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  1 / 12908 MEDLINE  
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[PMID]:29441969
[Au] Autor:Lin S; Wu J; Guo W; Zhu Y
[Ti] Título:Effects of leonurine on intracerebral haemorrhage by attenuation of perihematomal edema and neuroinflammation the JNK pathway.
[So] Source:Pharmazie;71(11):644-650, 2016 11 02.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:Perihematomal edema plays a critical role in secondary brain injury in intracerebral hemorrhage (ICH), which is associated with inflammation, hematoma toxicity and oxidative stress. In this work, we investigated the protective effects of leonurine, an alkaloid of Herbal Leonuri, and possible mechanisms to provide a basis for a new therapeutic approach for ICH treatment. In in vivo studies, we demonstrated for the first time that leonurine treatment substantially decreased perihematomal edema, ameliorated neurobehavioral function deficits, reduced apoptosis and protected injured cerebral tissue after ICH. These benefits appear to be ascribed to leonurine effectively attenuating bloodbrain barrier (BBB) breakdown in vivo, by inhibiting degradation of hemoglobin and alleviating inflammatory mediator release. In this study, BV-2 cells were exposed in vitro to oxyhemoglobin (OxyHb) at a concentration of 10 µM to mimic neuroinflammation after ICH. Consistent with the results of the in vivo study, leonurine significantly inhibited OxyHbinduced inflammatory proteins expression in BV-2 cells, mainly through inhibiting the c-Jun N-terminal kinase (JNK) signaling pathway. This is the first time that leonurine is proved to be capable to protect the injured cerebral tissue after ICH, based on alleviating neuroinflammation and attenuating BBB breakdown to ameliorate perihematomal edema.
[Mh] Termos MeSH primário: Edema Encefálico/tratamento farmacológico
Hemorragia Cerebral/tratamento farmacológico
Encefalite/tratamento farmacológico
Ácido Gálico/análogos & derivados
Hematoma/tratamento farmacológico
Proteínas Proto-Oncogênicas c-jun/efeitos dos fármacos
Transdução de Sinais/efeitos dos fármacos
[Mh] Termos MeSH secundário: Animais
Comportamento Animal/efeitos dos fármacos
Barreira Hematoencefálica/efeitos dos fármacos
Água Corporal/metabolismo
Edema Encefálico/patologia
Edema Encefálico/psicologia
Hemorragia Cerebral/psicologia
Encefalite/psicologia
Ácido Gálico/farmacologia
Hematoma/patologia
Hematoma/psicologia
Mediadores da Inflamação/metabolismo
Masculino
Metaloproteinase 9 da Matriz/metabolismo
Oxiemoglobinas/metabolismo
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Inflammation Mediators); 0 (Oxyhemoglobins); 0 (Proto-Oncogene Proteins c-jun); 09Q5W34QDA (leonurine); 632XD903SP (Gallic Acid); EC 3.4.24.35 (Matrix Metalloproteinase 9); EC 3.4.24.35 (Mmp9 protein, rat)
[Em] Mês de entrada:1803
[Cu] Atualização por classe:180308
[Lr] Data última revisão:
180308
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6692


  2 / 12908 MEDLINE  
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[PMID]:29441925
[Au] Autor:Cai QY; Liu XL; Zhang XQ; Liu YX; Li M; Zhao CZ; Zhang XM; Meng QH
[Ti] Título:Anti-neuroinflammation activity of acetylpuerarin mediated by a PKC-δ-dependent caspase signaling pathway: and studies.
[So] Source:Pharmazie;71(10):575-582, 2016 Oct 01.
[Is] ISSN:0031-7144
[Cp] País de publicação:Germany
[La] Idioma:eng
[Ab] Resumo:OBJECTIVE: This study was performed to evaluate the regulating effects of acetylpuerarin on inflammation in an Alzheimer's disease (AD) rat model and an inflammatory cell model. METHODS: Healthy female Wistar rats and mouse BV2 microglia cells were selected. AD rat models were established with the method of bilateral intrahippocampal amyloid-ß(Aß)1-42 injections and the inflammatory cell models were established using Aß25-35-induced mouse BV2 microglia cells. The cytotoxicity of acetylpuerarin on BV2 microglial cells was detected by MTT assay and the morphological changes of BV2 microglia cells were observed under inverted phase contrast microscope. As inflammatory parameters, the expressions of IL-1ß, iNOS, IL-6 and TNF-α were examined by Elisa, Immunohistochemistry, Quantitative real-time PCR (qRT-PCR), Western blot and Immunofluorescence analyses. We also examined the acetylpuerarin's effect on the activity of PKC-δ, IKKß and caspase-8/caspase-3 pathway. RESULTS: Acetylpuerarin exerted no significant cytotoxicity on BV2 microglia cells and was applied in all subsequent experiments. Acetylpuerarin treatment mitigated Aß25-35-induced morphological changes associated with microglia activation. Moreover, the expressions of caspase-8, cleaved caspase-3, PKC-δ, IKKß, iNOS, IL-1ß and TNF-α in Aß25-35-stimulated BV2 microglia cells were significantly suppressed by acetylpuerarin and in a dose-dependent manner. Additionally, the expression of IL-1ß in hippocampus and the level of IL-6 in serum of Aß1-42 treated rat were reduced by acetylpuerarin and in a concentration-dependent manner. CONCLUSION: Our results suggest that acetylpuerarin's anti-inflammation mechanism on AD may be mediated through the PKC-δ-dependent caspase signalling pathway.
[Mh] Termos MeSH primário: Caspases/efeitos dos fármacos
Encefalite/tratamento farmacológico
Isoflavonas/farmacologia
Proteína Quinase C-delta/efeitos dos fármacos
[Mh] Termos MeSH secundário: Doença de Alzheimer/induzido quimicamente
Doença de Alzheimer/tratamento farmacológico
Doença de Alzheimer/patologia
Peptídeos beta-Amiloides
Animais
Sobrevivência Celular/efeitos dos fármacos
Citocinas/metabolismo
Encefalite/induzido quimicamente
Feminino
Ativação de Macrófagos/efeitos dos fármacos
Camundongos
Microglia/efeitos dos fármacos
Fragmentos de Peptídeos
Ratos
Ratos Wistar
Transdução de Sinais/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Amyloid beta-Peptides); 0 (Cytokines); 0 (Isoflavones); 0 (Peptide Fragments); 0 (acetylpuerarin); 0 (amyloid beta-protein (1-42)); 0 (amyloid beta-protein (25-35)); EC 2.7.1.- (Prkcd protein, rat); EC 2.7.11.13 (Protein Kinase C-delta); EC 3.4.22.- (Caspases)
[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:180215
[St] Status:MEDLINE
[do] DOI:10.1691/ph.2016.6660


  3 / 12908 MEDLINE  
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[PMID]:27776205
[Au] Autor:Singh R; Bansal R
[Ad] Endereço:University Institute of Pharmaceutical Sciences, Panjab University , Chandigarh 160 014, India.
[Ti] Título:Investigations on 16-Arylideno Steroids as a New Class of Neuroprotective Agents for the Treatment of Alzheimer's and Parkinson's Diseases.
[So] Source:ACS Chem Neurosci;8(1):186-200, 2017 01 18.
[Is] ISSN:1948-7193
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Neuroinflammatory mechanisms mediated by activated glial and cytokines (TNF-α, IL-1ß) might contribute to neuronal degeneration leading to Alzheimer's (AD) and Parkinson's disease (PD). Lipopolysaccharide (LPS) is an inflammogen derived from the cell wall of Gram-negative bacteria, which promotes neuroinflammation and subsequent neurodegeneration. Dehydroepiandrosterone (DHEA) and testosterone have been reported as neuroprotective steroids useful for the treatment of various neurodegenerative disorders. In the present study, several 16-arylidene steroidal derivatives have been evaluated as neuroprotective agents in LPS-treated animal models. It was observed that 16-arylidene steroidal derivatives 1a-d and 6a-h considerably improve LPS-induced learning, memory, and movement deficits in animal models. Biochemical estimations of brain serum of treated animals revealed suppression of oxidative and nitrosative stress, acetylcholinesterase activity, and reduction in TNF-α levels, which were induced through LPS mediated neuroinflammatory mechanisms leading to neurodegeneration of brain. Of all the steroidal derivatives, 16-(4-pyridylidene) steroid 1c and its 4-aza analogue 6c were found to be the most active neuroprotective agents and produced effects comparable to standard drug celecoxib at a much lower dose and better than dexamethasone at the same dose in terms of behavioral, biochemical, and molecular aspects.
[Mh] Termos MeSH primário: Encefalite/tratamento farmacológico
Fármacos Neuroprotetores/química
Fármacos Neuroprotetores/uso terapêutico
Esteroides/uso terapêutico
[Mh] Termos MeSH secundário: Acetilcolinesterase/metabolismo
Análise de Variância
Animais
Catatonia/etiologia
Citocinas/metabolismo
Modelos Animais de Doenças
Encefalite/induzido quimicamente
Encefalite/complicações
Glutationa/metabolismo
Peroxidação de Lipídeos/efeitos dos fármacos
Lipopolissacarídeos/toxicidade
Masculino
Aprendizagem em Labirinto/efeitos dos fármacos
Camundongos
Modelos Moleculares
Simulação de Acoplamento Molecular
Fármacos Neuroprotetores/síntese química
Ratos
Esteroides/síntese química
Esteroides/química
Superóxido Dismutase/metabolismo
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Cytokines); 0 (Lipopolysaccharides); 0 (Neuroprotective Agents); 0 (Steroids); EC 1.15.1.1 (Superoxide Dismutase); EC 3.1.1.7 (Acetylcholinesterase); GAN16C9B8O (Glutathione)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:180223
[Lr] Data última revisão:
180223
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161025
[St] Status:MEDLINE
[do] DOI:10.1021/acschemneuro.6b00313


  4 / 12908 MEDLINE  
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[PMID]:28458341
[Au] Autor:Ikeda-Matsuo Y
[Ad] Endereço:Laboratory of Pharmacology, Department of Clinical Pharmacy, Faculty of Pharmaceutical Sciences, Hokuriku University.
[Ti] Título:The Role of mPGES-1 in Inflammatory Brain Diseases.
[So] Source:Biol Pharm Bull;40(5):557-563, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Prostaglandin E (PGE ) has been thought to be an important mediator of inflammation in peripheral tissues, but recent studies clearly show the involvement of PGE in inflammatory brain diseases. In some animal models of brain disease, the genetic disruption and chemical inhibition of cyclooxygenase (COX)-2 resulted in the reduction of PGE and amelioration of symptoms, and it had been thought that PGE produced by COX-2 may be involved in the progression of injuries. However, COX-2 produces not only PGE , but also some other prostanoids, and thus the protective effects of COX-2 inhibition, as well as severe side effects, may be caused by the inhibition of prostanoids other than PGE . Therefore, to elucidate the role of PGE , studies of microsomal prostaglandin E synthase-1 (mPGES-1), an inducible terminal enzyme for PGE synthesis, have recently been an active area of research. Studies from mPGES-1 deficient mice provide compelling evidence for its role in a variety of inflammatory brain diseases, such as ischemic stroke, Alzheimer's disease and epilepsy, and clues for developing new therapeutic treatments for brain diseases by targeting mPGES-1. Considering that COX inhibitors may non-selectively suppress the production of many types of prostanoids that are essential for normal physiological functioning of the brain and peripheral tissues, as well as induce gastro-intestinal, renal and cardiovascular complications, mPGES-1 inhibitors are expected to be injury-selective and have fewer side-effects when treating human brain diseases. Thus, this paper focuses on recent studies that have demonstrated the involvement of mPGES-1 in pathological brain diseases.
[Mh] Termos MeSH primário: Encefalopatias/genética
Dinoprostona/metabolismo
Encefalite/genética
Prostaglandina-E Sintases/genética
[Mh] Termos MeSH secundário: Animais
Encefalopatias/enzimologia
Encefalopatias/patologia
Encefalite/enzimologia
Encefalite/patologia
Seres Humanos
Doenças do Sistema Nervoso/enzimologia
Doenças do Sistema Nervoso/genética
Doenças do Sistema Nervoso/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Nm] Nome de substância:
EC 5.3.99.3 (PTGES protein, human); EC 5.3.99.3 (Prostaglandin-E Synthases); K7Q1JQR04M (Dinoprostone)
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-01026


  5 / 12908 MEDLINE  
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[PMID]:28458342
[Au] Autor:Katsuki H; Hijioka M
[Ad] Endereço:Department of Chemico-Pharmacological Sciences, Graduate School of Pharmaceutical Sciences, Kumamoto University.
[Ti] Título:Intracerebral Hemorrhage as an Axonal Tract Injury Disorder with Inflammatory Reactions.
[So] Source:Biol Pharm Bull;40(5):564-568, 2017.
[Is] ISSN:1347-5215
[Cp] País de publicação:Japan
[La] Idioma:eng
[Ab] Resumo:Intracerebral hemorrhage (ICH) is a neurological disorder frequently accompanied by severe dysfunction. Critical pathogenic events leading to poor prognosis should be identified for the development of novel effective therapies for ICH. Here we focus on the injury of the axonal tract, particularly of the internal capsule, with reference to its contribution to ICH pathology and potential therapeutic interventions in addition to its cellular mechanisms. Studies on human ICH patients and rodent models of ICH suggest that invasion of hematoma into the internal capsule greatly worsens the severity of post-ICH symptoms. A blood-derived protease thrombin may play an important role in the acute phase of axonal tract injury in the internal capsule that includes compromised axonal transport and fragmentation of axonal structures. Several agents such as clioquinol, melatonin and Am80 (a retinoic acid receptor agonist) have been shown to produce therapeutic effects on rodent models of ICH associated with injury of the internal capsule. In the course of examinations on the effect of Am80, we obtained evidence for the involvement of CXCL2, a neutrophil chemotactic factor, in the pathogenesis of ICH. Accordingly, we also refer to the potential roles of infiltrating neutrophils and inflammatory responses in axonal tract injury and resultant neurological dysfunction in ICH.
[Mh] Termos MeSH primário: Axônios/patologia
Hemorragia Cerebral/patologia
Encefalite/patologia
[Mh] Termos MeSH secundário: Animais
Seres Humanos
Camundongos
Ratos
Acidente Vascular Cerebral/patologia
[Pt] Tipo de publicação:JOURNAL ARTICLE; REVIEW
[Em] Mês de entrada:1802
[Cu] Atualização por classe:180212
[Lr] Data última revisão:
180212
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.1248/bpb.b16-01013


  6 / 12908 MEDLINE  
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[PMID]:29229308
[Au] Autor:Mangus LM; Beck SE; Queen SE; Brill SA; Shirk EN; Metcalf Pate KA; Muth DC; Adams RJ; Gama L; Clements JE; Mankowski JL
[Ad] Endereço:Department of Molecular and Comparative Pathobiology, Johns Hopkins University School of Medicine, Baltimore, Maryland.
[Ti] Título:Lymphocyte-Dominant Encephalitis and Meningitis in Simian Immunodeficiency Virus-Infected Macaques Receiving Antiretroviral Therapy.
[So] Source:Am J Pathol;188(1):125-134, 2018 01.
[Is] ISSN:1525-2191
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:A retrospective neuropathologic review of 30 SIV-infected pigtailed macaques receiving combination antiretroviral therapy (cART) was conducted. Seventeen animals with lymphocyte-dominant inflammation in the brain and/or meninges that clearly was morphologically distinct from prototypic SIV encephalitis and human immunodeficiency virus encephalitis were identified. Central nervous system (CNS) infiltrates in cART-treated macaques primarily comprised CD20 B cells and CD3 T cells with fewer CD68 macrophages. Inflammation was associated with low levels of SIV RNA in the brain as shown by in situ hybridization, and generally was observed in animals with episodes of cerebrospinal fluid (CSF) viral rebound or sustained plasma and CSF viremia during treatment. Although the lymphocytic CNS inflammation in these macaques shared morphologic characteristics with uncommon immune-mediated neurologic disorders reported in treated HIV patients, including CNS immune reconstitution inflammatory syndrome and neurosymptomatic CSF escape, the high prevalence of CNS lesions in macaques suggests that persistent adaptive immune responses in the CNS also may develop in neuroasymptomatic or mildly impaired HIV patients yet remain unrecognized given the lack of access to CNS tissue for histopathologic evaluation. Continued investigation into the mechanisms and outcomes of CNS inflammation in cART-treated, SIV-infected macaques will advance our understanding of the consequences of residual CNS HIV replication in patients on cART, including the possible contribution of adaptive immune responses to HIV-associated neurocognitive disorders.
[Mh] Termos MeSH primário: Antirretrovirais/uso terapêutico
Encéfalo/patologia
Encefalite/patologia
Linfócitos/patologia
Meningite/patologia
Síndrome de Imunodeficiência Adquirida dos Símios/patologia
[Mh] Termos MeSH secundário: Animais
Encefalite/complicações
Inflamação/patologia
Macaca nemestrina
Masculino
Meningite/complicações
Síndrome de Imunodeficiência Adquirida dos Símios/complicações
Síndrome de Imunodeficiência Adquirida dos Símios/tratamento farmacológico
Vírus da Imunodeficiência Símia
Carga Viral
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, N.I.H., EXTRAMURAL
[Nm] Nome de substância:
0 (Anti-Retroviral Agents)
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180131
[Lr] Data última revisão:
180131
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171213
[St] Status:MEDLINE


  7 / 12908 MEDLINE  
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[PMID]:28459229
[Au] Autor:Puca E; Majko J; Puca E; Qyra E; Gega A; Pipero P
[Ad] Endereço:University Hospital Center, Tirana, Albania. edmond_puca@yahoo.com.
[Ti] Título:Acute encephalitis as initial presentation of leptospirosis.
[So] Source:J Infect Dev Ctries;11(4):361-363, 2017 Apr 30.
[Is] ISSN:1972-2680
[Cp] País de publicação:Italy
[La] Idioma:eng
[Ab] Resumo:Encephalitis is an acute inflammation of the brain matter, very often associated with viral infections, but it can also be caused by non-viral pathogens such as leptospirosis. Leptospirosis is a systemic disease caused by bacteria of the Leptospira genus. Leptospiral infection has a broad spectrum of clinical manifestations ranging from subclinical or mild illness to a fulminant life-threatening illness. In this case report we describe a young patient from Southern Albania with isolated encephalitis caused by Leptospira, where acute encephalitis was the initial presentation of the disease.
[Mh] Termos MeSH primário: Encefalite/etiologia
Encefalite/patologia
Leptospira/isolamento & purificação
Leptospirose/diagnóstico
Leptospirose/patologia
[Mh] Termos MeSH secundário: Albânia
Seres Humanos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1801
[Cu] Atualização por classe:180109
[Lr] Data última revisão:
180109
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170502
[St] Status:MEDLINE
[do] DOI:10.3855/jidc.8613


  8 / 12908 MEDLINE  
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[PMID]:29175324
[Au] Autor:Cai HY; Yang JT; Wang ZJ; Zhang J; Yang W; Wu MN; Qi JS
[Ad] Endereço:Department of Microbiology and Immunology, Shanxi Medical University, 56 Xinjian South Road, Taiyuan, Shanxi Province, 030001, China. Electronic address: yancai1@163.com.
[Ti] Título:Lixisenatide reduces amyloid plaques, neurofibrillary tangles and neuroinflammation in an APP/PS1/tau mouse model of Alzheimer's disease.
[So] Source:Biochem Biophys Res Commun;495(1):1034-1040, 2018 01 01.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Type 2 diabetes mellitus (T2DM) has been identified as a high risk factor for Alzheimer's disease (AD). The impairment of insulin signaling has been found in AD brain. Glucagon-like peptide-1 (GLP-1) is an incretin hormone, normalises insulin signaling and acts as a neuroprotective growth factor. We have previously shown that the long-lasting GLP-1 receptor (GLP-1R) agonist lixisenatide plays an important role in memory formation, synaptic plasticity and cell proliferation of rats. In the follow-up study, we analysed the neuroprotective effect and mechanism of lixisenatide, injected for 60 days at 10 nmol/kg i.p. once daily in APP/PS1/tau female mice and C57BL/6J female mice (as control) aged 12 month. The results showed that lixisenatide could reduce amyloid plaques, neurofibrillary tangles and neuroinflammation in the hippocampi of 12-month-old APP/PS1/tau female mice; activation of PKA-CREB signaling pathway and inhibition of p38-MAPK might be the important mechanisms in the neuroprotective function of lixisenatide. The study demonstrated that GLP-1R agonists such as lixisenatide might have the potential to be developed as a novel therapy for AD.
[Mh] Termos MeSH primário: Doença de Alzheimer/tratamento farmacológico
Doença de Alzheimer/metabolismo
Encefalite/tratamento farmacológico
Encefalite/metabolismo
Emaranhados Neurofibrilares/efeitos dos fármacos
Peptídeos/administração & dosagem
[Mh] Termos MeSH secundário: Doença de Alzheimer/patologia
Precursor de Proteína beta-Amiloide/genética
Animais
Relação Dose-Resposta a Droga
Encefalite/patologia
Feminino
Receptor do Peptídeo Semelhante ao Glucagon 1/agonistas
Camundongos
Camundongos Endogâmicos C57BL
Camundongos Transgênicos
Emaranhados Neurofibrilares/metabolismo
Emaranhados Neurofibrilares/patologia
Fármacos Neuroprotetores/administração & dosagem
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Amyloid beta-Protein Precursor); 0 (Glp1r protein, rat); 0 (Glucagon-Like Peptide-1 Receptor); 0 (Neuroprotective Agents); 0 (Peptides); 74O62BB01U (lixisenatide)
[Em] Mês de entrada:1712
[Cu] Atualização por classe:180105
[Lr] Data última revisão:
180105
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:171128
[St] Status:MEDLINE


  9 / 12908 MEDLINE  
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[PMID]:29050399
[Au] Autor:Tobin WO; Guo Y; Krecke KN; Parisi JE; Lucchinetti CF; Pittock SJ; Mandrekar J; Dubey D; Debruyne J; Keegan BM
[Ad] Endereço:Department of Neurology, College of Medicine, Mayo Clinic, Rochester, MN, USA.
[Ti] Título:Diagnostic criteria for chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS).
[So] Source:Brain;140(9):2415-2425, 2017 Sep 01.
[Is] ISSN:1460-2156
[Cp] País de publicação:England
[La] Idioma:eng
[Ab] Resumo:Chronic lymphocytic inflammation with pontine perivascular enhancement responsive to steroids (CLIPPERS) is a central nervous system inflammatory syndrome predominantly affecting the brainstem, cerebellum, and spinal cord. Following its initial description, the salient features of CLIPPERS have been confirmed and expanded upon, but the lack of formalized diagnostic criteria has led to reports of patients with dissimilar features purported to have CLIPPERS. We evaluated clinical, radiological and pathological features of patients referred for suspected CLIPPERS and propose diagnostic criteria to discriminate CLIPPERS from non-CLIPPERS aetiologies. Thirty-five patients were evaluated for suspected CLIPPERS. Clinical and neuroimaging data were reviewed by three neurologists to confirm CLIPPERS by consensus agreement. Neuroimaging and neuropathology were reviewed by experienced neuroradiologists and neuropathologists, respectively, both of whom were blinded to the clinical data. CLIPPERS was diagnosed in 23 patients (18 male and five female) and 12 patients had a non-CLIPPERS diagnosis. CLIPPERS patients' median age of onset was 58 years (interquartile range, 24-72) and were followed a median of 44 months (interquartile range 38-63). Non-CLIPPERS patients' median age of onset was 52 years (interquartile range, 39-59) and were followed a median of 27 months (interquartile range, 14-47). Clinical symptoms of gait ataxia, diplopia, cognitive impairment, and facial paraesthesia did not discriminate CLIPPERS from non-CLIPPERS. Marked clinical and radiological corticosteroid responsiveness was observed in CLIPPERS (23/23), and clinical worsening occurred in all 12 CLIPPERS cases when corticosteroids were discontinued. Corticosteroid responsiveness was common but not universal in non-CLIPPERS [clinical improvement (8/12); radiological improvement (2/12); clinical worsening on discontinuation (3/8)]. CLIPPERS patients had brainstem predominant perivascular gadolinium enhancing lesions on magnetic resonance imaging that were discriminated from non-CLIPPERS by: homogenous gadolinium enhancing nodules <3 mm in diameter without ring-enhancement or mass effect, and homogenous T2 signal abnormality not significantly exceeding the T1 enhancement. Brain neuropathology on 14 CLIPPERS cases demonstrated marked CD3-positive T-lymphocyte, mild B-lymphocyte and moderate macrophage infiltrates, with perivascular predominance as well as diffuse parenchymal infiltration (14/14), present in meninges, white and grey matter, associated with variable tissue destruction, astrogliosis and secondary myelin loss. Clinical, radiological and pathological feature define CLIPPERS syndrome and are differentiated from non-CLIPPERS aetiologies by neuroradiological and neuropathological findings.
[Mh] Termos MeSH primário: Corticosteroides/uso terapêutico
Encefalite/diagnóstico
Inflamação/diagnóstico
[Mh] Termos MeSH secundário: Adulto
Idade de Início
Idoso
Encefalite/complicações
Encefalite/diagnóstico por imagem
Encefalite/patologia
Feminino
Gadolínio
Seres Humanos
Inflamação/complicações
Inflamação/diagnóstico por imagem
Inflamação/patologia
Imagem por Ressonância Magnética
Masculino
Meia-Idade
Estudos Retrospectivos
Síndrome
Adulto Jovem
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Adrenal Cortex Hormones); AU0V1LM3JT (Gadolinium)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171030
[Lr] Data última revisão:
171030
[Sb] Subgrupo de revista:AIM; IM
[Da] Data de entrada para processamento:171021
[St] Status:MEDLINE
[do] DOI:10.1093/brain/awx200


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[PMID]:28912034
[Au] Autor:Wadhwa M; Kumari P; Chauhan G; Roy K; Alam S; Kishore K; Ray K; Panjwani U
[Ad] Endereço:Defence Institute of Physiology and Allied Sciences (DIPAS), Defence Research and Development Organization (DRDO), Lucknow Road, Timarpur, Delhi, India.
[Ti] Título:Sleep deprivation induces spatial memory impairment by altered hippocampus neuroinflammatory responses and glial cells activation in rats.
[So] Source:J Neuroimmunol;312:38-48, 2017 Nov 15.
[Is] ISSN:1872-8421
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:We aimed to investigate the glial cells activation as a potential mechanism involved in the sleep deprivation (SD) induced cognitive impairment through changes in inflammatory cytokines. We analyzed the spatial memory, inflammatory cytokine levels, and gliosis during SD. SD induced spatial memory impairment, imbalance of inflammatory (increased pro- and decreased anti-) cytokines in both hippocampus and plasma in association with glial cells activation in the hippocampus of sleep-deprived rats were observed. Further analysis of the data presented a correlation between spatial memory impairment and activated microglia induced increased pro-inflammatory cytokines after 48h of SD.
[Mh] Termos MeSH primário: Encefalite/etiologia
Hipocampo/patologia
Transtornos da Memória/etiologia
Neuroglia/patologia
Privação do Sono/complicações
Privação do Sono/patologia
[Mh] Termos MeSH secundário: Animais
Peso Corporal/fisiologia
Proteínas de Ligação ao Cálcio/metabolismo
Citocinas/metabolismo
Ingestão de Alimentos/fisiologia
Ensaio de Imunoadsorção Enzimática
Proteína Glial Fibrilar Ácida/metabolismo
Masculino
Aprendizagem em Labirinto/fisiologia
Proteínas dos Microfilamentos/metabolismo
Ratos
Ratos Sprague-Dawley
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Aif1 protein, rat); 0 (Calcium-Binding Proteins); 0 (Cytokines); 0 (Glial Fibrillary Acidic Protein); 0 (Microfilament Proteins)
[Em] Mês de entrada:1710
[Cu] Atualização por classe:171011
[Lr] Data última revisão:
171011
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:170916
[St] Status:MEDLINE



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