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1.
Chinese Journal of Behavioral Medicine and Brain Science ; (12): 437-441, 2020.
Article in Chinese | WPRIM | ID: wpr-867076

ABSTRACT

Objective:To explore the characteristics of cognitive emotion regulation in patients with hepatolenticular degeneration, and the relationship with brain lesions.Methods:The Chinese version of cognitive emotion regulation (CERQ-C) was used to investigate 78 patients with hepatolenticular degeneration(WD group) and 84 healthy adults, and all patients were examined with brain 3.0 T magnetic resonance.The characteristics of cognitive and emotional regulation in WD group were analyzed when they encounterd negative life events, and the differences between WD group and healthy people.The relationship was further analyzed between different brain structure damage and cognitive emotion regulation combined with brain MRI.Results:(1)The scores of self censure, contemplation and catastrophes in WD group((11.41±2.46), (11.27±3.09), (9.53±2.85), respectively) were significantly higher than those in healthy control group(respectively(9.57±2.81), (9.79±2.63), (8.05±2.42))( t=4.417, 3.409, 3.563, P<0.01). The scores of refocus planning and positive reevaluation ((13.26±3.41), (13.49±3.14)) in MD group were significantly lower than those of the healthy control group ((14.88±2.57), (14.42±2.41))( t=-3.404, -2.103, P<0.05). (2)Multiple linear regression analysis showed that frontal lobe injury was the influencing factor of the score of positive re-evaluation ( B=-2.142, P=0.035), thalamic injury ( B=2.058, P=0.037) and putamen injury ( B=-2.348, P=0.011) were the influencing factors of the score of contemplation. Conclusion:WD patients are more likely to choose self censure, contemplation and catastrophes than healthy people when they encounter negative life events.Different brain regions have different effects on the choice of cognitive emotion regulation in WD patients.

2.
Chinese Journal of Nervous and Mental Diseases ; (12): 321-325, 2019.
Article in Chinese | WPRIM | ID: wpr-753920

ABSTRACT

Objective To explore cognitive impairment and related factors in patients with Wilson disease (WD) and to screen the risk factors of cognitive impairment in order to provide evidence for clinical intervention. Methods The Chinese Version Addenbrooke's Cognitive Examination-III (ACE-III-C) was used to assess the cognitive function. The WD patients with cognitive impairment were analyzed the difference between those with non-cognitive disorders in the Young scale, Baethel scale and biochemical indicators. Risk factors for cognitive impairment in WD patients were analyzed by multiple linear regression. Results Cognitive impairment occurred in 43 (59.7%) of 72 patients with WD. ACE-III-C total score, attention, memory, language fluency, visual spatial factor scores, Young scores, Barthel scores and serum copper levels were significantly different between patients with cognitive impairment and patients with non-cognitive impairment (P<0.01). Linear regression analysis showed that serum copper levels were the most important risk factors for ACE-III-C total score and cognitive subfields (P<0.01). Serum zinc levels as a secondary risk factor of language fluency and visual space (P<0.05). Age-related participation affected language fluency (P<0.05). Conclusions Serum copper and zinc levels may be the main risk factors of cognitive impairment. Modulation of serum copper and zinc levels may be the key for intervention to treat cognitive impairment in WD patients.

3.
Chinese Pharmacological Bulletin ; (12): 153-157, 2017.
Article in Chinese | WPRIM | ID: wpr-508253

ABSTRACT

Necrosis is also tightly controlled by signaling path-ways,thus it is called as regulated necrosis,which includes ne-croptosis,ferroptosis,parthanatos and CypD-mediated necrosis. It has been shown that regulated necrosis is closely related to the occurrence,development and prognosis of injury-relevant disea-ses such as myocardial infarction,stroke,neurodegenerative dis-eases.It will be significant for prevention and therapy of injury-relevant diseases to clarify the signal transductions and regulatory mechanisms for the regulated necrosis.

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