LIVIVO - Search results -

Search results

Result 1 - 10 of total 12

Search options

Article ; Online: Cognitive impairments in a Down syndrome model with abnormal hippocampal and prefrontal dynamics and cytoarchitecture.

Muza, Phillip M / Bush, Daniel / Pérez-González, Marta / Zouhair, Ines / Cleverley, Karen / Sopena, Miriam L / Aoidi, Rifdat / West, Steven J / Good, Mark / Tybulewicz, Victor L J / Walker, Matthew C / Fisher, Elizabeth M C / Chang, Pishan

iScience

2023 Volume 26, Issue 2, Page(s) 106073

Abstract: The Dp(10)2Yey mouse carries a ∼2.3-Mb intra-chromosomal duplication of mouse chromosome 10 (Mmu10) that has homology to human chromosome 21, making it an essential model for aspects of Down syndrome (DS, trisomy 21). In this study, we investigated ... ...

Abstract	The Dp(10)2Yey mouse carries a ∼2.3-Mb intra-chromosomal duplication of mouse chromosome 10 (Mmu10) that has homology to human chromosome 21, making it an essential model for aspects of Down syndrome (DS, trisomy 21). In this study, we investigated neuronal dysfunction in the Dp(10)2Yey mouse and report spatial memory impairment and anxiety-like behavior alongside altered neural activity in the medial prefrontal cortex (mPFC) and hippocampus (HPC). Specifically, Dp(10)2Yey mice showed impaired spatial alternation associated with increased sharp-wave ripple activity in mPFC during a period of memory consolidation, and reduced mobility in a novel environment accompanied by reduced theta-gamma phase-amplitude coupling in HPC. Finally, we found alterations in the number of interneuron subtypes in mPFC and HPC that may contribute to the observed phenotypes and highlight potential approaches to ameliorate the effects of human trisomy 21.
Language	English
Publishing date	2023-01-28
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2023.106073
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

This service is chargeable due to the Delivery terms set by subito. Orders including an article and supplementary material will be classified as separate orders. In these cases, fees will be demanded for each order.

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Increased dosage of DYRK1A leads to congenital heart defects in a mouse model of Down syndrome.

Science translational medicine

2024 Volume 16, Issue 731, Page(s) eadd6883

Abstract: Down syndrome (DS) is caused by trisomy of human chromosome 21 (Hsa21). DS is a gene dosage disorder that results in multiple phenotypes including congenital heart defects. This clinically important cardiac pathology is the result of a third copy of one ... ...

Abstract	Down syndrome (DS) is caused by trisomy of human chromosome 21 (Hsa21). DS is a gene dosage disorder that results in multiple phenotypes including congenital heart defects. This clinically important cardiac pathology is the result of a third copy of one or more of the approximately 230 genes on Hsa21, but the identity of the causative dosage-sensitive genes and hence mechanisms underlying this cardiac pathology remain unclear. Here, we show that hearts from human fetuses with DS and embryonic hearts from the Dp1Tyb mouse model of DS show reduced expression of mitochondrial respiration genes and cell proliferation genes. Using systematic genetic mapping, we determined that three copies of the dual-specificity tyrosine phosphorylation-regulated kinase 1A (
MeSH term(s)	Animals ; Humans ; Mice ; Disease Models, Animal ; Down Syndrome/genetics ; Genes, Mitochondrial ; Heart Defects, Congenital/genetics ; Myocytes, Cardiac ; Trisomy
Chemical Substances	Dyrk1a protein, mouse (EC 2.7.1.-)
Language	English
Publishing date	2024-01-24
Publishing country	United States
Document type	Journal Article
ZDB-ID	2518854-9
ISSN	1946-6242 ; 1946-6234
ISSN (online)	1946-6242
ISSN	1946-6234
DOI	10.1126/scitranslmed.add6883
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Zs.A 6941: Show issues

Location:
Je nach Verfügbarkeit (siehe Angabe bei Bestand)
bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular
ab Jg. 2022: Lesesaal (EG)

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Cognitive impairments in a Down syndrome model with abnormal hippocampal and prefrontal dynamics and cytoarchitecture

Phillip M. Muza / Daniel Bush / Marta Pérez-González / Ines Zouhair / Karen Cleverley / Miriam L. Sopena / Rifdat Aoidi / Steven J. West / Mark Good / Victor L.J. Tybulewicz / Matthew C. Walker / Elizabeth M.C. Fisher / Pishan Chang

iScience, Vol 26, Iss 2, Pp 106073- (2023)

2023

Abstract: Summary: The Dp(10)2Yey mouse carries a ∼2.3-Mb intra-chromosomal duplication of mouse chromosome 10 (Mmu10) that has homology to human chromosome 21, making it an essential model for aspects of Down syndrome (DS, trisomy 21). In this study, we ... ...

Abstract	Summary: The Dp(10)2Yey mouse carries a ∼2.3-Mb intra-chromosomal duplication of mouse chromosome 10 (Mmu10) that has homology to human chromosome 21, making it an essential model for aspects of Down syndrome (DS, trisomy 21). In this study, we investigated neuronal dysfunction in the Dp(10)2Yey mouse and report spatial memory impairment and anxiety-like behavior alongside altered neural activity in the medial prefrontal cortex (mPFC) and hippocampus (HPC). Specifically, Dp(10)2Yey mice showed impaired spatial alternation associated with increased sharp-wave ripple activity in mPFC during a period of memory consolidation, and reduced mobility in a novel environment accompanied by reduced theta-gamma phase-amplitude coupling in HPC. Finally, we found alterations in the number of interneuron subtypes in mPFC and HPC that may contribute to the observed phenotypes and highlight potential approaches to ameliorate the effects of human trisomy 21.
Keywords	Developmental neuroscience ; Transcriptomics ; Model organism ; Science ; Q
Language	English
Publishing date	2023-02-01T00:00:00Z
Publisher	Elsevier
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Fine-tuning of MEK signaling is pivotal for limiting B and T cell activation.

Houde, Nicolas / Beuret, Laurent / Bonaud, Amélie / Fortier-Beaulieu, Simon-Pierre / Truchon-Landry, Kim / Aoidi, Rifdat / Pic, Émilie / Alouche, Nagham / Rondeau, Vincent / Schlecht-Louf, Géraldine / Balabanian, Karl / Espéli, Marion / Charron, Jean

Cell reports

2022 Volume 38, Issue 2, Page(s) 110223

Abstract: MEK1 and MEK2, the only known activators of ERK, are attractive therapeutic candidates for both cancer and autoimmune diseases. However, how MEK signaling finely regulates immune cell activation is only partially understood. To address this question, we ... ...

Abstract	MEK1 and MEK2, the only known activators of ERK, are attractive therapeutic candidates for both cancer and autoimmune diseases. However, how MEK signaling finely regulates immune cell activation is only partially understood. To address this question, we specifically delete Mek1 in hematopoietic cells in the Mek2 null background. Characterization of an allelic series of Mek mutants reveals the presence of distinct degrees of spontaneous B cell activation, which are inversely proportional to the levels of MEK proteins and ERK activation. While Mek1 and Mek2 null mutants have a normal lifespan, 1Mek1 and 1Mek2 mutants retaining only one functional Mek1 or Mek2 allele in hematopoietic cell lineages die from glomerulonephritis and lymphoproliferative disorders, respectively. This establishes that the fine-tuning of the ERK/MAPK pathway is critical to regulate B and T cell activation and function and that each MEK isoform plays distinct roles during lymphocyte activation and disease development.
MeSH term(s)	Alleles ; Animals ; B-Lymphocytes/metabolism ; Female ; Humans ; Lymphocyte Activation/genetics ; Lymphocyte Activation/physiology ; MAP Kinase Kinase 1/metabolism ; MAP Kinase Kinase 1/physiology ; MAP Kinase Kinase 2/genetics ; MAP Kinase Kinase 2/metabolism ; MAP Kinase Kinase 2/physiology ; MAP Kinase Signaling System/genetics ; MAP Kinase Signaling System/physiology ; Male ; Mice ; Mice, 129 Strain ; Mitogen-Activated Protein Kinase 1/metabolism ; Phosphorylation ; Signal Transduction/physiology ; T-Lymphocytes/metabolism
Chemical Substances	Mitogen-Activated Protein Kinase 1 (EC 2.7.11.24) ; MAP Kinase Kinase 1 (EC 2.7.12.2) ; MAP Kinase Kinase 2 (EC 2.7.12.2) ; Map2k1 protein, mouse (EC 2.7.12.2) ; Map2k2 protein, mouse (EC 2.7.12.2)
Language	English
Publishing date	2022-01-12
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2649101-1
ISSN	2211-1247 ; 2211-1247
ISSN (online)	2211-1247
ISSN	2211-1247
DOI	10.1016/j.celrep.2021.110223
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Functional redundancy of the kinases MEK1 and MEK2: Rescue of the Mek1 mutant phenotype by Mek2 knock-in reveals a protein threshold effect.

Aoidi, Rifdat / Maltais, Annie / Charron, Jean

Science signaling

2016 Volume 9, Issue 412, Page(s) ra9

Abstract: The mammalian genome contains two mitogen-activated protein kinase (MAPK) kinase (MEK)-encoding genes, Mek1 and Mek2. MEKs phosphorylate and activate the two extracellular signal-regulated kinase (ERK) isoforms ERK1 and ERK2. Mek1(-/-) embryos die due to ...

Abstract	The mammalian genome contains two mitogen-activated protein kinase (MAPK) kinase (MEK)-encoding genes, Mek1 and Mek2. MEKs phosphorylate and activate the two extracellular signal-regulated kinase (ERK) isoforms ERK1 and ERK2. Mek1(-/-) embryos die due to placental defects, whereas Mek2(-/-) mice survive with a normal life span and fertility, suggesting that MEK1 has functions not shared by MEK2. However, most Mek1(+/-)Mek2(+/-) embryos also die from placental defects, indicating that both Mek genes contribute to placental development. To assess the functional specificity of the Mek1 and Mek2 genes, we produced a Mek1 knock-in allele in which the Mek2 coding sequences were placed under the control of Mek1 regulatory sequences (Mek1(2) allele). Mek1(2/2) mice were viable with no apparent phenotype, indicating rescue by MEK2 and functional redundancy between the two MEK proteins. However, Mek1(2/-) embryos with Mek2 in only one of the Mek1 alleles and the other Mek1 allele null died from abnormal placenta, suggesting a dosage effect. Analysis of mice from a Mek1 Mek2 allelic series revealed that the occurrence of the placenta phenotype correlated with the amount of MEK protein independently of which MEK isoform was produced. Thus, although MEK1 and MEK2 can substitute for each other, a minimum amount of MEK is critical for placenta development and embryo survival.
MeSH term(s)	Alleles ; Animals ; Crosses, Genetic ; Epitopes/chemistry ; Female ; Gene Knock-In Techniques ; Genotype ; Heterozygote ; Immunohistochemistry ; MAP Kinase Kinase 1/chemistry ; MAP Kinase Kinase 1/genetics ; MAP Kinase Kinase 2/chemistry ; MAP Kinase Kinase 2/genetics ; Mice ; Microscopy, Fluorescence ; Mutation ; Phenotype ; Phosphorylation ; Placenta/metabolism ; Pregnancy ; Pregnancy, Animal
Chemical Substances	Epitopes ; MAP Kinase Kinase 1 (EC 2.7.12.2) ; MAP Kinase Kinase 2 (EC 2.7.12.2) ; Map2k1 protein, mouse (EC 2.7.12.2) ; Map2k2 protein, mouse (EC 2.7.12.2)
Language	English
Publishing date	2016-01-26
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2417226-1
ISSN	1937-9145 ; 1945-0877
ISSN (online)	1937-9145
ISSN	1945-0877
DOI	10.1126/scisignal.aad5658
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: MEK2 Negatively Regulates Lipopolysaccharide-Mediated IL-1β Production through HIF-1α Expression.

Talwar, Harvinder / Bouhamdan, Mohamad / Bauerfeld, Christian / Talreja, Jaya / Aoidi, Rifdat / Houde, Nicolas / Charron, Jean / Samavati, Lobelia

Journal of immunology (Baltimore, Md. : 1950)

2019 Volume 202, Issue 6, Page(s) 1815–1825

Abstract: LPS-activated macrophages require metabolic reprogramming and glucose uptake mediated by hypoxia-inducible factor (HIF)-1 α and glucose transporter 1 (Glut1) expression for proinflammatory cytokine production, especially IL-1β. This process is tightly ... ...

Abstract	LPS-activated macrophages require metabolic reprogramming and glucose uptake mediated by hypoxia-inducible factor (HIF)-1 α and glucose transporter 1 (Glut1) expression for proinflammatory cytokine production, especially IL-1β. This process is tightly regulated through activation of MAPK kinases, including the MEK/ERK pathway as well as several transcription factors including HIF-1α. Although MAPK kinase (MEK) 2 deficiency had no significant effect on NO, TNF-α, or IL-12 production in response to LPS challenge, MEK2-deficient murine bone marrow-derived macrophages (BMDMs) exhibited lower IL-10 production. Importantly, MEK2-deficient BMDMs exhibited a preserved ERK1/2 phosphorylation, higher HIF-1α and Glut1 levels, and substantially increased IL-1β as well as IL-6 production in response to LPS stimulation. Knockdown of HIF-1α expression via short interference RNA decreased the level of HIF-1α expression in MEK2-deficient BMDMs and decreased IL-1β production in response to LPS treatment. Furthermore, we performed gain of function experiments by overexpressing MEK2 protein in RAW264.7 cells. LPS stimulation of MEK2 overexpressed in RAW264.7 cells led to a marked decreased IL-1β production. Finally, we investigated the role of
MeSH term(s)	Animals ; Hypoxia-Inducible Factor 1, alpha Subunit/immunology ; Hypoxia-Inducible Factor 1, alpha Subunit/metabolism ; Inflammation/chemically induced ; Inflammation/immunology ; Inflammation/metabolism ; Interleukin-1beta/immunology ; Interleukin-1beta/metabolism ; Lipopolysaccharides/toxicity ; MAP Kinase Kinase 2/immunology ; MAP Kinase Kinase 2/metabolism ; Macrophages/immunology ; Macrophages/metabolism ; Mice ; Mice, Mutant Strains ; RAW 264.7 Cells
Chemical Substances	Hif1a protein, mouse ; Hypoxia-Inducible Factor 1, alpha Subunit ; Interleukin-1beta ; Lipopolysaccharides ; MAP Kinase Kinase 2 (EC 2.7.12.2) ; Map2k2 protein, mouse (EC 2.7.12.2)
Language	English
Publishing date	2019-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	3056-9
ISSN	1550-6606 ; 0022-1767 ; 1048-3233 ; 1047-7381
ISSN (online)	1550-6606
ISSN	0022-1767 ; 1048-3233 ; 1047-7381
DOI	10.4049/jimmunol.1801477
Database	MEDical Literature Analysis and Retrieval System OnLINE

In stock of ZB MED Cologne/Königswinter

Ud II Zs.37: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 28: Show issues

Order via subito

Details ▾
- See ZB MED holdings
- Order with fees

Article ; Online: Lung development requires an active ERK/MAPK pathway in the lung mesenchyme.

Boucherat, Olivier / Landry-Truchon, Kim / Aoidi, Rifdat / Houde, Nicolas / Nadeau, Valérie / Charron, Jean / Jeannotte, Lucie

Developmental dynamics : an official publication of the American Association of Anatomists

2017 Volume 246, Issue 1, Page(s) 72–82

Abstract: Background: Reciprocal epithelial-mesenchymal communications are critical throughout lung development, dictating branching morphogenesis and cell specification. Numerous signaling molecules are involved in these interactions, but the way epithelial- ... ...

Abstract	Background: Reciprocal epithelial-mesenchymal communications are critical throughout lung development, dictating branching morphogenesis and cell specification. Numerous signaling molecules are involved in these interactions, but the way epithelial-mesenchymal crosstalk is coordinated remains unclear. The ERK/MAPK pathway transduces several important signals in lung formation. Epithelial inactivation of both Mek genes, encoding ERK/MAPK kinases, causes lung agenesis and death. Conversely, Mek mutation in mesenchyme results in lung hypoplasia, trachea cartilage malformations, kyphosis, omphalocele, and death. Considering the negative impact of kyphosis and omphalocele on intrathoracic space and, consequently, on lung growth, the exact role of ERK/MAPK pathway in lung mesenchyme remains unresolved. Results: To address the role of the ERK/MAPK pathway in lung mesenchyme in absence of kyphosis and omphalocele, we used the Tbx4 Conclusions: Lung development necessitates a functional ERK/MAPK pathway in the lung mesenchymal layer in order to coordinate efficient epithelial-mesenchymal interactions. Developmental Dynamics 246:72-82, 2017. © 2016 Wiley Periodicals, Inc.
Language	English
Publishing date	2017-01
Publishing country	United States
Document type	Journal Article
ZDB-ID	1102541-4
ISSN	1097-0177 ; 1058-8388
ISSN (online)	1097-0177
ISSN	1058-8388
DOI	10.1002/dvdy.24464
Database	MEDical Literature Analysis and Retrieval System OnLINE

Full text online

Accessible to users with ZB MED library card

In stock of ZB MED Cologne/Königswinter

Ub I Zs.60: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 2021: Bestellungen von Artikeln über das Online-Bestellformular ab Jg. 2022: Lesesaal (EG)
Zs.MG 64: Show issues

Order via subito

Details ▾

Article ; Online: Maternal iron deficiency perturbs embryonic cardiovascular development in mice.

Nature communications

2021 Volume 12, Issue 1, Page(s) 3447

Abstract: Congenital heart disease (CHD) is the most common class of human birth defects, with a prevalence of 0.9% of births. However, two-thirds of cases have an unknown cause, and many of these are thought to be caused by in utero exposure to environmental ... ...

Abstract	Congenital heart disease (CHD) is the most common class of human birth defects, with a prevalence of 0.9% of births. However, two-thirds of cases have an unknown cause, and many of these are thought to be caused by in utero exposure to environmental teratogens. Here we identify a potential teratogen causing CHD in mice: maternal iron deficiency (ID). We show that maternal ID in mice causes severe cardiovascular defects in the offspring. These defects likely arise from increased retinoic acid signalling in ID embryos. The defects can be prevented by iron administration in early pregnancy. It has also been proposed that teratogen exposure may potentiate the effects of genetic predisposition to CHD through gene-environment interaction. Here we show that maternal ID increases the severity of heart and craniofacial defects in a mouse model of Down syndrome. It will be important to understand if the effects of maternal ID seen here in mice may have clinical implications for women.
MeSH term(s)	Animals ; Aorta, Thoracic/abnormalities ; Biomarkers/metabolism ; Cardiovascular System/embryology ; Cell Differentiation ; Coronary Vessels/embryology ; Coronary Vessels/pathology ; Dietary Supplements ; Edema/pathology ; Embryo, Mammalian/abnormalities ; Embryo, Mammalian/pathology ; Embryonic Development ; Female ; Gene Expression Profiling ; Gene-Environment Interaction ; Green Fluorescent Proteins/metabolism ; Iron/metabolism ; Iron Deficiencies ; Lymphatic Vessels/embryology ; Lymphatic Vessels/pathology ; Mice, Inbred C57BL ; Myocardium/pathology ; Myocytes, Cardiac/metabolism ; Myocytes, Cardiac/pathology ; Penetrance ; Phenotype ; Pregnancy ; Signal Transduction ; Stem Cells/pathology ; Transgenes ; Tretinoin/metabolism ; Mice
Chemical Substances	Biomarkers ; Green Fluorescent Proteins (147336-22-9) ; Tretinoin (5688UTC01R) ; Iron (E1UOL152H7)
Language	English
Publishing date	2021-06-08
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-021-23660-5
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Article ; Online: Mek1

Aoidi, Rifdat / Houde, Nicolas / Landry-Truchon, Kim / Holter, Michael / Jacquet, Kevin / Charron, Louis / Krishnaswami, Suguna Rani / Yu, Benjamin D / Rauen, Katherine A / Bisson, Nicolas / Newbern, Jason / Charron, Jean

Disease models & mechanisms

2018 Volume 11, Issue 3

Abstract: The RAS/MAPK signaling pathway is one of the most investigated pathways, owing to its established role in numerous cellular processes and implication in cancer. Germline mutations in genes encoding members of the RAS/MAPK pathway also cause severe ... ...

Abstract	The RAS/MAPK signaling pathway is one of the most investigated pathways, owing to its established role in numerous cellular processes and implication in cancer. Germline mutations in genes encoding members of the RAS/MAPK pathway also cause severe developmental syndromes collectively known as RASopathies. These syndromes share overlapping characteristics, including craniofacial dysmorphology, cardiac malformations, cutaneous abnormalities and developmental delay. Cardio-facio-cutaneous syndrome (CFC) is a rare RASopathy associated with mutations in
MeSH term(s)	Alleles ; Amino Acid Sequence ; Animals ; Base Sequence ; Brain/pathology ; Cell Count ; Ectodermal Dysplasia/genetics ; Embryo, Mammalian/cytology ; Facies ; Failure to Thrive/genetics ; Fibroblasts/enzymology ; Gene Duplication ; Glial Fibrillary Acidic Protein/metabolism ; Heart Defects, Congenital/genetics ; Humans ; MAP Kinase Kinase 1/chemistry ; MAP Kinase Kinase 1/genetics ; MAP Kinase Signaling System/genetics ; Mice ; Mice, Mutant Strains ; Mutation/genetics ; Oligodendrocyte Transcription Factor 2/metabolism
Chemical Substances	Glial Fibrillary Acidic Protein ; Olig2 protein, mouse ; Oligodendrocyte Transcription Factor 2 ; MAP Kinase Kinase 1 (EC 2.7.12.2) ; Map2k1 protein, mouse (EC 2.7.12.2)
Language	English
Publishing date	2018-03-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ISSN	1754-8411
ISSN (online)	1754-8411
DOI	10.1242/dmm.031278
Database	MEDical Literature Analysis and Retrieval System OnLINE

Order via subito

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

Article ; Online: Maternal iron deficiency perturbs embryonic cardiovascular development in mice

Nature Communications, Vol 12, Iss 1, Pp 1-

2021 Volume 17

Abstract: From mouse experiments, the authors link iron deficiency in mothers with cardiovascular defects and increased retinoic acid signalling in their offspring, and giving iron early in pregnancy can prevent most defects. ...

Abstract	From mouse experiments, the authors link iron deficiency in mothers with cardiovascular defects and increased retinoic acid signalling in their offspring, and giving iron early in pregnancy can prevent most defects.
Keywords	Science ; Q
Language	English
Publishing date	2021-06-01T00:00:00Z
Publisher	Nature Portfolio
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

Full text online

Full text

Inter-library loan at ZB MED

Your chosen title can be delivered directly to ZB MED Cologne location if you are registered as a user at ZB MED Cologne.

To top

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

Inter-library loan at ZB MED

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

Full text online

More links

Kategorien

In stock of ZB MED Cologne/Königswinter

Order via subito

More links

Kategorien

Order via subito

More links

Kategorien

Order via subito

Inter-library loan at ZB MED

Full text online

More links

Kategorien

Inter-library loan at ZB MED