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1.
Ethn Dis ; 33(4): 180-193, 2023 Sep.
Artigo em Inglês | MEDLINE | ID: mdl-38854414

RESUMO

Introduction: Black and Hispanic adults are disproportionately burdened by cardiometabolic disorders. The aim of this systematic review was to examine the effectiveness of mobile health technologies to promote disease prevention and self-management among US adults in diverse communities. Methods: Potential studies were identified using a comprehensive search of the PubMed and EMBASE databases for recent studies published from December 2018 through 2021. Keywords and search strategies were established to focus on health disparity populations and the application of mobile health technology for cardiovascular disease risk reduction. Titles and abstracts were assessed and, if a study was eligible, 2 independent reviewers completed a full-length review with extraction in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines. Results: A total of 13 studies met our inclusion criteria. Study sample sizes ranged from 8 to 533 baseline participants. Studies were conducted in diverse communities (eg, North Carolina and California). Most studies used mobile applications (n=11) and a majority used accelerometers or similar technologies (eg, smartwatches) to assess changes in dietary behavior, blood pressure control, and physical activity. Overall, studies reported positive associations between mobile technology use and risk factor reduction actions and behaviors. Long-term adherence varied across studies. Those that prioritized culturally tailored approaches reported more significant impacts than those that did not. Conclusions: Evidence suggests that mobile technology may be useful in promoting disease self-management and risk reduction among populations at higher risk of cardiometabolic diseases. The use of mobile health technologies, particularly when tailored to target populations, may be a practical approach to advancing population health equity.


Assuntos
Doenças Cardiovasculares , Telemedicina , Humanos , Estados Unidos , Doenças Cardiovasculares/prevenção & controle , Doenças Cardiovasculares/etnologia , Aplicativos Móveis , Hispânico ou Latino/estatística & dados numéricos , Disparidades nos Níveis de Saúde , Disparidades em Assistência à Saúde/etnologia , Negro ou Afro-Americano
2.
Anticancer Res ; 37(2): 445-453, 2017 02.
Artigo em Inglês | MEDLINE | ID: mdl-28179289

RESUMO

BACKGROUND: Colorectal cancer is the third leading cause of cancer-related mortality in most developed countries. This mortality is mainly due to the metastatic progression to the liver with frequent recurrence. Colorectal cancer remains a therapeutic challenge and this has intensified the search for new drug targets. In an effort to establish a novel targeted-therapy, we studied the molecular mechanisms of cancer stem cell inhibitor salinomycin. MATERIALS AND METHODS: Co-immunoprecipitation was performed to examine STAT3-STAT1 protein interactions. Telomerase activity was measured by polymerase chain reaction (PCR) and ELISA assays. Apoptosis and cell stress arrays were analyzed to identify key proteins responding to salinomycin treatments. RESULTS: IL-6 and TNF-α induced STAT3 and STAT1 interactions, however the interactions were abolished by salinomycin challenge. Salinomycin reduced cancer stem cell phenotype and decreased telomerase activity of colorectal cancer cells. CONCLUSION: Our work uncovers a new mechanism through which salinomycin inhibits cancer stemness suggesting a novel targeted-therapy for metastatic colorectal cancer.


Assuntos
Neoplasias Colorretais/tratamento farmacológico , Piranos/farmacologia , Fator de Transcrição STAT1/antagonistas & inibidores , Fator de Transcrição STAT3/antagonistas & inibidores , Telomerase/antagonistas & inibidores , Benzamidas/farmacologia , Linhagem Celular Tumoral , Proliferação de Células/efeitos dos fármacos , Neoplasias Colorretais/enzimologia , Neoplasias Colorretais/metabolismo , Neoplasias Colorretais/patologia , Ensaio de Imunoadsorção Enzimática , Transição Epitelial-Mesenquimal , Células HT29 , Humanos , Imunoprecipitação , Interleucina-6/farmacologia , Fosforilação , Reação em Cadeia da Polimerase , Fator de Transcrição STAT1/metabolismo , Fator de Transcrição STAT3/metabolismo , Telomerase/metabolismo , Fator de Necrose Tumoral alfa/farmacologia , beta Catenina/biossíntese , Proteínas Quinases p38 Ativadas por Mitógeno/biossíntese
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