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Buch ; Online ; E-Book: Animal models of behavior genetics

Gewirtz, Jonathan C. / Kim, Yong-Kyu

(Advances in behavior genetics)

2016

Verfasserangabe	Jonathan C. Gewirtz, Yong-Kyu Kim editors
Serientitel	Advances in behavior genetics
Sprache	Englisch
Umfang	1 Online-Ressource (xvi, 389 Seiten), Illustrationen
Verlag	Springer
Erscheinungsort	New York
Erscheinungsland	Vereinigte Staaten
Dokumenttyp	Buch ; Online ; E-Book
Bemerkung	Zugriff für angemeldete ZB MED-Nutzerinnen und -Nutzer
HBZ-ID	HT019156962
ISBN	978-1-4939-3777-6 ; 9781493937752 ; 1-4939-3777-4 ; 1493937758
Datenquelle	ZB MED Katalog Medizin, Gesundheit, Ernährung, Umwelt, Agrar

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Artikel ; Online: Chromatin accessibility and H3K9me3 landscapes reveal long-term epigenetic effects of fetal-neonatal iron deficiency in rat hippocampus.

Liu, Shirelle X / Ramakrishnan, Aarthi / Shen, Li / Gewirtz, Jonathan C / Georgieff, Michael K / Tran, Phu V

BMC genomics

2024 Band 25, Heft 1, Seite(n) 301

Abstract: Background: Iron deficiency (ID) during the fetal-neonatal period results in long-term neurodevelopmental impairments associated with pervasive hippocampal gene dysregulation. Prenatal choline supplementation partially normalizes these effects, ... ...

Abstract	Background: Iron deficiency (ID) during the fetal-neonatal period results in long-term neurodevelopmental impairments associated with pervasive hippocampal gene dysregulation. Prenatal choline supplementation partially normalizes these effects, suggesting an interaction between iron and choline in hippocampal transcriptome regulation. To understand the regulatory mechanisms, we investigated epigenetic marks of genes with altered chromatin accessibility (ATAC-seq) or poised to be repressed (H3K9me3 ChIP-seq) in iron-repleted adult rats having experienced fetal-neonatal ID exposure with or without prenatal choline supplementation. Results: Fetal-neonatal ID was induced by limiting maternal iron intake from gestational day (G) 2 through postnatal day (P) 7. Half of the pregnant dams were given supplemental choline (5.0 g/kg) from G11-18. This resulted in 4 groups at P65 (Iron-sufficient [IS], Formerly Iron-deficient [FID], IS with choline [ISch], and FID with choline [FIDch]). Hippocampi were collected from P65 iron-repleted male offspring and analyzed for chromatin accessibility and H3K9me3 enrichment. 22% and 24% of differentially transcribed genes in FID- and FIDch-groups, respectively, exhibited significant differences in chromatin accessibility, whereas 1.7% and 13% exhibited significant differences in H3K9me3 enrichment. These changes mapped onto gene networks regulating synaptic plasticity, neuroinflammation, and reward circuits. Motif analysis of differentially modified genomic sites revealed significantly stronger choline effects than early-life ID and identified multiple epigenetically modified transcription factor binding sites. Conclusions: This study reveals genome-wide, stable epigenetic changes and epigenetically modifiable gene networks associated with specific chromatin marks in the hippocampus, and lays a foundation to further elucidate iron-dependent epigenetic mechanisms that underlie the long-term effects of fetal-neonatal ID, choline, and their interactions.
Mesh-Begriff(e)	Pregnancy ; Female ; Animals ; Rats ; Male ; Iron/metabolism ; Chromatin/genetics ; Chromatin/metabolism ; Animals, Newborn ; Rats, Sprague-Dawley ; Iron Deficiencies ; Epigenesis, Genetic ; Choline/pharmacology ; Choline/metabolism ; Hippocampus
Chemische Substanzen	Iron (E1UOL152H7) ; Chromatin ; Choline (N91BDP6H0X)
Sprache	Englisch
Erscheinungsdatum	2024-03-21
Erscheinungsland	England
Dokumenttyp	Journal Article
ZDB-ID	2041499-7
ISSN	1471-2164 ; 1471-2164
ISSN (online)	1471-2164
ISSN	1471-2164
DOI	10.1186/s12864-024-10230-4
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Behavioral predictors of individual differences in opioid addiction vulnerability as measured using i.v. self-administration in rats.

Swain, Yayi / Gewirtz, Jonathan C / Harris, Andrew C

Drug and alcohol dependence

2021 Band 221, Seite(n) 108561

Abstract: Background: Like other forms of psychopathology, vulnerability to opioid addiction is subject to wide individual differences. Animal behavioral models are valuable in advancing our understanding of mechanisms underlying vulnerability to the disorder's ... ...

Abstract	Background: Like other forms of psychopathology, vulnerability to opioid addiction is subject to wide individual differences. Animal behavioral models are valuable in advancing our understanding of mechanisms underlying vulnerability to the disorder's development and amenability to treatment. Methods: This review provides an overview of preclinical work on behavioral predictors of opioid addiction vulnerability as measured using the intravenous (i.v.) self-administration (SA) model in rats. We also highlight several new approaches to studying individual differences in opioid addiction vulnerability in preclinical models that could have greater sensitivity and lead to more clinically relevant findings. Results and conclusions: Evidence for the relationship between various behavioral traits and opioid SA in the preclinical literature is limited. With the possible exceptions of sensitivity to opioid agonist/withdrawal effects and stress reactivity, predictors of individual differences in SA of other drugs of abuse (e.g. sensation-seeking, impulsivity) do not predict vulnerability to opioid SA in rats. Refinement of SA measures and the use of multivariate designs and statistics could help identify predictors of opioid SA and lead to more clinically relevant studies on opioid addiction vulnerability.
Mesh-Begriff(e)	Analgesics, Opioid/administration & dosage ; Animals ; Impulsive Behavior ; Individuality ; Male ; Opioid-Related Disorders/psychology ; Rats ; Self Administration ; Substance Withdrawal Syndrome
Chemische Substanzen	Analgesics, Opioid
Sprache	Englisch
Erscheinungsdatum	2021-01-29
Erscheinungsland	Ireland
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	519918-9
ISSN	1879-0046 ; 0376-8716
ISSN (online)	1879-0046
ISSN	0376-8716
DOI	10.1016/j.drugalcdep.2021.108561
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Individual Differences in Different Measures of Opioid Self-Administration in Rats Are Accounted for by a Single Latent Variable.

Swain, Yayi / Waller, Niels G / Gewirtz, Jonathan C / Harris, Andrew C

Frontiers in psychiatry

2021 Band 12, Seite(n) 712163

Abstract: Individual differences in vulnerability to addiction have been widely studied through factor analysis (FA) in humans, a statistical method that identifies "latent" variables (variables that are not measured directly) that reflect the common variance ... ...

Abstract	Individual differences in vulnerability to addiction have been widely studied through factor analysis (FA) in humans, a statistical method that identifies "latent" variables (variables that are not measured directly) that reflect the common variance among a larger number of observed measures. Despite its widespread application in behavioral genetics, FA has not been used in preclinical opioid addiction research. The current study used FA to examine the latent factor structure of four measures of i.v. morphine self-administration (MSA) in rats (i.e., acquisition, demand elasticity, morphine/cue- and stress/cue-induced reinstatement). All four MSA measures are generally assumed in the preclinical literature to reflect "addiction vulnerability," and individual differences in multiple measures of abuse liability are best accounted for by a single latent factor in some human studies. A one-factor model was therefore fitted to the data. Two different regularized FAs indicated that a one-factor model fit our data well. Acquisition, elasticity of demand and morphine/cue-induced reinstatement loaded significantly onto a single latent factor while stress/cue-induced reinstatement did not. Consistent with findings from some human studies, our results indicated a common drug "addiction" factor underlying several measures of opioid SA. However, stress/cue-induced reinstatement loaded poorly onto this factor, suggesting that unique mechanisms mediate individual differences in this vs. other MSA measures. Further establishing FA approaches in drug SA and in preclinical neuropsychopathology more broadly will provide more reliable, clinically relevant core factors underlying disease vulnerability in animal models for further genetic analyses.
Sprache	Englisch
Erscheinungsdatum	2021-09-07
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article
ZDB-ID	2564218-2
ISSN	1664-0640
ISSN	1664-0640
DOI	10.3389/fpsyt.2021.712163
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Buch: Animal models of behavior genetics

Gewirtz, Jonathan C / Kim, Yong-Kyu

(Advances in behavior genetics)

2016

Verfasserangabe	Jonathan C. Gewirtz, Yong-Kyu Kim, editors
Serientitel	Advances in behavior genetics
Mesh-Begriff(e)	Genetics, Behavioral ; Behavior, Animal ; Cognition/physiology ; Models, Animal
Sprache	Englisch
Umfang	xvi, 389 pages :, illustrations.
Dokumenttyp	Buch
ISBN	9781493937752 ; 9781493937776 ; 1493937758 ; 1493937774
Datenquelle	Katalog der US National Library of Medicine (NLM)

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Artikel ; Online: Sex differences in adult social, cognitive, and affective behavioral deficits following neonatal phlebotomy-induced anemia in mice.

Matveeva, Tatyana M / Singh, Garima / Gisslen, Tate A / Gewirtz, Jonathan C / Georgieff, Michael K

Brain and behavior

2021 Band 11, Heft 3, Seite(n) e01780

Abstract: Introduction: Anemia is common in prematurely born infants due to blood loss resulting from frequent phlebotomies and may contribute to their neurobehavioral deficits. Preclinical models of phlebotomy-induced anemia (PIA) have revealed metabolic and ... ...

Abstract	Introduction: Anemia is common in prematurely born infants due to blood loss resulting from frequent phlebotomies and may contribute to their neurobehavioral deficits. Preclinical models of phlebotomy-induced anemia (PIA) have revealed metabolic and genomic changes in multiple brain structures of young mice, yet the impact of neonatal PIA on early-life and adult behavior has not been assessed. Methods: The present study employed a range of behavioral measures in phlebotomized anemic neonatal mice to investigate short- and long-term neurodevelopmental effects. PIA from postnatal (P) days 3 to 14 caused sex-specific changes in social behavior, novelty preference, and anxiety at P17 that persisted into adulthood. Results: Our preclinical model suggests that PIA may contribute to acute and long-term behavioral and affective deficits and warrants further substantiation of the observed behavioral phenomena in larger samples. Conclusions: We conclude that this model is a useful tool for beginning to better understand the lasting effect that early-life PIA might have on the developing brain. The differential impact of PIA on male and female subjects warrants further exploration for the development of appropriately targeted interventions.
Mesh-Begriff(e)	Anemia ; Animals ; Behavior, Animal ; Cognition ; Female ; Male ; Mice ; Phlebotomy ; Sex Characteristics
Sprache	Englisch
Erscheinungsdatum	2021-02-19
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	2623587-0
ISSN	2162-3279 ; 2162-3279
ISSN (online)	2162-3279
ISSN	2162-3279
DOI	10.1002/brb3.1780
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel: Prenatal Iron Deficiency and Choline Supplementation Interact to Epigenetically Regulate Jarid1b and Bdnf in the Rat Hippocampus into Adulthood

Liu, Shirelle X. / Barks, Amanda K. / Lunos, Scott / Gewirtz, Jonathan C. / Georgieff, Michael K. / Tran, Phu V.

Nutrients. 2021 Dec. 17, v. 13, no. 12

2021

Abstract: Early-life iron deficiency (ID) causes long-term neurocognitive impairments and gene dysregulation that can be partially mitigated by prenatal choline supplementation. The long-term gene dysregulation is hypothesized to underlie cognitive dysfunction. ... ...

Abstract	Early-life iron deficiency (ID) causes long-term neurocognitive impairments and gene dysregulation that can be partially mitigated by prenatal choline supplementation. The long-term gene dysregulation is hypothesized to underlie cognitive dysfunction. However, mechanisms by which iron and choline mediate long-term gene dysregulation remain unknown. In the present study, using a well-established rat model of fetal-neonatal ID, we demonstrated that ID downregulated hippocampal expression of the gene encoding JmjC-ARID domain-containing protein 1B (JARID1B), an iron-dependent histone H3K4 demethylase, associated with a higher histone deacetylase 1 (HDAC1) enrichment and a lower enrichment of acetylated histone H3K9 (H3K9ac) and phosphorylated cAMP response element-binding protein (pCREB). Likewise, ID reduced transcriptional capacity of the gene encoding brain-derived neurotrophic factor (BDNF), a target of JARID1B, associated with repressive histone modifications such as lower H3K9ac and pCREB enrichments at the Bdnf promoters in the adult rat hippocampus. Prenatal choline supplementation did not prevent the ID-induced chromatin modifications at these loci but induced long-lasting repressive chromatin modifications in the iron-sufficient adult rats. Collectively, these findings demonstrated that the iron-dependent epigenetic mechanism mediated by JARID1B accounted for long-term Bdnf dysregulation by early-life ID. Choline supplementation utilized a separate mechanism to rescue the effect of ID on neural gene regulation. The negative epigenetic effects of choline supplementation in the iron-sufficient rat hippocampus necessitate additional investigations prior to its use as an adjunctive therapeutic agent.
Schlagwörter	adulthood ; adults ; animal models ; choline ; chromatin ; cognitive disorders ; epigenetics ; genes ; hippocampus ; histone deacetylase ; histones ; iron ; rats ; therapeutics ; transcription (genetics)
Sprache	Englisch
Erscheinungsverlauf	2021-1217
Erscheinungsort	Multidisciplinary Digital Publishing Institute
Dokumenttyp	Artikel
ZDB-ID	2518386-2
ISSN	2072-6643
ISSN	2072-6643
DOI	10.3390/nu13124527
Datenquelle	NAL Katalog (AGRICOLA)

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Artikel ; Online: Causally mapping human threat extinction relevant circuits with depolarizing brain stimulation methods.

Webler, Ryan D / Oathes, Desmond J / van Rooij, Sanne J H / Gewirtz, Jonathan C / Nahas, Ziad / Lissek, Shmuel M / Widge, Alik S

Neuroscience and biobehavioral reviews

2022 Band 144, Seite(n) 105005

Abstract: Laboratory threat extinction paradigms and exposure-based therapy both involve repeated, safe confrontation with stimuli previously experienced as threatening. This fundamental procedural overlap supports laboratory threat extinction as a compelling ... ...

Abstract	Laboratory threat extinction paradigms and exposure-based therapy both involve repeated, safe confrontation with stimuli previously experienced as threatening. This fundamental procedural overlap supports laboratory threat extinction as a compelling analogue of exposure-based therapy. Threat extinction impairments have been detected in clinical anxiety and may contribute to exposure-based therapy non-response and relapse. However, efforts to improve exposure outcomes using techniques that boost extinction - primarily rodent extinction - have largely failed to date, potentially due to fundamental differences between rodent and human neurobiology. In this review, we articulate a comprehensive pre-clinical human research agenda designed to overcome these failures. We describe how connectivity guided depolarizing brain stimulation methods (i.e., TMS and DBS) can be applied concurrently with threat extinction and dual threat reconsolidation-extinction paradigms to causally map human extinction relevant circuits and inform the optimal integration of these methods with exposure-based therapy. We highlight candidate targets including the amygdala, hippocampus, ventromedial prefrontal cortex, dorsal anterior cingulate cortex, and mesolimbic structures, and propose hypotheses about how stimulation delivered at specific learning phases could strengthen threat extinction.
Mesh-Begriff(e)	Humans ; Extinction, Psychological/physiology ; Magnetic Resonance Imaging ; Brain ; Prefrontal Cortex/physiology ; Amygdala ; Brain Mapping
Sprache	Englisch
Erscheinungsdatum	2022-12-19
Erscheinungsland	United States
Dokumenttyp	Journal Article ; Review
ZDB-ID	282464-4
ISSN	1873-7528 ; 0149-7634
ISSN (online)	1873-7528
ISSN	0149-7634
DOI	10.1016/j.neubiorev.2022.105005
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Prenatal Iron Deficiency and Choline Supplementation Interact to Epigenetically Regulate

Liu, Shirelle X / Barks, Amanda K / Lunos, Scott / Gewirtz, Jonathan C / Georgieff, Michael K / Tran, Phu V

Nutrients

2021 Band 13, Heft 12

Abstract	Early-life iron deficiency (ID) causes long-term neurocognitive impairments and gene dysregulation that can be partially mitigated by prenatal choline supplementation. The long-term gene dysregulation is hypothesized to underlie cognitive dysfunction. However, mechanisms by which iron and choline mediate long-term gene dysregulation remain unknown. In the present study, using a well-established rat model of fetal-neonatal ID, we demonstrated that ID downregulated hippocampal expression of the gene encoding JmjC-ARID domain-containing protein 1B (JARID1B), an iron-dependent histone H3K4 demethylase, associated with a higher histone deacetylase 1 (HDAC1) enrichment and a lower enrichment of acetylated histone H3K9 (H3K9ac) and phosphorylated cAMP response element-binding protein (pCREB). Likewise, ID reduced transcriptional capacity of the gene encoding brain-derived neurotrophic factor (BDNF), a target of JARID1B, associated with repressive histone modifications such as lower H3K9ac and pCREB enrichments at the
Mesh-Begriff(e)	Animals ; Brain-Derived Neurotrophic Factor/genetics ; Brain-Derived Neurotrophic Factor/metabolism ; Choline/administration & dosage ; Choline/pharmacology ; DNA-Binding Proteins/genetics ; DNA-Binding Proteins/metabolism ; Dietary Supplements ; Epigenesis, Genetic ; Female ; Hippocampus/drug effects ; Hippocampus/metabolism ; Iron Deficiencies ; Jumonji Domain-Containing Histone Demethylases/genetics ; Jumonji Domain-Containing Histone Demethylases/metabolism ; Nuclear Proteins/metabolism ; Pregnancy ; Prenatal Exposure Delayed Effects ; Rats ; Repressor Proteins/metabolism
Chemische Substanzen	Bdnf protein, rat ; Brain-Derived Neurotrophic Factor ; DNA-Binding Proteins ; Nuclear Proteins ; Repressor Proteins ; Jumonji Domain-Containing Histone Demethylases (EC 1.14.11.-) ; Kdm5b protein, rat (EC 1.14.11.-) ; Choline (N91BDP6H0X)
Sprache	Englisch
Erscheinungsdatum	2021-12-17
Erscheinungsland	Switzerland
Dokumenttyp	Journal Article
ZDB-ID	2518386-2
ISSN	2072-6643 ; 2072-6643
ISSN (online)	2072-6643
ISSN	2072-6643
DOI	10.3390/nu13124527
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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Artikel ; Online: Repeated morphine exposure activates synaptogenesis and other neuroplasticity-related gene networks in the dorsomedial prefrontal cortex of male and female rats.

Liu, Shirelle X / Gades, Mari S / Swain, Yayi / Ramakrishnan, Aarthi / Harris, Andrew C / Tran, Phu V / Gewirtz, Jonathan C

Drug and alcohol dependence

2021 Band 221, Seite(n) 108598

Abstract: Background: Opioid abuse is a chronic disorder likely involving stable neuroplastic modifications. While a number of molecules contributing to these changes have been identified, the broader spectrum of genes and gene networks that are affected by ... ...

Abstract	Background: Opioid abuse is a chronic disorder likely involving stable neuroplastic modifications. While a number of molecules contributing to these changes have been identified, the broader spectrum of genes and gene networks that are affected by repeated opioid administration remain understudied. Methods: We employed Next-Generation RNA-sequencing (RNA-seq) followed by quantitative chromatin immunoprecipitation to investigate changes in gene expression and their regulation in adult male and female rats' dorsomedial prefrontal cortex (dmPFC) after a regimen of daily injection of morphine (5.0 mg/kg; 10 days). Ingenuity Pathway Analysis (IPA) was used to analyze affected molecular pathways, gene networks, and associated regulatory factors. A complementary behavioral study evaluated the effects of the same morphine injection regimen on locomotor activity, pain sensitivity, and somatic withdrawal signs. Results: Behaviorally, repeated morphine injection induced locomotor hyperactivity and hyperalgesia in both sexes. 90 % of differentially expressed genes (DEGs) in morphine-treated rats were upregulated in both males and females, with a 35 % overlap between sexes. A substantial number of DEGs play roles in synaptic signaling and neuroplasticity. Chromatin immunoprecipitation revealed enrichment of H3 acetylation, a transcriptionally activating chromatin mark. Although broadly similar, some differences were revealed in the gene ontology networks enriched in females and males. Conclusions: Our results cohere with findings from previous studies based on a priori gene selection. Our results also reveal novel genes and molecular pathways that are upregulated by repeated morphine exposure, with some common to males and females and others that are sex-specific.
Mesh-Begriff(e)	Analgesics, Opioid ; Animals ; Female ; Gene Regulatory Networks/drug effects ; Hyperalgesia/genetics ; Male ; Morphine/pharmacology ; Neurogenesis/drug effects ; Neuronal Plasticity/drug effects ; Opioid-Related Disorders/metabolism ; Opioid-Related Disorders/physiopathology ; Prefrontal Cortex/metabolism ; Prefrontal Cortex/physiology ; Rats
Chemische Substanzen	Analgesics, Opioid ; Morphine (76I7G6D29C)
Sprache	Englisch
Erscheinungsdatum	2021-02-13
Erscheinungsland	Ireland
Dokumenttyp	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	519918-9
ISSN	1879-0046 ; 0376-8716
ISSN (online)	1879-0046
ISSN	0376-8716
DOI	10.1016/j.drugalcdep.2021.108598
Datenquelle	MEDical Literature Analysis and Retrieval System OnLINE

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