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1.
Korean J Women Health Nurs ; 24(2): 185-195, 2018 Jun.
Artigo em Inglês | MEDLINE | ID: mdl-37684924

RESUMO

PURPOSE: To investigate factors related to cardio-cerebrovascular disease and groups disadvantaged by it in Korean middle-aged women, using the Korea National Health and Nutrition Examination Survey (KNHANES). METHODS: The present study was conducted with 1,627 middle-aged women, aged 40 to 64 years, who participated in the 7th (2016) Korea National Health and Nutrition Examination Survey conducted by the Korea Centers for Disease Control and Prevention. RESULTS: Cardio-cerebrovascular disease among middle-aged women was associated with quality of life, menopause, diabetes mellitus, body mass index, and family history of hypertension. The incidence of cardio-cerebrovascular disease in middle-aged women was found to be the most prevalent in women who have entered menopause, have a family history of hypertension, and have a body mass index greater than 30.0 kg/m². CONCLUSION: This study classifies the subjects according to the risk level of each disadvantaged group for cardio-cerebrovascular disease prevention and management in middle-aged women. The results provide evidence to support a tailored cardio- cerebrovascular disease prevention and management program based on the related factors of disadvantaged groups and to establish strategies in educational and practical aspects.

2.
FEBS J ; 275(23): 5969-81, 2008 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-19021771

RESUMO

Hypoxic preconditioning may afford protection against subsequent lethal hypoxia. As hypoxic tolerance induces changes in the expression of genes involved in DNA damage and repair response pathways, we investigated whether DNA-dependent protein kinase (DNA-PK), one of the DNA double-strand break repair proteins, could be involved in hypoxic preconditioning-induced protective signaling cascades. We showed that induction of hypoxia-inducible factor-1alpha expression during hypoxic preconditioning by repeated hypoxic exposure was associated with increased mRNA and protein levels of DNA-PK catalytic subunit (DNA-PKcs) and Ku70/Ku80, the DNA-PK components, in human hepatoma HepG2 cells, followed by upregulation of Hsp70/Hsp90 and Bcl-2 and concurrent downregulation of Bax. Additionally, loss of DNA-PKcs led to attenuated expression of Hsp70/Hsp90, accelerated hypoxia-inducible factor-1alpha degradation, and increased susceptibility to hypoxia-induced cell death. We also found that the mRNA and protein levels of heat shock factor-1 (HSF1) were progressively increased with DNA-PK activation during hypoxic preconditioning, and inhibition of HSF1 function by KNK437 resulted in a significant decrease in the level of protein kinase Akt as well as of DNA-PKcs, with downregulation of Hsp70/Hsp90 and HIF-1alpha. Our results suggest the possibility that DNA-PK-mediated signaling pathway is required for the increase in HIF-1alpha expression through activation of HSF1 and subsequent upregulation of heat shock proteins after hypoxic reconditioning.


Assuntos
Proteína Quinase Ativada por DNA/metabolismo , Proteínas de Choque Térmico/metabolismo , Subunidade alfa do Fator 1 Induzível por Hipóxia/metabolismo , Animais , Antígenos Nucleares/genética , Antígenos Nucleares/metabolismo , Apoptose/efeitos dos fármacos , Apoptose/genética , Apoptose/fisiologia , Compostos Benzidrílicos/farmacologia , Western Blotting , Hipóxia Celular/fisiologia , Linhagem Celular Transformada , Linhagem Celular Tumoral , Células Cultivadas , Inibidores de Cisteína Proteinase/farmacologia , Proteína Quinase Ativada por DNA/genética , Proteínas de Ligação a DNA/genética , Proteínas de Ligação a DNA/metabolismo , Proteínas de Choque Térmico HSP70/metabolismo , Proteínas de Choque Térmico HSP90/metabolismo , Fatores de Transcrição de Choque Térmico , Proteínas de Choque Térmico/genética , Humanos , Subunidade alfa do Fator 1 Induzível por Hipóxia/genética , Autoantígeno Ku , Camundongos , Camundongos Knockout , Camundongos SCID , Fosforilação/efeitos dos fármacos , Ligação Proteica/efeitos dos fármacos , Proteínas Proto-Oncogênicas c-bcl-2/genética , Proteínas Proto-Oncogênicas c-bcl-2/metabolismo , Pirrolidinonas/farmacologia , Reação em Cadeia da Polimerase Via Transcriptase Reversa , Fatores de Transcrição/genética , Fatores de Transcrição/metabolismo , Proteína X Associada a bcl-2/genética , Proteína X Associada a bcl-2/metabolismo
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