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[PMID]:28456003
[Au] Autor:Röhr D; Halfter H; Schulz JB; Young P; Gess B
[Ad] Endereço:Department of Sleep Medicine and Neuromuscular Disorders, University Hospital Muenster, Muenster, Germany.
[Ti] Título:Sodium-dependent Vitamin C transporter 2 deficiency impairs myelination and remyelination after injury: Roles of collagen and demethylation.
[So] Source:Glia;65(7):1186-1200, 2017 Jul.
[Is] ISSN:1098-1136
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Peripheral nerve myelination involves rapid production of tightly bound lipid layers requiring cholesterol biosynthesis and myelin protein expression, but also a collagen-containing extracellular matrix providing mechanical stability. In previous studies, we showed a function of ascorbic acid in peripheral nerve myelination and extracellular matrix formation in adult mice. Here, we sought the mechanism of action of ascorbic acid in peripheral nerve myelination using different paradigms of myelination in vivo and in vitro. We found impaired myelination and reduced collagen expression in Sodium-dependent Vitamin C Transporter 2 heterozygous mice (SVCT2 ) during peripheral nerve development and after peripheral nerve injury. In dorsal root ganglion (DRG) explant cultures, hypo-myelination could be rescued by precoating with different collagen types. The activity of the ascorbic acid-dependent demethylating Ten-eleven-translocation (Tet) enzymes was reduced in ascorbic acid deprived and SVCT2 DRG cultures. Further, in ascorbic acid-deprived DRG cultures, methylation of a CpG island in the collagen alpha1 (IV) and alpha2 (IV) bidirectional promoter region was increased compared to wild-type and ascorbic acid treated controls. Taken together, these results provide further evidence for the function of ascorbic acid in myelination and extracellular matrix formation in peripheral nerves and suggest a putative molecular mechanism of ascorbic acid function in Tet-dependent demethylation of collagen promoters.
[Mh] Termos MeSH primário: Colágeno/metabolismo
Desmetilação
Traumatismos dos Nervos Periféricos/genética
Traumatismos dos Nervos Periféricos/fisiopatologia
Remielinização/genética
Transportadores de Sódio Acoplados à Vitamina C/deficiência
[Mh] Termos MeSH secundário: Animais
Ácido Ascórbico/farmacologia
Células Cultivadas
Colágeno/genética
Modelos Animais de Doenças
Feminino
Transtornos Neurológicos da Marcha/etiologia
Gânglios Espinais/citologia
Masculino
Camundongos
Camundongos Transgênicos
Nervos Periféricos/patologia
Nervos Periféricos/ultraestrutura
RNA Mensageiro/metabolismo
Teste de Desempenho do Rota-Rod
Células Receptoras Sensoriais/metabolismo
Células Receptoras Sensoriais/patologia
Transportadores de Sódio Acoplados à Vitamina C/genética
Fatores de Tempo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (Slc23a2 protein, mouse); 0 (Sodium-Coupled Vitamin C Transporters); 9007-34-5 (Collagen); PQ6CK8PD0R (Ascorbic Acid)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180307
[Lr] Data última revisão:
180307
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170430
[St] Status:MEDLINE
[do] DOI:10.1002/glia.23152


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[PMID]:29169593
[Au] Autor:Tosti R; Eberlin KR
[Ad] Endereço:Department of Orthopedic Surgery, The Philadelphia Hand Center, Sidney Kimmel Medical College, Thomas Jefferson University, 834 Chestnut Street Suite G114, Philadelphia, PA 19107, USA.
[Ti] Título:"Damage Control" Hand Surgery: Evaluation and Emergency Management of the Mangled Hand.
[So] Source:Hand Clin;34(1):17-26, 2018 02.
[Is] ISSN:1558-1969
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mangled hand injuries are defined as those with significant damage to multiple structures, which may be limb threatening. Historically these injuries resulted in amputation or death, but modern surgical and perioperative advances allow for complex reconstruction and the possibility of a sensate and functional limb. Evaluation begins with surveying for life-threatening injuries followed by a systematic approach to identify injured structures; management begins with preserving all parts, minimizing warm ischemia time, performing débridement, and planning an operative approach to optimize the chance of a functional limb. With careful surgical planning and a well-executed reconstruction, most limbs can be salvaged.
[Mh] Termos MeSH primário: Traumatismos da Mão/cirurgia
[Mh] Termos MeSH secundário: Amputação
Antibacterianos/uso terapêutico
Medicina de Emergência
Seres Humanos
Traumatismos dos Nervos Periféricos/cirurgia
Cuidados Pós-Operatórios
Reimplante
Terapia de Salvação
Retalhos Cirúrgicos
Traumatismos dos Tendões/cirurgia
Lesões do Sistema Vascular/cirurgia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anti-Bacterial Agents)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180303
[Lr] Data última revisão:
180303
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171125
[St] Status:MEDLINE


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[PMID]:28743796
[Au] Autor:Roberts SL; Dun XP; Doddrell RDS; Mindos T; Drake LK; Onaitis MW; Florio F; Quattrini A; Lloyd AC; D'Antonio M; Parkinson DB
[Ad] Endereço:Plymouth University Peninsula Schools of Medicine and Dentistry, John Bull Building, Plymouth Science Park, Plymouth PL6 8BU, UK.
[Ti] Título:Sox2 expression in Schwann cells inhibits myelination and induces influx of macrophages to the nerve.
[So] Source:Development;144(17):3114-3125, 2017 09 01.
[Is] ISSN:1477-9129
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Correct myelination is crucial for the function of the peripheral nervous system. Both positive and negative regulators within the axon and Schwann cell function to ensure the correct onset and progression of myelination during both development and following peripheral nerve injury and repair. The Sox2 transcription factor is well known for its roles in the development and maintenance of progenitor and stem cell populations, but has also been proposed as a negative regulator of myelination in Schwann cells. We wished to test fully whether Sox2 regulates myelination and show here that, in mice, sustained Sox2 expression blocks myelination in the peripheral nerves and maintains Schwann cells in a proliferative non-differentiated state, which is also associated with increased inflammation within the nerve. The plasticity of Schwann cells allows them to re-myelinate regenerated axons following injury and we show that re-myelination is also blocked by Sox2 expression in Schwann cells. These findings identify Sox2 as a physiological regulator of Schwann cell myelination and its potential to play a role in disorders of myelination in the peripheral nervous system.
[Mh] Termos MeSH primário: Macrófagos/metabolismo
Bainha de Mielina/metabolismo
Nervos Periféricos/metabolismo
Fatores de Transcrição SOXB1/metabolismo
Células de Schwann/metabolismo
[Mh] Termos MeSH secundário: Animais
Biomarcadores/metabolismo
Caderinas/metabolismo
Proliferação Celular
Proteína 2 de Resposta de Crescimento Precoce/metabolismo
Proteínas de Fluorescência Verde/metabolismo
Camundongos Transgênicos
Atividade Motora
Condução Nervosa
Traumatismos dos Nervos Periféricos/metabolismo
Traumatismos dos Nervos Periféricos/patologia
Nervos Periféricos/patologia
Nervos Periféricos/ultraestrutura
Proteínas Proto-Oncogênicas c-jun/metabolismo
Ratos
Recuperação de Função Fisiológica
Células de Schwann/patologia
Transgenes
beta Catenina/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biomarkers); 0 (Cadherins); 0 (Early Growth Response Protein 2); 0 (Proto-Oncogene Proteins c-jun); 0 (SOXB1 Transcription Factors); 0 (beta Catenin); 147336-22-9 (Green Fluorescent Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180302
[Lr] Data última revisão:
180302
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.1242/dev.150656


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[PMID]:28459064
[Au] Autor:Zhou XH; Lin W; Ren YM; Liu S; Fan BY; Wei ZJ; Shi GD; Cheng X; Hao Y; Feng SQ
[Ad] Endereço:Department of Orthopedics, Tianjin Medical University General Hospital, Tianjin, China.
[Ti] Título:Comparison of DNA Methylation in Schwann Cells before and after Peripheral Nerve Injury in Rats.
[So] Source:Biomed Res Int;2017:5393268, 2017.
[Is] ISSN:2314-6141
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:This study aims to find the difference of genomewide DNA methylation in Schwann cells (SCs) before and after peripheral nerve system (PNS) injury by Methylated DNA Immunoprecipitation Sequencing (MeDIP-Seq) and seek meaningful differentially methylated genes related to repairment of injured PNS. SCs harvested from sciatic nerve were named as activated Schwann cells (ASCs), and the ones harvested from brachial plexus were named as normal Schwann cells (NSCs). Genomic DNA of ASCs and NSCs were isolated and MeDIP-Seq was conducted. Differentially methylated genes and regions were discovered and analyzed by bioinformatic methods. MeDIP-Seq analysis showed methylation differences were identified between ASCs and NSCs. The distribution of differentially methylated regions (DMRs) peaks in different components of genome was mainly located in distal intergenic regions. GO and KEGG analysis of these methylated genes were also conducted. The expression patterns of hypermethylated genes (Dgcr8, Zeb2, Dixdc1, Sox2, and Shh) and hypomethylated genes (Gpr126, Birc2) detected by qRT-PCR were opposite to the MeDIP analysis data with significance ( < 0.05), which proved MeDIP analysis data were real and believable. Our data serve as a basis for understanding the injury-induced epigenetic changes in SCs and the foundation for further studies on repair of PNS injury.
[Mh] Termos MeSH primário: Metilação de DNA/genética
Epigênese Genética/genética
Traumatismos dos Nervos Periféricos/genética
Células de Schwann/citologia
[Mh] Termos MeSH secundário: Animais
Traumatismos dos Nervos Periféricos/metabolismo
Ratos
Ratos Wistar
Células de Schwann/metabolismo
Análise de Sequência de DNA/métodos
Cicatrização/genética
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180227
[Lr] Data última revisão:
180227
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1155/2017/5393268


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[PMID]:28451639
[Au] Autor:Kanda H; Kobayashi K; Yamanaka H; Okubo M; Noguchi K
[Ad] Endereço:Department of Anatomy and Neuroscience, Hyogo College of Medicine, Nishinomiya, Hyogo 663-8501, Japan.
[Ti] Título:Microglial TNFα Induces COX2 and PGI2 Synthase Expression in Spinal Endothelial Cells during Neuropathic Pain.
[So] Source:eNeuro;4(2), 2017 Mar-Apr.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Prostaglandins (PGs) are typical lipid mediators that play a role in homeostasis and disease. They are synthesized from arachidonic acid by cyclooxygenase 1 (COX1) and COX2. Although COX2 has been reported to be upregulated in the spinal cord after nerve injury, its expression and functional roles in neuropathic pain remain unclear. In this study, we investigated the expression of Cox2, PGI2 synthase (Pgis), and prostaglandin I2 receptor (IP receptor) mRNA in the rat spinal cord after spared nerve injury (SNI). Levels of Cox2 and Pgis mRNA increased in endothelial cells from 24 to 48 h after nerve injury. IP receptor mRNA was constitutively expressed in dorsal horn neurons. A COX2 inhibitor and IP receptor antagonists attenuated pain behavior in the early phase of neuropathic pain. Furthermore, we examined the relationship between COX2 and tumor necrosis factor-α (TNFα) in the spinal cord of a rat SNI model. Levels of TNFα mRNA transiently increased in the spinal microglia 24 h after SNI. The TNF receptors Tnfr1 and Tnfr2 mRNA were colocalized with COX2. Intrathecal injection of TNFα induced Cox2 and Pgis mRNA expression in endothelial cells. These results revealed that microglia-derived TNFα induced COX2 and PGIS expression in spinal endothelial cells and that endothelial PGI2 played a critical role in neuropathic pain via neuronal IP receptor. These findings further suggest that the glia-endothelial cell interaction of the neurovascular unit via transient TNFα is involved in the generation of neuropathic pain.
[Mh] Termos MeSH primário: Ciclo-Oxigenase 2/metabolismo
Sistema Enzimático do Citocromo P-450/metabolismo
Células Endoteliais/enzimologia
Oxirredutases Intramoleculares/metabolismo
Microglia/metabolismo
Neuralgia/metabolismo
Medula Espinal/metabolismo
Fator de Necrose Tumoral alfa/metabolismo
[Mh] Termos MeSH secundário: Animais
Inflamação/enzimologia
Masculino
Traumatismos dos Nervos Periféricos/metabolismo
RNA Mensageiro
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (RNA, Messenger); 0 (Tumor Necrosis Factor-alpha); 9035-51-2 (Cytochrome P-450 Enzyme System); EC 1.14.99.1 (Cyclooxygenase 2); EC 1.14.99.1 (Ptgs2 protein, rat); EC 5.3.- (Intramolecular Oxidoreductases); EC 5.3.99.4 (prostacyclin synthetase)
[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


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[PMID]:29358641
[Au] Autor:Qian Y; Zhao X; Han Q; Chen W; Li H; Yuan W
[Ad] Endereço:School of Pharmacy, Shanghai Jiao Tong University, 800 Dongchuan Road, Shanghai, 200240, China.
[Ti] Título:An integrated multi-layer 3D-fabrication of PDA/RGD coated graphene loaded PCL nanoscaffold for peripheral nerve restoration.
[So] Source:Nat Commun;9(1):323, 2018 01 22.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:As a conductive nanomaterial, graphene has huge potentials in nerve function restoration by promoting electrical signal transduction and metabolic activities with unique topological properties. Polydopamine (PDA) and arginylglycylaspartic acid (RGD) can improve cell adhesion in tissue engineering. Here we report an integrated 3D printing and layer-by-layer casting (LBLC) method in multi-layered porous scaffold fabrication. The scaffold is composed of single-layered graphene (SG) or multi-layered graphene (MG) and polycaprolactone (PCL). The electrically conductive 3D graphene scaffold can significantly improve neural expression both in vitro and in vivo. It promotes successful axonal regrowth and remyelination after peripheral nerve injury. These findings implicate that graphene-based nanotechnology have great potentials in peripheral nerve restoration in preclinical and clinical application.
[Mh] Termos MeSH primário: Materiais Biocompatíveis/química
Grafite/química
Indóis/química
Regeneração Nervosa/efeitos dos fármacos
Oligopeptídeos/química
Polímeros/química
Engenharia Tecidual/métodos
Tecidos Suporte
[Mh] Termos MeSH secundário: Animais
Materiais Biocompatíveis/farmacologia
Adesão Celular/efeitos dos fármacos
Condutividade Elétrica
Grafite/farmacologia
Indóis/farmacologia
Masculino
Teste de Materiais
Nanotecnologia/métodos
Regeneração Nervosa/fisiologia
Oligopeptídeos/farmacologia
Traumatismos dos Nervos Periféricos/patologia
Traumatismos dos Nervos Periféricos/fisiopatologia
Traumatismos dos Nervos Periféricos/reabilitação
Poliésteres/química
Poliésteres/farmacologia
Polímeros/farmacologia
Porosidade
Cultura Primária de Células
Impressão Tridimensional
Ratos
Ratos Sprague-Dawley
Células de Schwann/citologia
Células de Schwann/efeitos dos fármacos
Células de Schwann/fisiologia
Nervo Isquiático/efeitos dos fármacos
Nervo Isquiático/lesões
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Biocompatible Materials); 0 (Indoles); 0 (Oligopeptides); 0 (Polyesters); 0 (Polymers); 0 (polydopamine); 24980-41-4 (polycaprolactone); 7782-42-5 (Graphite); 78VO7F77PN (arginyl-glycyl-aspartic acid)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180124
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02598-7


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[PMID]:29217355
[Au] Autor:Wang X; Zhang G; Qiao Y; Feng C; Zhao X
[Ad] Endereço:Department of Anesthesiology, The Second Hospital of Shandong University, 247 Bei Yuan Street, Jinan 250033, China.
[Ti] Título:Crocetin attenuates spared nerve injury-induced neuropathic pain in mice.
[So] Source:J Pharmacol Sci;135(4):141-147, 2017 Dec.
[Is] ISSN:1347-8648
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Crocetin is the main component of saffron and exhibits anti-oxidative and anti-inflammatory effects. Neuroinflammation and oxidative stress have been recognized to play a crucial role in the pathogenesis of neuropathic pain. We investigated the effect of crocetin in a mouse model with neuropathic pain induced by spared nerve injury (SNI). Crocetin was intrathecally perfused at various doses for up to 12 days starting 3 days before the surgery. Behavioral tests were performed to determine pain sensitivity. The concentrations of proinflammatory cytokines tumor necrosis factor (TNF-α) and interleukin-1ß (IL-1ß) were measured to assess neuroinflammation. In addition, the enzymatic activity of superoxide dismutase (SOD) was measured to reveal the oxidative stress level. We found that repeated treatment with crocetin dose-dependently attenuated mechanical and thermal allodynia in SNI mice. In addition, treatment with high dose of crocetin reduced SNI-induced increase of TNF-α and IL-1ß. Crocetin also restored the activity of mitochondrial MnSOD which was reduced in the sciatic nerve and the spinal cord of SNI mice. Collectively, our data demonstrate that crocetin effectively attenuates the neuropathic pain and significantly suppresses oxidative stress and neuroinflammation in the SNI mouse model, supporting the potential of crocetin in the treatment against neuropathic pain.
[Mh] Termos MeSH primário: Carotenoides/administração & dosagem
Carotenoides/farmacologia
Neuralgia/tratamento farmacológico
Neuralgia/etiologia
Traumatismos dos Nervos Periféricos/complicações
Fitoterapia
[Mh] Termos MeSH secundário: Animais
Anti-Inflamatórios
Antioxidantes
Biomarcadores
Carotenoides/isolamento & purificação
Crocus/química
Modelos Animais de Doenças
Relação Dose-Resposta a Droga
Mediadores da Inflamação/metabolismo
Interleucina-1beta/metabolismo
Masculino
Camundongos Endogâmicos
Neuralgia/diagnóstico
Neuralgia/metabolismo
Estresse Oxidativo
Nervo Isquiático/metabolismo
Medula Espinal
Superóxido Dismutase
Fator de Necrose Tumoral alfa/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Antioxidants); 0 (Biomarkers); 0 (Inflammation Mediators); 0 (Interleukin-1beta); 0 (Tumor Necrosis Factor-alpha); 20TC155L9C (crocetin); 36-88-4 (Carotenoids); EC 1.15.1.1 (Superoxide Dismutase)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171209
[St] Status:MEDLINE


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[PMID]:27771719
[Au] Autor:Lee H; Baek J; Min H; Cho IH; Yu SW; Lee SJ
[Ad] Endereço:Department of Neuroscience and Physiology, and Dental Research Institute, School of Dentistry, Seoul National University, Seoul, Republic of Korea.
[Ti] Título:Toll-Like Receptor 3 Contributes to Wallerian Degeneration after Peripheral Nerve Injury.
[So] Source:Neuroimmunomodulation;23(4):209-216, 2016.
[Is] ISSN:1423-0216
[Cp] País de publicação:Switzerland
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: It is well known that Schwann cells play an important role in Wallerian degeneration after peripheral nerve injury. Previously, we reported that toll-like receptor 3 (TLR3) is expressed on Schwann cells, implicating its role in Schwann cell activation during Wallerian degeneration. In this study, we tested this possibility using TLR3 knock-out mice. METHODS: Sciatic nerve-crush injury was induced in wild-type and TLR3 knock-out mice. Histological sections of the sciatic nerve were analyzed for Wallerian degeneration on days 3 and 7 after injury. The level of macrophage infiltration was measured by real-time RT-PCR, flow cytometry and immunohistochemistry. The macrophage-recruiting chemokine gene expressions in the injured nerve were determined by real-time RT-PCR. RESULTS: In TLR3 knock-out mice, the nerve injury-induced axonal degeneration and subsequent axonal debris clearance were reduced compared to in wild-type mice. In addition, nerve injury-induced macrophage infiltration into injury sites was attenuated in TLR3 knock-out mice and was accompanied by reduced expression of macrophage-recruiting chemokines such as CC-chemokine ligands (CCL)2/MCP-1, CCL4/MIP-1ß and CCL5/RANTES. These macrophage-recruiting chemokines were induced in primary Schwann cells upon TLR3 stimulation. Finally, intraneural injection of polyinosinic-polycytidylic acid, a synthetic TLR3 agonist, induced macrophage infiltration into the sciatic nerve in vivo. CONCLUSION: These data show that TLR3 signaling contributes to Wallerian degeneration after peripheral nerve injury by affecting Schwann cell activation and macrophage recruitment to injured nerves.
[Mh] Termos MeSH primário: Neuropatia Ciática/metabolismo
Neuropatia Ciática/patologia
Receptor 3 Toll-Like/deficiência
Degeneração Walleriana/metabolismo
Degeneração Walleriana/patologia
[Mh] Termos MeSH secundário: Animais
Células Cultivadas
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Knockout
Traumatismos dos Nervos Periféricos/metabolismo
Traumatismos dos Nervos Periféricos/patologia
Ratos
Ratos Sprague-Dawley
Células de Schwann/metabolismo
Células de Schwann/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (TLR3 protein, mouse); 0 (Toll-Like Receptor 3)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180213
[Lr] Data última revisão:
180213
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1159/000449134


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[PMID]:29280873
[Au] Autor:Hu CH; Chang TN; Lu JC; Laurence VG; Chuang DC
[Ad] Endereço:Taoyuan, Taiwan From the Department of Plastic Surgery, Chang Gung Memorial Hospital, Chang Gung Medical College and University.
[Ti] Título:Comparison of Surgical Strategies between Proximal Nerve Graft and/or Nerve Transfer and Distal Nerve Transfer Based on Functional Restoration of Elbow Flexion: A Retrospective Review of 147 Patients.
[So] Source:Plast Reconstr Surg;141(1):68e-79e, 2018 01.
[Is] ISSN:1529-4242
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Surgical strategy to treat incomplete brachial plexus injury with palsies of the shoulder and elbow by using proximal nerve graft/transfer or distal nerve transfer is still debated. The aim of this study was to compare both strategies with respect to the recovery of elbow flexion. METHODS: One hundred forty-seven patients were enrolled: 76 patients underwent reconstruction using proximal nerve graft/transfer, and 71 patients underwent reconstruction using distal nerve transfer. All patients were evaluated preoperatively and postoperatively to assess the recovery rate and muscle strength of elbow flexion. Shoulder abduction and hand grip power were also recorded to assess any concomitant postoperative changes between the two methods. RESULTS: The best recovery rate for functional elbow flexion (p = 0.006) and the fastest recovery to M3 strength (p < 0.001) were found in the double fascicular transfer group. However, recovery of shoulder abduction with proximal nerve graft/transfer was significantly better than with distal nerve transfer (80.3 percent versus 66.2 percent in shoulder abduction ≥60 degrees; and 56.6 percent versus 38.0 percent in shoulder abduction ≥90 degrees). A significant decrease in grip strength between the operative and nonoperative hands was also found in patients undergoing distal nerve transfer (p = 0.001). CONCLUSIONS: Proximal nerve graft/transfer offers more accurate diagnosis and proper treatment to restore shoulder and elbow function simultaneously. Distal nerve transfer can offer more efficient elbow flexion. Combined, both strategies in primary nerve reconstruction are especially recommended when there is no healthy or not enough donor nerve available. CLINICAL QUESTION/LEVEL OF EVIDENCE: Therapeutic, III.
[Mh] Termos MeSH primário: Plexo Braquial/lesões
Articulação do Cotovelo/fisiologia
Transferência de Nervo
Traumatismos dos Nervos Periféricos/cirurgia
Amplitude de Movimento Articular
[Mh] Termos MeSH secundário: Adulto
Plexo Braquial/cirurgia
Feminino
Seguimentos
Força da Mão
Seres Humanos
Masculino
Meia-Idade
Recuperação de Função Fisiológica
Estudos Retrospectivos
Resultado do Tratamento
[Pt] Tipo de publicação:COMPARATIVE STUDY; JOURNAL ARTICLE; VIDEO-AUDIO MEDIA
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171228
[St] Status:MEDLINE
[do] DOI:10.1097/PRS.0000000000003935


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[PMID]:29257018
[Au] Autor:Zhu D; Tapadia MD; Palispis W; Luu M; Wang W; Gupta R
[Ad] Endereço:Peripheral Nerve Research Laboratory, Department of Orthopaedic Surgery, University of California, Irvine, Irvine, California.
[Ti] Título:Attenuation of Robust Glial Scar Formation Facilitates Functional Recovery in Animal Models of Chronic Nerve Compression Injury.
[So] Source:J Bone Joint Surg Am;99(24):e132, 2017 Dec 20.
[Is] ISSN:1535-1386
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Late surgery for chronic nerve compression injuries usually improves sensation but rarely reverses motor atrophy. We hypothesized that a persistent glial scar after chronic nerve compression injury might account for poor motor recovery and that degradation of the glial scar as an adjunct to surgical decompression would improve functional recovery. METHODS: A previously described model of chronic nerve compression injury was created in C57BL/6 mice and Sprague-Dawley rats, and the nerves were harvested early or late after electrophysiological confirmation of the injury. Western blot, polymerase chain reaction, and quantitative immunohistochemical analyses were performed to determine levels of chondroitin sulfate proteoglycans and extracellular matrix molecules. Subsets of mice were treated either with surgical decompression alone or with decompression coupled with intraepineurial injection of a low dose (0.1 µgµL) or a high dose (0.2 µg/µL) of chondroitinase ABC at 6 weeks after injury. RESULTS: Aggrecan showed the greatest change in mRNA and protein levels at the early and late time points following creation of the chronic nerve compression injury. Quantitative immunohistochemical analysis revealed early aggrecan upregulation localized primarily to the endoneurium and late upregulation localized to the perineurium and epineurium (p < 0.0105). Quantitative immunohistochemical analysis for collagen IV, laminin-α2, and fibronectin also showed early upregulation with perineurial scarring. Quantitative immunohistochemical analysis and Western blot analysis for aggrecan demonstrated a marked increase in the endoneurium at the early time points and upregulation of expression in the epineurium and perineurium at the late time points. Decompression along with intraepineurial injection of high-dose chondroitinase ABC at 6 weeks after creation of the compression injury resulted in marked attenuation of decorin and aggrecan expression with functional improvement in nerve conduction velocity. CONCLUSIONS: Significant upregulation of chondroitin sulfate proteoglycans and other extracellular matrix components contributes to the pathogenesis of compression neuropathies in murine models. The administration of chondroitinase ABC degrades these chondroitin sulfate proteoglycans and improves functional recovery after chronic nerve compression injury; thus, it can be considered as a possible therapeutic adjunct.
[Mh] Termos MeSH primário: Condroitina ABC Liase/farmacologia
Cicatriz/prevenção & controle
Descompressão Cirúrgica/métodos
Síndromes de Compressão Nervosa/tratamento farmacológico
Traumatismos dos Nervos Periféricos/tratamento farmacológico
Traumatismos dos Nervos Periféricos/patologia
[Mh] Termos MeSH secundário: Agrecanas/farmacologia
Análise de Variância
Animais
Western Blotting
Doença Crônica
Modelos Animais de Doenças
Injeções Intralesionais
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Síndromes de Compressão Nervosa/patologia
Síndromes de Compressão Nervosa/cirurgia
Condução Nervosa/efeitos dos fármacos
Traumatismos dos Nervos Periféricos/cirurgia
RNA Mensageiro/efeitos dos fármacos
Distribuição Aleatória
Ratos
Ratos Sprague-Dawley
Reação em Cadeia da Polimerase em Tempo Real/métodos
Recuperação de Função Fisiológica/fisiologia
Sensibilidade e Especificidade
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aggrecans); 0 (RNA, Messenger); EC 4.2.2.20 (Chondroitin ABC Lyase)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:171227
[Lr] Data última revisão:
171227
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171220
[St] Status:MEDLINE
[do] DOI:10.2106/JBJS.17.00396



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