Patients\u27 and caregivers\u27 inside perspectives: living with a left-ventricular assist device as destination therapy

Left-ventricular assist devices (LVADs) have improved the quality of life for many patients with advanced heart failure. Past research focused on technology issues and survival rates, but patients\u27 and caregivers\u27 perspectives of living with an LVAD as a destination therapy (e.g., permanent alternative to transplant) was not explored. Roy\u27s adaptation model provided a framework to guide an understanding of how participants adjusted and accepted living with destination therapy. A hermeneutic-phenomenology as described by van Manen was used to explore and describe the essence of destination therapy from patients\u27 and caregivers\u27 perspectives in order to understand the meaning of this experience. Data saturation was achieved with 14 participants (7 men as patients, 71-76 years old; 1 man and 6 women as caregivers, 50-74 years old), who lived with destination therapy at home. Data was collected using open-ended interviews, thematic analysis was ongoing, and final themes were consensually validated. Procedures to ensure trustworthiness are described. Themes were consistent with Roy\u27s adaptation model. Participants illustrated a process of adjustment and eventually accepted the LVAD as part of their lives. Patients adjusted to the LVAD as part of their bodies, accepted the device as necessary to live, and exhibited an improved quality of life. Caregivers described persistent worry and stress and accepted caregiving as part of life. Dyadic perspectives reflected gratefulness for more time to live despite uncertainties about death and dying. Findings advance the knowledge of destination therapy management. These findings may direct a holistic approach to palliative and end of life care, and can heighten nurses\u27 awareness about the process of adaptation as a vital component for the promotion and maintenance of health and well-being among this growing population. Key words: left-ventricular assist devices, destination therapy, caregivers, hermeneutic phenomenology, Roy Adaptation Model

Phylogenesis and Clinical Aspects of Pandemic 2009 Influenza A (H1N1) Virus Infection

During the spring of 2009, a new influenza A (H1N1) virus of swine origin emerged and spread worldwide causing a pandemic influenza. Here, 329 naso-pharyngeal swabs collected from patients with flu-like symptoms were analyzed by real-time PCR for the presence of H1N1 2009 pandemic virus. Twenty-five samples collected from immunocompetent and immunodepressed patients contained the H1N1 pandemic virus. Phylogenetic analysis of the hemagglutinin and neuraminidase genes showed no obvious differences in terms of similarity and/or homology between the sequences identified in immunocompetent individuals and those obtained from immunocompromised patients. Pre-existing clinical conditions may influence the outcome of H1N1 disease

Modeling focal epileptic activity in the Wilson-Cowan model with depolarization block

Measurements of neuronal signals during human seizure activity and evoked epileptic activity in experimental models suggest that, in these pathological states, the individual nerve cells experience an activity driven depolarization block, i.e. they saturate. We examined the effect of such a saturation in the Wilson–Cowan formalism by adapting the nonlinear activation function; we substituted the commonly applied sigmoid for a Gaussian function. We discuss experimental recordings during a seizure that support this substitution. Next we perform a bifurcation analysis on the Wilson–Cowan model with a Gaussian activation function. The main effect is an additional stable equilibrium with high excitatory and low inhibitory activity. Analysis of coupled local networks then shows that such high activity can stay localized or spread. Specifically, in a spatial continuum we show a wavefront with inhibition leading followed by excitatory activity. We relate our model simulations to observations of spreading activity during seizures

Spatiotemporal coordination of rod and cone photoreceptor differentiation in goldfish retina

In this study, we have compared spatial and temporal aspects of development of new rods and cones in the adult goldfish by using a combination of bromodeoxyuridine immunocytochemistry and opsin in situ hybridization to determine the intervals between terminal mitosis (cell “birth”) and expression of opsin mRNA for each photoreceptor cell type. The goldfish opsins include rod opsin and four different cone opsins: red, green, blue, and ultraviolet. In a cohort of photoreceptors born at the same time, rods expressed opsin mRNA within 3 days of cell birth, while expression of cone opsin mRNA required at least 7 days. This temporal discrepancy in differentiation, coupled with a discordance in the site of cell genesis of rods and cones, allowed opsin expression to commence in both cell types in approximately the same retinal location. Commitment to the generic cone phenotype occurred within approximately 6 days throughout the cone cohort, as indicated by expression of interphotoreceptor retinoid-binding protein (IRBP) mRNA, but expression of a specific spectral phenotype was delayed until rods differentiated nearby. Onset of expression of cone opsin mRNA followed a phenotype-specific sequence: red, then green, then blue, and finally ultraviolet; in situ hybridization with two opsin probes confirmed that individual photoreceptors expressed only one type of opsin as they differentiated. This stepwise process of cone differentiation is consistent with the hypothesis that cell-cell interactions among developing photoreceptors may coordinate selection of specific photoreceptor phenotypes. J. Comp. Neurol. 382:272-284, 1997. © 1997 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/34448/1/10_ftp.pd

A study of knowledge and attitudes concerning the mentally retarded

There is no abstract available for this research paper.Thesis (M.A.

NAFLD and Chronic Kidney Disease

Non-alcoholic fatty liver disease (NAFLD) is the most common cause of chronic liver disease in developed countries and it is now considered a risk factor for cardiovascular disease. Evidence linking NAFLD to the development and progression of chronic kidney disease (CKD) is emerging as a popular area of scientific interest. The rise in simultaneous liver-kidney transplantation as well as the significant cost associated with the presence of chronic kidney disease in the NAFLD population make this entity a worthwhile target for screening and therapeutic intervention. While several cross-sectional and case control studies have been published to substantiate these theories, very little data exists on the underlying cause of NAFLD and CKD. In this review, we will discuss the most recent publications on the diagnosis of NAFLD as well new evidence regarding the pathophysiology of NAFLD and CKD as an inflammatory disorder. These mechanisms include the role of obesity, the renin-angiotensin system, and dysregulation of fructose metabolism and lipogenesis in the development of both disorders. Further investigation of these pathways may lead to novel therapies that aim to target the NAFLD and CKD. However, more prospective studies that include information on both renal and liver histology will be necessary in order to understand the relationship between these diseases