Recovery experiences of younger stroke survivors who are parents: A qualitative content analysis.

AIMS AND OBJECTIVES: To explore the experience of parenting for younger stroke survivors (aged 18 to 64 years at the time of the stroke). BACKGROUND: Stroke among younger adults increased 43% between 2000 and 2010. The social, emotional and physical functioning of younger adults affects multiple aspects of their lives including parenting. There is limited research on the experience of parenting after stroke. DESIGN: This is a qualitative descriptive study. METHODS: We conducted individual semi-structured interviews with 10 younger adults who were actively parenting children under the age of 18 years at the time of stroke. Conventional content analysis was used to analyse the data. We report the methods and results using the COREQ checklist. RESULTS: Impairments from stroke disrupted participants' identity, relationships and roles as a parent. The degree to which parenting abilities and behaviours were affected by stroke was contingent upon the type and severity of impairments as well as the children's age. Participants also observed emotional and behavioural changes in their children in response to their stroke. Support from family, friends, healthcare providers and children's school/day care was crucial to participants throughout their stroke recovery. Two major themes emerged: (a) finding a new normal; and (b) support for parenting post-stroke. CONCLUSIONS: Findings enable a deeper understanding of the distinct parenting challenges younger stroke survivors face and can inform future research on this population. RELEVANCE FOR CLINICAL PRACTICE: Study findings highlight the need for continual and tailored follow-up by nurses and other allied healthcare professionals to decrease the difficulty stroke survivors experience when trying to resume their role as parents.

Feasibility and Limitations of Proning Protocol for Nonintubated Patients With COVID-19.

Proning awake patients with COVID-19 is associated with lower mortality and intubation rates. However, these studies also demonstrate low participation rates and tolerance of awake proning. In this study, we attempt to understand barriers to proning. Medical and dental students surveyed nonintubated patients to understand factors affecting adherence to a proning protocol. Only patients who discussed proning with their medical team attempted the practice. Eight of nine patients who were informed about benefits of proning attempted the maneuver. Discomfort was the primary reason patients stopped proning. Addressing discomfort and implementing systematic patient education may increase adherence to proning.

Phosphatidylinositol-4,5-Bisphosphate Binding to Amphiphysin-II Modulates T-Tubule Remodeling: Implications for Heart Failure.

BIN1 (amphyphysin-II) is a structural protein involved in T-tubule (TT) formation and phosphatidylinositol-4,5-bisphosphate (PIP2) is responsible for localization of BIN1 to sarcolemma. The goal of this study was to determine if PIP2-mediated targeting of BIN1 to sarcolemma is compromised during the development of heart failure (HF) and is responsible for TT remodeling. Immunohistochemistry showed co-localization of BIN1, Cav1.2, PIP2, and phospholipase-Cß1 (PLCß1) in TTs in normal rat and human ventricular myocytes. PIP2 levels were reduced in spontaneously hypertensive rats during HF progression compared to age-matched controls. A PIP Strip assay of two native mouse cardiac-specific isoforms of BIN1 including the longest (cardiac BIN1 #4) and shortest (cardiac BIN1 #1) isoforms as well human skeletal BIN1 showed that all bound PIP2. In addition, overexpression of all three BIN1 isoforms caused tubule formation in HL-1 cells. A triple-lysine motif in a short loop segment between two helices was mutated and replaced by negative charges which abolished tubule formation, suggesting a possible location for PIP2 interaction aside from known consensus binding sites. Pharmacological PIP2 depletion in rat ventricular myocytes caused TT loss and was associated with changes in Ca2+ release typically found in myocytes during HF, including a higher variability in release along the cell length and a slowing in rise time, time to peak, and decay time in treated myocytes. These results demonstrate that depletion of PIP2 can lead to TT disruption and suggest that PIP2 interaction with cardiac BIN1 is required for TT maintenance and function.

T-tubule remodeling and increased heterogeneity of calcium release during the progression to heart failure in intact rat ventricle.

A highly organized transverse-tubule (TT) system is essential to normal Ca2+ cycling and cardiac function. We explored the relationship between the progressive disruption of TTs and resulting Ca2+ cycling during the development of heart failure (HF). Confocal imaging was used to measure Ca2+ transients and 2-D z-stack images in left ventricular epicardial myocytes of intact hearts from spontaneously hypertensive rats (SHR) and Wistar-Kyoto control rats. TT organization was measured as the organizational index (OI) derived from a fast Fourier transform of TT organization. We found little decrease in the synchrony of Ca2+ release with TT loss until TT remodeling was severe, suggesting a TT "reserve" characterized by a wide range of TT remodeling with little effect on synchrony of release but beyond which variability in release shows an accelerating sensitivity to TT loss. To explain this observation, we applied a computational model of spatially distributed Ca2+ signaling units to investigate the relationship between OI and excitation-contraction coupling. Our model showed that release heterogeneity exhibits a nonlinear relationship on both the spatial distribution of release units and the separation between L-type Ca2+ channels and ryanodine receptors. Our results demonstrate a unique relationship between the synchrony of Ca2+ release and TT organization in myocytes of intact rat ventricle that may contribute to both the compensated and decompensated phases of heart failure.