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[PMID]:28451635
[Au] Autor:Moyon S; Ma D; Huynh JL; Coutts DJC; Zhao C; Casaccia P; Franklin RJM
[Ad] Endereço:Department of Neuroscience, Icahn School of Medicine at Mount Sinai, New York, NY 10029.
[Ti] Título:Efficient Remyelination Requires DNA Methylation.
[So] Source:eNeuro;4(2), 2017 Mar-Apr.
[Is] ISSN:2373-2822
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Oligodendrocyte progenitor cells (OPCs) are the principal source of new myelin in the central nervous system. A better understanding of how they mature into myelin-forming cells is of high relevance for remyelination. It has recently been demonstrated that during developmental myelination, the DNA methyltransferase 1 (DNMT1), but not DNMT3A, is critical for regulating proliferation and differentiation of OPCs into myelinating oligodendrocytes (OLs). However, it remains to be determined whether DNA methylation is also critical for the differentiation of adult OPCs during remyelination. After lysolecithin-induced demyelination in the ventrolateral spinal cord white matter of adult mice of either sex, we detected increased levels of DNA methylation and higher expression levels of the DNA methyltransferase DNMT3A and lower levels of DNMT1 in differentiating adult OLs. To functionally assess the role of DNMT1 and DNMT3 in adult OPCs, we used mice with inducible and lineage-specific ablation of and/or (i.e., , ). Upon lysolecithin injection in the spinal cord of these transgenic mice, we detected defective OPC differentiation and inefficient remyelination in the null and null mice, but not in the null mice. Taken together with previous results in the developing spinal cord, these data suggest an age-dependent role of distinct DNA methyltransferases in the oligodendrocyte lineage, with a dominant role for DNMT1 in neonatal OPCs and for DNMT3A in adult OPCs.
[Mh] Termos MeSH primário: DNA (Citosina-5-)-Metiltransferase 1/metabolismo
DNA (Citosina-5-)-Metiltransferases/metabolismo
Metilação de DNA
Células Precursoras de Oligodendrócitos/metabolismo
Remielinização
Medula Espinal/metabolismo
[Mh] Termos MeSH secundário: Animais
DNA (Citosina-5-)-Metiltransferase 1/genética
DNA (Citosina-5-)-Metiltransferases/genética
Doenças Desmielinizantes/induzido quimicamente
Doenças Desmielinizantes/metabolismo
Feminino
Lisofosfatidilcolinas/administração & dosagem
Masculino
Camundongos Endogâmicos C57BL
Camundongos Knockout
Células Precursoras de Oligodendrócitos/ultraestrutura
Substância Branca/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Lysophosphatidylcholines); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferase 1); EC 2.1.1.37 (DNA (Cytosine-5-)-Methyltransferases); EC 2.1.1.37 (DNA methyltransferase 3A); EC 2.1.1.37 (Dnmt1 protein, mouse)
[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]:28457906
[Au] Autor:Üçal M; Haindl MT; Adzemovic MZ; Strasser J; Theisl L; Zeitelhofer M; Kraitsy K; Ropele S; Schäfer U; Fazekas F; Hochmeister S
[Ad] Endereço:Research Unit of Experimental Neurotraumatology, Department of Neurosurgery, Medical University Graz, Auenbruggerplatz 2.2, 8036 Graz, Austria.
[Ti] Título:Widespread cortical demyelination of both hemispheres can be induced by injection of pro-inflammatory cytokines via an implanted catheter in the cortex of MOG-immunized rats.
[So] Source:Exp Neurol;294:32-44, 2017 08.
[Is] ISSN:1090-2430
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Cortical demyelination is a common finding in patients with chronic multiple sclerosis (MS) and contributes to disease progression and overall disability. The exact pathomechanism that leads to cortical lesions is not clear. Research is limited by the fact that standard animal models of multiple sclerosis do not commonly affect the cortex, or if they do in some variants, the cortical demyelination is rather sparse and already remyelinated within a few days. In an attempt to overcome these limitations we implanted a tissue-compatible catheter into the cortex of Dark Agouti rats. After 14days the rats were immunized with 5µg myelin oligodendrocyte glycoprotein (MOG) in incomplete Freund's Adjuvant, which did not cause any clinical signs but animals developed a stable anti-MOG antibody titer. Then the animals received an injection of proinflammatory cytokines through the catheter. This led to a demyelination of cortical and subcortical areas starting from day 1 in a cone-like pattern spreading from the catheter area towards the subarachnoid space. On day 3 cortical demyelination already expanded to the contralateral hemisphere and reached its peak between days 9-15 after cytokine injection with a widespread demyelination of cortical and subcortical areas of both hemispheres. Clinically the animals showed only discrete signs of fatigue and recovered completely after day 15. Even on day 30 we still were able to detect demyelination in subpial and intracortical areas along with areas of partial and complete remyelination. Loss of cortical myelin was accompanied with marked microglia activation. A second injection of cytokines through the catheter on day 30 led to a second demyelination phase with the same symptoms, but again no detectable motor dysfunction. Suffering of the animals appeared minor compared to standard Experimental Autoimmune Encephalomyelitis and therefore, even long-term observation and repeated demyelination phases seem ethically acceptable.
[Mh] Termos MeSH primário: Córtex Cerebral/patologia
Citocinas/toxicidade
Doenças Desmielinizantes/induzido quimicamente
Doenças Desmielinizantes/patologia
Encefalomielite Autoimune Experimental/patologia
Lateralidade Funcional/fisiologia
[Mh] Termos MeSH secundário: Animais
Proteínas de Ligação ao Cálcio/metabolismo
Caspase 3/metabolismo
Citocinas/metabolismo
Modelos Animais de Doenças
Encefalomielite Autoimune Experimental/induzido quimicamente
Encefalomielite Autoimune Experimental/diagnóstico por imagem
Encefalomielite Autoimune Experimental/imunologia
Fibrina/metabolismo
Adjuvante de Freund/efeitos adversos
Lateralidade Funcional/efeitos dos fármacos
Imunização/efeitos adversos
Lipídeos/efeitos adversos
Masculino
Proteínas dos Microfilamentos/metabolismo
Microscopia Confocal
Atividade Motora
Proteína Proteolipídica de Mielina/metabolismo
Glicoproteína Associada a Mielina/efeitos adversos
Glicoproteína Associada a Mielina/sangue
Proteínas do Tecido Nervoso/metabolismo
Ratos
Estatísticas não Paramétricas
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, rat); 0 (Calcium-Binding Proteins); 0 (Cytokines); 0 (Lipids); 0 (Microfilament Proteins); 0 (Myelin Proteolipid Protein); 0 (Myelin-Associated Glycoprotein); 0 (Nerve Tissue Proteins); 0 (incomplete Freund's adjuvant); 9001-31-4 (Fibrin); 9007-81-2 (Freund's Adjuvant); EC 3.4.22.- (Caspase 3)
[Em] Mês de entrada:1708
[Cu] Atualização por classe:180218
[Lr] Data última revisão:
180218
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE


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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]:29384930
[Au] Autor:Xiong YJ; Zhao XL; Wang XY; Pan DJ; Tian DS
[Ad] Endereço:Department of Neurology.
[Ti] Título:Multiple cerebral gliomas mimicking central nervous system inflammatory demyelinating diseases: A rare case with review of literature.
[So] Source:Medicine (Baltimore);96(52):e9456, 2017 Dec.
[Is] ISSN:1536-5964
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:RATIONALE: Multiple cerebral gliomas (MCGs), usually classified into multifocal and multicentric subtypes, represent major diagnostic challenges as their clinical, radiologic, and pathohistological features are not uniform, often mimicking brain metastatic tumors or central nervous system inflammatory demyelinating diseases (IDD). PATIENT CONCERNS: Here, we report a rare case of MCGs with isolated seizures and 4 lesions in the brain, that was initially misdiagnosed as IDD during treatment. DIAGNOSIS: The pathological diagnosis was astrocytoma, which was classified as a World Health Organization grade II glioma. INTERVENTIONS: The patient was treated with dexamethasone and sodium valproate when he was misdiagnosed as having IDD. After the pathological diagnosis was obtained, he was treated with temozolomide and radiotherapy. OUTCOMES: Three months after the above treatment, the health of the patient had improved; he was asymptomatic, and presented with better radiological manifestations. LESSONS: Diagnostic imaging is valuable in differential diagnosis. Magnetic resonance spectroscopy is a promising technique for the assessment and characterization of lesions, though its role in definitive diagnosis is not yet defined. Brain tissue biopsy remains the golden standard for definitive diagnosis. In China, for various reasons, craniotomy biopsy is not performed routinely in patients with multiple intracranial lesions, and stereotactic cranial biopsy may be a more viable option because of its safety and cost-effectiveness. In summary, this case demonstrates that MCGs need to be included in the differential diagnosis of unknown intracranial multiple lesions.
[Mh] Termos MeSH primário: Neoplasias Encefálicas/diagnóstico
Doenças Desmielinizantes/diagnóstico
Glioma/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Neoplasias Encefálicas/terapia
Diagnóstico Diferencial
Glioma/terapia
Seres Humanos
Espectroscopia de Ressonância Magnética
Masculino
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180209
[Lr] Data última revisão:
180209
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:180201
[St] Status:MEDLINE
[do] DOI:10.1097/MD.0000000000009456


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[PMID]:29296000
[Au] Autor:Chavali M; Klingener M; Kokkosis AG; Garkun Y; Felong S; Maffei A; Aguirre A
[Ad] Endereço:Department of Pharmacological Sciences, Stony Brook University, Stony Brook, NY, 11794, USA.
[Ti] Título:Non-canonical Wnt signaling regulates neural stem cell quiescence during homeostasis and after demyelination.
[So] Source:Nat Commun;9(1):36, 2018 01 02.
[Is] ISSN:2041-1723
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Adult neural stem cells (NSCs) reside in a specialized microenvironment, the subventricular zone (SVZ), which provides them with unique signaling cues to control their basic properties and prevent their exhaustion. While the signaling mechanisms that regulate NSC lineage progression are well characterized, the molecular mechanisms that trigger the activation of quiescent NSCs during homeostasis and tissue repair are still unclear. Here, we uncovered that the NSC quiescent state is maintained by Rho-GTPase Cdc42, a downstream target of non-canonical Wnt signaling. Mechanistically, activation of Cdc42 induces expression of molecules involved in stem cell identity and anchorage to the niche. Strikingly, during a demyelination injury, downregulation of non-canonical Wnt-dependent Cdc42 activity is necessary to promote activation and lineage progression of quiescent NSCs, thereby initiating the process of tissue repair.
[Mh] Termos MeSH primário: Doenças Desmielinizantes
Homeostase
Células-Tronco Neurais/citologia
Transdução de Sinais
Proteínas Wnt/metabolismo
[Mh] Termos MeSH secundário: Animais
Proteína cdc42 de Ligação ao GTP/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Wnt Proteins); EC 3.6.5.2 (cdc42 GTP-Binding Protein)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180116
[Lr] Data última revisão:
180116
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180104
[St] Status:MEDLINE
[do] DOI:10.1038/s41467-017-02440-0


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[PMID]:29187683
[Au] Autor:Hoshino M; Suzuki Y; Akiyama H; Yamada K; Shima S; Mutoh T; Hasegawa Y
[Ad] Endereço:Department of Internal Medicine, Division of Neurology, St Marianna University School of Medicine.
[Ti] Título:[Efficacy of high-dose steroid pulse therapy for anti-galactocerebroside antibody-positive combined central and peripheral demyelination].
[So] Source:Rinsho Shinkeigaku;57(12):747-752, 2017 Dec 27.
[Is] ISSN:1882-0654
[Cp] País de publicação:Japan
[La] Idioma:jpn
[Ab] Resumo:A 59-year-old man had been admitted to another hospital because of diplopia and thirst at the beginning of March and was diagnosed with diabetic ketoacidosis. He was referred to our hospital because he had limb weakness, dysarthria, and bilateral sensory impairment of the upper limbs, which worsened rapidly from the middle of March, although plasma glucose had been well controlled after the initiation of insulin therapy in the previous hospital. Contrast spinal MRI in our hospital revealed hyperintense lesions at the level of C4 to C5 and T10. The level of myelin basic protein was high (1,260 pg/ml) in the cerebrospinal fluid and serum anti-neurofascin antibody was negative. Nerve conduction study showed typical findings of demyelination at least 2 regions. Although anti-neurofascin antibody was negative, he was diagnosed with combined central and peripheral demyelination (CCPD) based on these clinical findings. After the repeated methylprednisolone pulse therapy for five times, the hyperintense lesions of the spinal cord disappeared gradually. He was bedridden at the beginning of his hospitalization but could ambulate with a cane on discharge 2 months after the admission. Then we received the result of anti-galactocerebroside antibody test as positive. This case suggested that high-dose steroid pulse therapy is safe and may be effective for anti-galactocerebroside antibody-positive CCPD.
[Mh] Termos MeSH primário: Autoanticorpos/sangue
Doenças do Sistema Nervoso Central/diagnóstico
Doenças Desmielinizantes/diagnóstico
Galactosilceramidas/imunologia
Imunoglobulina G/sangue
Metilprednisolona/administração & dosagem
Doenças do Sistema Nervoso Periférico/diagnóstico por imagem
[Mh] Termos MeSH secundário: Biomarcadores/sangue
Moléculas de Adesão Celular/imunologia
Seres Humanos
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Proteína Básica da Mielina/sangue
Fatores de Crescimento Neural/imunologia
Pulsoterapia
Resultado do Tratamento
[Pt] Tipo de publicação:CASE REPORTS; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Autoantibodies); 0 (Biomarkers); 0 (Cell Adhesion Molecules); 0 (Galactosylceramides); 0 (Immunoglobulin G); 0 (Myelin Basic Protein); 0 (NFASC protein, human); 0 (Nerve Growth Factors); X4W7ZR7023 (Methylprednisolone)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180112
[Lr] Data última revisão:
180112
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171201
[St] Status:MEDLINE
[do] DOI:10.5692/clinicalneurol.cn-000977


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[PMID]:29026001
[Au] Autor:Martinez Sosa S; Smith KJ
[Ad] Endereço:Department of Neuroinflammation and Queen Square MS Centre, UCL Institute of Neurology, Queen Square, London WC1N 3BG, U.K.
[Ti] Título:Understanding a role for hypoxia in lesion formation and location in the deep and periventricular white matter in small vessel disease and multiple sclerosis.
[So] Source:Clin Sci (Lond);131(20):2503-2524, 2017 Oct 15.
[Is] ISSN:1470-8736
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:The deep and periventricular white matter is preferentially affected in several neurological disorders, including cerebral small vessel disease (SVD) and multiple sclerosis (MS), suggesting that common pathogenic mechanisms may be involved in this injury. Here we consider the potential pathogenic role of tissue hypoxia in lesion development, arising partly from the vascular anatomy of the affected white matter. Specifically, these regions are supplied by a sparse vasculature fed by long, narrow end arteries/arterioles that are vulnerable to oxygen desaturation if perfusion is reduced (as in SVD, MS and diabetes) or if the surrounding tissue is hypoxic (as in MS, at least). The oxygen crisis is exacerbated by a local preponderance of veins, as these can become highly desaturated 'sinks' for oxygen that deplete it from surrounding tissues. Additional haemodynamic deficiencies, including sluggish flow and impaired vasomotor reactivity and vessel compliance, further exacerbate oxygen insufficiency. The cells most vulnerable to hypoxic damage, including oligodendrocytes, die first, resulting in demyelination. Indeed, in preclinical models, demyelination is prevented if adequate oxygenation is maintained by raising inspired oxygen concentrations. In agreement with this interpretation, there is a predilection of lesions for the anterior and occipital horns of the lateral ventricles, namely regions located at arterial watersheds, or border zones, known to be especially susceptible to hypoperfusion and hypoxia. Finally, mitochondrial dysfunction due to genetic causes, as occurs in leucodystrophies or due to free radical damage, as occurs in MS, will compound any energy insufficiency resulting from hypoxia. Viewing lesion formation from the standpoint of tissue oxygenation not only reveals that lesion distribution is partly predictable, but may also inform new therapeutic strategies.
[Mh] Termos MeSH primário: Encefalopatias/patologia
Doenças Desmielinizantes/patologia
Hipóxia
Mitocôndrias/metabolismo
Esclerose Múltipla/patologia
Substância Branca/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Encefalopatias/sangue
Seres Humanos
Esclerose Múltipla/etiologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171017
[Lr] Data última revisão:
171017
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171014
[St] Status:MEDLINE
[do] DOI:10.1042/CS20170981


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[PMID]:28958376
[Au] Autor:Yarmohammadi H; Cunningham-Rundles C
[Ad] Endereço:Division of Clinical Immunology, Department of Medicine, Icahn School of Medicine at Mount Sinai, New York, New York. Electronic address: hale.yar@mssm.edu.
[Ti] Título:Idiopathic CD4 lymphocytopenia: Pathogenesis, etiologies, clinical presentations and treatment strategies.
[So] Source:Ann Allergy Asthma Immunol;119(4):374-378, 2017 Oct.
[Is] ISSN:1534-4436
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Idiopathic CD4 lymphocytopenia (ICL) is a rare condition characterized by an unexplained deficit of circulating CD4 T cells leading to increased risk of serious opportunistic infections. The pathogenesis, etiology, clinical presentation, and best treatment options remain unclear. OBJECTIVE: To describe the clinical presentation, treatment strategies, and outcome of patients with ICL seen in a single referral center. METHODS: In a retrospective study, from January 1993 to January 2014, the demographic characteristics, clinical presentation, and treatments of patients diagnosed with ICL were reviewed. RESULTS: Twenty-four patients (14 female [58%] and 10 male [42%]) were evaluated. The mean age was 45 ± 17.6 years (range 7-76 years). Mean CD4 and CD8 T-cell counts at the time of diagnosis were 119 ± 84/mm (range 4-294/mm ) and 219 ± 258/mm (range 7-630/mm ), respectively. Seventeen patients (71%) had opportunistic infections, 4 (17%) had malignancies, and 3 (13%) had unexplained demyelinating disease and neurologic problems. Most patients had normal levels of immunoglobulins. Thirteen patients had abnormally low to absent response to phytohemagglutinin, concanavalin A, and antigens (candida and tetanus). Three patients had resolution of warts and 1 had mycobacterial lung infection on interleukin-2 with increases in CD4 count. The 11 patients on trimethoprim and sulfamethoxazole had no further hospital admissions for infections. CONCLUSION: The pathogenesis of ICL remains unclear. Although only some patients are healthy, most patients present with opportunistic infections. There is no known standard treatment aside from prophylactic antibiotics.
[Mh] Termos MeSH primário: Antibacterianos/uso terapêutico
Doenças Desmielinizantes/tratamento farmacológico
Neoplasias/tratamento farmacológico
Infecções Oportunistas/tratamento farmacológico
T-Linfocitopenia Idiopática CD4-Positiva/tratamento farmacológico
[Mh] Termos MeSH secundário: Adolescente
Adulto
Idoso
Contagem de Linfócito CD4
Linfócitos T CD4-Positivos/efeitos dos fármacos
Linfócitos T CD4-Positivos/imunologia
Linfócitos T CD4-Positivos/patologia
Linfócitos T CD8-Positivos/efeitos dos fármacos
Linfócitos T CD8-Positivos/imunologia
Linfócitos T CD8-Positivos/patologia
Criança
Doenças Desmielinizantes/complicações
Doenças Desmielinizantes/diagnóstico
Doenças Desmielinizantes/imunologia
Gerenciamento Clínico
Feminino
Seres Humanos
Masculino
Meia-Idade
Neoplasias/complicações
Neoplasias/diagnóstico
Neoplasias/imunologia
Infecções Oportunistas/complicações
Infecções Oportunistas/diagnóstico
Infecções Oportunistas/imunologia
Estudos Retrospectivos
Sulfametoxazol/uso terapêutico
T-Linfocitopenia Idiopática CD4-Positiva/complicações
T-Linfocitopenia Idiopática CD4-Positiva/diagnóstico
T-Linfocitopenia Idiopática CD4-Positiva/imunologia
Trimetoprima/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents); AN164J8Y0X (Trimethoprim); JE42381TNV (Sulfamethoxazole)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171003
[Lr] Data última revisão:
171003
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170930
[St] Status:MEDLINE


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[PMID]:28934355
[Au] Autor:Rodionova NN; Allakhverdiev ES; Maksimov GV
[Ad] Endereço:Faculty of Biology, M.V. Lomonosov Moscow State University, Moscow, Russia.
[Ti] Título:Study of myelin structure changes during the nerve fibers demyelination.
[So] Source:PLoS One;12(9):e0185170, 2017.
[Is] ISSN:1932-6203
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Raman, NMR and EPR spectroscopy and electrophysiology methods were used to investigate the excitability and the packaging of myelin lipid layers and its viscosity during nerve exposure to pronase E. It was established that during exposure of nerve to pronase E the action potential (AP) conduction velocity and the Schwann cell (SC) (or myelin) water ordering increases, but the nerve myelin refractive index and internode incisions numbers decrease. This effect included two periods-short- and long-time period, probably, because the first one depends on SC protein changes and the second one-on the nerve fiber internode demyelination. It was concluded that high electrical resistance of myelin, which is important for a series of AP conduction velocity, not only depends on nerve fiber diameter and the myelin lipid composition, but also on the regularity of myelin lipid fatty acids and myelin lipid layer packing during the axoglial interaction.
[Mh] Termos MeSH primário: Doenças Desmielinizantes/metabolismo
Bainha de Mielina/química
Bainha de Mielina/metabolismo
Fibras Nervosas/metabolismo
[Mh] Termos MeSH secundário: Animais
Carotenoides/química
Carotenoides/metabolismo
Conformação Molecular
Bainha de Mielina/efeitos dos fármacos
Fibras Nervosas/efeitos dos fármacos
Fosfolipídeos/química
Fosfolipídeos/metabolismo
Pronase/farmacologia
Rana temporaria
Viscosidade/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Phospholipids); 36-88-4 (Carotenoids); EC 3.4.24.- (Pronase)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171024
[Lr] Data última revisão:
171024
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1371/journal.pone.0185170


  10 / 10475 MEDLINE  
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[PMID]:28931570
[Au] Autor:Madsen PM; Pinto M; Patel S; McCarthy S; Gao H; Taherian M; Karmally S; Pereira CV; Dvoriantchikova G; Ivanov D; Tanaka KF; Moraes CT; Brambilla R
[Ad] Endereço:The Miami Project To Cure Paralysis, Leonard M. Miller School of Medicine, University of Miami, Florida 33136.
[Ti] Título:Mitochondrial DNA Double-Strand Breaks in Oligodendrocytes Cause Demyelination, Axonal Injury, and CNS Inflammation.
[So] Source:J Neurosci;37(42):10185-10199, 2017 Oct 18.
[Is] ISSN:1529-2401
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Mitochondrial dysfunction has been implicated in the pathophysiology of neurodegenerative disorders, including multiple sclerosis (MS). To date, the investigation of mitochondrial dysfunction in MS has focused exclusively on neurons, with no studies exploring whether dysregulation of mitochondrial bioenergetics and/or genetics in oligodendrocytes might be associated with the etiopathogenesis of MS and other demyelinating syndromes. To address this question, we established a mouse model where mitochondrial DNA (mtDNA) double-strand breaks (DSBs) were specifically induced in myelinating oligodendrocytes (PLP:mtPstI mice) by expressing a mitochondrial-targeted endonuclease, mtPstI, starting at 3 weeks of age. In both female and male mice, DSBs of oligodendroglial mtDNA caused impairment of locomotor function, chronic demyelination, glial activation, and axonal degeneration, which became more severe with time of induction. In addition, after short transient induction of mtDNA DSBs, PLP:mtPstI mice showed an exacerbated response to experimental autoimmune encephalomyelitis. Together, our data demonstrate that mtDNA damage can cause primary oligodendropathy, which in turn triggers demyelination, proving PLP:mtPstI mice to be a useful tool to study the pathological consequences of mitochondrial dysfunction in oligodendrocytes. In addition, the demyelination and axonal loss displayed by PLP:mtPstI mice recapitulate some of the key features of chronic demyelinating syndromes, including progressive MS forms, which are not accurately reproduced in the models currently available. For this reason, the PLP:mtPstI mouse represents a unique and much needed platform for testing remyelinating therapies. In this study, we show that oligodendrocyte-specific mitochondrial DNA double-strand breaks in PLP:mtPstI mice cause oligodendrocyte death and demyelination associated with axonal damage and glial activation. Hence, PLP:mtPstI mice represent a unique tool to study the pathological consequences of mitochondrial dysfunction in oligodendrocytes, as well as an ideal platform to test remyelinating and neuroprotective agents.
[Mh] Termos MeSH primário: Axônios/patologia
Quebras de DNA de Cadeia Dupla
DNA Mitocondrial/genética
Doenças Desmielinizantes/genética
Doenças Desmielinizantes/patologia
Oligodendroglia/patologia
[Mh] Termos MeSH secundário: Animais
Sistema Nervoso Central/patologia
Sistema Nervoso Central/fisiologia
Encefalomielite Autoimune Experimental/genética
Encefalomielite Autoimune Experimental/patologia
Feminino
Inflamação/genética
Inflamação/patologia
Locomoção/fisiologia
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Degeneração Neural/genética
Degeneração Neural/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (DNA, Mitochondrial)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171103
[Lr] Data última revisão:
171103
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170922
[St] Status:MEDLINE
[do] DOI:10.1523/JNEUROSCI.1378-17.2017



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