Objectives: Caregiving stress process models suggest that heterogeneous contexts differentially contribute to caregivers' experiences of role overload and gains. End-of-life (EOL) caregivers, especially EOL dementia caregivers, facing unique challenges and care tasks, may experience role overload and gains in different ways than other caregivers. This study evaluates measurement invariance of role overload and gains between EOL caregivers and non-EOL caregivers and between EOL dementia and EOL non-dementia caregivers.
Methods: We utilized role gains and overload data from 1,859 family caregivers who participated in Round 7 of the National Study of Caregiving. We ran confirmatory factor analyses to investigate the factorial structure across all caregivers and then examined the structure's configural, metric, and scalar invariance between (a) EOL caregivers and non-EOL caregivers and (b) EOL dementia and EOL non-dementia caregivers.
Results: Across the entire sample, the two-factor overload and gains model had good fit (χ 2(19) = 121.37, p < .0001; RMSEA = .053, 90% CI = [.044, .062]; CFI = .954; TLI = .932). Tests of invariance comparing EOL caregivers to non-EOL caregivers and EOL dementia caregivers to EOL non-dementia caregivers maintained configural, metric, and partial scalar invariance. Latent mean comparisons revealed that EOL caregivers had higher role overload (p = .0002), but no different role gains (p = .45), than non-EOL caregivers. Likewise, EOL dementia caregivers had higher role overload (p = .05), but no different role gains (p = .42), than EOL non-dementia caregivers.
Discussion: Results offer both a deeper theoretical understanding of end-of-life dementia caregivers' experiences of role overload and gains, and a practical tool to measure those experiences.
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http://dx.doi.org/10.1093/geronb/gbac145 | DOI Listing |
Am J Physiol Heart Circ Physiol
January 2025
Department of Medicine, Division of Cardiovascular Disease, The University of Alabama at Birmingham, Birmingham, AL-35233.
Heart failure (HF) is a leading cause of death worldwide. We have shown that pressure overload (PO)-induced inflammatory cell recruitment leads to heart failure in IL-10 knockout (KO) mice. However, it's unclear if PO-induced inflammatory cells also target the gut mucosa, causing gut dysbiosis and leakage.
View Article and Find Full Text PDFFront Endocrinol (Lausanne)
January 2025
Inner Mongolia Key Laboratory of Disease-Related Biomarkers, The Second Affiliated Hospital, Baotou Medical College, Baotou, China.
Cardiac hypertrophy is an adaptive response to pressure or volume overload such as hypertension and ischemic heart diseases. Sustained cardiac hypertrophy eventually leads to heart failure. The pathophysiological alterations of hypertrophy are complex, involving both cellular and molecular systems.
View Article and Find Full Text PDFCirc Res
January 2025
Key Laboratory of Drug Targets and Translational Medicine for Cardio-cerebrovascular Diseases, Key Laboratory of Targeted Intervention of Cardiovascular Disease, Collaborative Innovation Center for Cardiovascular Disease Translational Medicine, The Affiliated Suzhou Hospital of Nanjing Medical University, Suzhou Municipal Hospital, Gusu School, Nanjing Medical University, Jiangsu, China (X.T., X.L., X.S., Y. Zhang, Y. Zu, Q.F., L.H., S.S., F.C., L.X., Y.J.).
Background: The decrease in S-nitrosoglutathione reductase (GSNOR) leads to an elevation of S-nitrosylation, thereby exacerbating the progression of cardiomyopathy in response to hemodynamic stress. However, the mechanisms under GSNOR decrease remain unclear. Here, we identify NEDD4 (neuronal precursor cell expressed developmentally downregulated 4) as a novel molecule that plays a crucial role in the pathogenesis of pressure overload-induced cardiac hypertrophy, by modulating GSNOR levels, thereby demonstrating significant therapeutic potential.
View Article and Find Full Text PDFFront Pharmacol
January 2025
Department of Emergency Intensive Care Unit, The First Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.
Introduction: In patients with acute respiratory distress syndrome, mechanical ventilation often leads to ventilation-induced lung injury (VILI), which is attributed to unphysiological lung strain (UPLS) in respiratory dynamics. Platelet endothelial cell adhesion molecule-1 (PECAM-1), a transmembrane receptor, senses mechanical signals. The Src/STAT3 pathway plays a crucial role in the mechanotransduction network, concurrently triggering pyroptosis related inflammatory responses.
View Article and Find Full Text PDFFront Cardiovasc Med
January 2025
School of Cardiovascular Medicine & Sciences, Faculty of Life Sciences & Medicine, King's College London, London, United Kingdom.
Aortic stenosis (AS) was historically considered a disease of the left side of the heart, with the main pathophysiological impact being predominantly on the left ventricle (LV). However, progressive pressure overload in AS can initiate a cascade of extra-valvular myocardial remodeling that could also precipitate maladaptive alterations in the structure and function of the right ventricle (RV). The haemodynamic and clinical importance of these changes in patients with AS have been largely underappreciated in the past.
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