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Article ; Online: Lysosomal degradation ensures accurate chromosomal segregation to prevent chromosomal instability.

Almacellas, Eugènia / Pelletier, Joffrey / Day, Charles / Ambrosio, Santiago / Tauler, Albert / Mauvezin, Caroline

2020 Volume 17, Issue 3, Page(s) 796–813

Abstract: Lysosomes, as primary degradative organelles, are the endpoint of different converging pathways, including macroautophagy. To date, lysosome degradative function has been mainly studied in interphase cells, while their role during mitosis remains ... ...

Abstract	Lysosomes, as primary degradative organelles, are the endpoint of different converging pathways, including macroautophagy. To date, lysosome degradative function has been mainly studied in interphase cells, while their role during mitosis remains controversial. Mitosis dictates the faithful transmission of genetic material among generations, and perturbations of mitotic division lead to chromosomal instability, a hallmark of cancer. Heretofore, correct mitotic progression relies on the orchestrated degradation of mitotic factors, which was mainly attributed to ubiquitin-triggered proteasome-dependent degradation. Here, we show that mitotic transition also relies on lysosome-dependent degradation, as impairment of lysosomes increases mitotic timing and leads to mitotic errors, thus promoting chromosomal instability. Furthermore, we identified several putative lysosomal targets in mitotic cells. Among them, WAPL, a cohesin regulatory protein, emerged as a novel SQSTM1-interacting protein for targeted lysosomal degradation. Finally, we characterized an atypical nuclear phenotype, the toroidal nucleus, as a novel biomarker for genotoxic screenings. Our results establish lysosome-dependent degradation as an essential event to prevent chromosomal instability.
MeSH term(s)	Animals ; Autophagy/physiology ; Chromosomal Instability/physiology ; Fibroblasts/metabolism ; HeLa Cells ; Humans ; Lysosomes/metabolism ; Mitosis/physiology ; Proteasome Endopeptidase Complex/metabolism ; Transcription Factors/metabolism ; Ubiquitin/metabolism
Chemical Substances	Transcription Factors ; Ubiquitin ; Proteasome Endopeptidase Complex (EC 3.4.25.1)
Language	English
Publishing date	2020-06-23
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2454135-7
ISSN	1554-8635 ; 1554-8627
ISSN (online)	1554-8635
ISSN	1554-8627
DOI	10.1080/15548627.2020.1764727
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Article ; Online: Phosphofructokinases Axis Controls Glucose-Dependent mTORC1 Activation Driven by E2F1.

Almacellas, Eugènia / Pelletier, Joffrey / Manzano, Anna / Gentilella, Antonio / Ambrosio, Santiago / Mauvezin, Caroline / Tauler, Albert

iScience

2019 Volume 20, Page(s) 434–448

Abstract: Cancer cells rely on mTORC1 activity to coordinate mitogenic signaling with nutrients availability for growth. Based on the metabolic function of E2F1, we hypothesize that glucose catabolism driven by E2F1 could participate on mTORC1 activation. Here, we ...

Abstract	Cancer cells rely on mTORC1 activity to coordinate mitogenic signaling with nutrients availability for growth. Based on the metabolic function of E2F1, we hypothesize that glucose catabolism driven by E2F1 could participate on mTORC1 activation. Here, we demonstrate that glucose potentiates E2F1-induced mTORC1 activation by promoting mTORC1 translocation to lysosomes, a process that occurs independently of AMPK activation. We showed that E2F1 regulates glucose metabolism by increasing aerobic glycolysis and identified the PFKFB3 regulatory enzyme as an E2F1-regulated gene important for mTORC1 activation. Furthermore, PFKFB3 and PFK1 were found associated to lysosomes and we demonstrated that modulation of PFKFB3 activity, either by substrate accessibility or expression, regulates the translocation of mTORC1 to lysosomes by direct interaction with Rag B and subsequent mTORC1 activity. Our results support a model whereby a glycolytic metabolon containing phosphofructokinases transiently interacts with the lysosome acting as a sensor platform for glucose catabolism toward mTORC1 activity.
Language	English
Publishing date	2019-10-01
Publishing country	United States
Document type	Journal Article
ISSN	2589-0042
ISSN (online)	2589-0042
DOI	10.1016/j.isci.2019.09.040
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Article ; Online: MYCN concurrence with SAHA-induced cell death in human neuroblastoma cells.

Cortés, Constanza / Kozma, Sara C / Tauler, Albert / Ambrosio, Santiago

Cellular oncology (Dordrecht)

2015 Volume 38, Issue 5, Page(s) 341–352

Abstract: Background: In the past, the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) has been shown to induce apoptosis in several human tumor types, including neuroblastomas. Amplification and over-expression of the MYCN oncogene is a diagnostic hallmark ...

Abstract	Background: In the past, the HDAC inhibitor suberoylanilide hydroxamic acid (SAHA) has been shown to induce apoptosis in several human tumor types, including neuroblastomas. Amplification and over-expression of the MYCN oncogene is a diagnostic hallmark and a poor prognostic indicator in high-risk neuroblastomas. Here, we studied the relationship between MYCN amplification and over-expression and the anti-tumor effect of SAHA to assess whether this drug may serve as a treatment option for high-risk neuroblastomas. Methods: Different human neuroblastoma cell lines, over-expressing or not over-expressing MYCN, were used in this study. Targeted knockdown and exogenous over-expression of MYCN were employed to examine correlations between MYCN expression levels and SAHA responses. After various time periods and concentration exposures to the drug, cell viability was measured by MTS assay, and variations in MYCN mRNA and protein levels were assessed by qPCR and Western blotting, respectively. Results: We found that SAHA decreased cell viability in all cell lines tested through apoptosis induction, and that SAHA had a stronger effect on cell lines carrying an amplified MYCN gene. A decrease in MYCN mRNA and protein levels was observed in the SAHA treated cell lines. Subsequent silencing and exogenous over-expression of MYCN changed the proliferation rate of the cells, but did not have any significant impact on the effect of SAHA on the viability of the cells. We also found that SAHA blocked the expression of MYCN and, by doing so, reduced the effects mediated by this protein. Conclusions: Our results suggest that SAHA may be used as a single-drug treatment option for neuroblastomas with an amplified MYCN gene, and as an adjuvant treatment option for all neuroblastomas.
MeSH term(s)	Apoptosis/drug effects ; Apoptosis/genetics ; Blotting, Western ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Proliferation/genetics ; Cell Survival/drug effects ; Cell Survival/genetics ; Dose-Response Relationship, Drug ; Gene Expression Regulation, Neoplastic/drug effects ; Histone Deacetylase Inhibitors/pharmacology ; Humans ; Hydroxamic Acids/pharmacology ; Microscopy, Fluorescence ; N-Myc Proto-Oncogene Protein ; Neuroblastoma/genetics ; Neuroblastoma/metabolism ; Neuroblastoma/pathology ; Nuclear Proteins/genetics ; Nuclear Proteins/metabolism ; Oncogene Proteins/genetics ; Oncogene Proteins/metabolism ; RNA Interference ; Reverse Transcriptase Polymerase Chain Reaction ; Time Factors
Chemical Substances	Histone Deacetylase Inhibitors ; Hydroxamic Acids ; MYCN protein, human ; N-Myc Proto-Oncogene Protein ; Nuclear Proteins ; Oncogene Proteins ; vorinostat (58IFB293JI)
Language	English
Publishing date	2015-10
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2595109-9
ISSN	2211-3436 ; 1875-8606 ; 2211-3428
ISSN (online)	2211-3436
ISSN	1875-8606 ; 2211-3428
DOI	10.1007/s13402-015-0233-9
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Article ; Online: Dopamine induces mitochondrial depolarization without activating PINK1-mediated mitophagy.

Bondi, Heather / Zilocchi, Mara / Mare, Maria Gabriella / D'Agostino, Gianluca / Giovannardi, Stefano / Ambrosio, Santiago / Fasano, Mauro / Alberio, Tiziana

Journal of neurochemistry

2016 Volume 136, Issue 6, Page(s) 1219–1231

Abstract: Parkinson's disease (PD) is one of the most prevalent neurodegenerative disorders, characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta. PD mostly occurs sporadically and its cause remains unknown, nevertheless the ... ...

Abstract	Parkinson's disease (PD) is one of the most prevalent neurodegenerative disorders, characterized by the loss of dopaminergic neurons in the substantia nigra pars compacta. PD mostly occurs sporadically and its cause remains unknown, nevertheless the discovery of familiar forms of PD, characterized by mutations of genes encoding proteins associated with mitochondria homeostasis, suggests a strong implication of the mitochondrial quality control system in PD. We investigated the effect of dopamine cytosolic accumulation in undifferentiated SH-SY5Y cells, an in vitro model widely used to reproduce impairment of dopamine homeostasis, an early step in PD pathogenesis. A strong depolarization of the mitochondrial membrane was observed after dopamine exposure. Nevertheless, mitochondrial network resulted to assume a peculiar morphology with a distinct pattern of OPA1 and MFN1, key regulators of mitochondrial dynamics. Moreover, selective elimination of dysfunctional mitochondria did not take place, suggesting an impairment of the mitophagic machinery induced by dopamine. Indeed, PINK1 did not accumulate on the outer mitochondrial membrane, nor was parkin recruited to depolarized mitochondria. Altogether, our results indicate that an improper handling of dysfunctional mitochondria may be a leading event in PD pathogenesis. Impaired dopamine (DA) homeostasis and oxidative stress play a key role in the pathogenesis of Parkinson's disease. Free cytosolic dopamine undergoes spontaneous oxidation and generates semiquinonic and quinonic species (DAQ) with the concurrent production of reactive oxygen species (ROS). Dopamine dissipates mitochondrial potential (Δψ
Language	English
Publishing date	2016-03
Publishing country	England
Document type	Journal Article
ZDB-ID	80158-6
ISSN	1471-4159 ; 0022-3042 ; 1474-1644
ISSN (online)	1471-4159
ISSN	0022-3042 ; 1474-1644
DOI	10.1111/jnc.13506
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Article: Histone deacetylase inhibition induces apoptosis and autophagy in human neuroblastoma cells

Francisco, Roser / Pérez-Perarnau, Alba / Cortés, Constanza / Gil, Joan / Tauler, Albert / Ambrosio, Santiago

Cancer letters. 2012 May 1, v. 318, no. 1

2012

Abstract: Neuroblastoma (NB) is the most common solid extracranial tumor in children. Here we showed that trichostatin A, a histone deacetylase inhibitor (HDACi), decreases cell viability in three NB cell lines of different phenotypes. The treatment leads to G2/M- ... ...

Abstract	Neuroblastoma (NB) is the most common solid extracranial tumor in children. Here we showed that trichostatin A, a histone deacetylase inhibitor (HDACi), decreases cell viability in three NB cell lines of different phenotypes. The treatment leads to G2/M-phase arrest, apoptosis and autophagy. Autophagy induction accompanies apoptosis in the most proliferative, N-Myc overexpressing cells. In contrast, autophagy precedes apoptosis and acts as a protective mechanism in the less proliferative, non-N-Myc overexpressing cells. Therefore, the autophagy induction is a relevant event in the NB response to HDACis, and it should be considered in the design of new treatments for this malignancy.
Keywords	apoptosis ; autophagy ; cell viability ; children ; histone deacetylase ; humans ; phenotype
Language	English
Dates of publication	2012-0501
Size	p. 42-52.
Publishing place	Elsevier Ireland Ltd
Document type	Article
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2011.11.036
Database	NAL-Catalogue (AGRICOLA)

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Article: Mechanisms of CPT1C-Dependent AMPAR Trafficking Enhancement.

Gratacòs-Batlle, Esther / Olivella, Mireia / Sánchez-Fernández, Nuria / Yefimenko, Natalia / Miguez-Cabello, Federico / Fadó, Rut / Casals, Núria / Gasull, Xavier / Ambrosio, Santiago / Soto, David

Frontiers in molecular neuroscience

2018 Volume 11, Page(s) 275

Abstract: In neurons, AMPA receptor (AMPAR) function depends essentially on their constituent components:the ion channel forming subunits and ion channel associated proteins. On the other hand, AMPAR trafficking is tightly regulated by a vast number of ... ...

Abstract	In neurons, AMPA receptor (AMPAR) function depends essentially on their constituent components:the ion channel forming subunits and ion channel associated proteins. On the other hand, AMPAR trafficking is tightly regulated by a vast number of intracellular neuronal proteins that bind to AMPAR subunits. It has been recently shown that the interaction between the GluA1 subunit of AMPARs and carnitine palmitoyltransferase 1C (CPT1C), a novel protein partner of AMPARs, is important in modulating surface expression of these ionotropic glutamate receptors. Indeed, synaptic transmission in CPT1C knockout (KO) mice is diminished supporting a positive trafficking role for that protein. However, the molecular mechanisms of such modulation remain unknown although a putative role of CPT1C in depalmitoylating GluA1 has been hypothesized. Here, we explore that possibility and show that CPT1C effect on AMPARs is likely due to changes in the palmitoylation state of GluA1. Based on
Language	English
Publishing date	2018-08-08
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2452967-9
ISSN	1662-5099
ISSN	1662-5099
DOI	10.3389/fnmol.2018.00275
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Article ; Online: V-ATPase: a master effector of E2F1-mediated lysosomal trafficking, mTORC1 activation and autophagy.

Meo-Evoli, Nathalie / Almacellas, Eugènia / Massucci, Francesco Alessandro / Gentilella, Antonio / Ambrosio, Santiago / Kozma, Sara C / Thomas, George / Tauler, Albert

Oncotarget

2015 Volume 6, Issue 29, Page(s) 28057–28070

Abstract: In addition to being a master regulator of cell cycle progression, E2F1 regulates other associated biological processes, including growth and malignancy. Here, we uncover a regulatory network linking E2F1 to lysosomal trafficking and mTORC1 signaling ... ...

Abstract	In addition to being a master regulator of cell cycle progression, E2F1 regulates other associated biological processes, including growth and malignancy. Here, we uncover a regulatory network linking E2F1 to lysosomal trafficking and mTORC1 signaling that involves v-ATPase regulation. By immunofluorescence and time-lapse microscopy we found that E2F1 induces the movement of lysosomes to the cell periphery, and that this process is essential for E2F1-induced mTORC1 activation and repression of autophagy. Gain- and loss-of-function experiments reveal that E2F1 regulates v-ATPase activity and inhibition of v-ATPase activity repressed E2F1-induced lysosomal trafficking and mTORC1 activation. Immunoprecipitation experiments demonstrate that E2F1 induces the recruitment of v-ATPase to lysosomal RagB GTPase, suggesting that E2F1 regulates v-ATPase activity by enhancing the association of V0 and V1 v-ATPase complex. Analysis of v-ATPase subunit expression identified B subunit of V0 complex, ATP6V0B, as a transcriptional target of E2F1. Importantly, ATP6V0B ectopic-expression increased v-ATPase and mTORC1 activity, consistent with ATP6V0B being responsible for mediating the effects of E2F1 on both responses. Our findings on lysosomal trafficking, mTORC1 activation and autophagy suppression suggest that pharmacological intervention at the level of v-ATPase may be an efficacious avenue for the treatment of metastatic processes in tumors overexpressing E2F1.
MeSH term(s)	Autophagy/physiology ; Blotting, Western ; Cell Line, Tumor ; Chromatin Immunoprecipitation ; E2F1 Transcription Factor/metabolism ; Fluorescent Antibody Technique ; Humans ; Immunoprecipitation ; Lysosomes/metabolism ; Mechanistic Target of Rapamycin Complex 1 ; Multiprotein Complexes/metabolism ; Neoplasms/pathology ; Protein Transport/physiology ; RNA, Small Interfering ; Real-Time Polymerase Chain Reaction ; TOR Serine-Threonine Kinases/metabolism ; Transfection ; Vacuolar Proton-Translocating ATPases/metabolism
Chemical Substances	E2F1 Transcription Factor ; E2F1 protein, human ; Multiprotein Complexes ; RNA, Small Interfering ; TOR Serine-Threonine Kinases (EC 2.7.1.1) ; Mechanistic Target of Rapamycin Complex 1 (EC 2.7.11.1) ; Vacuolar Proton-Translocating ATPases (EC 3.6.1.-)
Language	English
Publishing date	2015-09-29
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2560162-3
ISSN	1949-2553 ; 1949-2553
ISSN (online)	1949-2553
ISSN	1949-2553
DOI	10.18632/oncotarget.4812
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Article ; Online: Histone deacetylase inhibition induces apoptosis and autophagy in human neuroblastoma cells.

Francisco, Roser / Pérez-Perarnau, Alba / Cortés, Constanza / Gil, Joan / Tauler, Albert / Ambrosio, Santiago

Cancer letters

2012 Volume 318, Issue 1, Page(s) 42–52

Abstract	Neuroblastoma (NB) is the most common solid extracranial tumor in children. Here we showed that trichostatin A, a histone deacetylase inhibitor (HDACi), decreases cell viability in three NB cell lines of different phenotypes. The treatment leads to G2/M-phase arrest, apoptosis and autophagy. Autophagy induction accompanies apoptosis in the most proliferative, N-Myc overexpressing cells. In contrast, autophagy precedes apoptosis and acts as a protective mechanism in the less proliferative, non-N-Myc overexpressing cells. Therefore, the autophagy induction is a relevant event in the NB response to HDACis, and it should be considered in the design of new treatments for this malignancy.
MeSH term(s)	Acetylation/drug effects ; Apoptosis/drug effects ; Autophagy/drug effects ; Blotting, Western ; Cell Cycle/drug effects ; Cell Line, Tumor ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Histone Deacetylase Inhibitors/pharmacology ; Histone Deacetylases/chemistry ; Histone Deacetylases/metabolism ; Humans ; Hydroxamic Acids/pharmacology ; Neuroblastoma/pathology ; RNA, Messenger/genetics ; Real-Time Polymerase Chain Reaction
Chemical Substances	Histone Deacetylase Inhibitors ; Hydroxamic Acids ; RNA, Messenger ; trichostatin A (3X2S926L3Z) ; Histone Deacetylases (EC 3.5.1.98)
Language	English
Publishing date	2012-05-01
Publishing country	Ireland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	195674-7
ISSN	1872-7980 ; 0304-3835
ISSN (online)	1872-7980
ISSN	0304-3835
DOI	10.1016/j.canlet.2011.11.036
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Article ; Online: Understanding autophagy in cell death control.

Platini, Francesca / Pérez-Tomás, Ricardo / Ambrosio, Santiago / Tessitore, Luciana

Current pharmaceutical design

2009 Volume 16, Issue 1, Page(s) 101–113

Abstract: Autophagy is an evolutionarily conserved degradation pathway which primary functions as a cell survival adaptive mechanism during stress conditions. Autophagy is a tumor suppressor process and induction of the autophagic machinery can cause cell demise ... ...

Abstract	Autophagy is an evolutionarily conserved degradation pathway which primary functions as a cell survival adaptive mechanism during stress conditions. Autophagy is a tumor suppressor process and induction of the autophagic machinery can cause cell demise in apoptosis-resistant cancer. Thus, this metabolic pathway can act either to prevent or to promote carcinogenesis, as well as to modulate the response to anticancer therapies, included drug-induced apoptosis. Conventional therapies exert their cytotoxic activity mainly by inducing apoptosis. Massive activation of the apoptotic program in a tissue can result in cell loss providing a selective advantage for growth to displastic cells and tumor cell subpopulations with high levels of malignancy. This suggests that the activation of autophagy can counteract malignancy. On the contrary, therapeutic intervention-induced apoptosis can eliminate cells with pro-mutational biochemical alterations at risk for initiation, initiated cells and cells of focal and advanced preneoplastic and neoplastic lesions. Thus, pharmacological inhibition of autophagy may enhance apoptosis. Autophagy and apoptosis share common stimuli and signaling pathways, so that the final fate, life or death, depends on the cell response. Recently, accumulating data fuel novel potential therapeutic interventions to modulate autophagy to be beneficial in cancer therapy. This review highlights current knowledges aimed at unraveling the molecular interplay between autophagy and cell death as well as the possible therapeutic exploitation in cancer.
MeSH term(s)	Animals ; Antineoplastic Agents/therapeutic use ; Apoptosis ; Autophagy/drug effects ; Humans ; Neoplasms/drug therapy ; Neoplasms/pathology ; Signal Transduction/drug effects
Chemical Substances	Antineoplastic Agents
Language	English
Publishing date	2009-10-20
Publishing country	United Arab Emirates
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1304236-1
ISSN	1873-4286 ; 1381-6128
ISSN (online)	1873-4286
ISSN	1381-6128
DOI	10.2174/138161210789941810
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Zs.A 4714: Show issues

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Article: Dopamine induces TNFalpha and TNF-R1 expression in SH-SY5Y human neuroblastoma cells.

Gómez-Santos, Cristina / Francisco, Roser / Giménez-Xavier, Pol / Ambrosio, Santiago

Neuroreport

2007 Volume 18, Issue 16, Page(s) 1725–1728

Abstract: Cytotoxic concentrations of dopamine (100-500 microM DA) induce expression of tumour necrosis factor receptor-1 (TNF-R1) and tumour necrosis factor-alpha (TNFalpha) in SH-SY5Y human neuroblastoma cells. TNFalpha expression is dose-dependent and can also ... ...

Abstract	Cytotoxic concentrations of dopamine (100-500 microM DA) induce expression of tumour necrosis factor receptor-1 (TNF-R1) and tumour necrosis factor-alpha (TNFalpha) in SH-SY5Y human neuroblastoma cells. TNFalpha expression is dose-dependent and can also be detected after 6-hydroxydopamine (6-OHDA) or 1-methyl-4-phenylpyridinium iodide (MPP) treatment. The expression of TNF-R1 is also dose-dependent, but was not observed in 6-OHDA or MPP-treatment. Cells not expressing TNF-R1 were insensitive to TNFalpha, whereas those treated with DA showed a further decrease in viability when subsequently treated with TNFalpha. Thus, DA treatment confers sensitivity to TNFalpha. The decrease of cell viability caused by DA was in part prevented by neutralizing TNFalpha with anti-TNFalpha. As TNF-R1 is increased in substantia nigra of Parkinsonian brains, we suggest that nonvesiculated DA might also play a role in inducing TNF-R1 expression and predispose the neuron to the action of cytokines released in a microglia-mediated inflammatory response.
MeSH term(s)	1-Methyl-4-phenylpyridinium/pharmacology ; Antibodies/pharmacology ; Apoptosis/drug effects ; Apoptosis/physiology ; Cell Differentiation/drug effects ; Cell Differentiation/physiology ; Cell Line, Tumor ; Cell Survival/drug effects ; Cell Survival/physiology ; Dopamine/metabolism ; Dopamine/pharmacology ; Dose-Response Relationship, Drug ; Encephalitis/metabolism ; Encephalitis/physiopathology ; Humans ; Neuroblastoma ; Neurons/drug effects ; Neurons/metabolism ; Neurotoxins/pharmacology ; Oxidopamine/pharmacology ; Parkinson Disease/metabolism ; Parkinson Disease/physiopathology ; Receptors, Tumor Necrosis Factor, Type I/drug effects ; Receptors, Tumor Necrosis Factor, Type I/metabolism ; Substantia Nigra/metabolism ; Substantia Nigra/physiopathology ; Tumor Necrosis Factor-alpha/drug effects ; Tumor Necrosis Factor-alpha/metabolism ; Tumor Necrosis Factor-alpha/pharmacology ; Up-Regulation/drug effects ; Up-Regulation/physiology
Chemical Substances	Antibodies ; Neurotoxins ; Receptors, Tumor Necrosis Factor, Type I ; Tumor Necrosis Factor-alpha ; Oxidopamine (8HW4YBZ748) ; 1-Methyl-4-phenylpyridinium (R865A5OY8J) ; Dopamine (VTD58H1Z2X)
Language	English
Publishing date	2007-10-29
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	1049746-8
ISSN	1473-558X ; 0959-4965
ISSN (online)	1473-558X
ISSN	0959-4965
DOI	10.1097/WNR.0b013e3282f0d3db
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