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1.
Eur J Intern Med ; 82: 105-111, 2020 12.
Artigo em Inglês | MEDLINE | ID: mdl-33067121

RESUMO

BACKGROUND: In the mobile Atrial Fibrillation App (mAFA)-II trial, the use of mobile health (mHealth) technology, incorporating AF screening and integrated management strategy, was associated with improved short-term clinical outcomes. The aim of this study was to report adherence/persistence and long term (≥1 year) clinical outcomes of the mAFA-II trial, with mHealth-supported optimised stroke prevention, symptom control and comorbidity management. METHODS: We studied an adult population screened for AF, where identified patients could enter a structured program of holistic and integrated care based on the ABC (Atrial fibrillation Better Care) pathway using mHealth with a mAFA intervention. In this cluster randomised trial, comparing mHeath intervention to usual care, the primary composite outcome was 'stroke/thromboembolism, all-cause death and rehospitalization'. RESULTS: The 1261 subjects (mean age 67.0 years, 38.0% female) who were followed up over one year (mean follow-up 687 (standard deviation, SD 191) days) in the intervention arm, had a lower risk of the composite outcome of 'ischaemic stroke/systemic thromboembolism, death, and rehospitalization' (hazard ratio, HR 0.18, 95% confidence interval, CI: 0.13-0.25, P < 0.001), compared to usual care (1212 subjects, mean age 70.1 years, 42.1% female). Of 842 patients using their smart devices for 'Better symptom management', 70.8% had good management adherence (monitoring time/follow-up since initial monitoring ≥ 70%), with the persistence of use of 91.7%. CONCLUSION: Amongst AF patients with long term use (≥1 year) of mHealth technology for optimising stroke prevention, symptom control and comorbidity management, adherence/persistence was good and associated with a reduction in adverse clinical outcomes.


Assuntos
Fibrilação Atrial , Isquemia Encefálica , Prestação Integrada de Cuidados de Saúde , Acidente Vascular Cerebral , Telemedicina , Adulto , Idoso , Anticoagulantes , Fibrilação Atrial/diagnóstico , Tecnologia Biomédica , Feminino , Humanos , Fatores de Transcrição Maf Maior , Masculino , Tecnologia
2.
Int J Colorectal Dis ; 25(12): 1407-15, 2010 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-20730438

RESUMO

INTRODUCTION: Tea polyphenol has been shown to have anti-colorectal cancer and anti-gene mutation effects, although the mechanism of inhibition of microsatellite instability (MSI) colorectal cancer is not known. MATERIALS AND METHODS: Using LoVo, HCT-116, HT-29, and SW480 cells treated with an aqueous solution of tea polyphenol, cell proliferation was detected by the methyl thiazolyl tetrazolium method, changes in microsatellite sequences by the Genescan method and changes in the gene expression of LoVo cells using Illumina expression arrays. RESULTS: The proliferation inhibition rate of LoVo, HCT-116, HT-29, and SW480 cells treated with tea polyphenol increased with increasing drug concentration and showed an increasing tendency with time. The proliferation inhibition rate of LoVo and HCT-116 cells with tea polyphenols was higher than that of HT-29 and SW480 cells, and there was a significant difference in the proliferation inhibition rate at 24, 72 h and 1 week. The microsatellite sequence of LoVo cells treated with tea polyphenols remained stable. DISCUSSION: The gene expression arrays and quantitative RT-PCR suggested that tea polyphenol inhibited the gene expression of metallothionein 2A (MT2A), transcription factor (MAFA), hairy and enhancer of split 1 (HES1), and jagged1 (JAG1) nearly twofold over controls. It was also found that tea polyphenol inhibited the BAX and p38 genes with a more than twofold difference but did not significantly inhibited the NFκB pathway. CONCLUSION: Tea polyphenol significantly inhibited the proliferation of MSI colorectal cancer signals maintained stable at the microsatellite state in MSI colorectal cancer. Tea polyphenol inhibited the gene expression of HES1, JAG1, MT2A, and MAFA but upregulated the gene expression of BAX and downregulated that of (P)38. Further research is required to investigate how these pathways are interrelated.


Assuntos
Neoplasias Colorretais/tratamento farmacológico , Flavonoides/farmacologia , Regulação Neoplásica da Expressão Gênica , Instabilidade de Microssatélites/efeitos dos fármacos , Fenóis/farmacologia , Fatores de Transcrição Hélice-Alça-Hélice Básicos/genética , Proteínas de Ligação ao Cálcio/genética , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Neoplasias Colorretais/patologia , Relação Dose-Resposta a Droga , Proteínas de Homeodomínio/genética , Humanos , Peptídeos e Proteínas de Sinalização Intercelular/genética , Proteína Jagged-1 , Fatores de Transcrição Maf Maior/genética , Proteínas de Membrana/genética , Metalotioneína/genética , Polifenóis , Proteínas Serrate-Jagged , Chá/química , Fatores de Transcrição HES-1 , Proteína X Associada a bcl-2/genética , Proteínas Quinases p38 Ativadas por Mitógeno/genética
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