Poor Sleep and Impaired Self-Care: Towards a Comprehensive Model Linking Sleep, Cognition, and Heart Failure Outcomes

Background: Persons with heart failure (HF) have significantly lower sleep quantity and quality than persons without HF. The purpose of this article is to propose a conceptual model describing how poor sleep may contribute to inadequate self-care and untoward outcomes in persons with HF. Aims: Our overarching hypothesis is that sleep affects self-care and outcomes through its effects on cognition. Building on the work of others, we outline a conceptual model that illustrates that even transient sleep disruption prevents sleep-related restorative processes and contributes to cognitive dysfunction—especially in the 25–50% of HF patients with existing cognitive impairment. Poor sleep may be sufficient to impair cognition to a level that interferes with higher order functions involved in effective HF self-care practices. Through these mechanisms, inadequate sleep may contribute to poor outcomes such as low health-related quality of life and greater risk of unplanned hospitalization. Conclusion: The proposed model (1) bridges physical, neuropsychological and behavioral phenomena, (2) suggests a mechanism by which poor sleep affects daytime behavior, and (3) is empirically testable. Exploring factors that interfere with sleep may improve self-care and outcomes in persons with HF

Micro-Ethical Decision Making Among Baccalaureate Nursing Students: A Qualitative Investigation

Nursing students frequently encounter micro-ethical nursing practice problems during their clinical experience. The purpose of this study was to understand the lived experiences of senior-level baccalaureate students faced with making micro-ethical clinical decisions in practice settings. A descriptive qualitative design was used, and five central themes emerged. A dominant finding was the experience of unapplied and forgotten ethics education revealing a mismatch between what faculty perceived was taught and students’ experiences of that education. When faced with micro-ethical decisions, participants trusted and deferred to staff nurse recommendations, even if the advice contradicted best-practice standards. Contextual naivete was brought out of concealment, contributing to the experience of moral disequilibrium (i.e., students felt conflicted about what they learned in school as best practice and what they observed being role modeled in the clinical environment). This study resulted in theory-guided implications for nursing education and recommendations for future study

Weak Localization Effect in Superconductors by Radiation Damage

Large reductions of the superconducting transition temperature $T_{c}$ and the accompanying loss of the thermal electrical resistivity (electron-phonon interaction) due to radiation damage have been observed for several A15 compounds, Chevrel phase and Ternary superconductors, and $\rm{NbSe_{2}}$ in the high fluence regime. We examine these behaviors based on the recent theory of weak localization effect in superconductors. We find a good fitting to the experimental data. In particular, weak localization correction to the phonon-mediated interaction is derived from the density correlation function. It is shown that weak localization has a strong influence on both the phonon-mediated interaction and the electron-phonon interaction, which leads to the universal correlation of $T_{c}$ and resistance ratio.Comment: 16 pages plus 3 figures, revtex, 76 references, For more information, Plesse see http://www.fen.bilkent.edu.tr/~yjki

Resonant and off-resonant transients in electromagnetically induced transparency: Turn-on and turn-off dynamics

Published versio

Mutations in NR2E3 can cause dominant or recessive retinal degenerations in the same family.

NR2E3, a photoreceptor-specific nuclear receptor (PNR), represses cone-specific genes and activates several rod-specific genes. In humans, mutations in NR2E3 have been associated with the recessively-inherited enhanced short-wavelength sensitive S-cone syndrome (ESCS) and, recently, with autosomal dominant (ad) retinitis pigmentosa (RP) (adRP). In the present work, we describe two additional families affected by adRP that carry a heterozygous c.166G>A (p.G56R) mutation in the NR2E3 gene. Functional analysis determined the dominant negative activity of the p.G56R mutant protein as the molecular mechanism of adRP. Interestingly, in one pedigree, the most common causal variant for ESCS (p.R311Q) cosegregated with the adRP-linked p.G56R mutation, and the compound heterozygotes exhibited an ESCS-like phenotype, which in 1 of the 2 cases was strikingly "milder" than the patients carrying the p.G56R mutation alone. Impaired repression of cone-specific genes by the corepressors atrophin-1 (dentatorubral-pallidoluysian atrophy [DRPLA] gene product) and atrophin-2 (arginine-glutamic acid dipeptide repeat [RERE] protein) appeared to be a molecular mechanism mediating the beneficial effect of the p.R311Q mutation. Finally, the functional dominance of the p.R311Q variant to the p.G56R mutation is discussed