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1.
Neurol Res ; : 1-6, 2020 Sep 05.
Artigo em Inglês | MEDLINE | ID: mdl-32893753

RESUMO

BACKGROUND AND PURPOSE: Readmission within 30 days of index acute ischemic stroke (AIS) after hospitalization increases the burden on patients and healthcare expense. The purpose of our study was to investigate predictors and causes of 30-day readmission after AIS and investigate hospitalization expenses, length of stay (LOS) and in-hospital mortality of 30-day readmission. METHODS: This is a multicenter retrospective study. AIS were captured by International Classification of Diseases, Tenth Revision (ICD-10) diagnosis codes, patients with readmitted within 30 days after discharge were identified as readmission group. Multivariable logistic regression was used to identify independent predictors of 30-day readmissions. Hospitalization expenses, LOS and in-hospital mortality were compared for index admission and readmission. RESULTS: We identified 2371 patients with AIS, 176 patients died before discharge, 504(23.0%) patients were admitted within 30 days. Older age, prior stroke, non-neurology floor during index admission, indwelling urinary catheter and diabetes were independently associated with increased risk of 30-day readmission (P<0.05). The most common causes for 30-day readmission were infection (28.8%) and recurrent stroke and TIA (22.8%). Patients with 30-day readmission have longer LOS and higher hospitalization expenses on readmission compared with the mean of these metrics on index admission (P<0.001). The in-hospital mortality after a within 30-day readmission was higher than index admission (13.1% vs 8.0%; OR 1.88, 95% CI 2.5-5.3; P<0.001). CONCLUSIONS: Older age, stroke severity, prior stroke, diabetes, indwelling urinary catheter and admission to non-neurology floor during index admission were associated with 30-day readmission. 30-readmission after AIS increased hospitalization expenses, LOS and in-hospital mortality.

2.
J Vasc Res ; 53(5-6): 291-300, 2016.
Artigo em Inglês | MEDLINE | ID: mdl-27924795

RESUMO

Alisol A 24-acetate, a triterpenoid extracted from Alisma orientale, has shown antiatherosclerotic actions. The purpose of this study was to evaluate the inhibition of alisol A 24-acetate on oxidized low-density lipoprotein (Ox-LDL)-induced phenotypic transformation and migration of rat vascular smooth muscle cells (VSMCs), and to explore the underlying mechanisms. VSMCs were pretreated with alisol A 24-acetate and a specific extracellular signal-regulated kinase (ERK) inhibitor, U0126, and then stimulated with 50 mg/l Ox-LDL in vitro. The expression of VSMC phenotypic marker SM22α was determined using immunocytochemistry, and the migration of VSMCs was detected using a scratch-wound healing assay. The expression of matrix metalloproteinase (MMP)-9, MMP-2, phosphorylated ERK1/2 (pERK1/2) and total ERK was determined. Ox-LDL treatment caused a reduction in SM22α expression, VSMC transformation to the synthetic phenotype, increased MMP-2 and MMP-9 synthesis, the extension of VSMC migration distance and the upregulation of pERK1/2 expression, while the addition of alisol A 24-acetate or U0126 resulted in the elevation of SM22α expression, VSMC transformation to the contractile phenotype, a reduction in MMP-2 and MMP-9 expression, the shortening of cell migration distance and decreased pERK1/2 expression. The results of this study demonstrate that alisol A 24-acetate effectively reverses the phenotypic transformation and inhibits the migration of VSMCs, which may be associated with the suppression of the ERK1/2 signaling pathway.


Assuntos
Movimento Celular/efeitos dos fármacos , Colestenonas/farmacologia , Lipoproteínas LDL/toxicidade , Proteína Quinase 1 Ativada por Mitógeno/metabolismo , Proteína Quinase 3 Ativada por Mitógeno/metabolismo , Músculo Liso Vascular/efeitos dos fármacos , Miócitos de Músculo Liso/efeitos dos fármacos , Extratos Vegetais/farmacologia , Actinas/metabolismo , Alisma/química , Animais , Forma Celular/efeitos dos fármacos , Células Cultivadas , Colestenonas/isolamento & purificação , Relação Dose-Resposta a Droga , Masculino , Metaloproteinase 2 da Matriz/genética , Metaloproteinase 2 da Matriz/metabolismo , Metaloproteinase 9 da Matriz/genética , Metaloproteinase 9 da Matriz/metabolismo , Proteína Quinase 1 Ativada por Mitógeno/antagonistas & inibidores , Proteína Quinase 3 Ativada por Mitógeno/antagonistas & inibidores , Músculo Liso Vascular/enzimologia , Músculo Liso Vascular/patologia , Miócitos de Músculo Liso/enzimologia , Miócitos de Músculo Liso/patologia , Fenótipo , Extratos Vegetais/isolamento & purificação , Inibidores de Proteínas Quinases/farmacologia , Ratos Sprague-Dawley , Transdução de Sinais/efeitos dos fármacos , Fatores de Tempo
3.
Mol Med Rep ; 13(2): 1533-40, 2016 Feb.
Artigo em Inglês | MEDLINE | ID: mdl-26707062

RESUMO

ATP-binding cassette transporters A1 (ABCA1) and G1 (ABCG1), and macrophage scavenger receptor, cluster of differentiation (CD)36, function as key mediators of cholesterol efflux and influx from macrophages. In addition, they are associated with foam cell formation and the development of atherosclerosis (AS). The aim of the present study was to investigate the effects of extracellular signal-regulated kinases 1/2 (ERK1/2) inhibition on lipid balance in oxidized-low-density lipoprotein (Ox-LDL)-stimulated rat macrophages, and to examine the role of ERK1/2 inhibitors in AS. Rat peritoneal macrophages were treated with Ox-LDL alone or in combination with an ERK1/2 inhibitor, U0126, and untreated cells served as controls. Ox-LDL-induced lipid accumulation was detected by DiI fluorescence and oil red O staining. In addition, the mRNA and protein expression levels of ABCA1, ABCG1 and CD36 were determined using polymerase chain reaction and western blotting, respectively. Treatment with Ox-LDL significantly increased lipid accumulation and upregulated the mRNA and protein expression levels of ABCA1, ABCG1 and CD36 in macrophages. The addition of U0126 resulted in a marked reduction of lipid deposition, upregulation of ABCA1/G1 expression and suppression of CD36 expression in Ox-LDL-stimulated macrophages. The results of the present study indicated a novel association between ERK1/2 signaling and lipid metabolism, thus suggesting that inhibition of ERK1/2 may be considered a promising therapeutic strategy against AS.


Assuntos
Transportador 1 de Cassete de Ligação de ATP/biossíntese , Transportadores de Cassetes de Ligação de ATP/biossíntese , Antígenos CD36/biossíntese , Macrófagos/metabolismo , Transportador 1 de Cassete de Ligação de ATP/genética , Membro 1 da Subfamília G de Transportadores de Cassetes de Ligação de ATP , Transportadores de Cassetes de Ligação de ATP/genética , Animais , Butadienos/administração & dosagem , Antígenos CD36/genética , Colesterol/metabolismo , Regulação da Expressão Gênica/efeitos dos fármacos , Metabolismo dos Lipídeos/efeitos dos fármacos , Lipoproteínas LDL/administração & dosagem , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , Macrófagos/efeitos dos fármacos , Nitrilos/administração & dosagem , RNA Mensageiro/biossíntese , Ratos
4.
Neurol Res ; 37(6): 531-8, 2015 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-25023896

RESUMO

OBJECTIVES: Neuroglobin (Ngb), an identified globin in vertebrate brain, is a potential novel protective protein against brain ischemia. In our previous study, the human immunodeficiency virus trans-activator of transcription (TAT) protein transduction domain successfully delivered exogenous Ngb into neurons in the mouse, and protected the brain from cerebral ischemia-induced apoptosis. The aim of this study is to investigate the role of TAT-Ngb in attenuating oxygen-glucose deprivation (OGD) induced apoptosis and to explore the possible mechanism. METHODS: Nerve growth factor (NGF)-induced PC12 cells were divided into (1) the control group, (2) the OGD group (just OGD), (3) the Ngb treatment group (OGD and Ngb treatment), and (4) the TAT-Ngb treatment group (OGD and TAT-Ngb treatment). Cell viability and apoptosis were assessed by the MTT assay and the AnnexinV/propidium iodide (PI) staining, respectively. The mitochondrial transmembrane potential was measured by JC-1 staining. Caspase-3, Bcl-2, Bax, Stat3, Jak2, and Akt were determined by western blot analysis. RESULTS: Trans-activator of transcription effectively delivered Ngb into NGF-induced PC12 cells. Neuroglobin-mediated neuroprotection rescued cultured cells from OGD. We also confirmed previous findings that TAT-Ngb inhibited mitochondrial apoptosis following OGD. Inhibition of apoptosis by Ac-DEVD-CHO showed that caspase-3 was a crucial factor in OGD-induced apoptosis cascades. AG490, a specific Jak2 inhibitor, attenuated the protective effects of TAT-Ngb. The TAT-Ngb promoted expression of the anti-apoptotic protein Bcl-2 through the Jak2/Stat3 signal pathway, and inhibited apoptosis by blocking caspase-3 activation, while the Jak-Akt-Stat3 signal network was not involved. CONCLUSION: Our results demonstrate that TAT-Ngb can protect neuron-like cells against OGD-induced apoptosis by activating the Jak2/Stat3 pathway.


Assuntos
Apoptose/efeitos dos fármacos , Hipóxia Celular/efeitos dos fármacos , Globinas/administração & dosagem , Glucose/deficiência , Proteínas do Tecido Nervoso/administração & dosagem , Fármacos Neuroprotetores/administração & dosagem , Produtos do Gene tat do Vírus da Imunodeficiência Humana/genética , Animais , Apoptose/fisiologia , Western Blotting , Hipóxia Celular/fisiologia , Sobrevivência Celular/efeitos dos fármacos , Sobrevivência Celular/fisiologia , Sistemas de Liberação de Medicamentos , Inibidores Enzimáticos/farmacologia , Escherichia coli , Globinas/genética , Janus Quinase 2/antagonistas & inibidores , Janus Quinase 2/metabolismo , Potencial da Membrana Mitocondrial/efeitos dos fármacos , Potencial da Membrana Mitocondrial/fisiologia , Proteínas do Tecido Nervoso/genética , Neuroglobina , Células PC12 , Ratos , Proteínas Recombinantes de Fusão/administração & dosagem , Fator de Transcrição STAT3/metabolismo , Transdução de Sinais/efeitos dos fármacos , Tirfostinas/farmacologia , Produtos do Gene tat do Vírus da Imunodeficiência Humana/administração & dosagem
5.
Exp Neurol ; 227(1): 224-31, 2011 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-21093435

RESUMO

Neuroglobin (Ngb), a newly identified globin in vertebrate brain, has been suggested to be able to protect against brain hypoxic-ischemic injury. However, owing to its large size, the impermeability of the blood-brain barrier (BBB) to Ngb limits its application in brain injury. Recently, the 11-amino-acid human immunodeficiency virus trans-activator of transcription (TAT) protein transduction domain was shown to successfully deliver macromolecules into the brain. This study explored whether the TAT-Ngb fusion protein can cross the BBB and protect the brain from cerebral ischemia. The TAT-Ngb fusion protein generated from Escherichia coli BL21 (DE3) was efficiently delivered into mice brain tissues by intravenous injection as demonstrated by immunohistochemistry and Western blotting. Two groups of mice were treated with filamentous middle cerebral artery occlusion (MCAO) for 30min or 2h followed by reperfusion. Each group was then divided into sub-groups and was injected intravenously with TAT-Ngb, Ngb, or saline respectively before MCAO or immediately after reperfusion. Compared with the Ngb- and saline-treated group, the group with TAT-Ngb treated 2h before MCAO showed significantly less brain infarct volume and had better neurologic outcomes (p<0.05). Furthermore, a TAT-Ngb injection following a 30-min MCAO treatment significantly increased neuronal survival in the striatum (p<0.05). Our results demonstrated that the exogenous Ngb fusion protein containing the TAT protein transduction domain could be efficiently transduced into neurons in the mouse and protect the brain from mild or moderate ischemic injury.


Assuntos
Globinas/administração & dosagem , Infarto da Artéria Cerebral Média/prevenção & controle , Proteínas do Tecido Nervoso/administração & dosagem , Transativadores/metabolismo , Animais , Gasometria/métodos , Pressão Sanguínea/fisiologia , Infarto Encefálico/etiologia , Infarto Encefálico/prevenção & controle , Modelos Animais de Doenças , Vetores Genéticos/fisiologia , Humanos , Marcação In Situ das Extremidades Cortadas/métodos , Infarto da Artéria Cerebral Média/complicações , Camundongos , Camundongos Endogâmicos C57BL , Doenças do Sistema Nervoso/etiologia , Doenças do Sistema Nervoso/prevenção & controle , Neuroglobina , Fosfopiruvato Hidratase/metabolismo , Proteínas Recombinantes de Fusão/administração & dosagem , Proteínas Recombinantes de Fusão/genética , Fluxo Sanguíneo Regional/fisiologia , Fatores de Tempo , Transativadores/genética
6.
Neurobiol Aging ; 31(4): 647-53, 2010 Apr.
Artigo em Inglês | MEDLINE | ID: mdl-18621447

RESUMO

The association of R219K and V825I polymorphisms of ABCA1 gene with cerebral infarction has been rarely reported. Here we wish to address this issue. A total of 476 subjects from Chinese Han ethnic population were investigated, including 152 control individuals and 324 patients with cerebral infarction. Genotyping of R219K and V825I were performed by PCR-RFLP analysis. Data were analyzed using a statistical package. The R219K genotype frequency distributions were significantly different between patients with atherothrombotic cerebral infarction (ACI) and control individuals, with fewer KK genotypes and more RR genotypes in ACI patients (chi(2)=9.89, P<0.01). The K allele is less frequent among ACI patients than in controls (chi(2)=9.16, P<0.005). A significant association of KK with decreased ACI risk was exhibited, especially in male patients, aged patients and individuals with hypertension. These results indicate that the K allele of R219K polymorphism is an independent protective factor against ACI. In addition, though there is no association of V825I with ACI, this polymorphism may have certain synergistic effect with hypertension in susceptibility to ACI.


Assuntos
Transportadores de Cassetes de Ligação de ATP/genética , Grupo com Ancestrais do Continente Asiático/genética , Infarto Cerebral/genética , Predisposição Genética para Doença/genética , Arteriosclerose Intracraniana/genética , Polimorfismo Genético/genética , Transportador 1 de Cassete de Ligação de ATP , Adulto , Distribuição por Idade , Idoso , Idoso de 80 Anos ou mais , Infarto Cerebral/etnologia , Infarto Cerebral/metabolismo , China/etnologia , Análise Mutacional de DNA , Feminino , Frequência do Gene/genética , Marcadores Genéticos/genética , Testes Genéticos , Genótipo , Humanos , Hipertensão/complicações , Hipertensão/genética , Hipertensão/fisiopatologia , Arteriosclerose Intracraniana/etnologia , Arteriosclerose Intracraniana/metabolismo , Masculino , Pessoa de Meia-Idade , Distribuição por Sexo
7.
Neurol Res ; 32(2): 198-204, 2010 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-19433012

RESUMO

OBJECTIVES: This study was carried out to observe the effect of electroacupuncture (EA) on neurological deficits, proliferation and differentiation of nerve stem cells (NSCs) in adult rats with middle cerebral artery occlusion (MCAO) and to study its possible role in the treatment of cerebral ischemic injury. METHODS: A rat model of MCAO was established and interfered with EA. On days 4, 7, 14 and 21 after ischemic injury, neurological deficits were scored. On days 4, 7, 14 and 21 after injury, effect of EA interference on the proliferation and differentiation of rat NSCs was observed with BrdU/NeuN and BrdU/GFAP immunofluorescence double labeling. RESULTS: A significant difference was found in the scores of rat neurological deficits between the EA and model groups 7, 14 and 21 days after cerebral ischemic injury (p<0.05). BrdU positive cells were found in the subventricular zone (SVZ) 4, 7, 14 and 21 days after ischemic injury. The number of positive BrdU cells in the SVZ reached its peak 7 days after injury and was greater in the EA group than in the model group 7 and 14 days after injury (p<0.05). The number of BrdU/GFAP doubly labeled positive cells in the SVZ was greater in the EA group than in the model group 7 and 14 days after ischemic injury (p=0.012 and p=0.025, respectively). There was no difference in the number of BrdU/NeuN doubly labeled positive cells 4, 7 and 14 days in the striatum, but a significant difference 21 days (p=0.033) after ischemic injury between the two groups. DISCUSSION: Cerebral ischemic injury induces proliferation of NSCs, some of which will differentiate into both astroglia and neurons. EA may promote cells proliferation, stimulate the proliferating cells to differentiate into astroglia and mature into neurons, which may be one of the important reasons why EA can alleviate neurological deficits.


Assuntos
Isquemia Encefálica/patologia , Isquemia Encefálica/terapia , Diferenciação Celular , Proliferação de Células , Eletroacupuntura , Células-Tronco/citologia , Animais , Diferenciação Celular/fisiologia , Eletroacupuntura/métodos , Masculino , Neurônios/citologia , Neurônios/patologia , Ratos , Ratos Sprague-Dawley , Células-Tronco/patologia
8.
BMC Med Genet ; 9: 110, 2008 Dec 16.
Artigo em Inglês | MEDLINE | ID: mdl-19087291

RESUMO

BACKGROUND: Neuroglobin (Ngb), one of novel members of the globin superfamily, is expressed predominantly in brain neurons, and appears to modulate hypoxic-ischemic insults. The mechanisms underlying Ngb-mediated neuronal protection are still unclear. For it is one of the candidate protective factors for ischemic stroke, we conducted a case-control study to clarify the association of Ngb polymorphisms with ischemic stroke in the Southern Chinese Han population. METHODS: 355 cases and 158 controls were recruited. With brain imaging, cases were subdivided into large-artery atherosclerosis (LVD) and small-vessel occlusion (SVD) stroke. PCR amplified all the four exons of Ngb and flanking intron sequence for each exon. Genotyping for Ngb was achieved by direct sequencing and mismatched PCR-RFLP. Polymorphisms were studied both individually and as haplotypes in each group and subgroup which subdivided according to gender or age. RESULTS: Two intronic polymorphisms 89+104 c>t and 322-110 (6a)>5a were identified. The allele frequency of 89+104 t was decreased in stroke cases. The protective effect seems to be more pronounced in subgroups of female patients and age > 60 years. Also, we have confirmed decreased LDL-C level and reduced hypertension and hypercholesterolemia in 89+104 t allele carriers. In contrast, the 322-110 (6a)>5a genotype distribution was similar between cases and controls. However, the haplotype 89+104 c>t/322-110 (6a)>5a was related with LVD and SVD stroke. The haplotype c-5a was more frequent in both LVD and SVD groups while t-6a was more frequent in controls. CONCLUSION: Ngb polymorphism 89+104 t had protective effects on LVD and SVD in the Southern Chinese Han population. A "hitchhiking" effect was observed for the 89+104 t/322-110 (6a) genotype combination especially for LVD.


Assuntos
Isquemia Encefálica/genética , Globinas/genética , Proteínas do Tecido Nervoso/genética , Acidente Vascular Cerebral/genética , Adulto , Idoso , Idoso de 80 Anos ou mais , Alelos , Estudos de Casos e Controles , China , Feminino , Genótipo , Humanos , Modelos Logísticos , Masculino , Pessoa de Meia-Idade , Neuroglobina , Razão de Chances , Reação em Cadeia da Polimerase , Polimorfismo de Fragmento de Restrição , Polimorfismo de Nucleotídeo Único
9.
Dement Geriatr Cogn Disord ; 26(3): 234-8, 2008.
Artigo em Inglês | MEDLINE | ID: mdl-18841006

RESUMO

BACKGROUND: To date, 81 mutations of ATP-binding cassette transporter 1 (ABCA1) have been reported. However, no ABCA1 mutation has been reported in the Chinese population. METHODS: We used direct sequencing to screen for ABCA1 mutations in 72 patients with both atherosclerotic cerebral infarction (ACI) and plasma high-density lipoprotein cholesterol (HDL-C) < 0.8 mmol/l. The functionality of the mutation was verified using 200 unrelated controls and 76 patients with ACI and normal HDL-C by PCR-RFLP analysis. RESULTS: One patient with dementia prior to ACI was found to carry the heterozygous Y2206D mutation, which has not been reported previously. The patient had a medical history of atherosclerosis in the coronary and carotid arteries going back 40 years and splenohepatomegalia for 13 years, with a low plasma HDL-C level (0.66 mmol/l) and apolipoprotein A1 level (0.61 mmol/l). During the past decade, he had developed symptoms of dementia. Sixteen months prior to the study, he was admitted to hospital for an ACI. CONCLUSION: The results suggest that this patient is most likely a patient with familial hypoalphalipoproteinemia and that the Y2206D mutation may be associated with not only a lower level of HDL-C, but also with dementia.


Assuntos
Transportadores de Cassetes de Ligação de ATP/genética , Grupo com Ancestrais do Continente Asiático/genética , Demência/etnologia , Demência/genética , Arteriosclerose Intracraniana/etnologia , Arteriosclerose Intracraniana/genética , Transportador 1 de Cassete de Ligação de ATP , Idoso , Grupo com Ancestrais do Continente Asiático/estatística & dados numéricos , Infarto Cerebral/etnologia , Infarto Cerebral/genética , HDL-Colesterol/sangue , Humanos , Hipoalfalipoproteinemias/etnologia , Hipoalfalipoproteinemias/genética , Trombose Intracraniana/etnologia , Trombose Intracraniana/genética , Masculino , Pessoa de Meia-Idade , Mutação Puntual
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