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1.
Hypertension ; 80(11): 2318-2329, 2023 11.
Artigo em Inglês | MEDLINE | ID: mdl-37551594

RESUMO

BACKGROUND: It has long been hypothesized that the abnormal immune responses contribute to the essential hypertension (EH) and its subclinical target organ damage (STOD). However, the mechanism is unclear. This study aimed at exploring the potential association with abnormal T-cell responses and EH, STOD, and early atherosclerosis in patients with EH. METHODS: This cross-sectional study included 146 patients with EH and 73 age-matched normotensive individuals. The expressed peripheral TCR (T-cell receptor) ß repertoire was analyzed by high through-put sequencing. RESULTS: The TCRß repertoires of the patients with EH were significantly different, with significantly elevated certain TCR beta variable (TRBV) and joint (TRBJ) gene usages, significantly reduced TCRß diversity indexes (diversity 50s) and numbers of total TCRß clonal types, significantly elevated percentages of the biggest TCRß clones and numbers of clones accounting >0.1% sequences, compared with those in the normotensive controls. Decreased diversity 50s and increased biggest TCRß clone percentages were independently correlated with carotid intima-media thickness and subclinical carotid atherosclerosis (SCA) in the patients with EH. Moreover, the diversity 50s were further significantly reduced and the biggest TCRß clone percentages were significantly increased in the patients with EH with SCA (n=89) comparing to the patients with EH/patients without SCA (n=57), and in patients with EH/SCA with carotid plaque (n=22) comparing to patients with EH/SCA/patients without carotid plaque (n=67). Importantly, specific TCRß clones were identified in different subgroups of the patients with EH. CONCLUSIONS: These results reveal that abnormal T-cell responses may play important roles in the progression of EH and its SCA, especially the formation of carotid plaque. REGISTRATION: URL: https://www.chictr.org.cn; Unique identifier: ChiCTR2100054414.


Assuntos
Doenças das Artérias Carótidas , Espessura Intima-Media Carotídea , Humanos , Estudos Transversais , Hipertensão Essencial , Receptores de Antígenos de Linfócitos T , Fatores de Risco
2.
Front Psychiatry ; 13: 974045, 2022.
Artigo em Inglês | MEDLINE | ID: mdl-36569619

RESUMO

Background: Post-traumatic growth (PTG) refers to the positive psychological changes experienced with individuals after struggling with highly challenging life circumstances. Forgiveness can facilitate positive outcomes such as reduced distress, anxiety, and depression. Many studies have tested the relationships among forgiveness, social support, and PTG; however, a mechanism of social support has not been completely explored in hemodialysis patients. Objective: To test the relationship between forgiveness and post-traumatic growth and verify the mediating factor of social support on the relationship between forgiveness and PTG in hemodialysis patients. Materials and methods: In a descriptive cross-sectional study using convenience sampling from March to May 2021, 497 hemodialysis patients from nine hospitals filled out the Perceived Social Support Scale (PSSS), Heartland Forgiveness Scale (HFS), Post-traumatic Growth Inventory (PTGI), and general information. Data were analyzed using SPSS, and structural equation modeling was used to explore the relationships among forgiveness, social support, and PTG. Results: Forgiveness was significantly positively associated with PTG (P < 0.01). The proposed model provided a good fit to the data. Social support was found to play a partial mediating role between forgiveness and PTG (a*b = 0.122, BCa 95% CI: 0.078∼0.181). Conclusion: The results imply that forgiveness significantly directly and indirectly is related to PTG. Forgiveness in hemodialysis patients should be detected and effectively managed to ameliorate positive effects on PTG. It is necessary for nurses to consider implementing forgiveness interventions with an emphasis on building social support strategies to help hemodialysis patients enhance their PTG.

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