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Anderson G.,Office of Nursing Services | Anderson G.,Azusa Pacific University | Alt-White A.C.,Office of Nursing Services | Schaa K.L.,Office of Research and Development | And 4 more authors.
Worldviews on Evidence-Based Nursing | Year: 2015

Background: Nurses lack genome literacy, skill, and self-confidence in applying genomics to health care. Standardized curricula and evaluation tools are needed for wide spread uptake and application of genome science in nursing education, practice, and research. Aim: To determine whether psychometrically robust survey instruments exist to assess knowledge, skills, attitudes, and self-confidence in applying genomic nursing competency among students and registered nurses. Design: Psychometric systematic review. Data Sources: Medline, CINAHL, Academic Search Elite, Web of Science, and ProQuest Dissertations were searched from 1995 to 2014, with an English language restriction. Procedures: Critical analysis of the study elements and psychometric attributes was conducted after data were abstracted into analysis and synthesis tables. The synthesis assessed the design, methods, and measurement properties with a focus on reliability and validity using 16 criteria on a 4-point grading scale. Findings: Twelve studies were included in a detailed review that focused on assessment of genomic nursing core competencies. Six studies met the inclusion criteria. In terms of psychometric quality of the instruments, one study scored high, two moderate, two low, and one very low. Linking Evidence to Action: Most instruments assess self-perceived rather than objectively assessed competency. The highest quality instrument lacks clinical application. Knowledge-focused test questions based on up-to-date genome science that are relevant to practice need to be developed. © 2015. Source

Bailey A.L.,Charles George Veterans Affairs Medical Center | Bailey A.L.,Dorn Veterans Affairs Medical Center | Makela E.H.,Charles George Veterans Affairs Medical Center | Asberg K.,Charles George Veterans Affairs Medical Center
Journal of Psychiatric Practice | Year: 2016

Objective/Background: Because restless legs syndrome (RLS) is a problematic syndrome, demonstrating an association between use of selective serotonin reuptake inhibitors (SSRIs)- /serotonin-norepinephrine reuptake inhibitors (SNRIs) and RLS may help direct patient care. The goals of this study were (1) to establish the incidence of RLS in mental health patients being treated with SSRIs or SNRIs in a local Veterans Affairs medical center and (2) to evaluate the frequency with which certain SSRIs or SNRIs are associated with RLS and the trend in frequency of the diagnosis since the revision of the criteria for RLS offered by the International Restless Leg Syndrome Study Group (IRLSSG), the Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition (DSM-5), and the International Classification of Sleep Disorders,Revised (ICSD-3). Methods: A retrospective chart review was used to evaluate the number of patients receiving SSRI/SNRI therapy with and without a diagnosis of RLS, with the date of the RLS diagnosis and initiation of SSRI/SNRI therapy noted. The frequency with which certain SSRIs/SNRIs were associated with RLS, and the frequency of RLS diagnoses since January 2012 were also noted. Descriptive statistics and logistic regression were used for data analysis.Results: A total of 254 charts were reviewed. A majority of the patients (89.8%) were male, and 14 (5.5%) were diagnosed with RLS. A logistic regression equation approached significance in predicting RLS (P=0.053). Age and sex emerged as significant predictors of RLS. The prevalence of any individual SSRI or SNRI being associated with RLS was indeterminable. No difference was seen in the number of RLS diagnoses since the refining of the IRLSSG, DSM-5, and ICSD-3 criteria. Conclusions: The use of SSRIs/SNRIs does not seem to be associated with a diagnosis of RLS. In addition, the diagnosis of RLS does not seem to have become more common since the revision of the diagnostic criteria for the disorder. Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved. Source

Fadel J.R.,University of South Carolina | Reagan L.P.,University of South Carolina | Reagan L.P.,Dorn Veterans Affairs Medical Center
Current Opinion in Behavioral Sciences | Year: 2016

In peripheral tissues insulin activates signaling cascades to facilitate glucose uptake from the blood into tissues like liver, muscle and fat. Although insulin appears to play a minor role in the regulation of glucose uptake in the central nervous system (CNS), insulin is known to play a major role in regulating synaptic plasticity in brain regions like the hippocampus. The concept that insulin regulates hippocampal neuroplasticity is further supported from animal models of type 2 diabetes (T2DM) and Alzheimer's disease (AD). The goal of this review is to provide an overview of these studies, as well as the studies that have examined whether deficits in hippocampal insulin signaling are amenable to intervention strategies. © 2015 . Source

Sido J.M.,University of South Carolina | Jackson A.R.,University of South Carolina | Nagarkatti P.S.,University of South Carolina | Nagarkatti M.,University of South Carolina | Nagarkatti M.,Dorn Veterans Affairs Medical Center
Journal of Molecular Medicine | Year: 2016

Abstract: ∆9-Tetrahydrocannabinol (THC) is one of the major bioactive cannabinoids derived from the Cannabis sativa plant and is known for its anti-inflammatory properties. Delayed-type hypersensitivity (DTH) is driven by proinflammatory T helper cells including the classic inflammatory Th1 lineage as well as the more recently discovered Th17 lineage. In the current study, we investigated whether THC can alter the induction of Th1/Th17 cells involved in mBSA-induced DTH response. THC treatment (20 mg/kg) of C57BL/6 mice with DTH caused decreased swelling and infiltration of immune cells at the site of antigen rechallenge. Additionally, THC treatment decreased lymphocyte activation as well as Th1/Th17 lineage commitment, including reduced lineage-specific transcription factors and cytokines. Interestingly, while DTH caused an overexpression of miR-21, which increases Th17 differentiation via SMAD7 inhibition, and downregulation of miR-29b, an IFN-γ inhibitor, THC treatment reversed this microRNA (miR) dysregulation. Furthermore, when we transfected primary cells from DTH mice with miR-21 inhibitor or miR-29b mimic, as seen with THC treatment, the expression of target gene message was directly impacted increasing SMAD7 and decreasing IFN-γ expression, respectively. In summary, the current study suggests that THC treatment during DTH response can simultaneously inhibit Th1/Th17 activation via regulation of microRNA (miRNA) expression. Key messages: • THC treatment inhibits simultaneous Th1/Th17 driven inflammation. • THC treatment corrects DTH-mediated microRNA dysregulation. • THC treatment regulates proinflammatory cytokines and transcription factors. © 2016 Springer-Verlag Berlin Heidelberg Source

Elliott D.M.,University of South Carolina | Nagarkatti M.,University of South Carolina | Nagarkatti M.,Dorn Veterans Affairs Medical Center | Nagarkatti P.S.,University of South Carolina
Journal of Pharmacology and Experimental Therapeutics | Year: 2016

3,3'-Diindolylmethane (DIM), a natural indole found in cruciferous vegetables, has significant anti-cancer and anti-inflammatory properties. In this current study, we investigated the effects of DIM on acute lung injury (ALI) induced by exposure to staphylococcal enterotoxin B (SEB). We found that pretreatment of mice with DIM led to attenuation of SEB-induced inflammation in the lungs, vascular leak, and IFN-γ secretion. Additionally, DIM could induce cell-cycle arrest and cell death in SEB-activated T cells in a concentration-dependent manner. Interestingly, microRNA (miRNA) microarray analysis uncovered an altered miRNA profile in lung-infiltrating mononuclear cells after DIM treatment of SEB-exposed mice. Moreover, computational analysis of miRNA gene targets and regulation networks indicated that DIM alters miRNA in the cell death and cell-cycle progression pathways. Specifically, DIM treatment significantly downregulated several miRNA and a correlative increase associated gene targets. Furthermore, overexpression and inhibition studies demonstrated that DIM-induced cell death, at least in part, used miR-222. Collectively, these studies demonstrate for the first time that DIM treatment attenuates SEB-induced ALI and may do so through the induction of microRNAs that promote apoptosis and cell-cycle arrest in SEB-activated T cells. Source

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