RESUMEN
BACKGROUND: Type D personality, a newly specified personality type defined as the interaction of high levels of negative affectivity and social inhibition, is associated with poor health outcomes. Few interventional studies have been performed to improve health outcomes in this subpopulation. PURPOSE: This study was developed to examine the effects of an educational intervention on psychological health, health-promoting behaviors, and quality of life in coronary heart disease (CHD) patients with type D personality in China. METHODS: A randomized controlled trial was adopted. One hundred twenty-eight patients with CHD and type D personality were randomly assigned. The intervention group received the 12-week educational intervention in addition to usual care, whereas the control group received usual care only. Data on anxiety and depression, health-promoting behaviors, and quality of life were collected at baseline and at 1 and 3 months after enrollment. After controlling for the covariates, the generalized estimating equation model was used to examine the intervention effects. RESULTS: The mean age of the participants was 61.02 years, and more than 70% were male. Results of the generalized estimating equation analysis showed significantly greater improvements in anxiety, depression, and health-promoting behaviors in the intervention group than in the control group. In addition, quality of life, the domains of angina limitation, angina stability, and treatment satisfaction were found to have improved more significantly in the intervention group than the control group, whereas the posttest changes in angina frequency and disease perception were found to be similar in both groups. CONCLUSIONS/IMPLICATIONS FOR PRACTICE: The educational intervention was shown to be effective in improving psychological health, health-promoting behaviors, and certain domains of quality of life in patients with CHD and type D personality. Nurses should identify patients with this personality type and provide tailored care to improve their health outcomes in clinical practice.
Asunto(s)
Enfermedad Coronaria , Educación del Paciente como Asunto , Distrés Psicológico , Personalidad Tipo D , Femenino , Humanos , Masculino , Persona de Mediana Edad , Ansiedad , Enfermedad Coronaria/psicología , Salud Mental , Calidad de VidaRESUMEN
Purpose: To understand existing negative emotions in patients with coronary heart disease after percutaneous coronary stent implantation (PCI) and analyse its influencing factors. Methods: Patients with coronary heart disease after PCI in three tertiary hospitals in Changsha City from April to September 2018 were selected as the research subjects. The self-designed general information questionnaire assessed irritability, depression and anxiety (IDA) on a self-rating scale. It was used to examine patients' existing negative emotions with coronary heart disease after PCI and analyse the influencing factors. Results: 203 questionnaires were distributed, and 202 valid questionnaires were recovered, with an effective recovery rate of 99.5%. The IDA score of patients with coronary heart disease after PCI was 17.01±7.60 points, the incidence of negative emotions was 63.8%, and the incidences of depression, anxiety and irritability were 39.6%, 8.4% and 15.8%, respectively. Negative emotion was taken as the dependent variable and a patient's general data, such as lifestyle and disease, as the independent variables. A univariate analysis was conducted to obtain gender, age, educational level, marital status, work status, per capita monthly household income, sleep status, etc. Seven factors were identified as the influencing factors of negative emotions in patients with coronary heart disease after PCI, and the difference was statistically significant (P<0.05). Conclusion: Most patients with coronary heart disease after PCI tend to exhibit negative emotions such as anxiety and depression. Medical staff should attach great importance to evaluating any negative feelings in this group and take timely targeted intervention measures to prevent and mitigate the occurrence and development of these adverse emotions in patients with coronary heart disease after PCI.
RESUMEN
Glioma is characterized by high morbidity, high mortality and poor prognosis. Recent studies exhibited that lncRNA CCAT2 is overexpressed in glioma and promotes glioma progression, but the specific molecular biological mechanism remains to be determined. We performed qRT-PCR to evaluate the expression of related genes, Western blotting analysis to measure protein levels, colony formation assay to detect the proliferative ability of glioma cells, flow cytometry to measure cell apoptosis, bioinformatics analysis and dual luciferase assay to verify the binding sites and the targeted regulatory relationship in A172 and U251 cell lines and tube formation assay to determine endothelial angiogenesis. LncRNA CCAT2 and VEGFA were highly expressed, while miR-424 was expressed at low levels in NHA cells. Furthermore, knockdown of lncRNA CCAT2 decreased cell proliferation, increased cell apoptosis and inhibited endothelial angiogenesis in glioma. Moreover, lncRNA CCAT2 shared a complementary sequence with miR-424 which in turn directly bound to the 3'-UTR of VEGFA. Further investigation indicated that lncRNA CCAT2 promoted cell proliferation and endothelial angiogenesis by inducing the PI3K/AKT signalling pathway in glioma. The oncogenic lncRNA CCAT2 is highly associated with the development of glioma and exerts its function by upregulating VEGFA via miR-424.
Asunto(s)
Regulación Neoplásica de la Expresión Génica/genética , Glioma/metabolismo , MicroARNs/metabolismo , Neovascularización Patológica/metabolismo , ARN Largo no Codificante/metabolismo , Factor A de Crecimiento Endotelial Vascular/metabolismo , Regiones no Traducidas 3' , Apoptosis/genética , Línea Celular Tumoral , Proliferación Celular/genética , Células Endoteliales/metabolismo , Técnicas de Silenciamiento del Gen , Glioma/genética , Humanos , MicroARNs/genética , Neovascularización Patológica/genética , Oncogenes/genética , Fosfatidilinositol 3-Quinasas/metabolismo , Proteínas Proto-Oncogénicas c-akt/metabolismo , ARN Largo no Codificante/genética , ARN Interferente Pequeño , Transducción de Señal/genética , Regulación hacia Arriba , Factor A de Crecimiento Endotelial Vascular/genéticaRESUMEN
BACKGROUND: Glioma is a common malignant tumor of the human central nervous system, and the pathological characteristics include invasive growth, angiogenesis, and so on. Ectopic expression of miR-503 works as a critical factor in cancer cell proliferation, migration, and capillary-like tube formation. The potential mechanisms of miR-503 in angiogenesis of glioma cells are still not reported. METHODS: The expression levels of miR-503, LRIG2, and VEGFA mRNA and protein were performed by quantitative reverse transcription-PCR or Western blot assay. Dual-Luciferase reporter gene assay was used to determine the interaction between miR-503 and LRIG2. The concentration of VEGFA was measured using the ELISA method. The cell proliferation, migration, and angiogenesis of cocultured HCMEC/D3 cells were analyzed by MTT assay, transwell detection, and tube formation assay, respectively. RESULTS: The expression levels of LRIG2 and VEGFA were reduced in glioma cells with miR-503 overexpression and enhanced with miR-503 inhibition. Moreover, cell proliferation, migration, and angiogenesis of cocultured HCMEC/D3 cells were alleviated with miR-503 mimics transfection. VEGFA and miR-503 inhibitor promoted cell proliferation, cell migration, and angiogenesis. Luciferase reporter gene assay revealed that miR-503 could directly target LRIG2. Furthermore, knockdown of LRIG2 or addition of VEGF inhibitor bevacizumab could abrogate the effect of miR-503 inhibitor on VEGFA expression, as well as the promotion of cell proliferation, migration, and angiogenesis. CONCLUSION: MiR-503 mediated LRIG2 suppression and regulated the expression of VEGFA, thereby reducing cell proliferation, migration, and angiogenesis of glioma cells. These results provide new insight into the action mechanism of miR-503-modulated signaling pathway in angiogenesis of glioma cells.