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[PMID]: 27140190 [Au] Autor: Miyagishi H; Kosuge Y; Takano A; Endo M; Nango H; Yamagata-Murayama S; Hirose D; Kano R; Tanaka Y; Ishige K; Ito Y [Ad] Endereço: School of Pharmacy, Nihon University, 7-7-1 Narashinodai, Funabashi, Chiba, 274-8555, Japan. [Ti] Título: Increased Expression of 15-Hydroxyprostaglandin Dehydrogenase in Spinal Astrocytes During Disease Progression in a Model of Amyotrophic Lateral Sclerosis. [So] Source: Cell Mol Neurobiol;37(3):445-452, 2017 Apr. [Is] ISSN: 1573-6830 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Amyotrophic lateral sclerosis (ALS) is an adult-onset, progressive, and fatal neurodegenerative disease caused by selective loss of motor neurons. Both ALS model mice and patients with sporadic ALS have increased levels of prostaglandin E2 (PGE2). Furthermore, the protein levels of microsomal PGE synthase-1 and cyclooxygenase-2, which catalyze PGE2 biosynthesis, are significantly increased in the spinal cord of ALS model mice. However, it is unclear whether PGE2 metabolism in the spinal cord is altered. In the present study, we investigated the protein level of 15-hydroxyprostaglandin dehydrogenase (15-PGDH), a key enzyme in prostaglandin metabolism, in ALS model mice at three different disease stages. Western blotting revealed that the 15-PGDH level was significantly increased in the lumbar spinal cord at the symptomatic stage and end stage. Immunohistochemical staining demonstrated that 15-PGDH immunoreactivity was localized in glial fibrillary acidic protein (GFAP)-positive astrocytes at the end stage. In contrast, 15-PGDH immunoreactivity was not identified in NeuN-positive large cells showing the typical morphology of motor neurons in the anterior horn. Unlike 15-PGDH, the level of PGE2 in the spinal cord was increased only at the end stage. These results suggest that the significant increase of PGE2 at the end stage of ALS in this mouse model is attributable to an imbalance of the synthetic pathway and 15-PGDH-dependent scavenging system for PGE2, and that this drives the pathogenetic mechanism responsible for transition from the symptomatic stage. [Mh] Termos MeSH primário: Esclerose Amiotrófica Lateral/enzimologia Esclerose Amiotrófica Lateral/patologia Astrócitos/enzimologia Astrócitos/patologia Progressão da Doença Hidroxiprostaglandina Desidrogenases/metabolismo Medula Espinal/patologia [Mh] Termos MeSH secundário: Animais Dinoprostona/metabolismo Modelos Animais de Doenças Vértebras Lombares/metabolismo Vértebras Lombares/patologia Camundongos Transgênicos Neurônios Motores/enzimologia Neurônios Motores/patologia Corno Ventral da Medula Espinal/enzimologia Corno Ventral da Medula Espinal/patologia Regulação para Cima [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: EC 1.1.1.- (Hydroxyprostaglandin Dehydrogenases); EC 1.1.1.141 (15-hydroxyprostaglandin dehydrogenase); K7Q1JQR04M (Dinoprostone) [Em] Mês de entrada: 1703 [Cu] Atualização por classe: 171018 [Lr] Data última revisão: 171018 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 160504 [St] Status: MEDLINE [do] DOI: 10.1007/s10571-016-0377-9

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[PMID]: 27529273 [Au] Autor: Santos RI; Hermance ME; Gelman BB; Thangamani S [Ad] Endereço: Department of Pathology, University of Texas Medical Branch, Galveston, TX 77555, USA. roimarqu@utmb.edu. [Ti] Título: Spinal Cord Ventral Horns and Lymphoid Organ Involvement in Powassan Virus Infection in a Mouse Model. [So] Source: Viruses;8(8), 2016 Aug 12. [Is] ISSN: 1999-4915 [Cp] País de publicação: Switzerland [La] Idioma: eng [Ab] Resumo: Powassan virus (POWV) belongs to the family Flaviviridae and is a member of the tick-borne encephalitis serogroup. Transmission of POWV from infected ticks to humans has been documented in the USA, Canada, and Russia, causing fatal encephalitis in 10% of human cases and significant neurological sequelae in survivors. We used C57BL/6 mice to investigate POWV infection and pathogenesis. After footpad inoculation, infected animals exhibited rapid disease progression and 100% mortality. Immunohistochemistry and immunofluorescence revealed a very strong neuronal tropism of POWV infection. The central nervous system infection appeared as a meningoencephalitis with perivascular mononuclear infiltration and microglial activation in the brain, and a poliomyelitis-like syndrome with high level of POWV antigen at the ventral horn of the spinal cord. Pathological studies also revealed substantial infection of splenic macrophages by POWV, which suggests that the spleen plays a more important role in pathogenesis than previously realized. This report provides a detailed description of the neuroanatomical distribution of the lesions produced by POWV infection in C57BL/6 mice. [Mh] Termos MeSH primário: Vírus da Encefalite Transmitidos por Carrapatos/isolamento & purificação Vírus da Encefalite Transmitidos por Carrapatos/patogenicidade Encefalite Transmitida por Carrapatos/patologia Corno Ventral da Medula Espinal/patologia Baço/patologia [Mh] Termos MeSH secundário: Animais Modelos Animais de Doenças Vírus da Encefalite Transmitidos por Carrapatos/fisiologia Imuno-Histoquímica Masculino Camundongos Endogâmicos C57BL Microscopia de Fluorescência Análise de Sobrevida Tropismo Viral [Pt] Tipo de publicação: JOURNAL ARTICLE [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 170926 [Lr] Data última revisão: 170926 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 160817 [St] Status: MEDLINE

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[PMID]: 27225998 [Au] Autor: Sindou M; Georgoulis G [Ad] Endereço: University of Lyon 1, Lyon, France. [Ti] Título: Focal Dystonia in Hemiplegic Upper Limb: Favorable Effect of Cervical Microsurgical DREZotomy Involving the Ventral Horn - A Report of 3 Patients. [So] Source: Stereotact Funct Neurosurg;94(3):140-6, 2016. [Is] ISSN: 1423-0372 [Cp] País de publicação: Switzerland [La] Idioma: eng [Ab] Resumo: BACKGROUND: Focal dystonia in hemiplegic upper limbs is poorly responsive to medications or classical neurosurgical treatments. Only repeated botulinum toxin injections show efficacy, but in most severe cases effects are transient. OBJECTIVES: Cervical DREZ lesioning, which has proven efficacious in hyperspasticity when done deeply (3-5 mm) in the dorsal horn, may have favorable effects on the dystonic component when performed down to, and including, the base of the ventral horn (5-6 mm in depth). METHODS: Three patients underwent deep cervical microsurgical DREZotomy (MDT) for focal dystonia in the upper limb. RESULTS: Hypertonia was reduced, and sustained dystonic postures were suppressed. Residual motor function (hidden behind hypertonia) came to the surface. CONCLUSIONS: Cervical MDT may be a useful armamentarium for treating refractory focal dystonia in the upper limb. [Mh] Termos MeSH primário: Distúrbios Distônicos/cirurgia Hemiplegia/cirurgia Quadriplegia/cirurgia Corno Ventral da Medula Espinal/cirurgia [Mh] Termos MeSH secundário: Adulto Encefalopatias/complicações Lesões Encefálicas/complicações Vértebras Cervicais Eletrocoagulação Seres Humanos Masculino Microcirurgia Espasticidade Muscular/cirurgia Extremidade Superior Adulto Jovem [Pt] Tipo de publicação: JOURNAL ARTICLE [Em] Mês de entrada: 1709 [Cu] Atualização por classe: 170906 [Lr] Data última revisão: 170906 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 160527 [St] Status: MEDLINE [do] DOI: 10.1159/000446078

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[PMID]: 26600420 [Au] Autor: Morales AV; Espeso-Gil S; Ocaña I; Nieto-Lopez F; Calleja E; Bovolenta P; Lewandoski M; Diez Del Corral R [Ad] Endereço: Instituto Cajal, Consejo Superior de Investigaciones Científicas, Madrid, 28002, Spain. [Ti] Título: FGF signaling enhances a sonic hedgehog negative feedback loop at the initiation of spinal cord ventral patterning. [So] Source: Dev Neurobiol;76(9):956-71, 2016 09. [Is] ISSN: 1932-846X [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: A prevalent developmental mechanism for the assignment of cell identities is the production of spatiotemporal concentration gradients of extracellular signaling molecules that are interpreted by the responding cells. One of such signaling systems is the Shh gradient that controls neuronal subtype identity in the ventral spinal cord. Using loss and gain of function approaches in chick and mouse embryos, we show here that the fibroblast growth factor (FGF) signaling pathway is required to restrict the domains of ventral gene expression as neuroepithelial cells become exposed to Shh during caudal extension of the embryo. FGF signaling activates the expression of the Shh receptor and negative pathway regulator Patched 2 (Ptch2) and therefore can enhance a negative feedback loop that restrains the activity of the pathway. Thus, we identify one of the mechanisms by which FGF signaling acts as a modulator of the onset of Shh signaling activity in the context of coordination of ventral patterning and caudal axis extension. © 2015 Wiley Periodicals, Inc. Develop Neurobiol 76: 956-971, 2016. [Mh] Termos MeSH primário: Fatores de Crescimento de Fibroblastos/fisiologia Regulação da Expressão Gênica no Desenvolvimento/fisiologia Proteínas Hedgehog/fisiologia Transdução de Sinais/fisiologia Corno Ventral da Medula Espinal/fisiologia [Mh] Termos MeSH secundário: Animais Embrião de Galinha Seres Humanos Camundongos Corno Ventral da Medula Espinal/embriologia [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Hedgehog Proteins); 62031-54-3 (Fibroblast Growth Factors) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171121 [Lr] Data última revisão: 171121 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 151125 [St] Status: MEDLINE [do] DOI: 10.1002/dneu.22368

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[PMID]: 26506510 [Au] Autor: Allain AE; Cazenave W; Delpy A; Exertier P; Barthe C; Meyrand P; Cattaert D; Branchereau P [Ad] Endereço: Univ. Bordeaux, INCIA, UMR 5287, Site Talence, F33615 Pessac cedex, France. CNRS, INCIA, UMR 5287, Site Talence, F33615 Pessac cedex, France. [Ti] Título: Nonsynaptic glycine release is involved in the early KCC2 expression. [So] Source: Dev Neurobiol;76(7):764-79, 2016 07. [Is] ISSN: 1932-846X [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: The cation-chloride co-transporters are important regulators of the cellular Cl(-) homeostasis. Among them the Na(+) -K(+) -2Cl(-) co-transporter (NKCC1) is responsible for intracellular chloride accumulation in most immature brain structures, whereas the K(+) -Cl(-) co-transporter (KCC2) extrudes chloride from mature neurons, ensuring chloride-mediated inhibitory effects of GABA/glycine. We have shown that both KCC2 and NKCC1 are expressed at early embryonic stages (E11.5) in the ventral spinal cord (SC). The mechanisms by which KCC2 is prematurely expressed are unknown. In this study, we found that chronically blocking glycine receptors (GlyR) by strychnine led to a loss of KCC2 expression, without affecting NKCC1 level. This effect was not dependent on the firing of Na(+) action potentials but was mimicked by a Ca(2+) -dependent PKC blocker. Blocking the vesicular release of neurotransmitters did not impinge on strychnine effect whereas blocking volume-sensitive outwardly rectifying (VSOR) chloride channels reproduced the GlyR blockade, suggesting that KCC2 is controlled by a glycine release from progenitor radial cells in immature ventral spinal networks. Finally, we showed that the strychnine treatment prevented the maturation of rhythmic spontaneous activity. Thereby, the GlyR-activation is a necessary developmental process for the expression of functional spinal motor networks. © 2015 Wiley Periodicals, Inc. Develop Neurobiol 76: 764-779, 2016. [Mh] Termos MeSH primário: Canais de Cálcio/metabolismo Glicina/metabolismo Células-Tronco Neurais/metabolismo Proteína Quinase C/metabolismo Receptores da Glicina/metabolismo Corno Ventral da Medula Espinal/fisiologia Simportadores/metabolismo [Mh] Termos MeSH secundário: Animais Fenômenos Eletrofisiológicos Feminino Glicinérgicos/farmacologia Camundongos Gravidez Receptores da Glicina/efeitos dos fármacos Corno Ventral da Medula Espinal/embriologia Corno Ventral da Medula Espinal/metabolismo Estricnina/farmacologia [Pt] Tipo de publicação: JOURNAL ARTICLE [Nm] Nome de substância: 0 (Calcium Channels); 0 (Glycine Agents); 0 (Receptors, Glycine); 0 (Symporters); 0 (potassium-chloride symporters); EC 2.7.11.13 (Protein Kinase C); H9Y79VD43J (Strychnine); TE7660XO1C (Glycine) [Em] Mês de entrada: 1710 [Cu] Atualização por classe: 171120 [Lr] Data última revisão: 171120 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 151028 [St] Status: MEDLINE [do] DOI: 10.1002/dneu.22358

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[PMID]: 26084599 [Au] Autor: De Luca C; Savarese L; Colangelo AM; Bianco MR; Cirillo G; Alberghina L; Papa M [Ad] Endereço: Laboratory of Neuronal Networks, Department of Mental and Physical Health and Preventive Medicine, Second University of Naples, Via L. Armanni, 5, 80138, Naples, Italy. [Ti] Título: Astrocytes and Microglia-Mediated Immune Response in Maladaptive Plasticity is Differently Modulated by NGF in the Ventral Horn of the Spinal Cord Following Peripheral Nerve Injury. [So] Source: Cell Mol Neurobiol;36(1):37-46, 2016 Jan. [Is] ISSN: 1573-6830 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Reactive astrocytes and activated microglia are the key players in several pathophysiologic modifications of the central nervous system. We used the spared nerve injury (SNI) of the sciatic nerve to induce glial maladaptive response in the ventral horn of lumbar spinal cord and examine its role in the remodeling of the tripartite synapse plasticity. Imaging the ventral horn revealed that SNI was associated with both an early microglial and astrocytic activation, assessed, respectively, by analysis of Iba1 and GFAP expression. Microglia, in particular, localized peculiarly surrounding the motor neurons somata. Perineuronal astrocytes, which play a key role in maintaining the homeostasis of neuronal circuitry, underwent a substantial phenotypic change following peripheral axotomy, producing reactive gliosis. The gliosis was associated with the reduction of glial aminoacid transporters (GLT1 and GlyT1) and increase of neuronal glutamate transporter EAAC1. Although the expression of GABAergic neuronal marker GAD65/67 showed no change, glutamate increase, as demonstrated by HPLC analysis, shifted the excitatory/inhibitory balance as showed by the net increase of the glutamate/GABA ratio. Moreover, endogenous NGF levels were altered in SNI animals and not restored by the intrathecal NGF administration. This treatment reverted phenotypic changes associated with reactive astrocytosis, but failed to modify microglia activation. These findings on one hand confirm the correlation between gliopathy and maladaptive plasticity of the spinal synaptic circuitry, on the other hand add new data concerning the complex peculiar behavior of different glial cells in neuronal degenerative processes, defining a special role of microglia in sustaining the inflammatory response. [Mh] Termos MeSH primário: Astrócitos/metabolismo Imunidade/efeitos dos fármacos Microglia/metabolismo Fator de Crescimento Neural/farmacologia Plasticidade Neuronal/efeitos dos fármacos Traumatismos dos Nervos Periféricos/patologia Corno Ventral da Medula Espinal/patologia [Mh] Termos MeSH secundário: Animais Antígenos Nucleares/metabolismo Astrócitos/efeitos dos fármacos Biomarcadores/metabolismo Proteínas de Ligação ao Cálcio/metabolismo Cromatografia Líquida de Alta Pressão Gliose/patologia Glutamato Descarboxilase/metabolismo Ácido Glutâmico/metabolismo Vértebras Lombares/efeitos dos fármacos Vértebras Lombares/metabolismo Masculino Proteínas de Membrana Transportadoras/metabolismo Proteínas dos Microfilamentos/metabolismo Microglia/efeitos dos fármacos Proteínas do Tecido Nervoso/metabolismo Ratos Sprague-Dawley Nervo Isquiático/efeitos dos fármacos Nervo Isquiático/lesões Nervo Isquiático/patologia Corno Ventral da Medula Espinal/efeitos dos fármacos Ácido gama-Aminobutírico/metabolismo [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Aif1 protein, rat); 0 (Antigens, Nuclear); 0 (Biomarkers); 0 (Calcium-Binding Proteins); 0 (Membrane Transport Proteins); 0 (Microfilament Proteins); 0 (Nerve Tissue Proteins); 0 (NeuN protein, rat); 3KX376GY7L (Glutamic Acid); 56-12-2 (gamma-Aminobutyric Acid); 9061-61-4 (Nerve Growth Factor); EC 4.1.1.15 (Glutamate Decarboxylase) [Em] Mês de entrada: 1610 [Cu] Atualização por classe: 171018 [Lr] Data última revisão: 171018 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 150619 [St] Status: MEDLINE [do] DOI: 10.1007/s10571-015-0218-2

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[PMID]: 26334015 [Au] Autor: Tadros MA; Lim R; Hughes DI; Brichta AM; Callister RJ [Ad] Endereço: School of Biomedical Sciences & Pharmacy, Faculty of Health and Medicine, Hunter Medical Research Institute, The University of Newcastle, Callaghan, New South Wales, Australia; and. [Ti] Título: Electrical maturation of spinal neurons in the human fetus: comparison of ventral and dorsal horn. [So] Source: J Neurophysiol;114(5):2661-71, 2015 Nov. [Is] ISSN: 1522-1598 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: The spinal cord is critical for modifying and relaying sensory information to, and motor commands from, higher centers in the central nervous system to initiate and maintain contextually relevant locomotor responses. Our understanding of how spinal sensorimotor circuits are established during in utero development is based largely on studies in rodents. In contrast, there is little functional data on the development of sensory and motor systems in humans. Here, we use patch-clamp electrophysiology to examine the development of neuronal excitability in human fetal spinal cords (10-18 wk gestation; WG). Transverse spinal cord slices (300 µm thick) were prepared, and recordings were made, from visualized neurons in either the ventral (VH) or dorsal horn (DH) at 32°C. Action potentials (APs) could be elicited in VH neurons throughout the period examined, but only after 16 WG in DH neurons. At this age, VH neurons discharged multiple APs, whereas most DH neurons discharged single APs. In addition, at 16-18 WG, VH neurons also displayed larger AP and after-hyperpolarization amplitudes than DH neurons. Between 10 and 18 WG, the intrinsic properties of VH neurons changed markedly, with input resistance decreasing and AP and after-hyperpolarization amplitudes increasing. These findings are consistent with the hypothesis that VH motor circuitry matures more rapidly than the DH circuits that are involved in processing tactile and nociceptive information. [Mh] Termos MeSH primário: Potenciais de Ação Células do Corno Anterior/fisiologia Feto/fisiologia Células do Corno Posterior/fisiologia Corno Dorsal da Medula Espinal/embriologia Corno Ventral da Medula Espinal/embriologia [Mh] Termos MeSH secundário: Seres Humanos Corno Dorsal da Medula Espinal/fisiologia Corno Ventral da Medula Espinal/fisiologia [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Em] Mês de entrada: 1609 [Cu] Atualização por classe: 170220 [Lr] Data última revisão: 170220 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 150904 [St] Status: MEDLINE [do] DOI: 10.1152/jn.00682.2015

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[PMID]: 26139546 [Au] Autor: Wu SH; Huang SH; Lo YC; Chai CY; Lee SS; Chang KP; Lin SD; Lai CS; Yeh JL; Kwan AL [Ad] Endereço: Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung, Taiwan; Department of Anesthesia, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung, Taiwan. [Ti] Título: Autologous adipose-derived stem cells attenuate muscular atrophy and protect spinal cord ventral horn motor neurons in an animal model of burn injury. [So] Source: Cytotherapy;17(8):1066-75, 2015 Aug. [Is] ISSN: 1477-2566 [Cp] País de publicação: England [La] Idioma: eng [Ab] Resumo: BACKGROUND AIMS: Burn injuries might increase muscle mass loss, but the mechanisms are still unclear. In this study, we demonstrated that burn injury induced spinal cord ventral horn motor neuron (VHMN) apoptosis and subsequently caused muscle atrophy and revealed the potential protection of autologous adipose-derived stem cells (ASCs) transplantation on spinal cord VHMNs and muscle against burn injury. METHODS: Third-degree hind-paw burns were established by contact with a 75°C metal surface for 10 seconds. Adipose tissues were harvested from the groin fat pad, expanded in culture and labeled with chloromethyl-benzamido/1,1'-dioctadecyl-3,3,3',3'- tetramethyl indocarbocyanine perchlorate. The ASCs were transplanted into the injured hind paw at 4 weeks after burn injury. The lumbar spinal cord, sciatic nerve, gastrocnemius muscle and hind-paw skin were processed for immunofluorescent staining at 4 weeks after transplantation, including terminal deoxynucleotidyl transferase (TUNEL) assay, caspase-3, caspase-9, CD 90 and S100, and the gastrocnemius muscle was evaluated through the use of hematoxylin and eosin staining. RESULTS: Caspase-3-positive, caspase-9-positive and TUNEL-positive cells were significantly increased in the corresponding dermatome spinal cord VHMNs after burn injury. Moreover, the decrease of Schwann cells in sciatic nerve and the increase of denervation atrophy in gastrocnemius muscle were observed. Furthermore, ASCs transplantation significantly attenuated apoptotic death of VHMNs and the area of muscle denervation atrophy in the gastrocnemius muscle fibers. CONCLUSIONS: The animal model of third-degree burns in the hind paw showed significant apoptosis in the corresponding spinal cord VHMNs, which suggests that neuroprotection might be the potentially therapeutic target in burn-induced muscle atrophy. ASCs have potential neuroprotection against burn injuries through its anti-apoptotic effects. [Mh] Termos MeSH primário: Queimaduras/terapia Músculo Esquelético/patologia Atrofia Muscular/terapia Corno Ventral da Medula Espinal/patologia Transplante de Células-Tronco [Mh] Termos MeSH secundário: Adipócitos/citologia Tecido Adiposo/citologia Animais Antígenos CD/metabolismo Apoptose/fisiologia Queimaduras/patologia Caspases/metabolismo Modelos Animais de Doenças Marcação In Situ das Extremidades Cortadas Masculino Neurônios Motores/patologia Atrofia Muscular/patologia Atrofia Muscular/prevenção & controle Neuroproteção Ratos Ratos Sprague-Dawley Células de Schwann/patologia Nervo Isquiático/citologia Nervo Isquiático/patologia Células-Tronco/citologia [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Antigens, CD); EC 3.4.22.- (Caspases) [Em] Mês de entrada: 1601 [Cu] Atualização por classe: 150703 [Lr] Data última revisão: 150703 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 150704 [St] Status: MEDLINE

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[PMID]: 25914366 [Au] Autor: Spruill MM; Kuncl RW [Ad] Endereço: Department of Neurology and Pathology, Johns Hopkins University School of Medicine, Baltimore, Maryland. [Ti] Título: Calbindin-D28K is increased in the ventral horn of spinal cord by neuroprotective factors for motor neurons. [So] Source: J Neurosci Res;93(8):1184-91, 2015 Aug. [Is] ISSN: 1097-4547 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: Slow glutamate-mediated neuronal degeneration is implicated in the pathophysiology of motor neuron diseases such as amyotrophic lateral sclerosis (ALS). The calcium-binding proteins calbindin-D28K and parvalbumin have been reported to protect neurons against excitotoxic insults. Expression of calbindin-D28K is low in adult human motor neurons, and vulnerable motor neurons additionally may lack parvalbumin. Thus, it has been speculated that the lack of calcium-binding proteins may, in part, be responsible for early degeneration of the population of motor neurons most vulnerable in ALS. Using a rat organotypic spinal cord slice system, we examined whether the most potent neuroprotective factors for motor neurons can increase the expression of calbindin-D28K or parvalbumin proteins in the postnatal spinal cord. After 4 weeks of incubation of spinal cord slices with 1) glial cell line-derived neurotrophic factor (GDNF), 2) neurturin, 3) insulin-like growth factor I (IGF-I), or 4) pigment epithelium-derived factor (PEDF), the number of calbindin-D28K -immunopositive large neurons (>20 µm) in the ventral horn was higher under the first three conditions, but not after PEDF, compared with untreated controls. Under the same conditions, parvalbumin was not upregulated by any neuroprotective factor. The same calbindin increase was true of IGF-I and GDNF in a parallel glutamate toxicity model of motor neuron degeneration. Taken together with our previous reports from the same model, which showed that all these neurotrophic factors can potently protect motor neurons from slow glutamate injury, the data here suggest that upregulation of calbindin-D28K by some of these factors may be one mechanism by which motor neurons can be protected from glutamate-induced, calcium-mediated excitotoxicity. [Mh] Termos MeSH primário: Calbindina 1/biossíntese Neurônios Motores/metabolismo Fatores de Crescimento Neural/farmacologia Fármacos Neuroprotetores/farmacologia Corno Ventral da Medula Espinal/metabolismo [Mh] Termos MeSH secundário: Animais Animais Recém-Nascidos Neurônios Motores/efeitos dos fármacos Técnicas de Cultura de Órgãos Ratos Corno Ventral da Medula Espinal/efeitos dos fármacos [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Nm] Nome de substância: 0 (Calbindin 1); 0 (Nerve Growth Factors); 0 (Neuroprotective Agents) [Em] Mês de entrada: 1604 [Cu] Atualização por classe: 150622 [Lr] Data última revisão: 150622 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 150428 [St] Status: MEDLINE [do] DOI: 10.1002/jnr.23562

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[PMID]: 25695065 [Au] Autor: Wu SH; Huang SH; Cheng KI; Chai CY; Yeh JL; Wu TC; Hsu YC; Kwan AL [Ad] Endereço: Graduate Institute of Medicine, College of Medicine, Kaohsiung Medical University, Kaohsiung 80708, Taiwan ; Department of Anesthesia, Kaohsiung Medical University Hospital, Kaohsiung Medical University, Kaohsiung 80708, Taiwan ; Kaohsiung Municipal Hsiao-Kang Hospital, Kaohsiung Medical University, [Ti] Título: Third-degree hindpaw burn injury induced apoptosis of lumbar spinal cord ventral horn motor neurons and sciatic nerve and muscle atrophy in rats. [So] Source: Biomed Res Int;2015:372819, 2015. [Is] ISSN: 2314-6141 [Cp] País de publicação: United States [La] Idioma: eng [Ab] Resumo: BACKGROUND: Severe burns result in hypercatabolic state and concomitant muscle atrophy that persists for several months, thereby limiting patient recovery. However, the effects of burns on the corresponding spinal dermatome remain unknown. This study aimed to investigate whether burns induce apoptosis of spinal cord ventral horn motor neurons (VHMNs) and consequently cause skeletal muscle wasting. METHODS: Third-degree hindpaw burn injury with 1% total body surface area (TBSA) rats were euthanized 4 and 8 weeks after burn injury. The apoptosis profiles in the ventral horns of the lumbar spinal cords, sciatic nerves, and gastrocnemius muscles were examined. The Schwann cells in the sciatic nerve were marked with S100. The gastrocnemius muscles were harvested to measure the denervation atrophy. RESULT: The VHMNs apoptosis in the spinal cord was observed after inducing third-degree burns in the hindpaw. The S100 and TUNEL double-positive cells in the sciatic nerve increased significantly after the burn injury. Gastrocnemius muscle apoptosis and denervation atrophy area increased significantly after the burn injury. CONCLUSION: Local hindpaw burn induces apoptosis in VHMNs and Schwann cells in sciatic nerve, which causes corresponding gastrocnemius muscle denervation atrophy. Our results provided an animal model to evaluate burn-induced muscle wasting, and elucidate the underlying mechanisms. [Mh] Termos MeSH primário: Células do Corno Anterior/patologia Apoptose/fisiologia Queimaduras/patologia Membro Posterior/patologia Atrofia Muscular/patologia Nervo Isquiático/patologia Corno Ventral da Medula Espinal/patologia [Mh] Termos MeSH secundário: Animais Marcação In Situ das Extremidades Cortadas/métodos Masculino Músculo Esquelético/patologia Ratos Ratos Sprague-Dawley Células de Schwann/patologia [Pt] Tipo de publicação: JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T [Em] Mês de entrada: 1511 [Cu] Atualização por classe: 170220 [Lr] Data última revisão: 170220 [Sb] Subgrupo de revista: IM [Da] Data de entrada para processamento: 150220 [St] Status: MEDLINE [do] DOI: 10.1155/2015/372819

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