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Pesquisa : D12.776.157.530.400 [Categoria DeCS]
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[PMID]:29374927
[Au] Autor:You X; Wei ZR
[Ad] Endereço:Department of Plastic Surgery, the Affiliated Hospital of Zunyi Medical College, Zunyi, 563000, China.
[Ti] Título:[Advances in the research of function of Merkel cells in tactile formation of skin].
[So] Source:Zhonghua Shao Shang Za Zhi;34(1):51-54, 2018 Jan 20.
[Is] ISSN:1009-2587
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:Skin is the largest sense organ of human, with many mechanoreceptor cells under epidermis or dermis of skin and Merkel cell is one of them. It has been confirmed that Merkel cells play an important role in the process of mechanical transmission of mammalian soft tactile stimulation. Researches showed that Merkel cells had close relation to tactile formation and functioned by Merkel cell-neurite complexes and ion channels Piezo2. This article reviews Merkel cells and the function, problem and prospect of Merkel cells in tactile formation.
[Mh] Termos MeSH primário: Células de Merkel/fisiologia
Tato/fisiologia
[Mh] Termos MeSH secundário: Animais
Epiderme
Seres Humanos
Canais Iônicos
Mecanorreceptores
Pele
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Ion Channels)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180306
[Lr] Data última revisão:
180306
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180129
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.1009-2587.2018.01.010


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[PMID]:29416037
[Au] Autor:Zabara A; Chong JTY; Martiel I; Stark L; Cromer BA; Speziale C; Drummond CJ; Mezzenga R
[Ad] Endereço:Department of Health Sciences and Technology, ETH Zurich, Schmelzbergstrasse 9 LFO E23, 8092, Zürich, Switzerland.
[Ti] Título:Design of ultra-swollen lipidic mesophases for the crystallization of membrane proteins with large extracellular domains.
[So] Source:Nat Commun;9(1):544, 2018 02 07.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:In meso crystallization of membrane proteins from lipidic mesophases is central to protein structural biology but limited to membrane proteins with small extracellular domains (ECDs), comparable to the water channels (3-5 nm) of the mesophase. Here we present a strategy expanding the scope of in meso crystallization to membrane proteins with very large ECDs. We combine monoacylglycerols and phospholipids to design thermodynamically stable ultra-swollen bicontinuous cubic phases of double-gyroid (Ia3d), double-diamond (Pn3m), and double-primitive (Im3m) space groups, with water channels five times larger than traditional lipidic mesophases, and showing re-entrant behavior upon increasing hydration, of sequences Ia3d→Pn3m→Ia3d and Pn3m→Im3m→Pn3m, unknown in lipid self-assembly. We use these mesophases to crystallize membrane proteins with ECDs inaccessible to conventional in meso crystallization, demonstrating the methodology on the Gloeobacter ligand-gated ion channel (GLIC) protein, and show substantial modulation of packing, molecular contacts and activation state of the ensued proteins crystals, illuminating a general strategy in protein structural biology.
[Mh] Termos MeSH primário: Membrana Celular
Proteínas de Membrana/química
Fosfatidilgliceróis/química
[Mh] Termos MeSH secundário: Cristalização/métodos
Ácidos Graxos Monoinsaturados/química
Canais Iônicos
Transição de Fase
Domínios Proteicos
Termodinâmica
Água
Difração de Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Fatty Acids, Monounsaturated); 0 (Ion Channels); 0 (Membrane Proteins); 0 (Phosphatidylglycerols); 059QF0KO0R (Water); 4271ZA8WXO (distearoyl phosphatidylglycerol)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180209
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-018-02996-5


  3 / 34097 MEDLINE  
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[PMID]:29351552
[Au] Autor:Kropf J; Rössler W
[Ad] Endereço:Behavioral Physiology and Sociobiology (Zoology II), Biozentrum, University of Würzburg, Würzburg, Germany.
[Ti] Título:In-situ recording of ionic currents in projection neurons and Kenyon cells in the olfactory pathway of the honeybee.
[So] Source:PLoS One;13(1):e0191425, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:The honeybee olfactory pathway comprises an intriguing pattern of convergence and divergence: ~60.000 olfactory sensory neurons (OSN) convey olfactory information on ~900 projection neurons (PN) in the antennal lobe (AL). To transmit this information reliably, PNs employ relatively high spiking frequencies with complex patterns. PNs project via a dual olfactory pathway to the mushroom bodies (MB). This pathway comprises the medial (m-ALT) and the lateral antennal lobe tract (l-ALT). PNs from both tracts transmit information from a wide range of similar odors, but with distinct differences in coding properties. In the MBs, PNs form synapses with many Kenyon cells (KC) that encode odors in a spatially and temporally sparse way. The transformation from complex information coding to sparse coding is a well-known phenomenon in insect olfactory coding. Intrinsic neuronal properties as well as GABAergic inhibition are thought to contribute to this change in odor representation. In the present study, we identified intrinsic neuronal properties promoting coding differences between PNs and KCs using in-situ patch-clamp recordings in the intact brain. We found very prominent K+ currents in KCs clearly differing from the PN currents. This suggests that odor coding differences between PNs and KCs may be caused by differences in their specific ion channel properties. Comparison of ionic currents of m- and l-ALT PNs did not reveal any differences at a qualitative level.
[Mh] Termos MeSH primário: Abelhas/citologia
Abelhas/fisiologia
Condutos Olfatórios/citologia
Condutos Olfatórios/fisiologia
[Mh] Termos MeSH secundário: Potenciais de Ação
Animais
Antenas de Artrópodes/citologia
Antenas de Artrópodes/fisiologia
Encéfalo/citologia
Encéfalo/fisiologia
Fenômenos Eletrofisiológicos
Canais Iônicos/fisiologia
Transporte de Íons
Corpos Pedunculados/citologia
Corpos Pedunculados/fisiologia
Neurônios Receptores Olfatórios/citologia
Neurônios Receptores Olfatórios/fisiologia
Técnicas de Patch-Clamp
Olfato/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ion Channels)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180305
[Lr] Data última revisão:
180305
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180120
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0191425


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[PMID]:28451641
[Au] Autor:Yu J; Yang W; Liu H; Hao Y; Zhang Y
[Ad] Endereço:Department of Organismic and Evolutionary Biology, Center for Brain Science, Harvard University, Cambridge, MA 02138.
[Ti] Título:An Aversive Response to Osmotic Upshift in .
[So] Source:eNeuro;4(2), 2017 Mar-Apr.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Environmental osmolarity presents a common type of sensory stimulus to animals. While behavioral responses to osmotic changes are important for maintaining a stable intracellular osmolarity, the underlying mechanisms are not fully understood. In the natural habitat of , changes in environmental osmolarity are commonplace. It is known that the nematode acutely avoids shocks of extremely high osmolarity. Here, we show that also generates gradually increased aversion of mild upshifts in environmental osmolarity. Different from an acute avoidance of osmotic shocks that depends on the function of a transient receptor potential vanilloid channel, the slow aversion to osmotic upshifts requires the cGMP-gated sensory channel subunit TAX-2. TAX-2 acts in several sensory neurons that are exposed to body fluid to generate the aversive response through a motor network that underlies navigation. Osmotic upshifts activate the body cavity sensory neuron URX, which is known to induce aversion upon activation. Together, our results characterize the molecular and cellular mechanisms underlying a novel sensorimotor response to osmotic stimuli and reveal that engages different behaviors and the underlying mechanisms to regulate responses to extracellular osmolarity.
[Mh] Termos MeSH primário: Proteínas de Caenorhabditis elegans/metabolismo
Canais Iônicos/metabolismo
Osmorregulação
Células Receptoras Sensoriais/metabolismo
[Mh] Termos MeSH secundário: Animais
Caenorhabditis elegans
Locomoção
Pressão Osmótica
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Caenorhabditis elegans Proteins); 0 (Ion Channels); 0 (tax-2 protein, C elegans)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180228
[Lr] Data última revisão:
180228
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170429
[St] Status:MEDLINE


  5 / 34097 MEDLINE  
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[PMID]:29360451
[Au] Autor:Xu J; Yang F; Han D; Xu S
[Ad] Endereço:Key Laboratory for the Physics & Chemistry of Nanodevices, Department of Electronics, Peking University, Beijing, 100871, PR China.
[Ti] Título:Phenomena of synchronized response in biosystems and the possible mechanism.
[So] Source:Biochem Biophys Res Commun;496(2):661-666, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Phenomena of synchronized response is common among organs, tissues and cells in biosystems. We have analyzed and discussed three examples of synchronization in biosystems, including the direction-changing movement of paramecia, the prey behavior of flytraps, and the simultaneous discharge of electric eels. These phenomena and discussions support an electrical communication mechanism that in biosystems, the electrical signals are mainly soliton-like electromagnetic pulses, which are generated by the transient transmembrane ionic current through the ion channels and propagate along the dielectric membrane-based softmaterial waveguide network to complete synchronized responses. This transmission model implies that a uniform electrical communication mechanism might have been naturally developed in biosystem.
[Mh] Termos MeSH primário: Comunicação Animal
Fenômenos Eletrofisiológicos
Canais Iônicos/metabolismo
[Mh] Termos MeSH secundário: Animais
Membrana Celular/metabolismo
Eletricidade
Electrophorus/fisiologia
Transporte de Íons
Movimento
Paramecium/fisiologia
Sarraceniaceae/fisiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Ion Channels)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180216
[Lr] Data última revisão:
180216
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE


  6 / 34097 MEDLINE  
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[PMID]:28746810
[Au] Autor:Nánási PP; Magyar J; Varró A; Ördög B
[Ad] Endereço:a Department of Physiology, Faculty of Medicine, University of Debrecen, Debrecen, Hungary.
[Ti] Título:Beat-to-beat variability of cardiac action potential duration: underlying mechanism and clinical implications.
[So] Source:Can J Physiol Pharmacol;95(10):1230-1235, 2017 Oct.
[Is] ISSN:1205-7541
[Cp] País de publicação:Canada
[La] Idioma:eng
[Ab] Resumo:Beat-to-beat variability of cardiac action potential duration (short-term variability, SV) is a common feature of various cardiac preparations, including the human heart. Although it is believed to be one of the best arrhythmia predictors, the underlying mechanisms are not fully understood at present. The magnitude of SV is basically determined by the intensity of cell-to-cell coupling in multicellular preparations and by the duration of the action potential (APD). To compensate for the APD-dependent nature of SV, the concept of relative SV (RSV) has been introduced by normalizing the changes of SV to the concomitant changes in APD. RSV is reduced by I , I , and I while increased by I , suggesting that ion currents involved in the negative feedback regulation of APD tend to keep RSV at a low level. RSV is also influenced by intracellular calcium concentration and tissue redox potential. The clinical implications of APD variability is discussed in detail.
[Mh] Termos MeSH primário: Potenciais de Ação
Arritmias Cardíacas/fisiopatologia
Sistema de Condução Cardíaco/fisiopatologia
Frequência Cardíaca
[Mh] Termos MeSH secundário: Potenciais de Ação/efeitos dos fármacos
Animais
Antiarrítmicos/uso terapêutico
Arritmias Cardíacas/tratamento farmacológico
Arritmias Cardíacas/metabolismo
Sistema de Condução Cardíaco/efeitos dos fármacos
Sistema de Condução Cardíaco/metabolismo
Frequência Cardíaca/efeitos dos fármacos
Seres Humanos
Canais Iônicos/metabolismo
Modelos Cardiovasculares
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Arrhythmia Agents); 0 (Ion Channels)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180205
[Lr] Data última revisão:
180205
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1139/cjpp-2016-0597


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[PMID]:29376828
[Au] Autor:Chesler AT; Szczot M
[Ad] Endereço:National Center of Complementary and Integrative Health, National Institutes of Health, Bethesda, United States.
[Ti] Título:Portraits of a pressure sensor.
[So] Source:Elife;7, 2018 01 29.
[Is] ISSN:2050-084X
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Near atomic-resolution structures have provided insights into the mechanisms by which the Piezo1 ion channel senses and responds to mechanical stimuli.
[Mh] Termos MeSH primário: Canais Iônicos/química
[Mh] Termos MeSH secundário: Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE; COMMENT
[Nm] Nome de substância:
0 (Ion Channels)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180202
[Lr] Data última revisão:
180202
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180130
[St] Status:MEDLINE


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[PMID]:29263209
[Au] Autor:Oyrer J; Maljevic S; Scheffer IE; Berkovic SF; Petrou S; Reid CA
[Ad] Endereço:The Florey Institute of Neuroscience and Mental Health, University of Melbourne, Parkville, Melbourne, Australia (J.O., S.M., I.E.S., S.P., C.A.R.); Department of Medicine, Austin Health, University of Melbourne, Heidelberg West, Melbourne, Australia (I.E.S., S.F.B.); and Department of Paediatrics,
[Ti] Título:Ion Channels in Genetic Epilepsy: From Genes and Mechanisms to Disease-Targeted Therapies.
[So] Source:Pharmacol Rev;70(1):142-173, 2018 Jan.
[Is] ISSN:1521-0081
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epilepsy is a common and serious neurologic disease with a strong genetic component. Genetic studies have identified an increasing collection of disease-causing genes. The impact of these genetic discoveries is wide reaching-from precise diagnosis and classification of syndromes to the discovery and validation of new drug targets and the development of disease-targeted therapeutic strategies. About 25% of genes identified in epilepsy encode ion channels. Much of our understanding of disease mechanisms comes from work focused on this class of protein. In this study, we review the genetic, molecular, and physiologic evidence supporting the pathogenic role of a number of different voltage- and ligand-activated ion channels in genetic epilepsy. We also review proposed disease mechanisms for each ion channel and highlight targeted therapeutic strategies.
[Mh] Termos MeSH primário: Epilepsia/genética
Canais Iônicos/genética
[Mh] Termos MeSH secundário: Animais
Anticonvulsivantes/farmacologia
Anticonvulsivantes/uso terapêutico
Epilepsia/tratamento farmacológico
Epilepsia/metabolismo
Seres Humanos
Canais Iônicos/antagonistas & inibidores
Canais Iônicos/metabolismo
Terapia de Alvo Molecular
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anticonvulsants); 0 (Ion Channels)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180109
[Lr] Data última revisão:
180109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171222
[St] Status:MEDLINE
[do] DOI:10.1124/pr.117.014456


  9 / 34097 MEDLINE  
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[PMID]:29255213
[Au] Autor:Donahue HJ; Qu RW; Genetos DC
[Ad] Endereço:Department of Biomedical Engineering, Virginia Commonwealth University, 601 West Main Street, Richmond, Virginia 23284, USA.
[Ti] Título:Joint diseases: from connexins to gap junctions.
[So] Source:Nat Rev Rheumatol;14(1):42-51, 2017 Dec 19.
[Is] ISSN:1759-4804
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Connexons form the basis of hemichannels and gap junctions. They are composed of six tetraspan proteins called connexins. Connexons can function as individual hemichannels, releasing cytosolic factors (such as ATP) into the pericellular environment. Alternatively, two hemichannel connexons from neighbouring cells can come together to form gap junctions, membrane-spanning channels that facilitate cell-cell communication by enabling signalling molecules of approximately 1 kDa to pass from one cell to an adjacent cell. Connexins are expressed in joint tissues including bone, cartilage, skeletal muscle and the synovium. Indicative of their importance as gap junction components, connexins are also known as gap junction proteins, but individual connexin proteins are gaining recognition for their channel-independent roles, which include scaffolding and signalling functions. Considerable evidence indicates that connexons contribute to the function of bone and muscle, but less is known about the function of connexons in other joint tissues. However, the implication that connexins and gap junctional channels might be involved in joint disease, including age-related bone loss, osteoarthritis and rheumatoid arthritis, emphasizes the need for further research into these areas and highlights the therapeutic potential of connexins.
[Mh] Termos MeSH primário: Conexina 43/metabolismo
Conexinas/metabolismo
Junções Comunicantes/metabolismo
Artropatias/metabolismo
[Mh] Termos MeSH secundário: Animais
Artrite Reumatoide/metabolismo
Osso e Ossos/metabolismo
Cartilagem/metabolismo
Comunicação Celular/fisiologia
Diferenciação Celular/fisiologia
Conexinas/fisiologia
Conexinas/uso terapêutico
Junções Comunicantes/fisiologia
Seres Humanos
Ativação do Canal Iônico/fisiologia
Canais Iônicos/fisiologia
Camundongos
Camundongos Knockout
Sistema Musculoesquelético/metabolismo
Sistema Musculoesquelético/patologia
Osteoartrite/metabolismo
Osteoporose/metabolismo
Membrana Sinovial/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Connexin 43); 0 (Connexins); 0 (Ion Channels)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE
[do] DOI:10.1038/nrrheum.2017.204


  10 / 34097 MEDLINE  
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[PMID]:29194452
[Au] Autor:Lozano-Velasco E; Wangensteen R; Quesada A; Garcia-Padilla C; Osorio JA; Ruiz-Torres MD; Aranega A; Franco D
[Ad] Endereço:Cardiac and Skeletal Muscle Development Group, Department of Experimental Biology, University of Jaen, Jaen, Spain.
[Ti] Título:Hyperthyroidism, but not hypertension, impairs PITX2 expression leading to Wnt-microRNA-ion channel remodeling.
[So] Source:PLoS One;12(12):e0188473, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PITX2 is a homeobox transcription factor involved in embryonic left/right signaling and more recently has been associated to cardiac arrhythmias. Genome wide association studies have pinpointed PITX2 as a major player underlying atrial fibrillation (AF). We have previously described that PITX2 expression is impaired in AF patients. Furthermore, distinct studies demonstrate that Pitx2 insufficiency leads to complex gene regulatory network remodeling, i.e. Wnt>microRNAs, leading to ion channel impairment and thus to arrhythmogenic events in mice. Whereas large body of evidences has been provided in recent years on PITX2 downstream signaling pathways, scarce information is available on upstream pathways influencing PITX2 in the context of AF. Multiple risk factors are associated to the onset of AF, such as e.g. hypertension (HTN), hyperthyroidism (HTD) and redox homeostasis impairment. In this study we have analyzed whether HTN, HTD and/or redox homeostasis impact on PITX2 and its downstream signaling pathways. Using rat models for spontaneous HTN (SHR) and experimentally-induced HTD we have observed that both cardiovascular risk factors lead to severe Pitx2 downregulation. Interesting HTD, but not SHR, leads to up-regulation of Wnt signaling as well as deregulation of multiple microRNAs and ion channels as previously described in Pitx2 insufficiency models. In addition, redox signaling is impaired in HTD but not SHR, in line with similar findings in atrial-specific Pitx2 deficient mice. In vitro cell culture analyses using gain- and loss-of-function strategies demonstrate that Pitx2, Zfhx3 and Wnt signaling influence redox homeostasis in cardiomyocytes. Thus, redox homeostasis seems to play a pivotal role in this setting, providing a regulatory feedback loop. Overall these data demonstrate that HTD, but not HTN, can impair Pitx2>>Wnt pathway providing thus a molecular link to AF.
[Mh] Termos MeSH primário: Proteínas de Homeodomínio/genética
Hipertensão/genética
Hipertireoidismo/genética
Canais Iônicos/metabolismo
MicroRNAs/metabolismo
Fatores de Transcrição/genética
Proteínas Wnt/metabolismo
[Mh] Termos MeSH secundário: Animais
Camundongos
Camundongos Mutantes
Ratos
Ratos Wistar
Espécies Reativas de Oxigênio/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Homeodomain Proteins); 0 (Ion Channels); 0 (MicroRNAs); 0 (Reactive Oxygen Species); 0 (Transcription Factors); 0 (Wnt Proteins); 184787-43-7 (homeobox protein PITX2)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171226
[Lr] Data última revisão:
171226
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171202
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0188473



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