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Article: Genome-Wide Methylation Profiling in the Thalamus of Scrapie Sheep.

Hernaiz, Adelaida / Sanz, Arianne / Sentre, Sara / Ranera, Beatriz / Lopez-Pérez, Oscar / Zaragoza, Pilar / Badiola, Juan J / Filali, Hicham / Bolea, Rosa / Toivonen, Janne M / Martín-Burriel, Inmaculada

Frontiers in veterinary science

2022 Volume 9, Page(s) 824677

Abstract: Scrapie is a neurodegenerative disorder belonging to the group of transmissible spongiform encephalopathy (TSE). Scrapie occurs in sheep and goats, which are considered good natural animal models of these TSE. Changes in DNA methylation occur in the ... ...

Abstract	Scrapie is a neurodegenerative disorder belonging to the group of transmissible spongiform encephalopathy (TSE). Scrapie occurs in sheep and goats, which are considered good natural animal models of these TSE. Changes in DNA methylation occur in the central nervous system (CNS) of patients suffering from prion-like neurodegenerative diseases, such as Alzheimer's disease. Nevertheless, potential DNA methylation alterations have not yet been investigated in the CNS of any prion disease model or naturally infected cases, neither in humans nor in animals. Genome-wide DNA methylation patterns were studied in the thalamus obtained from sheep naturally infected with scrapie at a clinical stage (
Language	English
Publishing date	2022-02-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2834243-4
ISSN	2297-1769
ISSN	2297-1769
DOI	10.3389/fvets.2022.824677
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Article ; Online: Cerebrospinal Fluid and Plasma Small Extracellular Vesicles and miRNAs as Biomarkers for Prion Diseases.

López-Pérez, Óscar / Sanz-Rubio, David / Hernaiz, Adelaida / Betancor, Marina / Otero, Alicia / Castilla, Joaquín / Andréoletti, Olivier / Badiola, Juan José / Zaragoza, Pilar / Bolea, Rosa / Toivonen, Janne M / Martín-Burriel, Inmaculada

International journal of molecular sciences

2021 Volume 22, Issue 13

Abstract: Diagnosis of transmissible spongiform encephalopathies (TSEs), or prion diseases, is based on the detection of proteinase K (PK)-resistant ... ...

Abstract	Diagnosis of transmissible spongiform encephalopathies (TSEs), or prion diseases, is based on the detection of proteinase K (PK)-resistant PrP
MeSH term(s)	Biomarkers ; Exosomes/metabolism ; Extracellular Vesicles/metabolism ; Extracellular Vesicles/ultrastructure ; MicroRNAs/blood ; MicroRNAs/cerebrospinal fluid ; MicroRNAs/genetics ; Prion Diseases/blood ; Prion Diseases/cerebrospinal fluid ; Prion Diseases/genetics ; Prion Diseases/metabolism
Chemical Substances	Biomarkers ; MicroRNAs
Language	English
Publishing date	2021-06-25
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms22136822
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Article ; Online: Circulating Cytokines Could Not Be Good Prognostic Biomarkers in a Mouse Model of Amyotrophic Lateral Sclerosis.

Moreno-Martínez, Laura / de la Torre, Miriam / Toivonen, Janne M / Zaragoza, Pilar / García-Redondo, Alberto / Calvo, Ana Cristina / Osta, Rosario

Frontiers in immunology

2019 Volume 10, Page(s) 801

Abstract: Background: ...

Abstract	Background:
MeSH term(s)	Amyotrophic Lateral Sclerosis/blood ; Amyotrophic Lateral Sclerosis/diagnosis ; Amyotrophic Lateral Sclerosis/mortality ; Animals ; Biomarkers ; Cytokines/blood ; Disease Models, Animal ; Disease Progression ; Female ; Male ; Mice ; Mice, Transgenic ; Prognosis
Chemical Substances	Biomarkers ; Cytokines
Language	English
Publishing date	2019-04-12
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2606827-8
ISSN	1664-3224 ; 1664-3224
ISSN (online)	1664-3224
ISSN	1664-3224
DOI	10.3389/fimmu.2019.00801
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Article: Endocrine regulation of aging and reproduction in Drosophila.

Toivonen, Janne M / Partridge, Linda

Molecular and cellular endocrinology

2008 Volume 299, Issue 1, Page(s) 39–50

Abstract: Hormonal signals can modulate lifespan and reproductive capacity across the animal kingdom. The use of model organisms such as worms, flies and mice has been fundamentally important for aging research in the discovery of genetic alterations that can ... ...

Abstract	Hormonal signals can modulate lifespan and reproductive capacity across the animal kingdom. The use of model organisms such as worms, flies and mice has been fundamentally important for aging research in the discovery of genetic alterations that can extend healthy lifespan. The effects of mutations in the insulin and insulin-like growth factor-like signaling (IIS) pathways are evolutionarily conserved in that they can increase lifespan in all three animal models. Additionally, steroids and other lipophilic signaling molecules modulate lifespan in diverse organisms. Here we shall review how major hormonal pathways in the fruit fly Drosophila melanogaster interact to influence reproductive capacity and aging.
MeSH term(s)	Aging/physiology ; Animals ; Biogenic Amines/physiology ; Drosophila/physiology ; Endocrine System/physiology ; Insulin/physiology ; Models, Animal ; Models, Biological ; Reproduction/physiology ; Signal Transduction/physiology ; Somatomedins/physiology
Chemical Substances	Biogenic Amines ; Insulin ; Somatomedins
Language	English
Publishing date	2008-07-17
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	187438-x
ISSN	1872-8057 ; 0303-7207
ISSN (online)	1872-8057
ISSN	0303-7207
DOI	10.1016/j.mce.2008.07.005
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Article ; Online: MicroRNA Alterations in a Tg501 Mouse Model of Prion Disease.

Toivonen, Janne M / Sanz-Rubio, David / López-Pérez, Óscar / Marín-Moreno, Alba / Bolea, Rosa / Osta, Rosario / Badiola, Juan J / Zaragoza, Pilar / Espinosa, Juan-Carlos / Torres, Juan-Maria / Martín-Burriel, Inmaculada

Biomolecules

2020 Volume 10, Issue 6

Abstract: MicroRNAs (miRNAs) may contribute to the development and pathology of many neurodegenerative diseases, including prion diseases. They are also promising biomarker candidates due to their stability in body fluids. We investigated miRNA alterations in a ... ...

Abstract	MicroRNAs (miRNAs) may contribute to the development and pathology of many neurodegenerative diseases, including prion diseases. They are also promising biomarker candidates due to their stability in body fluids. We investigated miRNA alterations in a Tg501 mouse model of prion diseases that expresses a transgene encoding the goat prion protein (
MeSH term(s)	Animals ; Disease Models, Animal ; Gene Expression Profiling ; Gene Expression Regulation ; Gene Regulatory Networks ; Goat Diseases/genetics ; Goat Diseases/pathology ; Goats ; Mice ; Mice, Transgenic ; MicroRNAs/genetics ; Prion Diseases/genetics ; Prion Diseases/pathology ; Prion Diseases/veterinary ; Sequence Analysis, RNA
Chemical Substances	MicroRNAs
Language	English
Publishing date	2020-06-15
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2701262-1
ISSN	2218-273X ; 2218-273X
ISSN (online)	2218-273X
ISSN	2218-273X
DOI	10.3390/biom10060908
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Article ; Online: Xenobiotics that affect oxidative phosphorylation alter differentiation of human adipose-derived stem cells at concentrations that are found in human blood.

Llobet, Laura / Toivonen, Janne M / Montoya, Julio / Ruiz-Pesini, Eduardo / López-Gallardo, Ester

Disease models & mechanisms

2015 Volume 8, Issue 11, Page(s) 1441–1455

Abstract: Adipogenesis is accompanied by differentiation of adipose tissue-derived stem cells to adipocytes. As part of this differentiation, biogenesis of the oxidative phosphorylation system occurs. Many chemical compounds used in medicine, agriculture or other ... ...

Abstract	Adipogenesis is accompanied by differentiation of adipose tissue-derived stem cells to adipocytes. As part of this differentiation, biogenesis of the oxidative phosphorylation system occurs. Many chemical compounds used in medicine, agriculture or other human activities affect oxidative phosphorylation function. Therefore, these xenobiotics could alter adipogenesis. We have analyzed the effects on adipocyte differentiation of some xenobiotics that act on the oxidative phosphorylation system. The tested concentrations have been previously reported in human blood. Our results show that pharmaceutical drugs that decrease mitochondrial DNA replication, such as nucleoside reverse transcriptase inhibitors, or inhibitors of mitochondrial protein synthesis, such as ribosomal antibiotics, diminish adipocyte differentiation and leptin secretion. By contrast, the environmental chemical pollutant tributyltin chloride, which inhibits the ATP synthase of the oxidative phosphorylation system, can promote adipocyte differentiation and leptin secretion, leading to obesity and metabolic syndrome as postulated by the obesogen hypothesis.
MeSH term(s)	Adipocytes/drug effects ; Adipocytes/metabolism ; Adipocytes/secretion ; Adipogenesis/drug effects ; Adipose Tissue/cytology ; Cell Shape/drug effects ; Cells, Cultured ; DNA Replication/drug effects ; DNA, Mitochondrial/biosynthesis ; DNA, Mitochondrial/drug effects ; Humans ; Leptin/secretion ; Mitochondria/drug effects ; Mitochondria/metabolism ; Oxidative Phosphorylation/drug effects ; Phenotype ; Stem Cells/drug effects ; Stem Cells/metabolism ; Stem Cells/secretion ; Time Factors ; Trialkyltin Compounds/toxicity ; Xenobiotics/blood ; Xenobiotics/pharmacology ; Xenobiotics/toxicity
Chemical Substances	DNA, Mitochondrial ; Leptin ; Trialkyltin Compounds ; Xenobiotics ; tributyltin (4XDX163P3D)
Language	English
Publishing date	2015-11
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1754-8411
ISSN (online)	1754-8411
DOI	10.1242/dmm.021774
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Article ; Online: Tetanus toxin C-fragment: the courier and the cure?

Toivonen, Janne M / Oliván, Sara / Osta, Rosario

Toxins

2010 Volume 2, Issue 11, Page(s) 2622–2644

Abstract: In many neurological disorders strategies for a specific delivery of a biological activity from the periphery to the central nervous system (CNS) remains a considerable challenge for successful therapy. Reporter assays have established that the non-toxic ...

Abstract	In many neurological disorders strategies for a specific delivery of a biological activity from the periphery to the central nervous system (CNS) remains a considerable challenge for successful therapy. Reporter assays have established that the non-toxic C-fragment of tetanus toxin (TTC), provided either as protein or encoded by non-viral naked DNA plasmid, binds pre-synaptic motor neuron terminals and can facilitate the retrograde axonal transport of desired therapeutic molecules to the CNS. Alleviated symptoms in animal models of neurological diseases upon delivery of therapeutic molecules offer a hopeful prospect for TTC therapy. This review focuses on what has been learned on TTC-mediated neuronal targeting, and discusses the recent discovery that, instead of being merely a carrier molecule, TTC itself may well harbor neuroprotective properties.
MeSH term(s)	Animals ; Axonal Transport/drug effects ; Disease Models, Animal ; Gene Targeting ; Genetic Therapy ; Humans ; Molecular Targeted Therapy ; Motor Neuron Disease/drug therapy ; Motor Neuron Disease/genetics ; Motor Neurons/drug effects ; Neural Pathways/drug effects ; Neurodegenerative Diseases/drug therapy ; Neurodegenerative Diseases/genetics ; Neuromuscular Junction ; Neuroprotective Agents ; Peptide Fragments/genetics ; Peptide Fragments/therapeutic use ; Presynaptic Terminals/drug effects ; Tetanus Toxin/genetics ; Tetanus Toxin/therapeutic use
Chemical Substances	Neuroprotective Agents ; Peptide Fragments ; Tetanus Toxin ; tetanus toxin fragment C
Language	English
Publishing date	2010-10-29
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2518395-3
ISSN	2072-6651 ; 2072-6651
ISSN (online)	2072-6651
ISSN	2072-6651
DOI	10.3390/toxins2112622
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Article ; Online: Granulocyte Colony-Stimulating Factor Ameliorates Skeletal Muscle Dysfunction in Amyotrophic Lateral Sclerosis Mice and Improves Proliferation of SOD1-G93A Myoblasts in vitro.

Rando, Amaya / Gasco, Samanta / de la Torre, Miriam / García-Redondo, Alberto / Zaragoza, Pilar / Toivonen, Janne M / Osta, Rosario

Neuro-degenerative diseases

2017 Volume 17, Issue 1, Page(s) 1–13

Abstract: Background: Amyotrophic lateral sclerosis (ALS) causes loss of upper and lower motor neurons as well as skeletal muscle (SKM) dysfunction and atrophy. SKM is one of the tissues involved in the development of ALS pathology, and studies in a SOD1-G93A ... ...

Abstract	Background: Amyotrophic lateral sclerosis (ALS) causes loss of upper and lower motor neurons as well as skeletal muscle (SKM) dysfunction and atrophy. SKM is one of the tissues involved in the development of ALS pathology, and studies in a SOD1-G93A mouse model of ALS have demonstrated alterations in SKM degeneration/regeneration marker expression in vivo and defective mutant myoblast proliferation in vitro. Granulocyte colony-stimulating factor (G-CSF) has been shown to alleviate SOD1-G93A pathology. However, it is unknown whether G-CSF may have a direct effect on SKM or derived myoblasts. Objective: To investigate effects of G-CSF and its analog pegfilgrastim (PEGF) on SOD1-G93A- associated SKM markers in vivo and those of G-CSF on myoblast proliferation in vitro. Methods: The effect of PEGF treatment on hematopoietic stem cell mobilization, survival, and motor function was determined. RNA expression of SKM markers associated with mutant SOD1 expression was quantified in response to PEGF treatment in vivo, and the effect of G-CSF on the proliferation of myoblasts derived from mutant and control muscles was determined in vitro. Results: Positive effects of PEGF on hematopoietic stem cell mobilization, survival, and functional assays in SOD1-G93A animals were confirmed. In vivo PEGF treatment augmented the expression of its receptor Csf3r and alleviated typical markers for mutant SOD1 muscle. Additionally, G-CSF was found to directly increase the proliferation of SOD1-G93A, but not wild-type primary myoblasts in vitro. Conclusion: Our results support the beneficial role of the G-CSF analog PEGF in a SOD1-G93A model of ALS. Thus, G-CSF and its analogs may be directly beneficial in diseases where the SKM function is compromised.
MeSH term(s)	Amyotrophic Lateral Sclerosis/drug therapy ; Amyotrophic Lateral Sclerosis/metabolism ; Amyotrophic Lateral Sclerosis/pathology ; Animals ; Cell Proliferation/drug effects ; Cell Proliferation/physiology ; Cell Survival/drug effects ; Cell Survival/physiology ; Cells, Cultured ; Disease Models, Animal ; Female ; Filgrastim ; Granulocyte Colony-Stimulating Factor/pharmacology ; Hematopoietic Stem Cells/drug effects ; Hematopoietic Stem Cells/metabolism ; Humans ; Male ; Mice, Transgenic ; Motor Activity/drug effects ; Motor Activity/physiology ; Muscle, Skeletal/drug effects ; Muscle, Skeletal/metabolism ; Muscle, Skeletal/pathology ; Myoblasts/drug effects ; Myoblasts/metabolism ; Myoblasts/pathology ; Neuromuscular Agents/pharmacology ; Polyethylene Glycols ; Recombinant Proteins/pharmacology ; Superoxide Dismutase-1/genetics ; Superoxide Dismutase-1/metabolism
Chemical Substances	Neuromuscular Agents ; Recombinant Proteins ; SOD1 protein, human ; Granulocyte Colony-Stimulating Factor (143011-72-7) ; Polyethylene Glycols (30IQX730WE) ; pegfilgrastim (3A58010674) ; Superoxide Dismutase-1 (EC 1.15.1.1) ; Filgrastim (PVI5M0M1GW)
Language	English
Publishing date	2017
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2143569-8
ISSN	1660-2862 ; 1660-2854
ISSN (online)	1660-2862
ISSN	1660-2854
DOI	10.1159/000446113
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Zs.A 5918: Show issues			Location: Je nach Verfügbarkeit (siehe Angabe bei Bestand) bis Jg. 1994: Bestellungen von Artikeln über das Online-Bestellformular Jg. 1995 - 2021: Lesesall (2.OG) ab Jg. 2022: Lesesaal (EG)
Zs.MO 567: Show issues

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Article ; Online: MicroRNA-206: a potential circulating biomarker candidate for amyotrophic lateral sclerosis.

Toivonen, Janne M / Manzano, Raquel / Oliván, Sara / Zaragoza, Pilar / García-Redondo, Alberto / Osta, Rosario

PloS one

2014 Volume 9, Issue 2, Page(s) e89065

Abstract: Amyotrophic lateral sclerosis (ALS) is a lethal motor neuron disease that progressively debilitates neuronal cells that control voluntary muscle activity. Biomarkers are urgently needed to facilitate ALS diagnosis and prognosis, and as indicators of ... ...

Abstract	Amyotrophic lateral sclerosis (ALS) is a lethal motor neuron disease that progressively debilitates neuronal cells that control voluntary muscle activity. Biomarkers are urgently needed to facilitate ALS diagnosis and prognosis, and as indicators of therapeutic response in clinical trials. microRNAs (miRNAs), small posttranscriptional modifiers of gene expression, are frequently altered in disease conditions. Besides their important regulatory role in variety of biological processes, miRNAs can also be released into the circulation by pathologically affected tissues and display remarkable stability in body fluids. In a mouse model of ALS that expresses mutated human superoxide dismutase 1 (SOD1-G93A) skeletal muscle is one of the tissues affected early by mutant SOD1 toxicity. To find biomarkers for ALS, we studied miRNA alterations from skeletal muscle and plasma of SOD1-G93A mice, and subsequently tested the levels of the affected miRNAs in the serum from human ALS patients. Fast-twitch and slow-twitch muscles from symptomatic SOD1-G93A mice (age 90 days) and their control littermates were first studied using miRNA microarrays and then evaluated with quantitative PCR from five age groups from neonatal to the terminal disease stage (10-120 days). Among those miRNA changed in various age/gender/muscle groups (miR-206, -1, -133a, -133b, -145, -21, -24), miR-206 was the only one consistently altered during the course of the disease pathology. In both sexes, mature miR-206 was increased in fast-twitch muscles preferably affected in the SOD1-G93A model, with highest expression towards the most severely affected animals. Importantly, miR-206 was also increased in the circulation of symptomatic animals and in a group of 12 definite ALS patients tested. We conclude that miR-206 is elevated in the circulation of symptomatic SOD1-G93A mice and possibly in human ALS patients. Although larger scale studies on ALS patients are warranted, miR-206 is a promising candidate biomarker for this motor neuron disease.
MeSH term(s)	Amyotrophic Lateral Sclerosis/blood ; Amyotrophic Lateral Sclerosis/genetics ; Animals ; Biomarkers/blood ; Female ; Gene Expression Regulation ; Humans ; Male ; Mice ; Mice, Transgenic ; MicroRNAs/blood ; MicroRNAs/genetics ; Middle Aged ; Muscle Fibers, Fast-Twitch/metabolism ; Muscle Fibers, Slow-Twitch/metabolism ; Superoxide Dismutase/genetics ; Superoxide Dismutase-1
Chemical Substances	Biomarkers ; MicroRNAs ; Mirn206 microRNA, mouse ; SOD1 protein, human ; Sod1 protein, mouse (EC 1.15.1.1) ; Superoxide Dismutase (EC 1.15.1.1) ; Superoxide Dismutase-1 (EC 1.15.1.1)
Language	English
Publishing date	2014-02-20
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0089065
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Article ; Online: Chemotherapeutic agent 5-fluorouracil increases survival of SOD1 mouse model of ALS.

Rando, Amaya / de la Torre, Miriam / Martinez-Muriana, Anna / Zaragoza, Pilar / Musaro, Antonio / Hernández, Sara / Navarro, Xavier / Toivonen, Janne M / Osta, Rosario

PloS one

2019 Volume 14, Issue 1, Page(s) e0210752

Abstract: Amyotrophic lateral sclerosis (ALS) is a lethal motor neuron disease with no cure. Currently there are only two ALS drugs approved by the FDA, both with a limited therapeutic effect. In the search for drug candidates for ALS, we studied the effect of ... ...

Abstract	Amyotrophic lateral sclerosis (ALS) is a lethal motor neuron disease with no cure. Currently there are only two ALS drugs approved by the FDA, both with a limited therapeutic effect. In the search for drug candidates for ALS, we studied the effect of known stem cell mobilizing agents (treatment) and antimetabolite 5-fluorouracil (5-FU) (anti-treatment) in SOD1G93A model of ALS. Surprisingly, we found that anti-cancer drug 5-FU increases lifespan, delays the disease onset and improves motor performance in ALS mice. Although we were not able to demonstrate the mechanistic basis of the beneficial 5-FU action in ALS mice, our findings suggest that 5-FU or similar drugs are possible drug candidates for the treatment of motor neuron diseases through drug repurposing.
MeSH term(s)	Amyotrophic Lateral Sclerosis/drug therapy ; Amyotrophic Lateral Sclerosis/genetics ; Amyotrophic Lateral Sclerosis/physiopathology ; Animals ; Antimetabolites, Antineoplastic/therapeutic use ; Bone Marrow Cells/drug effects ; Disease Models, Animal ; Drug Repositioning ; Female ; Fluorouracil/therapeutic use ; Humans ; Leukocyte Count ; Male ; Mice ; Mice, Transgenic ; Motor Activity/drug effects ; Motor Neurons/drug effects ; Motor Neurons/pathology ; Motor Neurons/physiology ; Muscles/drug effects ; Muscles/physiopathology ; Superoxide Dismutase/genetics
Chemical Substances	Antimetabolites, Antineoplastic ; SOD1 G93A protein (EC 1.15.1.1) ; Superoxide Dismutase (EC 1.15.1.1) ; Fluorouracil (U3P01618RT)
Language	English
Publishing date	2019-01-14
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ISSN	1932-6203
ISSN (online)	1932-6203
DOI	10.1371/journal.pone.0210752
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