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1.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-1031760

RESUMO

@#Parkinson disease (PD) is a common neurodegenerative disease. Cognitive dysfunction seriously affects the quality of life of patients with PD, increasing their family burden. Currently, there are no clinically identified biomarkers to assist with the early diagnosis of cognitive impairment in patients with PD. Event-related potential P300 is a sensitive electrophysiological indicator to detect early insidious cognitive decline in PD. This article reviews the diagnostic value and clinical application of P300 for cognitive impairment in patients with PD.

2.
Biomed Res Int ; 2018: 6473580, 2018.
Artigo em Inglês | MEDLINE | ID: mdl-29770336

RESUMO

BACKGROUND/AIMS: Epigallocatechin-3-gallate (EGCG) has neuroprotective effects and the ability to resist amyloidosis. This study observed the protective effect of EGCG against neuronal injury in rat models of middle cerebral artery occlusion (MCAO) and investigated the mechanism of action of PI3K/AKT/eNOS signaling pathway. METHODS: Rat models of permanent MCAO were established using the suture method. Rat behavior was measured using neurological deficit score. Pathology and apoptosis were measured using HE staining and TUNEL. Oxidative stress and brain injury markers were examined using ELISA. Apoptosis-related proteins and PI3K/AKT/eNOS signaling pathway were determined using western blot assay and immunohistochemistry. RESULTS: EGCG decreased neurological function score, protected nerve cells, inhibited neuronal apoptosis, and inhibited oxidative stress injury and brain injury markers level after MCAO. EGCG reduced the apoptotic rate of neurons, increased the expression of Bcl-2, and decreased the expression of Caspase-3 and Bax. After LY294002 suppressed the PI3K pathway, the protective effect of EGCG decreased after administration of PI3K inhibitors. CONCLUSION: EGCG has a protective effect on rat brain injury induced by MCAO, possibly by modulating the PI3K/AKT/eNOS signaling pathway.


Assuntos
Apoptose/efeitos dos fármacos , Catequina/análogos & derivados , Infarto da Artéria Cerebral Média/tratamento farmacológico , Óxido Nítrico Sintase Tipo III/metabolismo , Fosfatidilinositol 3-Quinases/metabolismo , Proteínas Proto-Oncogênicas c-akt/metabolismo , Transdução de Sinais/efeitos dos fármacos , Animais , Isquemia Encefálica/tratamento farmacológico , Isquemia Encefálica/metabolismo , Catequina/farmacologia , Cromonas/farmacologia , Infarto da Artéria Cerebral Média/metabolismo , Masculino , Morfolinas/farmacologia , Fármacos Neuroprotetores/farmacologia , Ratos , Ratos Sprague-Dawley , Traumatismo por Reperfusão/tratamento farmacológico , Traumatismo por Reperfusão/metabolismo
3.
Chinese Journal of Geriatrics ; (12): 902-906, 2016.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-502423

RESUMO

It was believed that there were only two patterns of cell death named after necrosis and apoptosis in the past.With the progress of research,scholars have found that there also existed other cell death patterns.However,the mechanisms and relationships between cell death patterns are still unclear,especially in the neuronal cell death.This review focuses on the cell death patterns and their relationships during ischemic stroke,in order to provide the theoretical basis and new ideas for the further study of neuronal cell death,and for the treatment of ischemic stroke.

4.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-485251

RESUMO

Objective To evaluate the predictive values of ABCD,ABCD2 ,SPI-Ⅱ and ESSEN score models for the patients with high-risk transient ischemic attack (TIA)to develop to cerebral infarction in short and long term. Methods The ABCD, ABCD2 , SPI-Ⅱ and ESSEN scores of 235 cases of TIA patients were retrospectively analyzed.The incidence of cerebral infarction was followed up for 7 d and 1 year, and the receiver operating characteristic curve (ROC)was drawn to calculate the area under curve (AUC)to assess the accuracy of the score models,and compared with the original model and the relative risk (RR)value was calculated.Results The 7 d-incidence and 1 year-incidence of cerebral infarction in the 235 TIA patients were 9.36 % and 20.43%.The AUC of ABCD,ABCD2 ,SPI-Ⅱ and ESSEN models for 7 d were 0.70,0.74,0.67,and 0.62.The AUC of 1 year were 0.62,0.62,0.64,and 0.65.Compared with the orginal models,the RRs for 7 d of ABCD score model of the TIA patients in low,middle,and high risk groups were 0.09,0.92,and 0.72;the RRs of ABCD2 score model were 0.49,0.59,and 0.65;the RRs of SPI-Ⅱ score model were 0.58,0.87,and 0.55;the RRs of ESSEN score model were 0.11,0.18,and 0.55.Conclusion ABCD,ABCD2 ,SPI-Ⅱ and ESSEN score models can be used to assess the risk of cerebral infarction after TIA in Chinese population.The ABCD2 score model is of great value for short-term risk prediction,and the ESSEN score model is more value for long-term risk prediction.

6.
Chinese Journal of Neurology ; (12): 379-382, 2009.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-394556

RESUMO

Objective To report clinical features,diagnosis and treatment in a case of adult onset Still's disease (AOSD) accompanied by demyelinating encephalopathy.Methods We reported a case of Stills disease with signs of encephalopathy.We also reviewed and discussed the literature on the neurological manifestations in AOSD.Results The 35-year-old patient had recurrent fever and arthralgias for 3 years,headache for 1 month and transient loss of consciousness.Laboratory tests showed non-specific immunological activity.MRI showed tumor-like lesions at left parietal and occipital lobes surrounded by sleeve-like edema.The lesion had significant occupation effect.Biopsy proved the presence of demyelinating changes.The patient recovered favorably after administration of corticosteroids and immunoglobulin.The lesions had almost disappeared on follow-up MRI 4 months later.Conclusions Demyelinating encephalopathy may develop in patient with AOSD.MRI may show tumor-like damage,which is rarely reported in the literature.Diagnosis depends on history,clinical manifestation and neuroimaging.Biopsy provides important information in making diagnosis.Treatment with corticosteroids and intravenous immunoglobulin was found to achieve good recovery.

7.
Artigo em Chinês | WPRIM (Pacífico Ocidental) | ID: wpr-407364

RESUMO

BACKGROUND: We can investigate mechanism of endogenous neuroprotection in rat cerebral hypoxic tolerance trial. OBJECTIVE: To observe the characteristics of cerebral hypoxic tolerance in rat models with cerebral hypoxic preconditioning. DESIGN: Randomized controlled observation. SETTING: Department of Neurology, China-Japanese Friendship Hospital, Jilin University. MATERIALS: The experiment was performed in the Basic Animal Experimental Center, China-Japan Friendship Hospital, Jilin University from April 2003 to April 2004. Inbred line healthy Wistar rats, of either sex, with the body mass of 200-300 g, were randomly assigned into normal control group (n=6), sham operation group (n=6), ischemic control group (n=20), hypoxic preconditioning (3 hours, 8% O2 and 92% N2) plus ischemic group (n=60) (according to different hypoxic phases, there were 5 time phases: 30 minutes, 1, 3, 5 and 6 hours with 12 rats in each time phase), hypoxic preconditioning group (n=18) [according to different hypoxic phases, there were 3 time phases: 1, 3 and 5 hours with 6 rats in each time phase, 3 rats received TTC staining and 3 rats received hematoxylin and eosin (HE) staining]. METHODS: ①Hypoxic preconditioning: Firstly, natrica calx was put into closed glass container to absorb CO2 and O2, secondly, mixed gas of 8% O2 and 92% N2 was input, and then animals were put into the container, 3 rats each time. Temperature and humidity were kept steadily. ②Permanent ischemic middle cerebral artery rat models were established. ③The models were determined with a series in procedures: neurological score, infarcted volume evaluation, pathological sample preparation, immunohistochemical staining, imaging analysis and so on. ④The data were compared in groups with variance analysis.MAIN OUTCOME MEASURES: Changes in cerebral infarcted volume, neurological score and pathological morphology in rats of experimental group and control group. RESULTS: Neurological score in the hypoxic preconditioning (8% O2, at hours 1, 3 and 5) plus ischemic group was lower than in the ischemic control group(P<0.01). Neurological score at minute 30 and hour 6 after hypoxia (8% O2) had insignificant difference in the ischemic control group. Mean cerebral infarcted volume ratio in the hypoxic preconditioning (8% O2, at hours 1, 3 and 5) plus ischemic group was lower than in the ischemic control group(P<0.01). Mean cerebral infarcted volume ratio after hypoxia (8% O2, at minute 30 and hour 6) had insignificant difference with ischemic control group (P>0.05). CONCLUSION: Hypoxic preconditioning in rats can effectively release nerve injury induced by focal cerebral ischemia, suggesting that it has protective effect on brain. The procedure of establishing cerebral ischemic tolerance models with hypoxic preconditioning, which is simple and stable, with little injury on experimental animals, is a useful tool for studying cerebral ischemic tolerance.

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