BSN-IN-10 Health Policy Project

The overall purpose of this qualitative, narrative analysis project was to elicit perceptions of the Association of periOperative Registered Nurses (AORN) of Central Ohio regarding Ohio’s Nursing 2015, BSN-IN-10 Initiative,through focus group interaction. The project sought to answer the question: Do we need to legislate that newly licensed registered nurses in Ohio obtain a baccalaureate degree within ten years of initial licensure? After viewing a presentation (using digital storytelling media) entitled, “BSN-IN-10: What is Your Opinion?” that reflects improved patient outcomes related to higher education, AORN participants were given an opportunity in a guided interaction setting to discuss and debate issues surrounding Ohio’s Nursing 2015, BSN-IN-10 Initiative. Data from this focus group discussion was analyzed in relation to key themes. Seven theme clusters emerged and were incorporated under the following three main theme categories: Lack of Knowledge; Lack of Resources; AORN Values Higher Education. Findings noted under these categories suggest that today’s nursing workforce is not informed about the urgent need for more BSN prepared nurses and the available resources that are present to assist them in obtaining this goal. This information has been shared with Ohio’s Nursing 2015 Initiative, Yellow Team Task Force as well as Ohio’s newly forming Action Coalition as it implies that healthcare policy advocates need to find alternative means to communicate the development of Ohio’s BSN-IN-10 Initiative.A three-year embargo was granted for this item

Prevalence, 12-Month Prognosis, and Clinical Management Need of Depression in Coronary Heart Disease Patients: A Prospective Cohort Study

Background: Screening for depression in patients with coronary heart disease (CHD) remains controversial. There is limited data on the actual depression management need in routine care. The aim of this study was to examine the prevalence, treatment rates, prognosis, and management need of clinical and subclinical depression in CHD patients according to the American Heart Association recommendations and the National Institute for Health and Care Excellence (NICE) guideline Depression in Adults with a Chronic Physical Health Problem. Methods: Patients were recruited at 2 German university clinics between 2012 and 2014. Depressive disorders were assessed according to the DSM-IV and depressive symptom severity at baseline and during follow-up was evaluated with the Patient Health Questionnaire (PHQ-9). Depression management need was determined by the severity and longitudinal course of depression symptoms. Results: Of 1,024 patients (19% women), 12% had clinical depression (depressive disorder) and 45% had subclinical depression (PHQ-9 score >= 5) at baseline. Among those with clinical depression, 46% were in treatment at least once during 12 months; 26% were continuously in treatment during follow-up. Depressive disorder and depressive symptoms were significant risk factor-adjusted predictors of the 12-months mortality (adjusted HR = 3.19; 95% CI 1.32-7.69, and adjusted HR = 1.09; 95% CI 1.02-1.16, respectively). Depressive symptoms persisted in 85% of the clinically depressed and in 47% of the subclinically depressed patients. According to current recommendations, 29% of all CHD patients would require depression management within 1 year. Conclusions: There is a need for enhanced recognition, referral, and continuous and improved clinical management of depression in CHD patients

A map for successful CCNE accreditation

The purpose of this article is to provide nurse educators with recommendations on how to develop the needed structures and processes that lead to accreditation success. We provide a comprehensive list of 28 recommendations, a timeline for completion of tasks, and specific information on how to document the achievement of the four CCNE Standards. The first two recommendations deal with two vital structures that comprise a well-functioning program: an effective committee structure and a robust evaluation plan. Recommendations 3 to 12 concern the process steps for preparing for an accreditation visit and are aligned with a timeline for completion. The remaining recommendations address how to document compliance with each CCNE standard

X-linked susceptibility to mycobacteria is caused by mutations in NEMO impairing CD40-dependent IL-12 production

Germline mutations in five autosomal genes involved in interleukin (IL)-12–dependent, interferon (IFN)-γ–mediated immunity cause Mendelian susceptibility to mycobacterial diseases (MSMD). The molecular basis of X-linked recessive (XR)–MSMD remains unknown. We report here mutations in the leucine zipper (LZ) domain of the NF-κB essential modulator (NEMO) gene in three unrelated kindreds with XR-MSMD. The mutant proteins were produced in normal amounts in blood and fibroblastic cells. However, the patients' monocytes presented an intrinsic defect in T cell–dependent IL-12 production, resulting in defective IFN-γ secretion by T cells. IL-12 production was also impaired as the result of a specific defect in NEMO- and NF-κB/c-Rel–mediated CD40 signaling after the stimulation of monocytes and dendritic cells by CD40L-expressing T cells and fibroblasts, respectively. However, the CD40-dependent up-regulation of costimulatory molecules of dendritic cells and the proliferation and immunoglobulin class switch of B cells were normal. Moreover, the patients' blood and fibroblastic cells responded to other NF-κB activators, such as tumor necrosis factor-α, IL-1β, and lipopolysaccharide. These two mutations in the NEMO LZ domain provide the first genetic etiology of XR-MSMD. They also demonstrate the importance of the T cell– and CD40L-triggered, CD40-, and NEMO/NF-κB/c-Rel–mediated induction of IL-12 by monocyte-derived cells for protective immunity to mycobacteria in humans

Congenital Hydrocephalus and Abnormal Subcommissural Organ Development in Sox3 Transgenic Mice

Congenital hydrocephalus (CH) is a life-threatening medical condition in which excessive accumulation of CSF leads to ventricular expansion and increased intracranial pressure. Stenosis (blockage) of the Sylvian aqueduct (Aq; the narrow passageway that connects the third and fourth ventricles) is a common form of CH in humans, although the genetic basis of this condition is unknown. Mouse models of CH indicate that Aq stenosis is associated with abnormal development of the subcommmissural organ (SCO) a small secretory organ located at the dorsal midline of the caudal diencephalon. Glycoproteins secreted by the SCO generate Reissner's fibre (RF), a thread-like structure that descends into the Aq and is thought to maintain its patency. However, despite the importance of SCO function in CSF homeostasis, the genetic program that controls SCO development is poorly understood. Here, we show that the X-linked transcription factor SOX3 is expressed in the murine SCO throughout its development and in the mature organ. Importantly, overexpression of Sox3 in the dorsal diencephalic midline of transgenic mice induces CH via a dose-dependent mechanism. Histological, gene expression and cellular proliferation studies indicate that Sox3 overexpression disrupts the development of the SCO primordium through inhibition of diencephalic roof plate identity without inducing programmed cell death. This study provides further evidence that SCO function is essential for the prevention of hydrocephalus and indicates that overexpression of Sox3 in the dorsal midline alters progenitor cell differentiation in a dose-dependent manner

Immunohistochemical identification and synaptic inputs to the diffuse bipolar cell type DB1 in macaque retina.

Detailed analysis of the synaptic inputs to the primate DB1 bipolar cell has been precluded by the absence of a suitable immunohistochemical marker. Here we demonstrate that antibodies for the EF-hand calcium-binding protein, secretagogin, strongly label the DB1 bipolar cell as well as a mixed population of GABAergic amacrine cells in the macaque retina. Using secretagogin as a marker, we show that the DB1 bipolar makes synaptic contact with both L/M as well as S-cone photoreceptors and only minimal contact with rod photoreceptors. Electron microscopy showed that the DB1 bipolar makes flat contacts at both triad-associated and nontriad-associated positions on the cone pedicle. Double labeling with various glutamate receptor subunit antibodies failed to conclusively determine the subunit composition of the glutamate receptors on DB1 bipolar cells. In the IPL, DB1 bipolar cell axon terminals expressed the glycine receptor, GlyRα1, at sites of contact with AII amacrine cells, suggesting that these cells receive input from the rod pathway

Association of FKBP5 genotype with depressive symptoms in patients with coronary heart disease: a prospective study

Depression and coronary heart disease (CHD) are prevalent and often co-occurring disorders. Both have been associated with a dysregulated stress system. As a central element of the stress system, the FKBP5 gene has been shown to be associated with depression. In a prospective design, this study aims to investigate the association of FKBP5 with depressive symptoms in CHD patients. N = 268 hospitalized CHD patients were included. Depressive symptoms were measured using the Hospital Anxiety and Depression Scale (HADS-D) at four time points (baseline, and after 1 month, 6 months, and 12 months). The functional FKBP5 single-nucleotide polymorphism (SNP) rs1360780 was selected for genotyping. Linear regression models showed that a higher number of FKBP5 C alleles was associated with more depressive symptoms in CHD patients both at baseline (p = 0.015) and at 12-months follow-up (p = 0.025) after adjustment for confounders. Further analyses revealed that this effect was driven by an interaction of FKBP5 genotype with patients' prior CHD course. Specifically, only in patients with a prior myocardial infarction or coronary revascularization, more depressive symptoms were associated with a higher number of C alleles (baseline: p = 0.046; 1-month: p = 0.026; 6-months: p = 0.028). Moreover, a higher number of C alleles was significantly related to a greater risk for dyslipidemia (p = .016). Our results point to a relevance of FKBP5 in the association of the two stress-related diseases depression and CHD

Time-Dependent Nanomechanics of Cartilage

In this study, atomic force microscopy-based dynamic oscillatory and force-relaxation indentation was employed to quantify the time-dependent nanomechanics of native (untreated) and proteoglycan (PG)-depleted cartilage disks, including indentation modulus Eind, force-relaxation time constant τ, magnitude of dynamic complex modulus |E∗|, phase angle δ between force and indentation depth, storage modulus E′, and loss modulus E″. At ∼2 nm dynamic deformation amplitude, |E∗| increased significantly with frequency from 0.22 ± 0.02 MPa (1 Hz) to 0.77 ± 0.10 MPa (316 Hz), accompanied by an increase in δ (energy dissipation). At this length scale, the energy dissipation mechanisms were deconvoluted: the dynamic frequency dependence was primarily governed by the fluid-flow-induced poroelasticity, whereas the long-time force relaxation reflected flow-independent viscoelasticity. After PG depletion, the change in the frequency response of |E∗| and δ was consistent with an increase in cartilage local hydraulic permeability. Although untreated disks showed only slight dynamic amplitude-dependent behavior, PG-depleted disks showed great amplitude-enhanced energy dissipation, possibly due to additional viscoelastic mechanisms. Hence, in addition to functioning as a primary determinant of cartilage compressive stiffness and hydraulic permeability, the presence of aggrecan minimized the amplitude dependence of |E∗| at nanometer-scale deformation

X-linked susceptibility to mycobacteria is caused by mutations in NEMO impairing CD40-dependent IL-12 production

Germline mutations in five autosomal genes involved in interleukin (IL)-12-dependent, interferon (IFN)-gamma-mediated immunity cause Mendelian susceptibility to mycobacterial diseases (MSMD). The molecular basis of X-linked recessive (XR)-MSMD remains unknown. We report here mutations in the leucine zipper (LZ) domain of the NF-kappa B essential modulator (NEMO) gene in three unrelated kindreds with XR-MSMD. The mutant proteins were produced in normal amounts in blood and fibroblastic cells. However, the patients’ monocytes presented an intrinsic defect in T cell-dependent IL-12 production, resulting in defective IFN-gamma secretion by T cells. IL-12 production was also impaired as the result of a specific defect in NEMO- and NF-kappa B/c-Rel-mediated CD40 signaling after the stimulation of monocytes and dendritic cells by CD40L-expressing T cells and fibroblasts, respectively. However, the CD40-dependent up-regulation of costimulatory molecules of dendritic cells and the proliferation and immunoglobulin class switch of B cells were normal. Moreover, the patients’ blood and fibroblastic cells responded to other NF-kappa B activators, such as tumor necrosis factor-alpha, IL-beta, and lipopolysaccharide. These two mutations in the NEMO LZ domain provide the first genetic etiology of XR-MSMD. They also demonstrate the importance of the T cell- and CD40L-triggered, CD40-, and NEMO/NF-kappa B/c-Rel-mediated induction of IL-12 by monocyte-derived cells for protective immunity to mycobacteria in humans