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1.
Chinese Journal of Neurology ; (12): 45-50, 2012.
Article in Chinese | WPRIM | ID: wpr-428274

ABSTRACT

ObjectiveTo investigate the effect of focal ischemic preconditioning (IPC) on the expression of protein kinase-like endoplasmic reticulum kinase ( PERK ) and glucose-regulated protein 78 (GRP78) mRNA and protein after focal cerebral ischemia/reperfusion (I/R) in rats.MethodsAll 120 male SD rats were randomly divided into three groups: sham-operation group,middle cerebral artery occlusion (MCAO) group and brain ischemia preconditioning (BIP) group.Each group was further divided into 4 subgroups according to 12 h,1,2 and 3 d after I/R.The IPC models were made in order to measure the expression of PERK,GRP78 mRNA and protein by in situ hybridization and Western blot,and the apoptosis rate of neuron by flow cytometry. Results ①The expression of PERK mRNA increased and reached the peak at 12 h,then decreased continuously after 1 d.BIP could decrease its expression.The expression of PERK protein increased at 12 h and reached the peak at 24 h,then decreased continuously after 2 d.BIP could decrease its expression.②The expression both of GRP78 mRNA and its protein all increased and reached the peak at 12 h,then decreased continuously.BIP could increase their expression (mRNA:12 h: 136.70±9.53,F=32.265; 24 h:147.54 ±9.97,F=54.920; 2 d:158.16 ±9.44,F=45.374; 3d: 165.85±10.26,F=16.493,P<0.05; protein:12 h: 1.319±0.116,F=5.619,P<0.05; 24 h: 1.226±0.108,F=33.742,P<0.01; 2 d:1.183 ±0.112,F =46.556,P <0.01; 3 d:1.115± 0.098,F =11.730,P<0.05).③The rate of apoptosis neuron of rats in MCAO increased markedly at 12 h after reperfusion,and reached the peak at 1 d,then decreased continuously.BIP could decrease the rate of apoptosis neuron. Conclusion BIP can protect neurons through inhibiting the expression of PERK and inducing the expression of GRP78 after endoplasmic reticulum stress in rats.

2.
China Journal of Traditional Chinese Medicine and Pharmacy ; (12)2005.
Article in Chinese | WPRIM | ID: wpr-563610

ABSTRACT

This thesis discourse upon blood stagnant in cerebral venation is the pivotal pathogenesis of cerebral ischemia stroke,and discuss once the cerebral ischemia occur,it can derive more phlegms,toxic heat and other pathological outcomes,resulting in inflammatory injury of cerebral ischemia,forming a vicious circle of "inflammation-thrombus",so that aggravating the injury with ischemia and anoxia of never cells,even causing inreversible putrescence of cerebral ischemia.And this condition should be the springs of the development and aggravation of the illness.Therefore,applying promoting blood circulation for removing blood stasis measures can removing blood stasis,eliminating pathogenic wind-fire and cleanning out phlegm,so the pyogenic infections can be dispelled,and the pathological state of inflammation,injury and microcirculation obstacle in the brain can be meliorated.Then,the brain vascula become smooth and the blood supply resume,the symptoms with never functional impairment alleviate or meliorate,thereby,the rate of death and cripple decrease obviously.

3.
Chinese Journal of Rehabilitation Theory and Practice ; (12): 764-765, 2005.
Article in Chinese | WPRIM | ID: wpr-978554

ABSTRACT

@#ObjectiveTo explore the effect of rehabilitation in open wards on chronic schizophrenic patients.Methods48 chronic schizophrenic patients were shifted to open wards with comprehensive rehabilitational therapy.They were evaluated with Positive And Negative Symptoms Scale(PANSS),Nurse's Observation Scale for Inpatient Evaluation(NOSIE),Social Disability Screening Schedule (SDSS) before and 6 months after the shifting.ResultsThere was significant difference in the total scores, negative symptoms scales score, general psychopathological scales score and response deficient factor score of PANSS, all the factors scores except psychiatric manifestations and depression of NOSIE, and scores of SDSS pre- and post-shifting(P<0.01).ConclusionRehabilitation in open wards can improve the negative symptoms and social function of chronic schizophrenics.

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