Innovative Approach to New Nurse Residency, Meaningful Use and Health Care Reform

The project’s aim was to examine the financial impact of replacing registered nurse (RN) travelers, RN registry and RN overtime with new graduate RNs. Newly graduated RNs are often viewed by hospital administrators as a more costly staffing resource. This project contributes knowledge regarding the potential cost savings with the utilization of a centralized float pool incorporating new graduates. In addition, it contributes a novel idea for reducing organizational costs of implementing an electronic medical record with the utilization of new graduates as super users. A new graduate program, which incorporated the use of a formal preceptor and mentoring program, was designed to train 100 nurses over the next four years. New graduates were hired as non-benefited employees into a centralized float pool. The first two cohorts consisting of 54 new graduates completed training in April 2013 and June 2013. Data were collected over a 12 month period using organizational financial reports and group discussions with the new graduates. Overtime decreased in the areas new graduates were hired and traveler/registry usage decreased to 26.4 FTE below the budgeted level. From April 2013 through September 2013 the savings contributed to the new graduate project was two million dollars. In October 2013 an additional $500,000 was saved due to the new graduate project and this monthly savings is expected to continue. Utilizing new graduates as super users also saved the organization 375,000 dollars. Implementing a new graduate program and replacing RN traveler, registry and overtime hours proved to be cost effective

Effects of varying Notch1 signal strength on embryogenesis and vasculogenesis in compound mutant heterozygotes

<p>Abstract</p> <p>Background</p> <p>Identifying developmental processes regulated by Notch1 can be addressed in part by characterizing mice with graded levels of Notch1 signaling strength. Here we examine development in embryos expressing various combinations of <it>Notch1 </it>mutant alleles. Mice homozygous for the hypomorphic <it>Notch1</it>^{12<it>f </it>}allele, which removes the single <it>O</it>-fucose glycan in epidermal growth factor-like repeat 12 (EGF12) of the Notch1 ligand binding domain (lbd), exhibit reduced growth after weaning and defective T cell development. Mice homozygous for the inactive <it>Notch1</it>^{<it>lbd </it>}allele express Notch1 missing an ~20 kDa internal segment including the canonical Notch1 ligand binding domain, and die at embryonic day ~E9.5. The embryonic and vascular phenotypes of compound heterozygous <it>Notch1</it>^{12<it>f</it>/<it>lbd </it>}embryos were compared with <it>Notch1</it>^{+/12<it>f</it>}, <it>Notch1</it>^{12<it>f</it>/12<it>f</it>}, and <it>Notch1</it>^{<it>lbd</it>/<it>lbd </it>}embryos. Embryonic stem (ES) cells derived from these embryos were also examined in Notch signaling assays. While Notch1 signaling was stronger in <it>Notch1</it>^{12<it>f</it>/<it>lbd </it>}compound heterozygotes compared to <it>Notch1</it>^{<it>lbd</it>/<it>lbd </it>}embryos and ES cells, Notch1 signaling was even stronger in embryos carrying <it>Notch1</it>^{12<it>f </it>}and a null <it>Notch1 </it>allele.</p> <p>Results</p> <p>Mouse embryos expressing the hypomorphic <it>Notch1</it>^{12<it>f </it>}allele, in combination with the inactive <it>Notch1</it>^{<it>lbd </it>}allele which lacks the Notch1 ligand binding domain, died at ~E11.5-12.5. <it>Notch1</it>^{12<it>f</it>/<it>lbd </it>}ES cells signaled less well than <it>Notch1</it>^{12<it>f</it>/12<it>f </it>}ES cells but more strongly than <it>Notch1</it>^{<it>lbd</it>/<it>lbd </it>}ES cells. However, vascular defects in <it>Notch1</it>^{12<it>f</it>/<it>lbd </it>}yolk sac were severe and similar to <it>Notch1</it>^{<it>lbd</it>/<it>lbd </it>}yolk sac. By contrast, vascular disorganization was milder in <it>Notch1</it>^{12<it>f</it>/<it>lbd </it>}compared to <it>Notch1</it>^{<it>lbd</it>/<it>lbd </it>}embryos. The expression of Notch1 target genes was low in <it>Notch1</it>^{12<it>f</it>/<it>lbd </it>}yolk sac and embryo head, whereas Vegf and Vegfr2 transcripts were increased. The severity of the compound heterozygous <it>Notch1</it>^{12<it>f</it>/<it>lbd </it>}yolk sac phenotype suggested that the allelic products may functionally interact. By contrast, compound heterozygotes with <it>Notch1</it>^{12<it>f </it>}in combination with a <it>Notch1 </it>null allele (<it>Notch1</it>^tm1Con) were capable of surviving to birth.</p> <p>Conclusions</p> <p>Notch1 signaling in <it>Notch1</it>^{12<it>f</it>/<it>lbd </it>}compound heterozygous embryos is more defective than in compound heterozygotes expressing a hypomorphic <it>Notch1</it>^{12<it>f </it>}allele and a <it>Notch1 </it>null allele. The data suggest that the gene products Notch1^lbdand Notch1^12finteract to reduce the activity of Notch1^12f.</p

A review of scientific theories used to justify the delivery of school-based mindfulness programmes . A protocol for a scoping review

The research is funded by the National Institute for Health and Care Research (NIHR133712) using UK aid from the UK Government to support global health research.Preprin

A protocol for a critical realist synthesis of school mindfulness interventions designed to promote pupils' mental wellbeing

The research is funded by the National Institute for Health and Care Research (GB) (NIHR 133712) using UK aid from the UK Government to support global health research. The funders did not and will not have a role in study design, data collection and analysis, the decision to publish, or preparation of the manuscript. The funders did not and will not have a role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.Peer reviewe

MGAT1 and Complex N-Glycans Regulate ERK Signaling During Spermatogenesis

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In vivo consequences of deleting EGF repeats 8–12 including the ligand binding domain of mouse Notch1

<p>Abstract</p> <p>Background</p> <p>Notch signaling is highly conserved in the metazoa and is critical for many cell fate decisions. Notch activation occurs following ligand binding to Notch extracellular domain. <it>In vitro </it>binding assays have identified epidermal growth factor (EGF) repeats 11 and 12 as the ligand binding domain of Drosophila Notch. Here we show that an internal deletion in mouse Notch1 of EGF repeats 8–12, including the putative ligand binding domain (lbd), is an inactivating mutation <it>in vivo</it>. We also show that maternal and zygotic <it>Notch1</it>^{<it>lbd</it>/<it>lbd </it>}mutant embryos develop through gastrulation to mid-gestation.</p> <p>Results</p> <p><it>Notch1</it>^{<it>lbd</it>/<it>lbd </it>}embryos died at mid-gestation with a phenotype indistinguishable from <it>Notch1 </it>null mutants. In embryonic stem (ES) cells, Notch1^lbdwas expressed on the cell surface at levels equivalent to wild type Notch1, but Delta1 binding was reduced to the same level as in <it>Notch1 </it>null cells. In an ES cell co-culture assay, Notch signaling induced by Jagged1 or Delta1 was reduced to a similar level in <it>Notch1</it>^{<it>lbd</it><it/>}and <it>Notch1 </it>null cells. However, the <it>Notch1</it>^{<it>lbd</it>/<it>lbd </it>}allele was expressed similarly to wild type Notch1 in <it>Notch1</it>^{<it>lbd</it>/<it>lbd </it>}ES cells and embryos at E8.75, indicating that Notch1 signaling is not essential for the <it>Notch1 </it>gene to be expressed. In addition, maternal and zygotic <it>Notch1 </it>mutant blastocysts developed through gastrulation.</p> <p>Conclusion</p> <p>Mouse Notch1 lacking the ligand binding domain is expressed at the cell surface but does not signal in response to the canonical Notch ligands Delta1 and Jagged1. Homozygous <it>Notch1</it>^{<it>lbd</it>/<it>lbd </it>}mutant embryos die at ~E10 similar to <it>Notch1 </it>null embryos. While Notch1 is expressed in oocytes and blastocysts, Notch1 signaling via canonical ligands is dispensable during oogenesis, blastogenesis, implantation and gastrulation.</p

A protocol for a critical realist synthesis of school mindfulness interventions designed to promote pupils' mental wellbeing

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This research was funded by the National Institute for Health and Care Research (NIHR 133712) using UK aid from the UK Government to support global health research.Peer reviewedPublisher PD

Synergistic regulation of Notch signaling by different O-glycans promotes hematopoiesis

Glycosylation of Notch receptors by O-fucose glycans regulates Notch ligand binding and Notch signaling during hematopoiesis. However, roles in hematopoiesis for other O-glycans that modify Notch receptors have not been determined. Here we show that the EGF domain specific GlcNAc transferase EOGT is required in mice for the optimal production of lymphoid and myeloid cells. The phenotype of Eogt null mice was largely cell-autonomous, and Notch target gene expression was reduced in T cell progenitors. Moreover, EOGT supported residual Notch signaling following conditional deletion of Pofut1 in hematopoietic stem cells (HSC). Eogt : Pofut1 double mutant HSC had more severe defects in bone marrow and in T and B cell development in thymus and spleen, compared to deletion of Pofut1 alone. The combined results show that EOGT and O-GlcNAc glycans are required for optimal hematopoiesis and T and B cell development, and that they act synergistically with POFUT1 and O-fucose glycans to promote Notch signaling in lymphoid and myeloid differentiation

Financial Deepening, Private Domestic Savings and Per Capita Gdp Growth in Nigeria

A general way of evaluating the economic welfare or living standards of country is through its per capita GDP, This study investigates empirically the impact of financial deepening on per capita GDP growth, the interaction effect of financial deepening and private domestic savings on Nigeria’s GDP per capita growth and how per capita GDP respond to shocks in financial deepening in Nigeria. Financial deepening is represented by, the ratio of private sector credit to gross domestic product (PSC/GDP). This study used quarterly data from 1986 to 2014 and was generated from both the CBN (2015) statistical bulletin and World Bank (2015) database. Concerning the Impact of Financial Deepening on GDP per capita and the Interaction effect of private domestic Savings and Financial deepening on GDP per capita, ARDL model was implore,. This thesis therefore, makes a modest contribution to the literature having identified that  financial deepening can contribute to GDP per capita growth, if there is an improvement in domestic resources mobilization, and efficiency in capital allocation in the country. Simply put, these results appear to reveal that various financial development policies have not contributed enough to Nigeria’s per capita growth. However, if government and financial institutions can encourage mobilization of domestic savings; develop credit and equity markets; minimise financial risk; and ensure efficiency of capital allocation, Nigerians can benefit from the deepening of the financial sector and domestic savings in the long-run development of the country