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Article ; Online: Identification of ER/SR resident proteins as biomarkers for ER/SR calcium depletion in skeletal muscle cells.

Greer, Lacey K / Meilleur, Katherine G / Harvey, Brandon K / Wires, Emily S

2022 Volume 17, Issue 1, Page(s) 225

Abstract: Background: Aberrations to endoplasmic/sarcoplasmic reticulum (ER/SR) calcium concentration can result in the departure of endogenous proteins in a phenomenon termed exodosis. Redistribution of the ER/SR proteome can have deleterious effects to cell ... ...

Abstract	Background: Aberrations to endoplasmic/sarcoplasmic reticulum (ER/SR) calcium concentration can result in the departure of endogenous proteins in a phenomenon termed exodosis. Redistribution of the ER/SR proteome can have deleterious effects to cell function and cell viability, often contributing to disease pathogenesis. Many proteins prone to exodosis reside in the ER/SR via an ER retention/retrieval sequence (ERS) and are involved in protein folding, protein modification, and protein trafficking. While the consequences of their extracellular presence have yet to be fully delineated, the proteins that have undergone exodosis may be useful for biomarker development. Skeletal muscle cells rely upon tightly coordinated ER/SR calcium release for muscle contractions, and perturbations to calcium homeostasis can result in myopathies. Ryanodine receptor type-1 (RYR1) is a calcium release channel located in the SR. Mutations to the RYR1 gene can compromise calcium homeostasis leading to a vast range of clinical phenotypes encompassing hypotonia, myalgia, respiratory insufficiency, ophthalmoplegia, fatigue and malignant hyperthermia (MH). There are currently no FDA approved treatments for RYR1-related myopathies (RYR1-RM). Results: Here we examine the exodosis profile of skeletal muscle cells following ER/SR calcium depletion. Proteomic analysis identified 4,465 extracellular proteins following ER/SR calcium depletion with 1,280 proteins significantly different than vehicle. A total of 54 ERS proteins were identified and 33 ERS proteins significantly increased following ER/SR calcium depletion. Specifically, ERS protein, mesencephalic astrocyte-derived neurotrophic factor (MANF), was elevated following calcium depletion, making it a potential biomarker candidate for human samples. Despite no significant elevation of MANF in plasma levels among healthy volunteers and RYR1-RM individuals, MANF plasma levels positively correlated with age in RYR1-RM individuals, presenting a potential biomarker of disease progression. Selenoprotein N (SEPN1) was also detected only in extracellular samples following ER/SR calcium depletion. This protein is integral to calcium handling and SEPN1 variants have a causal role in SEPN1-related myopathies (SEPN1-RM). Extracellular presence of ER/SR membrane proteins may provide new insight into proteomic alterations extending beyond ERS proteins. Pre-treatment of skeletal muscle cells with bromocriptine, an FDA approved drug recently found to have anti-exodosis effects, curbed exodosis of ER/SR resident proteins. Conclusion: Changes to the extracellular content caused by intracellular calcium dysregulation presents an opportunity for biomarker development and drug discovery.
MeSH term(s)	Biomarkers/metabolism ; Calcium/metabolism ; Endoplasmic Reticulum/metabolism ; Humans ; Muscle Fibers, Skeletal/metabolism ; Muscle, Skeletal/metabolism ; Muscular Diseases/genetics ; Proteins/metabolism ; Proteomics ; Ryanodine Receptor Calcium Release Channel/genetics ; Ryanodine Receptor Calcium Release Channel/metabolism ; Sarcoplasmic Reticulum/metabolism
Chemical Substances	Biomarkers ; Proteins ; Ryanodine Receptor Calcium Release Channel ; Calcium (SY7Q814VUP)
Language	English
Publishing date	2022-06-13
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Research Support, N.I.H., Extramural
ZDB-ID	2225857-7
ISSN	1750-1172 ; 1750-1172
ISSN (online)	1750-1172
ISSN	1750-1172
DOI	10.1186/s13023-022-02368-9
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Article ; Online: Nucleic Acid-Based Therapeutic Approach for Spinal and Bulbar Muscular Atrophy and Related Neurological Disorders.

Hirunagi, Tomoki / Sahashi, Kentaro / Meilleur, Katherine G / Katsuno, Masahisa

Genes

2022 Volume 13, Issue 1

Abstract: The recent advances in nucleic acid therapeutics demonstrate the potential to treat hereditary neurological disorders by targeting their causative genes. Spinal and bulbar muscular atrophy (SBMA) is an X-linked and adult-onset neurodegenerative disorder ... ...

Abstract	The recent advances in nucleic acid therapeutics demonstrate the potential to treat hereditary neurological disorders by targeting their causative genes. Spinal and bulbar muscular atrophy (SBMA) is an X-linked and adult-onset neurodegenerative disorder caused by the expansion of trinucleotide cytosine-adenine-guanine repeats, which encodes a polyglutamine tract in the
MeSH term(s)	Animals ; Bulbo-Spinal Atrophy, X-Linked/genetics ; Bulbo-Spinal Atrophy, X-Linked/pathology ; Bulbo-Spinal Atrophy, X-Linked/therapy ; Humans ; Nervous System Diseases/genetics ; Nervous System Diseases/pathology ; Nervous System Diseases/therapy ; Oligonucleotides, Antisense/administration & dosage ; RNA, Small Interfering/administration & dosage
Chemical Substances	Oligonucleotides, Antisense ; RNA, Small Interfering
Language	English
Publishing date	2022-01-05
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2527218-4
ISSN	2073-4425 ; 2073-4425
ISSN (online)	2073-4425
ISSN	2073-4425
DOI	10.3390/genes13010109
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Article: Nucleic Acid-Based Therapeutic Approach for Spinal and Bulbar Muscular Atrophy and Related Neurological Disorders

Hirunagi, Tomoki / Sahashi, Kentaro / Meilleur, Katherine G. / Katsuno, Masahisa

Genes. 2022 Jan. 05, v. 13, no. 1

2022

Abstract	The recent advances in nucleic acid therapeutics demonstrate the potential to treat hereditary neurological disorders by targeting their causative genes. Spinal and bulbar muscular atrophy (SBMA) is an X-linked and adult-onset neurodegenerative disorder caused by the expansion of trinucleotide cytosine-adenine-guanine repeats, which encodes a polyglutamine tract in the androgen receptor gene. SBMA belongs to the family of polyglutamine diseases, in which the use of nucleic acids for silencing a disease-causing gene, such as antisense oligonucleotides and small interfering RNAs, has been intensively studied in animal models and clinical trials. A unique feature of SBMA is that both motor neuron and skeletal muscle pathology contribute to disease manifestations, including progressive muscle weakness and atrophy. As both motor neurons and skeletal muscles can be therapeutic targets in SBMA, nucleic acid-based approaches for other motor neuron diseases and myopathies may further lead to the development of a treatment for SBMA. Here, we review studies of nucleic acid-based therapeutic approaches in SBMA and related neurological disorders and discuss current limitations and perspectives to apply these approaches to patients with SBMA.
Keywords	androgen receptors ; animals ; genes ; motor neurons ; muscles ; muscular atrophy ; neurodegenerative diseases ; oligonucleotides ; skeletal muscle ; therapeutics
Language	English
Dates of publication	2022-0105
Publishing place	Multidisciplinary Digital Publishing Institute
Document type	Article
ZDB-ID	2527218-4
ISSN	2073-4425
ISSN	2073-4425
DOI	10.3390/genes13010109
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Article: Differential inclusion of

Silverstein, Sarah / Orbach, Rotem / Syeda, Safoora / Foley, A Reghan / Gorokhova, Svetlana / Meilleur, Katherine G / Leach, Meganne E / Uapinyoying, Prech / Chao, Katherine R / Donkervoort, Sandra / Bönnemann, Carsten G

medRxiv : the preprint server for health sciences

2024

Abstract: Biallelic pathogenic variants in the gene encoding nebulin ( ...

Abstract	Biallelic pathogenic variants in the gene encoding nebulin (
Language	English
Publishing date	2024-03-26
Publishing country	United States
Document type	Preprint
DOI	10.1101/2024.03.25.24304535
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Article ; Online: Review of RyR1 pathway and associated pathomechanisms.

Witherspoon, Jessica W / Meilleur, Katherine G

Acta neuropathologica communications

2016 Volume 4, Issue 1, Page(s) 121

Abstract: Ryanodine receptor isoform-1 (RyR1) is a major calcium channel in skeletal muscle important for excitation-contraction coupling. Mutations in the RYR1 gene yield RyR1 protein dysfunction that manifests clinically as RYR1-related congenital myopathies ( ... ...

Abstract	Ryanodine receptor isoform-1 (RyR1) is a major calcium channel in skeletal muscle important for excitation-contraction coupling. Mutations in the RYR1 gene yield RyR1 protein dysfunction that manifests clinically as RYR1-related congenital myopathies (RYR1-RM) and/or malignant hyperthermia susceptibility (MHS). Individuals with RYR1-RM and/or MHS exhibit varying symptoms and severity. The symptoms impair quality of life and put patients at risk for early mortality, yet the cause of varying severity is not well understood. Currently, there is no Food and Drug Administration (FDA) approved treatment for RYR1-RM. Discovery of effective treatments is therefore critical, requiring knowledge of the RyR1 pathway. The purpose of this review is to compile work published to date on the RyR1 pathway and to implicate potential regions as targets for treatment. The RyR1 pathway is comprised of protein-protein interactions, protein-ligand interactions, and post-translational modifications, creating an activation/regulatory macromolecular complex. Given the complexity of this pathway, we divided these interactions and modifications into six regulatory groups. Three of several RyR1 interacting proteins, FK506-binding protein 12 (FKBP12), triadin, and calmodulin, were identified as playing important roles across all groups and may serve as promising target sites for treatment. Also, variability in disease severity may be influenced by prolongation or hyperactivity of post-translational modifications resulting from RyR1 dysfunction.
MeSH term(s)	Animals ; Humans ; Muscle, Skeletal/metabolism ; Ryanodine Receptor Calcium Release Channel/metabolism
Chemical Substances	Ryanodine Receptor Calcium Release Channel
Language	English
Publishing date	2016-11-17
Publishing country	England
Document type	Journal Article ; Review
ZDB-ID	2715589-4
ISSN	2051-5960 ; 2051-5960
ISSN (online)	2051-5960
ISSN	2051-5960
DOI	10.1186/s40478-016-0392-6
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Article ; Online: Ryanodine Receptor 1-Related Myopathies: Diagnostic and Therapeutic Approaches.

Lawal, Tokunbor A / Todd, Joshua J / Meilleur, Katherine G

Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics

2018 Volume 15, Issue 4, Page(s) 885–899

Abstract: Ryanodine receptor type 1-related myopathies (RYR1-RM) are the most common class of congenital myopathies. Historically, RYR1-RM classification and diagnosis have been guided by histopathologic findings on muscle biopsy. Main histological subtypes of ... ...

Abstract	Ryanodine receptor type 1-related myopathies (RYR1-RM) are the most common class of congenital myopathies. Historically, RYR1-RM classification and diagnosis have been guided by histopathologic findings on muscle biopsy. Main histological subtypes of RYR1-RM include central core disease, multiminicore disease, core-rod myopathy, centronuclear myopathy, and congenital fiber-type disproportion. A range of RYR1-RM clinical phenotypes has also emerged more recently and includes King Denborough syndrome, RYR1 rhabdomyolysis-myalgia syndrome, atypical periodic paralysis, congenital neuromuscular disease with uniform type 1 fibers, and late-onset axial myopathy. This expansion of the RYR1-RM disease spectrum is due, in part, to implementation of next-generation sequencing methods, which include the entire RYR1 coding sequence rather than being restricted to hotspot regions. These methods enhance diagnostic capabilities, especially given historic limitations of histopathologic and clinical overlap across RYR1-RM. Both dominant and recessive modes of inheritance have been documented, with the latter typically associated with a more severe clinical phenotype. As with all congenital myopathies, no FDA-approved treatments exist to date. Here, we review histopathologic, clinical, imaging, and genetic diagnostic features of the main RYR1-RM subtypes. We also discuss the current state of treatments and focus on disease-modulating (nongenetic) therapeutic strategies under development for RYR1-RM. Finally, perspectives for future approaches to treatment development are broached.
MeSH term(s)	Animals ; Humans ; Muscular Diseases/diagnosis ; Muscular Diseases/genetics ; Muscular Diseases/therapy ; Ryanodine Receptor Calcium Release Channel/genetics ; Ryanodine Receptor Calcium Release Channel/metabolism
Chemical Substances	Ryanodine Receptor Calcium Release Channel
Language	English
Publishing date	2018-11-01
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	2316693-9
ISSN	1878-7479 ; 1933-7213
ISSN (online)	1878-7479
ISSN	1933-7213
DOI	10.1007/s13311-018-00677-1
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Article ; Online: Rare genetic variants impact muscle strength.

Huang, Yunfeng / Bodnar, Dora / Chen, Chia-Yen / Sanchez-Andrade, Gabriela / Sanderson, Mark / Shi, Jun / Meilleur, Katherine G / Hurles, Matthew E / Gerety, Sebastian S / Tsai, Ellen A / Runz, Heiko

Nature communications

2023 Volume 14, Issue 1, Page(s) 3449

Abstract: Muscle strength is highly heritable and predictive for multiple adverse health outcomes including mortality. Here, we present a rare protein-coding variant association study in 340,319 individuals for hand grip strength, a proxy measure of muscle ... ...

Abstract	Muscle strength is highly heritable and predictive for multiple adverse health outcomes including mortality. Here, we present a rare protein-coding variant association study in 340,319 individuals for hand grip strength, a proxy measure of muscle strength. We show that the exome-wide burden of rare protein-truncating and damaging missense variants is associated with a reduction in hand grip strength. We identify six significant hand grip strength genes, KDM5B, OBSCN, GIGYF1, TTN, RB1CC1, and EIF3J. In the example of the titin (TTN) locus we demonstrate a convergence of rare with common variant association signals and uncover genetic relationships between reduced hand grip strength and disease. Finally, we identify shared mechanisms between brain and muscle function and uncover additive effects between rare and common genetic variation on muscle strength.
MeSH term(s)	Humans ; Hand Strength ; Muscle Strength/genetics ; Muscular Diseases ; Mutation, Missense ; Genetic Predisposition to Disease ; Carrier Proteins
Chemical Substances	GIGYF1 protein, human ; Carrier Proteins
Language	English
Publishing date	2023-06-10
Publishing country	England
Document type	Journal Article
ZDB-ID	2553671-0
ISSN	2041-1723 ; 2041-1723
ISSN (online)	2041-1723
ISSN	2041-1723
DOI	10.1038/s41467-023-39247-1
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Article ; Online: Unusually severe muscular dystrophy upon in-frame deletion of the dystrophin rod domain and lack of compensation by membrane-localized utrophin.

Gorokhova, Svetlana / Schessl, Joachim / Zou, Yaqun / Yang, Michele L / Heydemann, Peter T / Sufit, Robert L / Meilleur, Katherine / Donkervoort, Sandra / Medne, Livija / Finkel, Richard S / Bönnemann, Carsten G

Med (New York, N.Y.)

2023 Volume 4, Issue 4, Page(s) 245–251.e3

Abstract: Background: Utrophin, a dystrophin homolog, is consistently upregulated in muscles of patients with Duchenne muscular dystrophy (DMD) and is believed to partially compensate for the lack of dystrophin in dystrophic muscle. Even though several animal ... ...

Abstract	Background: Utrophin, a dystrophin homolog, is consistently upregulated in muscles of patients with Duchenne muscular dystrophy (DMD) and is believed to partially compensate for the lack of dystrophin in dystrophic muscle. Even though several animal studies support the idea that utrophin can modulate DMD disease severity, human clinical data are scarce. Methods: We describe a patient with the largest reported in-frame deletion in the DMD gene, including exons 10-60 and thus encompassing the entire rod domain. Findings: The patient presented with an unusually early and severe progressive weakness, initially suggesting congenital muscular dystrophy. Immunostaining of his muscle biopsy showed that the mutant protein was able to localize at the sarcolemma and stabilize the dystrophin-associated complex. Strikingly, utrophin protein was absent from the sarcolemmal membrane despite the upregulation of utrophin mRNA. Conclusions: Our results suggest that the internally deleted and dysfunctional dystrophin lacking the entire rod domain may exert a dominant-negative effect by preventing upregulated utrophin protein from reaching the sarcolemmal membrane and thus blocking its partial rescue of muscle function. This unique case may set a lower size limit for similar constructs in potential gene therapy approaches. Funding: This work was supported by a grant from MDA USA (MDA3896) and by grant number R01AR051999 from NIAMS/NIH to C.G.B.
MeSH term(s)	Animals ; Humans ; Dystrophin/genetics ; Dystrophin/metabolism ; Utrophin/genetics ; Utrophin/metabolism ; Utrophin/therapeutic use ; Muscular Dystrophy, Duchenne/genetics ; Muscular Dystrophy, Duchenne/pathology ; Muscles/metabolism ; Muscles/pathology ; Sarcolemma/metabolism ; Sarcolemma/pathology
Chemical Substances	Dystrophin ; Utrophin
Language	English
Publishing date	2023-03-10
Publishing country	United States
Document type	Case Reports ; Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Research Support, N.I.H., Intramural
ISSN	2666-6340
ISSN (online)	2666-6340
DOI	10.1016/j.medj.2023.02.005
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Article ; Online: Rycal S48168 (ARM210) for

Todd, Joshua J / Lawal, Tokunbor A / Chrismer, Irene C / Kokkinis, Angela / Grunseich, Christopher / Jain, Minal S / Waite, Melissa R / Biancavilla, Victoria / Pocock, Shavonne / Brooks, Kia / Mendoza, Christopher J / Norato, Gina / Cheung, Ken / Riekhof, Willa / Varma, Pooja / Colina-Prisco, Claudia / Emile-Backer, Magalie / Meilleur, Katherine G / Marks, Andrew R /

Webb, Yael / Marcantonio, Eugene E / Foley, A Reghan / Bönnemann, Carsten G / Mohassel, Payam

EClinicalMedicine

2024 Volume 68, Page(s) 102433

Abstract: Background: RYR1: Methods: Participants received 120 mg (n = 3) or 200 mg (n = 4) S48168 (ARM210) daily for 29 days. The primary endpoint was safety and tolerability. Exploratory endpoints included S48168 (ARM210) pharmacokinetics (PK), target ... ...

Abstract	Background: RYR1 Methods: Participants received 120 mg (n = 3) or 200 mg (n = 4) S48168 (ARM210) daily for 29 days. The primary endpoint was safety and tolerability. Exploratory endpoints included S48168 (ARM210) pharmacokinetics (PK), target engagement, motor function measure (MFM)-32, hand grip and pinch strength, timed functional tests, PROMIS fatigue scale, semi-quantitative physical exam strength measurements, and oxidative stress biomarkers. The trial was registered with clinicaltrials.gov (NCT04141670) and was conducted at the National Institutes of Health Clinical Center between October 28, 2019 and December 12, 2021. Findings: S48168 (ARM210) was well-tolerated, did not cause any serious adverse events, and exhibited a dose-dependent PK profile. Three of four participants who received the 200 mg/day dose reported improvements in PROMIS-fatigue at 28 days post-dosing, and also demonstrated improved proximal muscle strength on physical examination. Interpretation: S48168 (ARM210) demonstrated favorable safety, tolerability, and PK, in Funding: NINDS and NINR Intramural Research Programs, NIH Clinical Center Bench to Bedside Award (2017-551673), ARMGO Pharma Inc., and its development partner Les Laboratoires Servier.
Language	English
Publishing date	2024-01-25
Publishing country	England
Document type	Journal Article
ISSN	2589-5370
ISSN (online)	2589-5370
DOI	10.1016/j.eclinm.2024.102433
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Article ; Online: Ryanodine receptor 1-related disorders: an historical perspective and proposal for a unified nomenclature.

Lawal, Tokunbor A / Todd, Joshua J / Witherspoon, Jessica W / Bönnemann, Carsten G / Dowling, James J / Hamilton, Susan L / Meilleur, Katherine G / Dirksen, Robert T

Skeletal muscle

2020 Volume 10, Issue 1, Page(s) 32

Abstract: The RYR1 gene, which encodes the sarcoplasmic reticulum calcium release channel or type 1 ryanodine receptor (RyR1) of skeletal muscle, was sequenced in 1988 and RYR1 variations that impair calcium homeostasis and increase susceptibility to malignant ... ...

Abstract	The RYR1 gene, which encodes the sarcoplasmic reticulum calcium release channel or type 1 ryanodine receptor (RyR1) of skeletal muscle, was sequenced in 1988 and RYR1 variations that impair calcium homeostasis and increase susceptibility to malignant hyperthermia were first identified in 1991. Since then, RYR1-related myopathies (RYR1-RM) have been described as rare, histopathologically and clinically heterogeneous, and slowly progressive neuromuscular disorders. RYR1 variants can lead to dysfunctional RyR1-mediated calcium release, malignant hyperthermia susceptibility, elevated oxidative stress, deleterious post-translational modifications, and decreased RyR1 expression. RYR1-RM-affected individuals can present with delayed motor milestones, contractures, scoliosis, ophthalmoplegia, and respiratory insufficiency.Historically, RYR1-RM-affected individuals were diagnosed based on morphologic features observed in muscle biopsies including central cores, cores and rods, central nuclei, fiber type disproportion, and multi-minicores. However, these histopathologic features are not always specific to RYR1-RM and often change over time. As additional phenotypes were associated with RYR1 variations (including King-Denborough syndrome, exercise-induced rhabdomyolysis, lethal multiple pterygium syndrome, adult-onset distal myopathy, atypical periodic paralysis with or without myalgia, mild calf-predominant myopathy, and dusty core disease) the overlap among diagnostic categories is ever increasing. With the continuing emergence of new clinical subtypes along the RYR1 disease spectrum and reports of adult-onset phenotypes, nuanced nomenclatures have been reported (RYR1- [related, related congenital, congenital] myopathies). In this narrative review, we provide historical highlights of RYR1 research, accounts of the main diagnostic disease subtypes and propose RYR1-related disorders (RYR1-RD) as a unified nomenclature to describe this complex and evolving disease spectrum.
MeSH term(s)	Animals ; Humans ; Neuromuscular Diseases/genetics ; Neuromuscular Diseases/metabolism ; Neuromuscular Diseases/pathology ; Phenotype ; Ryanodine Receptor Calcium Release Channel/genetics ; Ryanodine Receptor Calcium Release Channel/metabolism ; Ryanodine Receptor Calcium Release Channel/standards ; Terminology as Topic
Chemical Substances	RYR1 protein, human ; Ryanodine Receptor Calcium Release Channel
Language	English
Publishing date	2020-11-16
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, N.I.H., Intramural ; Review
ZDB-ID	2595637-1
ISSN	2044-5040 ; 2044-5040
ISSN (online)	2044-5040
ISSN	2044-5040
DOI	10.1186/s13395-020-00243-4
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