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[PMID]:29395086
[Au] Autor:Deng S; Ai Y; Gong H; Feng Q; Li X; Chen C; Liu Z; Wang Y; Peng Q; Zhang L
[Ad] Endereço:Department of Critical Care Medicine, Xiangya Hospital, Central South University, Changsha, 410008, PR China. Electronic address: dengsy2014@foxmail.com.
[Ti] Título:Mitochondrial dynamics and protective effects of a mitochondrial division inhibitor, Mdivi-1, in lipopolysaccharide-induced brain damage.
[So] Source:Biochem Biophys Res Commun;496(3):865-871, 2018 02 12.
[Is] ISSN:1090-2104
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sepsis is one of the most common reasons for mortality in Intensive Care Units. As a common but severe neurological complication, sepsis associated encephalopathy (SAE) has always been ignored and there is no generally accepted treatment. In this study, we demonstrated that Mdivi-1 ameliorated brain damage assessed by Nissl staining. Furthermore, Mdivi-1 reduced TUNEL-positive cells in hippocampus, and inhibited S100 calcium binding protein B (S100B) and neuron-specific enolase (NSE) release into plasma. Biochemical analysis also showed that Mdivi-1 protected hippocampus from oxidative stresses. Western blot analysis revealed that Mdivi-1, as a Drp1 inhibitor, inhibited LPS induced dynamin-related GTPase (Drp1) increase. Interestingly, it can also attenuate LPS induced optic atrophy 1 (OPA1) and phosphorylated Drp1 (p-Drp1) decrease. Thus Mdivi-1 protected rats from SAE, and this protective effect could be associated with its inhibition of Drp1 and its activation of p-Drp1 and OPA1. Mitochondrial dynamics may be a potential pharmacological therapeutic target for treating SAE.
[Mh] Termos MeSH primário: Encéfalo/metabolismo
Encéfalo/patologia
Mitocôndrias/efeitos dos fármacos
Mitocôndrias/metabolismo
Quinazolinonas/administração & dosagem
Encefalopatia Associada a Sepse/tratamento farmacológico
Encefalopatia Associada a Sepse/patologia
[Mh] Termos MeSH secundário: Animais
Encéfalo/efeitos dos fármacos
Relação Dose-Resposta a Droga
Dinaminas/metabolismo
Lipopolissacarídeos
Masculino
Mitocôndrias/patologia
Fármacos Neuroprotetores/administração & dosagem
Ratos
Ratos Sprague-Dawley
Encefalopatia Associada a Sepse/metabolismo
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (3-(2,4-dichloro-5-methoxyphenyl)-2-sulfanyl-4(3H)-quinazolinone); 0 (Lipopolysaccharides); 0 (Neuroprotective Agents); 0 (Quinazolinones); EC 3.6.5.5 (Drp1 protein, rat); EC 3.6.5.5 (Dynamins)
[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:180204
[St] Status:MEDLINE


  2 / 33 MEDLINE  
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[PMID]:27979475
[Au] Autor:Li Y; Wang F; Luo Y
[Ad] Endereço:Department of Anesthesiology, Ruijin Hospital, Shanghai JiaoTong University School of Medicine, Shanghai, China.
[Ti] Título:Ginsenoside Rg1 protects against sepsis-associated encephalopathy through beclin 1-independent autophagy in mice.
[So] Source:J Surg Res;207:181-189, 2017 Jan.
[Is] ISSN:1095-8673
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Sepsis-associated encephalopathy (SAE), a commonly complicated syndrome, is associated with increased mortality in patients with sepsis. Currently, no specific diagnostic test or effective intervention exists to improve long-term consequences on cerebral function. Ginsenoside Rg1 (Rg1), a major component in ginseng, was reported to have pleiotropic properties including anti-inflammation and neuroprotection. The aim of our study was to investigate the protective effect of Rg1 on SAE and the potential mechanism. MATERIALS AND METHODS: SAE model was prepared by inducing cecal ligation and puncture (CLP) in mice. Rg1 was injected 1 h before the CLP operation. Survival rate within 7 d after operation was analyzed. Surviving mice were subjected to Morris water maze tests and the brains were collected for histopathologic evaluation and immunohistochemistry. The hippocampus was obtained for Western blot, real time polymerase chain reaction, and enzyme-linked immunosorbent assay analysis. RESULTS: Rg1 improved the postoperative survival rate and protected against sepsis-associated learning and memory impairments (Morris water maze). Besides, Rg1 was able to attenuate brain histopathologic changes (hematoxylin and eosin staining), suppress Iba1 activation, decrease the expressions of inflammatory cytokines (tumor necrosis factor α, interleukin 1ß, and interleukin 6), and reduce neuronal apoptosis (cleaved caspase 3 activation) in hippocampus. Furthermore, the mechanism study showed that Rg1 suppressed the expressions of light chain 3-II and p62 in hippocampus but not beclin 1. CONCLUSIONS: These findings suggested that Rg1 improved the survival rate and ameliorated cognitive impairments partially through regulating cerebral inflammation and apoptosis. In addition, the action mechanism might be noncanonical beclin 1-independent autophagy pathway. Rg1 may be a promising treatment strategy for SAE.
[Mh] Termos MeSH primário: Autofagia/efeitos dos fármacos
Ginsenosídeos/uso terapêutico
Fármacos Neuroprotetores/uso terapêutico
Encefalopatia Associada a Sepse/prevenção & controle
Sepse/complicações
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Autofagia/fisiologia
Beclina-1/metabolismo
Biomarcadores/metabolismo
Western Blotting
Ensaio de Imunoadsorção Enzimática
Ginsenosídeos/farmacologia
Hipocampo/efeitos dos fármacos
Hipocampo/metabolismo
Imuno-Histoquímica
Masculino
Camundongos
Camundongos Endogâmicos C57BL
Fármacos Neuroprotetores/farmacologia
Distribuição Aleatória
Encefalopatia Associada a Sepse/etiologia
Resultado do Tratamento
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Beclin-1); 0 (Biomarkers); 0 (Ginsenosides); 0 (Neuroprotective Agents); PJ788634QY (ginsenoside Rg1)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170719
[Lr] Data última revisão:
170719
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161217
[St] Status:MEDLINE


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[PMID]:27913953
[Au] Autor:Gao R; Ji MH; Gao DP; Yang RH; Zhang SG; Yang JJ; Shen JC
[Ad] Endereço:Department of Emergency and Intensive Care Medicine, Nanjing Integrated Traditional Chinese and Western Medicine Hospital, Affiliated with Nanjing University of Chinese Medicine, Nanjing, 210014, China.
[Ti] Título:Neuroinflammation-Induced Downregulation of Hippocampacal Neuregulin 1-ErbB4 Signaling in the Parvalbumin Interneurons Might Contribute to Cognitive Impairment in a Mouse Model of Sepsis-Associated Encephalopathy.
[So] Source:Inflammation;40(2):387-400, 2017 Apr.
[Is] ISSN:1573-2576
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sepsis-associated encephalopathy (SAE) is a common complication associated with poor prognosis in septic patients, but the underlying mechanism remains unclear. We hypothesized that disturbed neuregulin 1 (NRG1)-ErbB4 signaling in the parvalbumin interneurons was involved in sepsis-induced cognitive impairment in a mouse model of SAE. The SAE model was induced by cecal ligation/perforation (CLP). Animals were randomly divided into the following six groups: sham + vehicle group, sham + NRG1 group, CLP + vehicle group, CLP + NRG1 group, CLP + NRG1 + AG1478 (ErbB4 inhibitor) group, and CLP + minocycline group. Behavioral tests and in vivo electrophysiology were performed at the indicated time points. The brain tissues were harvested to determine the levels of hippocampcal cytokines, IBA1-positive cells, NRG1, ErbB4, and parvalbumin. In the present study, sepsis induced the anxiety-like behavior and hippocampal-dependent cognitive impairment, as reflected by significantly increased distance spent in the open field test and decreased freezing time to context in the fear conditioning test. The abnormal behavioral changes co-occurred with significant increases in hippocampal IBA1-positive cells, IL-1ß and IL-6 levels, and decreased NRG1, ErbB4, parvalbumin expressions, and evoked gamma activity. NRG1 treatment attenuated the sepsis-induced cognitive impairment and the associated biochemical markers, which were abolished by AG1478 administration. Notably, minocycline treatment attenuated neuroinflammation and mimicked the beneficial effects of NRG1 treatment. In summary, we provided additional evidence that the disruption of NRG1-ErbB4 signaling in the parvalbumin interneurons mediated by neuroinflammation might lead to abnormal gamma oscillations and thus contribute to cognitive impairment in a mouse model of SAE.
[Mh] Termos MeSH primário: Encefalite/patologia
Hipocampo/metabolismo
Hipocampo/fisiopatologia
Neuregulina-1/metabolismo
Receptor ErbB-4/metabolismo
Encefalopatia Associada a Sepse/fisiopatologia
[Mh] Termos MeSH secundário: Animais
Disfunção Cognitiva/tratamento farmacológico
Disfunção Cognitiva/etiologia
Modelos Animais de Doenças
Regulação para Baixo
Inibidores Enzimáticos/farmacologia
Inibidores Enzimáticos/uso terapêutico
Ritmo Gama
Hipocampo/química
Interneurônios/metabolismo
Camundongos
Parvalbuminas
Quinazolinas/farmacologia
Quinazolinas/uso terapêutico
Receptor ErbB-4/antagonistas & inibidores
Transdução de Sinais/efeitos dos fármacos
Tirfostinas/farmacologia
Tirfostinas/uso terapêutico
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Enzyme Inhibitors); 0 (Neuregulin-1); 0 (Nrg1 protein, mouse); 0 (Parvalbumins); 0 (Quinazolines); 0 (Tyrphostins); 170449-18-0 (tyrphostin AG 1478); EC 2.7.10.1 (Erbb4 protein, mouse); EC 2.7.10.1 (Receptor, ErbB-4)
[Em] Mês de entrada:1705
[Cu] Atualização por classe:171020
[Lr] Data última revisão:
171020
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:161204
[St] Status:MEDLINE
[do] DOI:10.1007/s10753-016-0484-2


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[PMID]:27434564
[Au] Autor:Wang G; Wang S; Zhou Y; Chen X; Ma X; Tong D
[Ad] Endereço:Department of Neurology, Shuyang People' Hospital Affiliated to Xuzhou Medical University, Shuyang 223600, Jiangsu, China (Wang GS, Chen XD, Tong DM); Department of General Surgery, Shuyang People' Hospital Affiliated to Xuzhou Medical University, Shuyang 223600, Jiangsu, China (Zhou YT); Department of Critical Care Medicine, Shuyang People' Hospital Affiliated to Xuzhou Medical University, Shuyang 223600, Jiangsu, China (Wang SD); Department of Science and Education, Shuyang People' Hospital Affiliated to Xuzhou Medical University, Shuyang 223600, Jiangsu, China (Ma XB). Corresponding author: Tong Daoming, Email: tongdaoming@163.com.
[Ti] Título:[Sepsis associated encephalopathy is an independently risk factor for nosocomial coma in patients with supratentorial intracerebral hemorrhage: a retrospective cohort study of 261 patients].
[So] Source:Zhonghua Wei Zhong Bing Ji Jiu Yi Xue;28(8):723-8, 2016 Aug.
[Is] ISSN:2095-4352
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To investigate whether the presence of sepsis associated encephalopathy (SAE) would predict nosocomial coma (NC) and poor outcome in patients with supratentorial intracerebral hemorrhage (SICH). METHODS: A retrospective cohort study was conducted. The adult acute SICH patients with or without coma admitted to intensive care unit (ICU) of Shuyang People' Hospital Affiliated to Xuzhou Medical University from December 2012 to December 2015 were enrolled. Brain computed tomography (CT) scans were analyzed and the patients were divided into pre-hospital coma (PC) and NC groups. The clinical data and the incidence of SAE of patients in two groups were compared, and the 30-day prognosis was followed up. Univariate and Cox regression analyses were performed to analyze whether SAE would predict NC and poor outcome in patients with SICH. RESULTS: A total of 330 patients with acute SICH and coma were enrolled, excluding 60 cases of infratentorial cerebral hemorrhage, 3 cases of primary intraventricular hemorrhage, and 6 cases of unknown volume hematoma. Finally, 261 patients were included, with 111 patients of NC events, and 150 patients of PC events. 69 (62.2%) SAE in SICH with NC and 33 (22.2%) SAE in SICH with PC was diagnosed, and the incidence of SAE between two groups was statistically significant (P < 0.01). Compared with PC group, SICH patients in the NC group had lower incidence of hypertension (81.1% vs. 96.0%), longer time from onset to NC [days: 2.3 (23.9) vs. 0 (0.5)] and length of ICU stay [days: 5.0 (34.0) vs. 3.0 (12.0)], higher initial Glasgow coma score (GCS, 10.2±1.5 vs. 6.6±1.6) and sequential organ failure assessment (SOFA) score [4.0 (6.0) vs. 3.0 (3.0)], lower initial National Institutes of Health Stroke Scale (NIHSS) score (19.4±6.6 vs. 30.2±6.8), as well as more frequent sepsis (78.4% vs. 38.0%), vegetative state (24.3% vs. 14.0%), acute respiratory failure (24.3% vs. 10.0%), pneumonia (37.8% vs. 24.0%), septic shock (8.1% vs. 0), acute liver failure (5.4% vs. 0), hypernatremia (8.1% vs. 0), CT indicating that more frequent vasogenic edema (64.9% vs. 16.0%) and white matter lesion (13.5% vs. 2.0%), and less mannitol usage (94.6% vs. 100.0%), and less brain midline shift (32.4% vs. 68.0%) and hematoma enlargement (8.1% vs. 30.0%), less hematoma volume (mL: 28.0±18.8 vs. 38.3±24.4) in CT, and higher 30-day mortality (54.1% vs. 26.0%) with statistical differences (all P < 0.05). It was shown by Cox regression analyses that SAE [hazard ratio (HR) = 3.5, 95% confidence interval (95%CI) = 1.346-6.765, P = 0.000] and SOFA score (HR = 1.8, 95%CI = 1.073-1.756, P = 0.008) were independent risk factors of death of SICH patients with NC, and hematoma enlargement was independent risk factor of death of SICH patients with PC (HR = 3.0, 95%CI = 1.313-5.814, P = 0.000). CONCLUSIONS: SAE is the independent factor of inducing NC event and poor prognosis in SICH patients.
[Mh] Termos MeSH primário: Hemorragia Cerebral/epidemiologia
Coma/epidemiologia
Encefalopatia Associada a Sepse/epidemiologia
[Mh] Termos MeSH secundário: Adulto
Encéfalo/patologia
Escala de Coma de Glasgow
Seres Humanos
Hipertensão/epidemiologia
Incidência
Unidades de Terapia Intensiva
Escores de Disfunção Orgânica
Prognóstico
Estudos Retrospectivos
Fatores de Risco
Sepse/epidemiologia
Choque Séptico/epidemiologia
Tomografia Computadorizada por Raios X
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170328
[Lr] Data última revisão:
170328
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160720
[St] Status:MEDLINE
[do] DOI:10.3760/cma.j.issn.2095-4352.2016.08.011


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[PMID]:27411454
[Au] Autor:Zhang LN; Wang XH; Wu L; Huang L; Zhao CG; Peng QY; Ai YH
[Ad] Endereço:Department of Critical Care Medicine, Xiangya Hospital, Central South University, Changsha, Hunan 410008, China.
[Ti] Título:Diagnostic and Predictive Levels of Calcium-binding Protein A8 and Tumor Necrosis Factor Receptor-associated Factor 6 in Sepsis-associated Encephalopathy: A Prospective Observational Study.
[So] Source:Chin Med J (Engl);129(14):1674-81, 2016 Jul 20.
[Is] ISSN:0366-6999
[Cp] País de publicação:China
[La] Idioma:eng
[Ab] Resumo:BACKGROUND: Despite its high prevalence, morbidity, and mortality, sepsis-associated encephalopathy (SAE) is still poorly understood. The aim of this prospective and observational study was to investigate the clinical significance of calcium-binding protein A8 (S100A8) in serum and tumor necrosis factor receptor-associated factor 6 (TRAF6) in peripheral blood mononuclear cells (PBMCs) in diagnosing SAE and predicting its prognosis. METHODS: Data of septic patients were collected within 24 h after Intensive Care Unit admission from July 2014 to March 2015. Healthy medical personnel served as the control group. SAE was defined as cerebral dysfunction in the presence of sepsis that fulfilled the exclusion criteria. The biochemical indicators, Glasgow Coma Scale, Acute Physiology and Chronic Health Evaluation score II, TRAF6 in PBMC, serum S100A8, S100ß, and neuron-specific enolase were evaluated in SAE patients afresh. TRAF6 and S100A8 were also measured in the control group. RESULTS: Of the 57 enrolled patients, 29 were diagnosed with SAE. The S100A8 and TRAF6 concentrations in SAE patients were both significantly higher than that in no-encephalopathy (NE) patients, and higher in NE than that in controls (3.74 ± 3.13 vs. 1.08 ± 0.75 vs. 0.37 ± 0.14 ng/ml, P < 0.01; 3.18 ± 1.55 vs. 1.02 ± 0.63 vs. 0.47 ± 0.10, P < 0.01). S100A8 levels of 1.93 ng/ml were diagnostic of SAE with 92.90% specificity and 69.00% sensitivity in the receiver operating characteristic (ROC) curve, and the area under the curve was 0.86 (95% confidence interval [CI]: 0.76-0.95). TRAF6-relative levels of 1.44 were diagnostic of SAE with 85.70% specificity and 86.20% sensitivity, and the area under the curve was 0.94 (95% CI: 0.88-0.99). In addition, S100A8 levels of 2.41 ng/ml predicted 28-day mortality of SAE with 90.00% specificity and 73.70% sensitivity in the ROC curve, and the area under the curve was 0.88. TRAF6 relative levels of 2.94 predicted 28-day mortality of SAE with 80.00% specificity and 68.40% sensitivity, and the area under the curve was 0.77. Compared with TRAF6, the specificity of serum S100A8 in diagnosing SAE and predicting mortality was higher, although the sensitivity was low. In contrast, the TRAF6 had higher sensitivity for diagnosis. CONCLUSIONS: Peripheral blood levels of S100A8 and TRAF6 in SAE patients were elevated and might be related to the severity of SAE and predict the outcome of SAE. The efficacy and specificity of S100A8 for SAE diagnosis were superior, despite its weak sensitivity. S100A8 might be a better biomarker for diagnosis of SAE and predicting prognosis.
[Mh] Termos MeSH primário: Calmodulina/sangue
Encefalopatia Associada a Sepse/diagnóstico
Fator 6 Associado a Receptor de TNF/sangue
[Mh] Termos MeSH secundário: Adulto
Idoso
Biomarcadores/sangue
Calgranulina A/sangue
Feminino
Seres Humanos
Masculino
Meia-Idade
Estudos Prospectivos
Subunidade beta da Proteína Ligante de Cálcio S100/sangue
Encefalopatia Associada a Sepse/sangue
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Biomarkers); 0 (CALN1 protein, human); 0 (Calgranulin A); 0 (Calmodulin); 0 (S100 Calcium Binding Protein beta Subunit); 0 (TNF Receptor-Associated Factor 6)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170313
[Lr] Data última revisão:
170313
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160715
[St] Status:MEDLINE
[do] DOI:10.4103/0366-6999.185860


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[PMID]:27400829
[Au] Autor:Zhu SZ; Huang WP; Huang LQ; Han YL; Han QP; Zhu GF; Wen MY; Deng YY; Zeng HK
[Ad] Endereço:Southern Medical University, Guangzhou, Guangdong, China; Department of Emergency and Critical Care Medicine, Guangdong General Hospital & Guangdong Academy of Medical Sciences, Guangzhou, Guangdong, China; Department of Emergency, Guangzhou Medical University Affiliated Third Hospital, Guangzho
[Ti] Título:Huperzine A protects sepsis associated encephalopathy by promoting the deficient cholinergic nervous function.
[So] Source:Neurosci Lett;631:70-8, 2016 Sep 19.
[Is] ISSN:1872-7972
[Cp] País de publicação:Ireland
[La] Idioma:eng
[Ab] Resumo:Neuroinflammatory deregulation in the brain plays a crucial role in the pathogenesis of sepsis associated encephalopathy (SAE). Given the mounting evidence of anti-inflammatory and neuroprotective effects of the cholinergic nervous system, it is surprising that there is little information about its changes in the brain during sepsis. To elucidate the role of the cholinergic nervous system in SAE, hippocampal choline acetyltransferase, muscarinic acetylcholine receptor-1, acetylcholinesterase and acetylcholine were evaluated in LPS-induced sepsis rats. Expression of pro-inflammatory cytokines, neuronal apoptosis, and animal cognitive performance were also assessed. Furthermore, therapeutic effects of the acetylcholinesterase inhibitor Huperzine A (HupA) on the hippocampal cholinergic nervous function and neuroinflammation were evaluated. A deficiency of the cholinergic nervous function was revealed in SAE, accompanied with over-expressed pro-inflammatory cytokines, increase in neuronal apoptosis and brain cognitive impairment. HupA remarkably promoted the deficient cholinergic nervous function and attenuated the abnormal neuroinflammation in SAE, paralleled with the recovery of brain function. We suggest that the deficiency of the cholinergic nervous function and the abnormal neuroinflammation are synergistically implicated in the pathogenesis of SAE. Thus, HupA is a potential therapeutic candidate for SAE, as it improves the deficient cholinergic nervous function and exerts anti-inflammatory action.
[Mh] Termos MeSH primário: Acetilcolina/metabolismo
Acetilcolinesterase/metabolismo
Alcaloides/administração & dosagem
Anti-Inflamatórios/administração & dosagem
Colina O-Acetiltransferase/metabolismo
Encefalite/metabolismo
Receptores Muscarínicos/metabolismo
Encefalopatia Associada a Sepse/metabolismo
Sesquiterpenos/administração & dosagem
[Mh] Termos MeSH secundário: Animais
Apoptose/efeitos dos fármacos
Inibidores da Colinesterase/administração & dosagem
Encefalite/etiologia
Hipocampo/efeitos dos fármacos
Hipocampo/metabolismo
Lipopolissacarídeos
Masculino
Ratos
Ratos Wistar
Encefalopatia Associada a Sepse/induzido quimicamente
Encefalopatia Associada a Sepse/complicações
Aprendizagem Espacial/efeitos dos fármacos
Memória Espacial/efeitos dos fármacos
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Alkaloids); 0 (Anti-Inflammatory Agents); 0 (Cholinesterase Inhibitors); 0 (Lipopolysaccharides); 0 (Receptors, Muscarinic); 0 (Sesquiterpenes); 0111871I23 (huperzine A); EC 2.3.1.6 (Choline O-Acetyltransferase); EC 3.1.1.7 (Acetylcholinesterase); N9YNS0M02X (Acetylcholine)
[Em] Mês de entrada:1707
[Cu] Atualização por classe:170726
[Lr] Data última revisão:
170726
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160713
[St] Status:MEDLINE


  7 / 33 MEDLINE  
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[PMID]:27398623
[Au] Autor:Berisavac II; Padjen VV; Ercegovac MD; Beslac-Bumbasirevic LjG; Stanarcevic PDj; Stefanovic-Budimkic MS; Radovic MM; Jovanovic DR
[Ad] Endereço:Department of Emergency Neurology, Neurology Clinic, Clinical Centre of Serbia, Belgrade, Serbia; University of Belgrade, Faculty of Medicine, Belgrade, Serbia. Electronic address: ivanaberisavac@gmail.com.
[Ti] Título:Focal epileptic seizures, electroencephalography and outcome of sepsis associated encephalopathy-A pilot study.
[So] Source:Clin Neurol Neurosurg;148:60-6, 2016 Sep.
[Is] ISSN:1872-6968
[Cp] País de publicação:Netherlands
[La] Idioma:eng
[Ab] Resumo:OBJECTIVES: Sepsis associated encephalopathy (SAE) represents a diffuse and/or multifactorial cerebral dysfunction during response to systemic infection. Study aim was to compare clinical and electroencephalogram (EEG) characteristics and intrahospital survival rate among SAE patients. PATIENTS AND METHODS: A prospective study, during 42 months' period, included 39 SAE patients assigned in two groups according the outcome (survival: 19, and death: 20 patients). All the patients' features were registered: demography, neurological status, infection type, seizure appearance, brain computerized tomography (CT), EEG, EEG reactivity, Glasgow Coma Score (GCS) and Acute Physiology and Chronic Health Evaluation II (APACHE II) Score. The analysis included EEGs obtained during patients' consciousness change (improvement or deterioration) and the level of consciousness during and at the end of hospitalization. RESULTS: SAE was detected in 29.5% of patients with encephalopathy (2.8% of all patients hospitalized). Patients with lethal outcome were more likely to be female (p=0.0011), to have focal seizures (p=0.034), lower values of GCS during hospitalization (p<0.05) and longer lasting nosocomial infections (p=0.029). At the time of clinical exacerbation, patients were more likely to have suppression on EEG and less likely theta activity. Delta waves, TW waves and suppression of EEG activity were the most common findings 24h prior to death (p=0.0004). The lack of EEG reactivity was associated with death (p=0.00043). CONCLUSION: Presence of focal seizures, EEG suppression at the time of exacerbation in SAE elderly patients, particularly women, with longer infection duration and lower values of GCS, is associated with intrahospital death.
[Mh] Termos MeSH primário: Eletroencefalografia/métodos
Avaliação de Resultados (Cuidados de Saúde)/estatística & dados numéricos
Convulsões/fisiopatologia
Encefalopatia Associada a Sepse/fisiopatologia
[Mh] Termos MeSH secundário: Idoso
Idoso de 80 Anos ou mais
Feminino
Seres Humanos
Masculino
Meia-Idade
Projetos Piloto
Estudos Prospectivos
Convulsões/epidemiologia
Convulsões/mortalidade
Encefalopatia Associada a Sepse/epidemiologia
Encefalopatia Associada a Sepse/mortalidade
Fatores Sexuais
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170817
[Lr] Data última revisão:
170817
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160712
[St] Status:MEDLINE


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[PMID]:27374440
[Au] Autor:Li Y; Su Y; Qu Y; Mu D; Li X
[Ad] Endereço:Pediatric Intensive Care Unit, West China Second University Hospital, Sichuan University, Chengdu 610041, China.
[Ti] Título:[Autophagy in hippocampal nerve cells from rats with sepsis-associated encephalopathy].
[So] Source:Zhong Nan Da Xue Xue Bao Yi Xue Ban;41(6):571-7, 2016 Jun 28.
[Is] ISSN:1672-7347
[Cp] País de publicação:China
[La] Idioma:chi
[Ab] Resumo:OBJECTIVE: To show evidence of the autophagy in hippocampal nerve cells from rats with sepsis-associated encephalopathy (SAE) in vivo and to investigate the expression of microtubule-associated protein 1 light chain 3 (LC3). 
 METHODS: A rat model of sepsis was established by the cecal ligation and puncture (CLP). A total of 60 male Wistar rats (30 days old) were randomly divided into a sham group (n=10) and a CLP group (n=50). At 12 hours after CLP, the electroencephalogram (EEG) and somatosensory evoked potential (SEP) changes in rats were monitored and the neurobehavioral score was measured. According to the occurrence of SAE, the CLP group was further divided into an SAE(+) group and an SAE(-) group. Histopathological changes in hippocampus were observed by hematoxylin-eosin staining. An electron microscope was used to observe autophagosome formation and lysosome activation in the hippocampal nerve cells. Expressions of LC3-I and LC3-II protein were measured by Western blot. 
 RESULTS: Five of 50 rats in CLP group died in 12 hours after CLP. According to the low neurobehavioral score and abnormal EEG and SEP, 16 rats were diagnosed as SAE. The incidence of SAE was 35.56% (16/45). Compared with the sham group or the SAE(-) group, the frequency of α wave in SAE(+) group was significantly decreased at 12 hours after CLP, the δ wave increased, the P1 amplitude decreased, and the latency of SEP waves (P1 and N1) was prolonged (P<0.05). The morphology of hippocampal nerve cells was obvious in a status of edema. Pyramidal cells decreased significantly, even dissolved, and cell arrangement was in disorder in the SAE(+) group. But these cells were normal in the sham group and the SAE(-) group. The structure of hippocampal nerve cells was disordered, and the autophagy, granular matrix and square or rectangular crystals were found in the SAE(+) group. However, there was no autophagy both in the sham group and the SAE(-) group. LC3-II/LC3-I ratio in the hippocampal nerve cells was increased significantly at 12 hours after CLP in the SAE(+) group when compared with that in the sham or the SAE(-) group (P<0.05). 
 CONCLUSION: There is autophagy in hippocampal nerve cells from rats with SAE and the LC3-II/LC3-I ratio is increased significantly.
[Mh] Termos MeSH primário: Autofagia
Hipocampo
Encefalopatia Associada a Sepse
[Mh] Termos MeSH secundário: Animais
Masculino
Proteínas Associadas aos Microtúbulos
Neurônios
Ratos
Ratos Wistar
[Pt] Tipo de publicação:JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Microtubule-Associated Proteins)
[Em] Mês de entrada:1703
[Cu] Atualização por classe:170320
[Lr] Data última revisão:
170320
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160705
[St] Status:MEDLINE
[do] DOI:10.11817/j.issn.1672-7347.2016.06.004


  9 / 33 MEDLINE  
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[PMID]:27172727
[Au] Autor:Fesenko OV; Sinopal'nikov AI; Filatov VV; Danishevsky SV; Styrt EA
[Ti] Título:[CLINICAL ASPECTS OF SEPTIC ENCEPHALOPATHY].
[So] Source:Klin Med (Mosk);94(1):67-70, 2016.
[Is] ISSN:0023-2149
[Cp] País de publicação:Russia (Federation)
[La] Idioma:rus
[Ab] Resumo:Septic encephalopathy is a form of general cerebral dysfunction caused by a systemic inflammatory reaction. Its investigation encounters enormous difficulties for the lack of reliable biological markers of neuronal lesions and methods for the evaluation of consciousness in severely ill patients. Hence, the importance of correct clinical interpretation of the character and magnitude of CNS activity. Examples are presented demonstrating the difficulty of interpreting disorders in CNS activity associated with evere community-acquired pneumonia.
[Mh] Termos MeSH primário: Antibacterianos/administração & dosagem
Pneumonia
Encefalopatia Associada a Sepse
[Mh] Termos MeSH secundário: Encéfalo/patologia
Encéfalo/fisiopatologia
Diagnóstico Diferencial
Gerenciamento Clínico
Evolução Fatal
Seres Humanos
Masculino
Meia-Idade
Exame Neurológico/métodos
Pneumonia/complicações
Pneumonia/diagnóstico
Pneumonia/tratamento farmacológico
Pneumonia/fisiopatologia
Encefalopatia Associada a Sepse/diagnóstico
Encefalopatia Associada a Sepse/etiologia
Encefalopatia Associada a Sepse/fisiopatologia
Tomografia Computadorizada por Raios X/métodos
Inconsciência/etiologia
Adulto Jovem
[Pt] Tipo de publicação:CASE REPORTS; ENGLISH ABSTRACT; JOURNAL ARTICLE
[Nm] Nome de substância:
0 (Anti-Bacterial Agents)
[Em] Mês de entrada:1606
[Cu] Atualização por classe:160513
[Lr] Data última revisão:
160513
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160514
[St] Status:MEDLINE


  10 / 33 MEDLINE  
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[PMID]:26924896
[Au] Autor:Sui DM; Xie Q; Yi WJ; Gupta S; Yu XY; Li JB; Wang J; Wang JF; Deng XM
[Ad] Endereço:Department of Anesthesiology and Intensive Care, Changhai Hospital, Second Military Medical University, 168 Changhai Road, Shanghai 200433, China; Department of Anesthesiology, Chengdu Military General Hospital, 270 Tianhui Road, Chengdu 610083, China.
[Ti] Título:Resveratrol Protects against Sepsis-Associated Encephalopathy and Inhibits the NLRP3/IL-1ß Axis in Microglia.
[So] Source:Mediators Inflamm;2016:1045657, 2016.
[Is] ISSN:1466-1861
[Cp] País de publicação:United States
[La] Idioma:eng
[Ab] Resumo:Sepsis-associated encephalopathy (SAE) is characterized as brain dysfunction associated with sepsis. In this study we sought to investigate the effects of resveratrol in mice with SAE, as well as its effects in NLRP3 inflammasome and IL-1ß, which were critical in the pathogenesis of SAE. SAE was induced in mice via cecal ligation and puncture (CLP), and resveratrol was administered at two doses after surgery. Spatial learning memory functions were evaluated by Morris water maze testing. Apoptosis in the hippocampus was quantified using TUNEL assay. Inflammation in the hippocampus was quantified by measuring the levels of microglial activation, NLRP3, and IL-1ß. CLP mice treated with resveratrol demonstrated a better spatial memory during water maze training. The TUNEL assay demonstrated significantly attenuated rates of apoptosis, in resveratrol treated mice, while decreasing the number of iba-1 positive microglia in the hippocampus region. NLRP3 expression and IL-1ß cleavage were well inhibited by resveratrol dose-dependently. The in vitro results showed that in the BV2 cell lines resveratrol prevents ATP induced NLRP3 activation and IL-1ß cleavage, which were reversed by the sirtuin 1 inhibitor, nicotinamide. In conclusion, resveratrol improves the spatial memory in mice with SAE and inhibits the NLRP3/IL-1ß axis in the microglia.
[Mh] Termos MeSH primário: Interleucina-1beta/metabolismo
Microglia/efeitos dos fármacos
Microglia/metabolismo
Proteína 3 que Contém Domínio de Pirina da Família NLR/metabolismo
Encefalopatia Associada a Sepse/tratamento farmacológico
Encefalopatia Associada a Sepse/metabolismo
Estilbenos/uso terapêutico
[Mh] Termos MeSH secundário: Animais
Linhagem Celular
Masculino
Camundongos
Camundongos Endogâmicos C57BL
[Pt] Tipo de publicação:JOURNAL ARTICLE; RESEARCH SUPPORT, NON-U.S. GOV'T
[Nm] Nome de substância:
0 (Interleukin-1beta); 0 (NLR Family, Pyrin Domain-Containing 3 Protein); 0 (Nlrp3 protein, mouse); 0 (Stilbenes); Q369O8926L (resveratrol)
[Em] Mês de entrada:1612
[Cu] Atualização por classe:170220
[Lr] Data última revisão:
170220
[Sb] Subgrupo de revista:IM
[Da] Data de entrada para processamento:160301
[St] Status:MEDLINE
[do] DOI:10.1155/2016/1045657



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