Mapping the Cardiometabolic Patient Experience and Self-Care Behaviors to Inform Design, Implementation, and Persistent Use of Digital Health Care Solutions: Mixed Methods Study.

BACKGROUND: Cardiometabolic conditions including acute coronary syndrome (ACS) and type 2 diabetes (T2D) require comprehensive care and patient engagement in self-care behaviors, and the drivers of those behaviors at the individual and health system level are still poorly understood. OBJECTIVE: We aim to gain insights into self-care behaviors of individuals with cardiometabolic conditions. METHODS: A convenience sample of 98 adult patients with ACS and T2D was recruited in the United States, Germany, and Taiwan to participate in a mixed methods study using ethnographic methods. All participants completed 7-day web-based diaries tracking their level of engagement, and 48 completed 90-minute web-based semistructured interviews between February 4, 2021, and March 27, 2021, focusing on themes including moments of engagement. Qualitative analysis identified factors influencing self-care practices and a Patient Mind States Model prototype. RESULTS: Patient reports indicate that many patients feel social pressure to adhere to treatment. Patients' experience can be understood within 5 categories defined in terms of their degree of engagement and adherence ("ignoring," "struggling," "juggling," "controlling," and "reframing"). CONCLUSIONS: For people living with ACS and T2D, the self-care journey is defined by patterns of patient experiences, which can identify areas that tailored digital health care interventions may play a meaningful role.

Peroxisome proliferator-activated receptor-γ agonist rosiglitazone prevents albuminuria but not glomerulosclerosis in experimental diabetes.

BACKGROUNDS/AIMS: Renal inflammation and nephrin downregulation contribute to albuminuria in diabetes. We studied, in streptozotocin-induced diabetic rats, the effect of rosiglitazone (RSG), a peroxisome proliferator-activated receptor-γ agonist, on renal macrophage infiltration, MCP1, and nephrin expression in relation to albuminuria. METHODS: We investigated control and diabetic rats treated or untreated with RSG. Animals were sacrificed at 1, 3, and 9 months. Renal MCP1 and nephrin expression were studied by immunoblotting, renal macrophage infiltration by immunohistochemistry, and albuminuria by ELISA. Electron microscopy was used to assess glomerular ultrastructural morphology. In vitro experiments were conducted in isolated cultured rat glomeruli. RESULTS: Glycaemic control was similar in diabetic rats treated and untreated with RSG, and blood pressure was comparable in all groups. RSG prevented diabetes-induced albuminuria at 9 months, and renal macrophage infiltration and MCP1 upregulation at 3 and 9 months. Diabetes-mediated nephrin downregulation was abolished by RSG. Diabetes-induced glomerulosclerosis, glomerular basement membrane thickening, and foot process fusion were not affected by RSG. In isolated glomeruli, MCP1 directly induced nephrin downregulation and this was prevented by RSG. RSG had no effect on nephrin expression. CONCLUSION: RSG prevents albuminuria and nephrin downregulation in experimental diabetes independently of glycaemic and blood pressure control. This effect likely occurs via correction of diabetes-induced inflammatory processes.

Circulating vascular progenitor cells in patients with type 1 diabetes and microalbuminuria.

OBJECTIVE: Patients with type 1 diabetes and microalbuminuria are at increased risk of cardiovascular disease (CVD). Abnormalities in vascular progenitor cells, which participate in vascular repair, may be implicated in this susceptibility. RESEARCH DESIGN AND METHODS: We studied the number and function of vascular progenitor cells in 22 type 1 diabetic patients with history of microalbuminuria (MA(+)) and 22 type 1 diabetic patients without history of microalbuminuria (MA(-)), of similar age, diabetes duration, glycemic control, renal function, and no history of CVD. RESULTS: MA(+) patients had lower circulating CD34(+) and CD34(+)/CD133(+) cell numbers compared with MA(-) patients (P < 0.006). In in vitro functional assays, MA(+) patients had a significantly lower number of colony-forming units and impaired vascular endothelial growth factor (VEGF)-A-mediated tube formation, when compared with MA(-) patients (P < 0.01). CONCLUSIONS: In type 1 diabetic patients with microalbuminuria, a marker of microvascular injury and a risk factor for CVD, circulating vascular progenitor cell number is reduced and function is impaired.

Mechanical forces and TGFbeta1 reduce podocyte adhesion through alpha3beta1 integrin downregulation.

BACKGROUND: Podocyturia is a marker of diabetic nephr- opathy, a possible determinant of its progression and a powerful risk factor for cardiovascular disease. A reduction in podocyte adhesion to the glomerular basement membrane (GBM) via downregulation of alpha3beta1 integrin expression, the main podocyte anchoring dimer to the GBM, may represent one of the mechanisms of podocyturia in glomerular disease. This study investigated the role of mechanical forces and transforming growth factor beta1 (TGFbeta1) in podocyte adhesion and integrin expression. METHODS: Conditionally immortalized murine podocytes were exposed to mechanical stretch and/or TGFbeta1 for 48 h. Podocyte adhesion, apoptosis and alpha3beta1 integrin expression were assessed. RESULTS: Stretch and TGFbeta1 significantly reduced podocyte adhesion and alpha3beta1 integrin expression, events paralleled by increased apoptosis. Blockade of beta1 integrin, with a specific antibody, demonstrated a reduced podocyte adhesion indicating that beta1 integrin downregulation was required for the loss of podocyte adhesion. This was linked to an increase in podocyte apoptosis. The role of apoptosis in podocyte adhesion was further investigated using caspase-3 inhibitors. Podocyte apoptosis inhibition did not affect stretch- and TGFbeta1-mediated integrin downregulation and the loss of podocyte adhesion, suggesting that alpha3beta1 integrin downregulation is sufficient to alter cell adhesion. Although stretch significantly increased podocyte TGFbeta type I, II and III receptors but not podocyte TGFbeta1 secretion, the combination of stretch and TGFbeta1 did not show any additive or synergistic effects on podocyte adhesion and alpha3beta1 integrin expression. CONCLUSIONS: These results suggest that downregulation of alpha3beta1 integrin expression, by mechanical forces or TGFbeta1, is per se sufficient to reduce podocyte adhesion. Apoptosis may represent a parallel important determinant of the podocyte loss from the GBM.