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[PMID]:29280843
[Au] Autor:Nahabedian MY; Nahabedian AG
[Ad] Endereço:Maurice Y. Nahabedian is an attending plastic surgeon at the National Center for Plastic Surgery in McLean, Va., and at the Inova Fairfax Hospital in Falls Church, Va. Anissa G. Nahabedian is an RN at Sibley Hospital in Washington, D.C.
[Ti] Título:Closing the gap for patients with rectus abdominis diastasis.
[So] Source:Nursing;48(1):49-52, 2018 Jan.
[Is] ISSN:1538-8689
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Doenças Musculares/enfermagem
Relações Enfermeiro-Paciente
Educação de Pacientes como Assunto
Reto do Abdome
[Mh] Termos MeSH secundário: Seres Humanos
Doenças Musculares/etiologia
Diagnóstico de Enfermagem
Enfermagem Perioperatória
Complicações Pós-Operatórias
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180222
[Lr] Data última revisão:
180222
[Sb] Subgrupo de revista:N
[Da] Data de entrada para processamento:171228
[St] Status:MEDLINE
[do] DOI:10.1097/01.NURSE.0000527601.09592.14


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[PMID]:29307828
[Au] Autor:Wang X; Min S; Xie F; Yang J; Li L; Chen J
[Ad] Endereço:Department of Anesthesiology, First Affiliated Hospital of Chongqing Medical University, Chongqing, China.
[Ti] Título:Glial cell-derived neurotrophic factor alleviates sepsis-induced neuromuscular dysfunction by decreasing the expression of γ- and α7-nicotinic acetylcholine receptors in an experimental rat model of neuromyopathy.
[So] Source:Biochem Biophys Res Commun;496(2):260-266, 2018 02 05.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sepsis-induced neuromuscular dysfunction results from up-regulation of the expression of γ- and α7-nicotinic acetylcholine receptors (nAChR). Although glial cell derived neurotrophic factor (GDNF) has been implicated in repairing and supporting neurons, little is known about the effects of GDNF on demyelination of nerves in sepsis. In this study, we tested the hypothesis that GDNF could alleviate sepsis-induced neuromuscular dysfunction by decreasing the expression of γ- and α7-nAChR in an experimental rat model of neuromyopathy. Rats were randomly divided into a sham group and a sepsis group. Levels of inflammatory factors, muscle function, and nicotinic acetylcholine receptors were tested in rats after cecal ligation and puncture (CLP). At 24 h after CLP, GDNF was injected around the sciatic nerve of sepsis rats, cytokines were detected by enzyme-linked immunosorbent assay (ELISA), and immunofluorescence staining was used to detect the expression of nAChRs. GDNF and its downstream effector (Erk1/2 and GFR-α), neuregulin-1 (NRG-1) and γ- and α7-nAChR were measured using Western blot analysis. The expression of GDNF reached a minimum at 24 h after CLP. Compared with the sham group, the release of cytokines and the expression of γ- and α7-nAChR were significantly increased in the sepsis group. The administration of GDNF significantly alleviated sepsis-induced neuromuscular dysfunction, as well as reducing the expression of γ- and α7-nAChR. In addition, the expression of Erk1/2, GFR-α, NRG-1 were significantly increased after GDNF treatment. GDNF administration may improve patient outcomes by reducing the demyelination of nerves and the expression of γ- and α7-nAChR.
[Mh] Termos MeSH primário: Anti-Inflamatórios/farmacologia
Doenças Desmielinizantes/tratamento farmacológico
Fator Neurotrófico Derivado de Linhagem de Célula Glial/farmacologia
Doenças Musculares/tratamento farmacológico
Fármacos Neuroprotetores/farmacologia
Sepse/tratamento farmacológico
Receptor Nicotínico de Acetilcolina alfa7/genética
[Mh] Termos MeSH secundário: Animais
Citocinas/genética
Citocinas/metabolismo
Doenças Desmielinizantes/genética
Doenças Desmielinizantes/metabolismo
Doenças Desmielinizantes/patologia
Modelos Animais de Doenças
Regulação da Expressão Gênica
Fatores de Troca do Nucleotídeo Guanina/genética
Fatores de Troca do Nucleotídeo Guanina/metabolismo
Masculino
Proteína Quinase 1 Ativada por Mitógeno/genética
Proteína Quinase 1 Ativada por Mitógeno/metabolismo
Proteína Quinase 3 Ativada por Mitógeno/genética
Proteína Quinase 3 Ativada por Mitógeno/metabolismo
Doenças Musculares/genética
Doenças Musculares/metabolismo
Doenças Musculares/patologia
Neuregulina-1/genética
Neuregulina-1/metabolismo
Junção Neuromuscular/efeitos dos fármacos
Junção Neuromuscular/metabolismo
Junção Neuromuscular/patologia
Isoformas de Proteínas/antagonistas & inibidores
Isoformas de Proteínas/genética
Isoformas de Proteínas/metabolismo
Ratos
Ratos Sprague-Dawley
Nervo Isquiático/efeitos dos fármacos
Nervo Isquiático/metabolismo
Nervo Isquiático/patologia
Sepse/genética
Sepse/metabolismo
Sepse/patologia
Transdução de Sinais
Receptor Nicotínico de Acetilcolina alfa7/antagonistas & inibidores
Receptor Nicotínico de Acetilcolina alfa7/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Anti-Inflammatory Agents); 0 (Cytokines); 0 (Glial Cell Line-Derived Neurotrophic Factor); 0 (Guanine Nucleotide Exchange Factors); 0 (Neuregulin-1); 0 (Neuroprotective Agents); 0 (Nrg1 protein, rat); 0 (Protein Isoforms); 0 (alpha7 Nicotinic Acetylcholine Receptor); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 1); EC 2.7.11.24 (Mitogen-Activated Protein Kinase 3)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180214
[Lr] Data última revisão:
180214
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180109
[St] Status:MEDLINE


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[PMID]:29307884
[Au] Autor:Dumancas CY; Reyes HAG; Cosico J; Savadkar A; Lah S
[Ad] Endereço:Department of Medicine, New York Medical College, Metropolitan Hospital Center, New York, NY, USA.
[Ti] Título:Streptococcus pneumoniae-Related Hemophagocytic Lymphohistiocytosis Treated with IVIG and Steroids.
[So] Source:Am J Case Rep;19:25-28, 2018 Jan 08.
[Is] ISSN:1941-5923
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND Hemophagocytic lymphohistiocytosis (HLH) is a rare life-threatening condition that has a poor prognosis due to the ensuing cytokine storm leading to severe organ damage. Current treatment guidelines suggest using a combination of steroid- and etoposide-based chemotherapy. CASE REPORT The authors present a case of a 41-year-old African-American female who presented with symptoms of foodborne illness and who developed multi-organ dysfunction. HLH was suspected because of poor response to broad-spectrum antibiotics with a constellation of findings, including cytopenia, hypofibrinogenemia, hypertriglyceridemia, and hyperferritinemia. Clinical improvement was noted after administration of intravenous immunoglobulin and dexamethasone while waiting for the soluble interleukin-2 receptor levels; therefore, chemotherapy was not administered.  CONCLUSIONS Despite the variable and poor prognosis of HLH, early treatment with steroids and immunosuppressive therapy is crucial to improving the survival rate. The inclusion of immunoglobulin therapy should be considered a treatment option for HLH.
[Mh] Termos MeSH primário: Dexametasona/administração & dosagem
Glucocorticoides/administração & dosagem
Imunoglobulinas Intravenosas/administração & dosagem
Fatores Imunológicos/administração & dosagem
Linfo-Histiocitose Hemofagocítica/microbiologia
Linfo-Histiocitose Hemofagocítica/terapia
Streptococcus pneumoniae/isolamento & purificação
[Mh] Termos MeSH secundário: Adulto
Antibacterianos/administração & dosagem
Índice de Massa Corporal
Diabetes Mellitus Tipo 2/complicações
Quimioterapia Combinada
Feminino
Seres Humanos
Linfo-Histiocitose Hemofagocítica/diagnóstico
Uso da Maconha/efeitos adversos
Insuficiência de Múltiplos Órgãos/tratamento farmacológico
Insuficiência de Múltiplos Órgãos/etiologia
Doenças Musculares/etiologia
Doenças Musculares/reabilitação
Transferência de Pacientes
Prognóstico
Fatores de Risco
Streptococcus pneumoniae/patogenicidade
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); 0 (Glucocorticoids); 0 (Immunoglobulins, Intravenous); 0 (Immunologic Factors); 7S5I7G3JQL (Dexamethasone)
[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:180109
[St] Status:MEDLINE


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[PMID]:29342166
[Au] Autor:Benetti E; Mastrocola R; Chiazza F; Nigro D; D'Antona G; Bordano V; Fantozzi R; Aragno M; Collino M; Minetto MA
[Ad] Endereço:Dipartimento di Scienza e Tecnologia del Farmaco, University of Turin, Turin, Italy.
[Ti] Título:Effects of vitamin D on insulin resistance and myosteatosis in diet-induced obese mice.
[So] Source:PLoS One;13(1):e0189707, 2018.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Epidemiological studies pointed out to a strong association between vitamin D deficiency and type 2 diabetes prevalence. However, the role of vitamin D supplementation in the skeletal muscle, a tissue that play a crucial role in the maintenance of glucose homeostasis, has been scarcely investigated so far. On this basis, this study aimed to evaluate the effect of vitamin D supplementation in a murine model of diet-induced insulin resistance with particular attention to the effects evoked on the skeletal muscle. Male C57BL/6J mice (n = 40) were fed with a control or a High Fat-High Sugar (HFHS) diet for 4 months. Subsets of animals were treated for 2 months with vitamin D (7 µg·kg-1, i.p. three times/week). HFHS diet induced body weight increase, hyperglycemia and impaired glucose tolerance. HFHS animals showed an impaired insulin signaling and a marked fat accumulation in the skeletal muscle. Vitamin D reduced body weight and improved systemic glucose tolerance. In addition, vitamin D restored the impaired muscle insulin signaling and reverted myosteatosis evoked by the diet. These effects were associated to decreased activation of NF-κB and lower levels of TNF-alpha. Consistently, a significantly decreased activation of the SCAP/SREBP lipogenic pathway and lower levels of CML protein adducts and RAGE expression were observed in skeletal muscle of animals treated with vitamin D. Collectively, these data indicate that vitamin D-induced selective inhibition of signaling pathways (including NF-κB, SCAP/SREBP and CML/RAGE cascades) within the skeletal muscle significantly contributed to the beneficial effects of vitamin D supplementation against diet-induced metabolic derangements.
[Mh] Termos MeSH primário: Resistência à Insulina
Doenças Musculares/prevenção & controle
Vitamina D/farmacologia
[Mh] Termos MeSH secundário: Animais
Dieta Hiperlipídica
Carboidratos da Dieta/administração & dosagem
Teste de Tolerância a Glucose
Insulina/metabolismo
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Obesos
Músculo Esquelético/metabolismo
Doenças Musculares/metabolismo
Transdução de Sinais
Vitamina D/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Dietary Carbohydrates); 0 (Insulin); 1406-16-2 (Vitamin D)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180129
[Lr] Data última revisão:
180129
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180118
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0189707


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[PMID]:29298145
[Au] Autor:Kennedy KR; Wang AL
[Ad] Endereço:University of Alabama at Birmingham, Birmingham, AL kcreal@uab.edu.
[Ti] Título:Poland Syndrome.
[So] Source:N Engl J Med;378(1):72, 2018 Jan 04.
[Is] ISSN:1533-4406
[Cp] País de publicação:United States
[La] Idioma:eng
[Mh] Termos MeSH primário: Dedos/anormalidades
Doenças Musculares
Músculos Peitorais/anormalidades
Síndrome de Poland/patologia
[Mh] Termos MeSH secundário: Idoso de 80 Anos ou mais
Seres Humanos
Masculino
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180118
[Lr] Data última revisão:
180118
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE


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[PMID]:29183798
[Au] Autor:McElhanon KE; Bhattacharya S
[Ad] Endereço:Department of Physiology and Cell Biology, Davis Heart and Lung Research Institute, The Ohio State University Wexner Medical Center, 473 W. 12th Ave, Columbus, OH 43210-1252, United States.
[Ti] Título:Altered membrane integrity in the progression of muscle diseases.
[So] Source:Life Sci;192:166-172, 2018 Jan 01.
[Is] ISSN:1879-0631
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:Sarcolemmal integrity is orchestrated through the interplay of preserving membrane strength and fast tracking the membrane repair process during an event of compromised membrane fragility. Several molecular players have been identified that act in a concerted fashion to maintain the barrier function of the muscle membrane. Substantial research findings in the field of muscle biology point out the importance of maintaining membrane integrity as a key contributory factor to cellular homeostasis. Innumerable data on the progression of membrane pathology associated with compromised muscle membrane integrity support targeting sarcolemmal integrity in skeletal and cardiac muscle as a model therapeutic strategy to alleviate some of the pathologic conditions. This review will discuss strategies that researchers have undertaken to compensate for an imbalance in sarcolemma membrane fragility and membrane repair to maintain muscle membrane integrity.
[Mh] Termos MeSH primário: Membranas/patologia
Doenças Musculares/patologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Músculo Esquelético/patologia
Miocárdio/patologia
Miócitos Cardíacos/patologia
Sarcolema/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180108
[Lr] Data última revisão:
180108
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171130
[St] Status:MEDLINE


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[PMID]:28466399
[Au] Autor:Rosenson RS; Gandra SR; McKendrick J; Dent R; Wieffer H; Cheng LI; Catapano AL; Oh P; Kees Hovingh G; Stroes ES
[Ad] Endereço:Icahn School of Medicine at Mount Sinai, 1425 Madison Ave, MC1 Level, New York, NY, 10029, USA. robert.rosenson@mssm.edu.
[Ti] Título:Identification and Management of Statin-Associated Symptoms in Clinical Practice: Extension of a Clinician Survey to 12 Further Countries.
[So] Source:Cardiovasc Drugs Ther;31(2):187-195, 2017 Apr.
[Is] ISSN:1573-7241
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:PURPOSE: Statins are the first-choice pharmacological treatment for patients with hypercholesterolemia and at risk for cardiovascular disease; however, a minority of patients experience statin-associated symptoms (SAS) and are considered to have reduced statin tolerance. The objective of this study was to establish how patients with SAS are identified and managed in clinical practice in Austria, Belgium, Colombia, Croatia, the Czech Republic, Denmark, Portugal, Switzerland, Russia, Saudi Arabia, Turkey, and the United Arab Emirates. METHODS: A cross-sectional survey was conducted (2015-2016) among clinicians (n = 60 per country; Croatia: n = 30) who are specialized/experienced in the treatment of hypercholesterolemia. Participants were asked about their experience of patients presenting with potential SAS and how such patients were identified and treated. RESULTS: Muscle-related symptoms were the most common presentation of potential SAS (average: 51%; range across countries [RAC] 17-74%); other signs/symptoms included persistent elevation in transaminases. To establish whether symptoms are due to statins, clinicians required rechallenge after discontinuation of statin treatment (average: 77%; RAC 40-90%); other requirements included trying at least one alternative statin. Clinicians reported that half of high-risk patients with confirmed SAS receive a lower-dose statin (average: 53%; RAC 43-72%), and that most receive another non-statin lipid-lowering therapy with or without a concomitant statin (average: 65%; RAC 52-83%). CONCLUSIONS: The specialists and GPs surveyed use stringent criteria to establish causality between statin use and signs or symptoms, and persevere with statin treatment where possible.
[Mh] Termos MeSH primário: Inibidores de Hidroximetilglutaril-CoA Redutases/efeitos adversos
Hipercolesterolemia/tratamento farmacológico
Músculo Esquelético/efeitos dos fármacos
Doenças Musculares/diagnóstico
Doenças Musculares/terapia
Padrões de Prática Médica
[Mh] Termos MeSH secundário: Colômbia/epidemiologia
Estudos Transversais
Relação Dose-Resposta a Droga
Substituição de Medicamentos
Europa (Continente)/epidemiologia
Pesquisas sobre Serviços de Saúde
Seres Humanos
Inibidores de Hidroximetilglutaril-CoA Redutases/administração & dosagem
Hipercolesterolemia/diagnóstico
Hipercolesterolemia/epidemiologia
Doenças Musculares/induzido quimicamente
Doenças Musculares/epidemiologia
Valor Preditivo dos Testes
Prevalência
Medição de Risco
Fatores de Risco
Arábia Saudita/epidemiologia
Emirados Árabes Unidos/epidemiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; MULTICENTER STUDY
[Nm] Nome de substância:
0 (Hydroxymethylglutaryl-CoA Reductase Inhibitors)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170504
[St] Status:MEDLINE
[do] DOI:10.1007/s10557-017-6727-0


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[PMID]:29203373
[Au] Autor:Preciado LM; Rey-Suárez P; Henao IC; Pereañez JA
[Ad] Endereço:Programa de Ofidismo/Escorpionismo, Facultad de Ciencias Farmacéuticas y Alimentarias, Universidad de Antioquia UdeA, Calle 70 No. 52-21, Medellín, Colombia.
[Ti] Título:Betulinic, oleanolic and ursolic acids inhibit the enzymatic and biological effects induced by a P-I snake venom metalloproteinase.
[So] Source:Chem Biol Interact;279:219-226, 2018 Jan 05.
[Is] ISSN:1872-7786
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Betulinic acid (BA), Oleanolic acid (OA) and Ursolic acid (UA), are pentacyclic triterpenoids with widespread occurrence throughout the plant kingdom, these compounds are widely recognized by their pharmacological and biological properties, such as, anti-tumoral, anti-inflammatory, anti-microbial and hepatoprotective activity. In this work we determined the inhibitory ability of these compounds on the enzymatic, hemorrhagic, myotoxic and edema-inducing activities of Batx-I, a P-I metalloproteinase isolated from Bothrops atrox venom. BA, UA and OA inhibited the proteolytic activity of Batx-I on gelatin with IC values of 115.3, 223.0 and 357.3 µM, respectively. Additionally, these compounds showed inhibition of the hemorrhagic activity of Batx-I in skin with IC 345.7, 643.5 and 1077.0 µM for BA, UA and OA in preincubation experiments. In studies with independent-injection, in which Batx-I was injected and then, at the same site, a concentration of 600 µM of each compound were administered at either 0, 5 or 10 min, BA showed a significant reduction of hemorrhage at 0 and 5 min. In addition, these compounds inhibited myotoxicity and edema-forming activity of Batx-I at 600 µM concentration. Molecular docking studies suggested that these compounds could occupy part of the substrate binding cleft of the enzyme affecting its catalytic cycle. In this manner, triterpenic acids are candidates for the development of inhibitors for the prevention of local tissue damage in snakebite envenomation.
[Mh] Termos MeSH primário: Venenos de Crotalídeos/enzimologia
Metaloproteases/metabolismo
Ácido Oleanólico/farmacologia
Triterpenos/farmacologia
[Mh] Termos MeSH secundário: Animais
Bothrops/fisiologia
Edema/induzido quimicamente
Edema/prevenção & controle
Hemorragia/induzido quimicamente
Hemorragia/prevenção & controle
Metaloproteases/genética
Camundongos
Estrutura Molecular
Doenças Musculares/induzido quimicamente
Doenças Musculares/prevenção & controle
Ácido Oleanólico/química
Triterpenos/química
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Crotalid Venoms); 0 (Triterpenes); 4G6A18707N (betulinic acid); 6SMK8R7TGJ (Oleanolic Acid); EC 3.4.- (Metalloproteases); P3M2575F3F (ursolic acid)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180103
[Lr] Data última revisão:
180103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171206
[St] Status:MEDLINE


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[PMID]:28177127
[Au] Autor:Bohnert KR; McMillan JD; Kumar A
[Ad] Endereço:Department of Anatomical Sciences Neurobiology, University of Louisville School of Medicine, Louisville, Kentucky.
[Ti] Título:Emerging roles of ER stress and unfolded protein response pathways in skeletal muscle health and disease.
[So] Source:J Cell Physiol;233(1):67-78, 2018 Jan.
[Is] ISSN:1097-4652
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Skeletal muscle is the most abundant tissue in the human body and can adapt its mass as a consequence of physical activity, metabolism, growth factors, and disease conditions. Skeletal muscle contains an extensive network of endoplasmic reticulum (ER), called sarcoplasmic reticulum, which plays an important role in the regulation of proteostasis and calcium homeostasis. In many cell types, environmental and genetic factors that disrupt ER function cause an accumulation of misfolded and unfolded proteins in the ER lumen that ultimately leads to ER stress. To alleviate the stress and restore homeostasis, the ER activates a signaling network called the unfolded protein response (UPR). The UPR has three arms, which regulate protein synthesis and expression of many ER chaperone and regulatory proteins. However, the role of individual UPR pathways in skeletal muscle has just begun to be investigated. Recent studies suggest that UPR pathways play pivotal roles in muscle stem cell homeostasis, myogenic differentiation, and regeneration of injured skeletal muscle. Moreover, markers of ER stress and the UPR are activated in skeletal muscle in diverse conditions such as exercise, denervation, starvation, high fat diet, cancer cachexia, and aging. Accumulating evidence also suggests that ER stress may have important roles in the pathogenesis of inflammatory myopathies and genetic muscle disorders. The purpose of this review article is to discuss the role and potential mechanisms by which ER stress and the individual arms of the UPR regulate skeletal muscle formation, plasticity, and function in various physiological and pathophysiological conditions.
[Mh] Termos MeSH primário: Estresse do Retículo Endoplasmático
Retículo Endoplasmático/metabolismo
Proteínas Musculares/metabolismo
Músculo Esquelético/metabolismo
Doenças Musculares/metabolismo
Resposta a Proteínas não Dobradas
[Mh] Termos MeSH secundário: Adaptação Fisiológica
Envelhecimento
Animais
Retículo Endoplasmático/patologia
Metabolismo Energético
Exercício
Homeostase
Seres Humanos
Desenvolvimento Muscular
Músculo Esquelético/patologia
Músculo Esquelético/fisiopatologia
Atrofia Muscular/metabolismo
Atrofia Muscular/patologia
Atrofia Muscular/fisiopatologia
Doenças Musculares/patologia
Doenças Musculares/fisiopatologia
Regeneração
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Muscle Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171212
[Lr] Data última revisão:
171212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170209
[St] Status:MEDLINE
[do] DOI:10.1002/jcp.25852


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[PMID]:28745680
[Au] Autor:Belousova ED
[Ad] Endereço:Department of Psychoneurology and Epileptology ,Research and Clincal Institute of Pediatrics, Pirogov Russian National Research Medical University, Moscow, Russia.
[Ti] Título:[The decreased level of plasma carnitine in patients with epilepsy].
[Ti] Título:Snizhenie kontsentratsii karnitina u patsientov s épilepsiei..
[So] Source:Zh Nevrol Psikhiatr Im S S Korsakova;117(6):106-110, 2017.
[Is] ISSN:1997-7298
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Antiepileptic drugs (AEDs) have long been known to affect carnitine metabolism, dropping the plasma free carnitine. Valproate (VPA) was considered to be the strongest carnitine-reducing agent. VPA-induced hyperammonemic encephalopathy and hepatotoxicity are well known, and pre-existing carnitine deficiency can be a predisposing factor, especially in congenital metabolic disorders. Several studies have shown that carnitine supplementation in patients receiving VPA to result in subjective and objective improvements and to prevent VPA-induced hepatotoxicity and encephalopathy, in parallel with increases in carnitine serum concentrations. Level of free plasma carnitine <20 micromol/l (syn. carnitine deficiency) in patients with epilepsy (in 15-30% of cases) may occur not only with administration of VPA but with administration of other AEDs (phenobarbital, phenytoin, carbamazepine) and low nutritional intake of carnitine. Some findings indicate that the number of AEDs used is a risk factor for carnitine deficiency. It was established that body weight, height and multidrug therapy are significantly associated with low level of free plasma in epileptic patients. Carnitine deficiency can have severe consequences; but most epileptic patients suffering from it are asymptomatic. Although carnitine deficiency is not uncommon among patients receiving AEDs, it seems not necessary to routinely monitor carnitine levels in epileptic ambulatory patients, this is reasonable only in groups of risk. L-carnitine supplementation is clearly indicated in case of VPA-induced hepatotoxicity (i.v. administration) VPA overdose (i.v. administration), primary carnitine-transporter defect and is strongly recommended in specific secondary carnitine deficiency syndromes, symptomatic VPA-associated hyperammonemia, infants and young children receiving VPA, especially those younger than 2 years, patients with a complex neurologic disorder, who are receiving multiple AEDs, patients who have risk factors for hepatotoxicity and carnitine insufficiency. In the absence of double blind trials, clinical practice is based on empiric observation, clinical experience, and theory. Well-designed studies of specific and general uses of L-carnitine replacement therapy in patients with epilepsy are needed.
[Mh] Termos MeSH primário: Anticonvulsivantes/efeitos adversos
Cardiomiopatias/induzido quimicamente
Carnitina/sangue
Carnitina/deficiência
Epilepsia/sangue
Epilepsia/tratamento farmacológico
Hiperamonemia/induzido quimicamente
Doenças Musculares/induzido quimicamente
[Mh] Termos MeSH secundário: Anticonvulsivantes/uso terapêutico
Peso Corporal
Carbamazepina/efeitos adversos
Carbamazepina/uso terapêutico
Cardiomiopatias/tratamento farmacológico
Carnitina/uso terapêutico
Criança
Feminino
Seres Humanos
Hiperamonemia/tratamento farmacológico
Lactente
Masculino
Doenças Musculares/tratamento farmacológico
Síndromes Neurotóxicas/tratamento farmacológico
Síndromes Neurotóxicas/etiologia
Fatores de Risco
Ácido Valproico/efeitos adversos
Ácido Valproico/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
0 (Anticonvulsants); 33CM23913M (Carbamazepine); 614OI1Z5WI (Valproic Acid); S7UI8SM58A (Carnitine)
[Em] Mês de entrada:1711
[Cu] Atualização por classe:171128
[Lr] Data última revisão:
171128
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170727
[St] Status:MEDLINE
[do] DOI:10.17116/jnevro201711761106-110



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