Phenomenon of ordinariness in nursing

This phenomenological research aimed to illuminate the nature and effects of ordinariness in nursing and to discover whether the phenomenon enhanced the nursing encounter. The researcher worked as a participant observer with six registered nurses in a Professorial Nursing Unit. Following each interaction, the researcher wrote her impressions in a personal-professional journal and audiotaped conversations with the respective nurses and patients to gain their impressions. Using a theoretical framework of the phenomenological concepts of lived experience, Dasein, Being-in-the-world and fusion of horizons as an underpinning methodology, an initial hermeneutical analysis and interpretation of the impressions generated qualities and activities indicative of the aspects of the phenomenon of ordinariness in nursing. The second phase of the analysis and interpretation sought to illuminate the nature of the phenomenon itself. Eight actualities of the nature of the phenomenon emerged: \u27allowingness,\u27 \u27straightforwardness,\u27 \u27self-likeness,\u27 \u27homeliness,\u27 \u27favourableness,\u27 \u27intuneness,\u27 \u27lightheartedness\u27 and \u27connectedness.\u27 These actualities were described in relation to the phenomenon of interest. The effects of the phenomenon were the creative potential to enhance the nursing encounter and included many and various effects of facilitation, fair play, familiarity, family, favouring, feelings, fun and friendship. The research found that nurses and patients shared a common sense of humanity, which enhanced the nursing encounter. Within the context of caring, the nurses were ordinary people, perceived as being extraordinarily effective, by the very ways in which their humanness shone through their knowledge and skills, to make their whole being with patients something more than just professional helping. The shared sense of ordinariness between nurses and patients made them as one in then- humanness and created a special place, in which the relative strangeness of the experience of being in a health care setting, could be made familiar and manageable

Brief of Professors at Law and Business Schools as \u3cem\u3eAmici Curiae\u3c/em\u3e in Support of Respondents: \u3cem\u3eOmnicare, Inc., et al. v. Laborers District Council Construction Industry Pension Fund, et al.\u3c/em\u3e

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Germline deletion of FAK-related non-kinase delays post-natal cardiomyocyte mitotic arrest

The cardiomyocyte phenotypic switch from a proliferative to terminally differentiated state impacts normal heart development and pathologic myocardial remodeling, yet the signaling mechanisms that regulate this vital process are incompletely understood. Studies from our lab and others indicate that focal adhesion kinase (FAK) is a critical regulator of cardiac growth and remodeling and we found that expression of the endogenous FAK inhibitor, FAK-related non kinase (FRNK) coincided with postnatal cardiomyocyte arrest. Mis-expression of FRNK in the embryonic heart led to pre-term lethality associated with reduced cardiomyocyte proliferation and led us to speculate that the postnatal FRNK surge might be required to promote quiescence in this growth promoting environment. Herein, we provide strong evidence that endogenous FRNK contributes to post-mitotic arrest. Depletion of FRNK promoted DNA synthesis in post-natal day (P) 10 hearts accompanied by a transient increase in DNA content and multi-nucleation by P14, indicative of DNA replication without cell division. Interestingly, a reduction in tri- and tetra-nucleated cardiomyocytes, concomitant with an increase in bi-nucleated cells by P21, indicated the possibility that FRNK-depleted cardiomyocytes underwent eventual cytokinesis. In support of this conclusion, Aurora B-labeled central spindles (a hallmark of cytokinesis) were observed in tetra-nucleated P20 FRNK−/− but not wt cardiomyocytes, while no evidence of apoptosis was observed. Moreover, hearts from FRNK null mice developed ventricular enlargement that persisted until young adulthood which resulted from myocyte expansion rather than myocyte hypertrophy or interstitial growth. These data indicate that endogenous FRNK serves an important role in limiting DNA synthesis and regulating the un-coupling between DNA synthesis and cytokinesis in the post-natal myocardium

Adhesion Stimulates Direct PAK1/ERK2 Association and Leads to ERK-dependent PAK1 Thr 212 Phosphorylation

The Rac1/Cdc42 effector p21-activated kinase (PAK) is activated by various signaling cascades including receptor-tyrosine kinases and integrins and regulates a number of processes such as cell proliferation and motility. PAK activity has been shown to be required for maximal activation of the canonical Ras/Raf/MEK/ERK Map kinase signaling cascade, likely because of PAK co-activation of Raf and MEK. Herein, we found that adhesion signaling also stimulates an association between PAK1 and ERK1/2. PAK1 and ERK1/2 co-immunoprecipitated from rat aortic smooth muscle cells (SMC) plated on fibronectin, and the two proteins co-localized in membrane ruffles and adhesion complexes following PDGF-BB or sphingosine 1-phosphate treatment, respectively. Far Western analysis demonstrated a direct association between the two proteins, and peptide mapping identified an ERK2 binding site within the autoinhibitory domain of PAK1. Interestingly, deletion of a major ERK binding site in PAK attenuates activation of an ERK-dependent serum-responsive element (SRE)-luciferase reporter gene, indicating that association between PAK and ERK is required to facilitate ERK signaling. We also show that ERK2 phosphorylates PAK1 on Thr(212) in vitro and that Thr(212) is phosphorylated in smooth muscle cells following PDGF-BB treatment in an adhesion- and MEK/ERK-dependent fashion. Expression of a phosphomimic variant, PAK-T212E, does not alter ERK association, but markedly attenuates downstream ERK signaling. Taken together, these data suggest that PAK1 may facilitate ERK signaling by serving as a scaffold to recruit Raf, MEK, and ERK to adhesion complexes, and that subsequent growth factor-stimulated phosphorylation of PAK-Thr(212) by ERK may serve to provide a negative feedback signal to control coordinate activation of ERK by growth factor- and matrix-induced signals

Empirical approach to the analysis of university student absenteeism. Proposal of a questionnaire for students to evaluate the possible causes

Works on student absenteeism in the universities have not been preferential for the authors in the field of educational research. Usually, what has been made is an approach to the available absenteeism data as an intervening variable or as a variable characteristic of the educational process, but not as a dependent variable in the strict sense of the term. In this work, we intend to make an empirical approach to the possible reasons of student absenteeism. There is a double point of view: the students" and the professors"; the reasons that justify it according to its protagonists are studied. This paper focuses on the six university degrees taught at the School of Economy and Business of the University of Barcelona (Facultat d"Economia i Empresa de la Universitat de Barcelona). An"ad-hoc" questionnaire has been prepared and the opinions of 1,162 undergraduates have been analyzed. The reasons given by each population differ in hierarchy and motivations

An Endogenous Inhibitor of Focal Adhesion Kinase Blocks Rac1/JNK but Not Ras/ERK-dependent Signaling in Vascular Smooth Muscle Cells

Humoral factors and extracellular matrix are critical co-regulators of smooth muscle cell (SMC) migration and proliferation. We reported previously that focal adhesion kinase (FAK)-related non-kinase (FRNK) is expressed selectively in SMC and can inhibit platelet-derived growth factor BB homodimer (PDGF-BB)-induced proliferation and migration of SMC by attenuating FAK activity. The goal of the current studies was to identify the mechanism by which FAK/FRNK regulates SMC growth and migration in response to diverse mitogenic signals. Transient overexpression of FRNK in SMC attenuated autophosphorylation of FAK at Tyr-397, reduced Src family-dependent tyrosine phosphorylation of FAK at Tyr-576, Tyr-577, and Tyr-881, and reduced phosphorylation of the FAK/Src substrates Cas and paxillin. However, FRNK expression did not alter the magnitude or dynamics of ERK activation induced by PDGF-BB or angiotensin II. Instead, FRNK expression markedly attenuated PDGF-BB-, angiotensin II-, and integrin-stimulated Rac1 activity and attenuates downstream signaling to JNK. Importantly, constitutively active Rac1 rescued the proliferation defects in FRNK expressing cells. Based on these observations, we hypothesize that FAK activation is required to integrate integrin signals with those from receptor tyrosine kinases and G protein-coupled receptors through downstream activation of Rac1 and that in SMC, FRNK may control proliferation and migration by buffering FAK-dependent Rac1 activation

The LIM Protein Leupaxin Is Enriched in Smooth Muscle and Functions As an Serum Response Factor Cofactor to Induce Smooth Muscle Cell Gene Transcription

Leupaxin is a LIM-domain containing adapter protein belonging to the paxillin family that has been previously reported to be preferentially expressed in hematopoeitic cells. Herein, we identified leupaxin in a screen for FAK binding partners in aortic smooth muscle, show that leupaxin is enriched in human and mouse vascular smooth muscle, and that leupaxin expression is dynamically regulated during development. In addition, our studies reveal that leupaxin can undergo cytoplasmic/nuclear shuttling and functions as an SRF-cofactor in the nucleus. We found that leupaxin forms a complex with SRF, associates with CArG-containing regions of SM promoters, and that ectopic expression of leupaxin induces SM marker gene expression in both 10T1/2 cells and rat aortic smooth muscle cells (SMC). Subsequent studies indicated that enhanced FAK activity (induced by fibronectin or expression of constitutively active FAK) attenuates the nuclear accumulation of leupaxin and limits the ability of leupaxin to enhance SRF-dependent gene transcription. Thus, these studies indicate that modulation of the sub-cellular localization of SRF-cofactors is one mechanism by which extracellular matrix-dependent signals might regulate phenotypic switching of SMC

Blood pressure–associated polymorphism controls ARHGAP42 expression via serum response factor DNA binding

We recently demonstrated that selective expression of the Rho GTPase-activating protein ARHGAP42 in smooth muscle cells (SMCs) controls blood pressure by inhibiting RhoA-dependent contractility, providing a mechanism for the blood pressure–associated locus within the ARHGAP42 gene. The goals of the current study were to identify polymorphisms that affect ARHGAP42 expression and to better assess ARHGAP42’s role in the development of hypertension. Using DNase I hypersensitivity methods and ENCODE data, we have identified a regulatory element encompassing the ARHGAP42 SNP rs604723 that exhibits strong SMC-selective, allele-specific activity. Importantly, CRISPR/Cas9–mediated deletion of this element in cultured human SMCs markedly reduced endogenous ARHGAP42 expression. DNA binding and transcription assays demonstrated that the minor T allele variation at rs604723 increased the activity of this fragment by promoting serum response transcription factor binding to a cryptic cis-element. ARHGAP42 expression was increased by cell stretch and sphingosine 1-phosphate in a RhoA-dependent manner, and deletion of ARHGAP42 enhanced the progression of hypertension in mice treated with DOCA-salt. Our analysis of a well-characterized cohort of untreated borderline hypertensive patients suggested that ARHGAP42 genotype has important implications in regard to hypertension risk. Taken together, our data add insight into the genetic mechanisms that control blood pressure and provide a potential target for individualized antihypertensive therapies

Research protocol – Assessing Post-Stroke Psychology Longitudinal Evaluation (APPLE) study : A prospective cohort study in stroke

Acknowledgements The following experts provided advice on the design and conduct of the APPLE study: Prof Jonathan Evans (University of Glasgow); Prof Gillian Mead (University of Edinburgh); Prof Sarah T Pendlebury (University of Oxford) Funding This work was supported by the Chief Scientist Office and Stroke Association (funders reference PPA 2015/01_CSO).Peer reviewedPublisher PD

Illinois Cave Amphipod ( Gammarus acherondytes ) Recovery Plan

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