherapy-induced cognitive changes is a major burden on a substantial number of cancer survivors. The mechanism of this sequel is unknown. In this study, we followed long-term effects of early in life mithramycin (MTR) treatment on behaviour and on the normal course of alterations of gene expression in brain. Between post-natal days (PND) 7 and 10, male rats were divided into 2 groups, 1 receiving MTR (0.1 mg/kg s.c. per day) and the other receiving saline. At PND11, frontal cortex tissue samples were dissected from 4 rats from each group. At PND 65 the remaining rats underwent behavioural tests after which all the rats were decapitated and their prefrontal cortex incised. Rats treated transiently with MTR early in life, showed impairments in spatial working memory and anxious-like behaviour in adulthood. The immediate molecular effect of MTR was expressed in a limited number of altered genes of different unconnected trajectories, which were simultaneously distorted by the drug. In contrast, 3 months later we observed a change in the expression of more than 1000 genes that converged into specific cellular processes. Time-dependent gene expression dynamics of several genes was significantly different between treated and untreated rats. The differences in the total number of altered genes and in gene expression trends, immediately and long after MTR treatment cessation, suggest the evolution of a new cellular homeostatic set point, which can lead to behavioural abnormalities following chemotherapy treatment.
Mesh-Begriff(e)	Animals ; Anxiety/complications ; Cognitive Dysfunction/chemically induced ; Cognitive Dysfunction/complications ; Cognitive Dysfunction/genetics ; Cognitive Dysfunction/physiopathology ; Gene Expression Regulation/drug effects ; Male ; Memory, Short-Term/drug effects ; Phenotype ; Plicamycin/adverse effects ; Rats ; Spatial Memory/drug effects
Chemische Substanzen	Plicamycin (NIJ123W41V)
Sprache	Englisch
Erscheinungsdatum	2018-07-11
Erscheinungsland	Australia
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	189277-0
ISSN	1440-1681 ; 0305-1870 ; 0143-9294
ISSN (online)	1440-1681
ISSN	0305-1870 ; 0143-9294
DOI	10.1111/1440-1681.12975
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Gene environment interaction in periphery and brain converge to modulate behavioral outcomes: Insights from the SP1 transient early in life interference rat model.

Asor, Eyal / Ben-Shachar, Dorit

World journal of psychiatry

2016 Band 6, Heft 3, Seite(n) 294–302

Abstract: It is generally assumed that behavior results from an interaction between susceptible genes and environmental stimuli during critical life stages. The present article reviews the main theoretical and practical concepts in the research of gene environment ...

Abstract	It is generally assumed that behavior results from an interaction between susceptible genes and environmental stimuli during critical life stages. The present article reviews the main theoretical and practical concepts in the research of gene environment interaction, emphasizing the need for models simulating real life complexity. We review a novel approach to study gene environment interaction in which a brief post-natal interference with the expression of multiple genes, by hindering the activity of the ubiquitous transcription factor specificity protein 1 (Sp1) is followed by later-in-life exposure of rats to stress. Finally, this review discusses the role of peripheral processes in behavioral responses, with the Sp1 model as one example demonstrating how specific behavioral patterns are linked to modulations in both peripheral and central physiological processes. We suggest that models, which take into account the tripartite reciprocal interaction between the central nervous system, peripheral systems and environmental stimuli will advance our understanding of the complexity of behavior.
Sprache	Englisch
Erscheinungsdatum	2016-09-22
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Review
ISSN	2220-3206
ISSN	2220-3206
DOI	10.5498/wjp.v6.i3.294
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Platelets: A possible glance into brain biological processes in schizophrenia.

Asor, Eyal / Ben-Shachar, Dorit

World journal of psychiatry

2013 Band 2, Heft 6, Seite(n) 124–133

Abstract: Schizophrenia is a severe mental disorder, characterized by behavioral, emotional and cognitive disturbances, which commonly follows a chronic course. Diagnostic accuracy, management plans, treatment evaluation and prognosis are dependent on relatively ... ...

Abstract	Schizophrenia is a severe mental disorder, characterized by behavioral, emotional and cognitive disturbances, which commonly follows a chronic course. Diagnostic accuracy, management plans, treatment evaluation and prognosis are dependent on relatively subjective assessments. Despite extensive research and improvement in imaging technology, as well as modern genetic and molecular methodologies, the biological basis of this disease is still unclear. Therefore, there is a need for objective and valid biological markers. Platelets have often been used as a model in neurobiological research. The accessibility of platelets and their similarities with neurons turns them into an attractive candidate to search for biological markers for diagnosis and for unraveling pathophysiological processes relevant to the etiology of brain disorders, including schizophrenia. The present review addresses the main changes in platelet physiology observed in schizophrenia and its response to antipsychotic medication. We summarize numerous studies demonstrating impaired metabolism, uptake and receptor kinetics of schizophrenia-relevant neurotransmitters, abnormalities in membrane derived phospholipids and polyunsaturated fatty acids, as well as dysfunctions in the mitochondria. These changes fit with the various hypotheses raised for the etiology of schizophrenia, including the dopamine-glutamate hypothesis, the autoimmune hypothesis, the polyunsaturated fatty acid hypothesis and the impaired energy metabolism hypothesis. Despite extensive research in platelets, no conclusive reliable biomarker has been identified yet. This review suggests that the clinical heterogeneity and the biological complexity of schizophrenia lead to the inevitable conclusion that biomarkers will be identified only for subgroups characterized according to the different diagnostic criteria. Moreover, any biomarker would have to be an array of interrelated factors or even a set of several such arrays.
Sprache	Englisch
Erscheinungsdatum	2013-07-01
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Review
ISSN	2220-3206
ISSN	2220-3206
DOI	10.5498/wjp.v2.i6.124
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: The role of branched chain amino acid and tryptophan metabolism in rat's behavioral diversity: Intertwined peripheral and brain effects.

Asor, Eyal / Stempler, Shiri / Avital, Avi / Klein, Ehud / Ruppin, Eytan / Ben-Shachar, Dorit

European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology

2015 Band 25, Heft 10, Seite(n) 1695–1705

Abstract: Previously, we showed that a transient early-in-life interference with the expression of multiple genes by mithramycin (MTR) followed by later-in-life exposure to chronic stress, leads to a "daring" and novelty seeking behavior in rats. In this study we ... ...

Abstract	Previously, we showed that a transient early-in-life interference with the expression of multiple genes by mithramycin (MTR) followed by later-in-life exposure to chronic stress, leads to a "daring" and novelty seeking behavior in rats. In this study we searched for molecular changes that contribute to this behavioral alteration. We applied a non-hypothesis driven strategy using whole genome cDNA array analysis (WGA) followed by Genome Scale Metabolic modeling analysis (GSMM). Gene expression validation was performed by qRT-PCR and immunoblotting. Brain and serum amino acids levels were measured by HPLC. WGA data directed us towards metabolic pathways and GSMM pointed at branched chain amino acids (BCAA) pathway. Out of 21 amino acids analyzed in the prefrontal cortex of MTR+Stress rats only tryptophan, whose brain levels depend on serum BCAA levels, showed a significant decrease. No change was observed in serotonin or kynurenine levels. However, a significant reduction in mRNA and protein levels of the large neutral amino acid transporter (LAT1), which transports BCAA and tryptophan into the brain, as well as in serum levels of tryptophan/BCAA ratio were observed. The latter may be attributed to the failure to increase serum insulin, following stress, in rats pre-exposed to mithramycin. Finally, significant correlations were observed between the anxiety index and tryptophan and between T-maze errors and LAT1. This study shows a specific behavioral pattern, which is linked to modulations in fluxes of amino acids both peripheral and central, which converge and reciprocally interact, and may thus be equally important targets for therapeutic intervention.
Mesh-Begriff(e)	Amino Acids, Branched-Chain/metabolism ; Animals ; Anxiety/metabolism ; Blood Glucose/metabolism ; Disease Models, Animal ; Exploratory Behavior/physiology ; Insulin/blood ; Kynurenine/metabolism ; Large Neutral Amino Acid-Transporter 1/metabolism ; Male ; Maze Learning/physiology ; Plicamycin/pharmacology ; Prefrontal Cortex/drug effects ; Prefrontal Cortex/growth & development ; Prefrontal Cortex/metabolism ; Protein Synthesis Inhibitors/pharmacology ; RNA, Messenger/metabolism ; Random Allocation ; Rats, Wistar ; Serotonin/metabolism ; Stress, Psychological/metabolism ; Tryptophan/metabolism
Chemische Substanzen	Amino Acids, Branched-Chain ; Blood Glucose ; Insulin ; Large Neutral Amino Acid-Transporter 1 ; Protein Synthesis Inhibitors ; RNA, Messenger ; Serotonin (333DO1RDJY) ; Kynurenine (343-65-7) ; Tryptophan (8DUH1N11BX) ; Plicamycin (NIJ123W41V)
Sprache	Englisch
Erscheinungsdatum	2015-10
Erscheinungsland	Netherlands
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1082947-7
ISSN	1873-7862 ; 0924-977X
ISSN (online)	1873-7862
ISSN	0924-977X
DOI	10.1016/j.euroneuro.2015.07.009
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Risk for molecular contamination of tissue samples evaluated for targeted anti-cancer therapy.

Asor, Eyal / Stav, Michael Y / Simon, Einav / Fahoum, Ibrahim / Sabo, Edmond / Ben-Izhak, Ofer / Hershkovitz, Dov

PloS one

2017 Band 12, Heft 3, Seite(n) e0173760

Abstract: With the increasing usage of sensitive PCR technology for pharmacogenetics, cross contamination becomes a significant concern. Researchers employed techniques which basically include replacing laboratory equipment after each sample preparation; however, ... ...

Abstract	With the increasing usage of sensitive PCR technology for pharmacogenetics, cross contamination becomes a significant concern. Researchers employed techniques which basically include replacing laboratory equipment after each sample preparation; however, there are no recommended guidelines. In the present work we wanted to evaluate the risk of cross contamination during tissue processing using the routine precaution measures. Twenty-one surgical samples of lung adenocarcinoma were used, of which 7 contained EGFR exon 19 mutation, 7 contained EGFR exon 21 mutation (p.L858R) and 7 were EGFR wild-type. The samples were ordered by alternating the mutation group to maximize the potential for cross contamination and underwent tissue sectioning and de-paraffinization. The entire process was performed using the same tools. Following DNA extraction all samples underwent PCR amplification and were scrutinized for small fractions of EGFR mutation using deep sequencing with the Ion torrent PGM technology. Twenty samples yielded results. The fraction of mutated copies was 41 ± 23% (range 11-66) for the cases with known exon 19 mutation and 48±24% (range 0-65) for the cases with known exon 21 mutations. No in-frame exon 19 deletion mutations were identified in the wild-type (WT) and exon 21 groups. The fraction of EGFR exon 21 (codon 858) mutations was 0.018±0.014% (range 0-0.05%) in the WT and exon 19 groups, which was not statistically different than the background sequencing artifact noise for the same base-pair alteration (p = 0.21). Our results suggest that standard precautions are sufficient for molecular pathology diagnosis of surgical samples and are not associated with increased risk of cross contamination.
Mesh-Begriff(e)	Adenocarcinoma/genetics ; Adenocarcinoma/pathology ; Adenocarcinoma of Lung ; ErbB Receptors/genetics ; Exons ; Humans ; Limit of Detection ; Lung Neoplasms/genetics ; Lung Neoplasms/pathology ; Molecular Targeted Therapy ; Mutation ; Mutation Rate ; Paraffin Embedding/methods ; Paraffin Embedding/standards ; Pathology, Molecular/methods ; Pathology, Molecular/standards ; Polymerase Chain Reaction/methods ; Tissue Fixation/methods ; Tissue Fixation/standards
Chemische Substanzen	EGFR protein, human (EC 2.7.10.1) ; ErbB Receptors (EC 2.7.10.1)
Sprache	Englisch
Erscheinungsdatum	2017-03-13
Erscheinungsland	United States
Dokumenttyp	Journal Article
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0173760
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Predictive factors of early mortality in children with developmental disabilities: a case-comparison analysis.

Cohen, Ayala / Asor, Eyal / Tirosh, Emanuel

Journal of child neurology

2008 Band 23, Heft 5, Seite(n) 536–542

Abstract: The aim of this study was to identify the risk factors for early mortality in children with neurodevelopmental disabilities. Of 1000 children who were sequentially referred to the same child developmental center over the period 1975-1985, 81 children ... ...

Abstract	The aim of this study was to identify the risk factors for early mortality in children with neurodevelopmental disabilities. Of 1000 children who were sequentially referred to the same child developmental center over the period 1975-1985, 81 children died between the ages of 6 months and 22 years (mean, 8.04 years; 6.1 SD). A group of 81 age-matched children and another group of 81 developmentally and age-matched children also referred to the center served as comparison groups. Following multivariate analysis, low developmental quotient, restricted mobility, assisted feeding, and genetic etiology were risk factors for early mortality when compared to the age-matched group (P < .01). In comparison to the developmentally matched group, restricted mobility, genetic etiology, and hearing deficit were identified as significant risk factors (P < .01). Comprehensive treatment at the child development center was demonstrated to be a significant protective factor (P = .004). Socioeconomic variables were not significant in predicting an increased mortality risk in disabled individuals. In conclusion, in addition to mobility and feeding skills, a genetic etiology and hearing deficit are risk factors for early mortality, whereas socioeconomic variables are not. A comprehensive treatment program was found to be a protective factor.
Mesh-Begriff(e)	Adolescent ; Adult ; Age Factors ; Case-Control Studies ; Chi-Square Distribution ; Child ; Child, Preschool ; Developmental Disabilities/epidemiology ; Developmental Disabilities/mortality ; Family ; Female ; Follow-Up Studies ; Humans ; Infant ; Kaplan-Meier Estimate ; Male ; Predictive Value of Tests ; Prognosis ; Retrospective Studies ; Risk Factors
Sprache	Englisch
Erscheinungsdatum	2008-05
Erscheinungsland	United States
Dokumenttyp	Comparative Study ; Journal Article
ZDB-ID	639288-x
ISSN	1708-8283 ; 0883-0738
ISSN (online)	1708-8283
ISSN	0883-0738
DOI	10.1177/0883073807309795
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Isolated Mitochondria Transfer Improves Neuronal Differentiation of Schizophrenia-Derived Induced Pluripotent Stem Cells and Rescues Deficits in a Rat Model of the Disorder.

Robicsek, Odile / Ene, Hila M / Karry, Rachel / Ytzhaki, Ofer / Asor, Eyal / McPhie, Donna / Cohen, Bruce M / Ben-Yehuda, Rotem / Weiner, Ina / Ben-Shachar, Dorit

Schizophrenia bulletin

2017 Band 44, Heft 2, Seite(n) 432–442

Abstract: Dysfunction of mitochondria, key players in various essential cell processes, has been repeatedly reported in schizophrenia (SZ). Recently, several studies have reported functional recovery and cellular viability following mitochondrial transplantation, ... ...

Abstract	Dysfunction of mitochondria, key players in various essential cell processes, has been repeatedly reported in schizophrenia (SZ). Recently, several studies have reported functional recovery and cellular viability following mitochondrial transplantation, mostly in ischemia experimental models. Here, we aimed to demonstrate beneficial effects of isolated active normal mitochondria (IAN-MIT) transfer in vitro and in vivo, using SZ-derived induced pluripotent stem cells (iPSCs) differentiating into glutamatergic neuron, as well as a rodent model of SZ. First, we show that IAN-MIT enter various cell types without manipulation. Next, we show that IAN-MIT transfer into SZ-derived lymphoblasts induces long-lasting improvement in various mitochondrial functions including cellular oxygen consumption and mitochondrial membrane potential (Δ ψ m). We also demonstrate improved differentiation of SZ-derived iPSCs into neurons, by increased expression of neuronal and glutamatergic markers β3-tubulin, synapsin1, and Tbr1 and by an activation of the glutamate-glutamine cycle. In the animal model, we show that intra-prefrontal cortex injection of IAN-MIT in adolescent rats exposed prenatally to a viral mimic prevents mitochondrial Δ ψ m and attentional deficit at adulthood. Our results provide evidence for a direct link between mitochondrial function and SZ-related deficits both in vitro and in vivo and suggest a therapeutic potential for IAN-MIT transfer in diseases with bioenergetic and neurodevelopmental abnormalities such as SZ.
Mesh-Begriff(e)	Animals ; Attention/physiology ; Behavior, Animal/physiology ; Cell Differentiation/physiology ; Cells, Cultured ; Cognitive Dysfunction/metabolism ; Cognitive Dysfunction/physiopathology ; Cognitive Dysfunction/therapy ; Disease Models, Animal ; Female ; Humans ; Induced Pluripotent Stem Cells/metabolism ; Male ; Mitochondria/metabolism ; Mitochondria/transplantation ; Neurons/metabolism ; Prefrontal Cortex ; Rats ; Rats, Wistar ; Schizophrenia/metabolism ; Schizophrenia/therapy
Sprache	Englisch
Erscheinungsdatum	2017-07-13
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	439173-1
ISSN	1745-1701 ; 0586-7614
ISSN (online)	1745-1701
ISSN	0586-7614
DOI	10.1093/schbul/sbx077
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Early postnatal interference with the expression of multiple Sp1 regulated genes leads to disparate behavioral response to sub-chronic and chronic stress in rats.

Asor, Eyal / Belhanes, Hila / Kavushansky, Alexandra / Zubedat, Salman / Klein, Ehud / Avital, Avi / Ben-Shachar, Dorit

Psychoneuroendocrinology

2013 Band 38, Heft 10, Seite(n) 2173–2183

Abstract: Background: It is currently accepted that complex behavior and mental disorder results from a combination of biological susceptibility and exposure to environmental stimuli. Most of the gene-environment interaction models focus on the interaction ... ...

Abstract	Background: It is currently accepted that complex behavior and mental disorder results from a combination of biological susceptibility and exposure to environmental stimuli. Most of the gene-environment interaction models focus on the interaction between the stimuli and a single candidate gene. We suggest that an alternative approach is interference with the expression of multiple genes followed by exposure to environmental insults. Methods: Early interference with gene transcription was performed by treatment of 7 days old Wistar male rats for 4 days with the Sp1/DNA binding inhibitor, mithramycin. Environmental insult was mimicked by exposing these rats during adulthood (34 days) to sub-chronic (12 days, n=30) or chronic stress (28 days, n=48). The effects of mithramycin and stress treatment on the behavioral response and serum corticosterone concentration were assessed. Results: Exposure of mithramycin treated rats to sub-chronic stress led to anxious behavior in the open field test, high startle response, low sucrose preference, indifference to novel objects and high serum corticosterone concentration. However, exposure to chronic stress resulted in normal sucrose preference, startle response and serum corticosterone, novelty seeking behavior and reduced anxiety. In saline treated rats the extension of stress duration led to behavioral and hormonal adaptation to stress. Conclusion: Our study suggests that postnatal temporal interference with multiple gene expression can lead to hyper-responsiveness to environmental stimuli, the features of which affects the phenotypic outcomes. Such a paradigm may be used to model gene-environmental interaction in the etiology of behavioral disorders.
Mesh-Begriff(e)	Animals ; Animals, Newborn ; Behavior, Animal/drug effects ; Chronic Disease ; Exploratory Behavior/drug effects ; Female ; Gene Expression Regulation, Developmental/drug effects ; Gene-Environment Interaction ; Male ; Nucleic Acid Synthesis Inhibitors/pharmacology ; Plicamycin/pharmacology ; Pregnancy ; Rats ; Rats, Wistar ; Sp1 Transcription Factor/physiology ; Stress, Psychological/genetics ; Stress, Psychological/physiopathology ; Time Factors
Chemische Substanzen	Nucleic Acid Synthesis Inhibitors ; Sp1 Transcription Factor ; Plicamycin (NIJ123W41V)
Sprache	Englisch
Erscheinungsdatum	2013-10
Erscheinungsland	England
Dokumenttyp	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	197636-9
ISSN	1873-3360 ; 0306-4530
ISSN (online)	1873-3360
ISSN	0306-4530
DOI	10.1016/j.psyneuen.2013.04.005
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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