Dorn Veterans Affairs Medical Center

Columbia, United States

Dorn Veterans Affairs Medical Center

Columbia, United States
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Wagner S.E.,University of Georgia | Burch J.B.,University of South Carolina | Burch J.B.,Dorn Veterans Affairs Medical Center | Bottai M.,University of South Carolina | And 7 more authors.
Cancer Causes and Control | Year: 2011

Objective: This ecologic study tested the hypothesis that census tracts with elevated groundwater uranium and more frequent groundwater use have increased cancer incidence. Methods: Data sources included: incident total, leukemia, prostate, breast, colorectal, lung, kidney, and bladder cancers (1996-2005, SC Central Cancer Registry); demographic and groundwater use (1990 US Census); and groundwater uranium concentrations (n = 4,600, from existing federal and state databases). Kriging was used to predict average uranium concentrations within tracts. The relationship between uranium and standardized cancer incidence ratios was modeled among tracts with substantial groundwater use via linear or semiparametric regression, with and without stratification by the proportion of African Americans in each area. Results: A total of 134,685 cancer cases were evaluated. Tracts with ≥50% groundwater use and uranium concentrations in the upper quartile had increased risks for colorectal, breast, kidney, prostate, and total cancer compared to referent tracts. Some of these relationships were more likely to be observed among tracts populated primarily by African Americans. Conclusion: SC regions with elevated groundwater uranium and more groundwater use may have an increased incidence of certain cancers, although additional research is needed since the design precluded adjustment for race or other predictive factors at the individual level. © 2010 Springer Science+Business Media B.V.


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.


Yang F.,University of South Carolina | Yang X.,University of South Carolina | Yang X.,Dorn Veterans Affairs Medical Center | Yang X.,Dorn Research Institute | And 7 more authors.
Biomicrofluidics | Year: 2010

Separation of colorectal cancer cells from other biological materials is important for stool-based diagnosis of colorectal cancer. In this paper, we use conventional dielectrophoresis in a microfluidic chip to manipulate and isolate HCT116 colorectal cancer cells. It is noticed that at a particular alternating current frequency band, the HCT116 cells are clearly deflected to a side channel from the main channel after the electric activation of an electrode pair. This motion caused by negative dielectrophoresis can be used to simply and rapidly separate cancer cells from other cells. In this manuscript, we report the chip design, flow conditions, dielectrophoretic spectrum of the cancer cells, and the enrichment factor of the colorectal cancer cells from other cells. © 2010 American Institute of Physics.


Grillo C.A.,University of South Carolina | Mulder P.,University of South Carolina | Macht V.A.,University of South Carolina | Kaigler K.F.,University of South Carolina | And 5 more authors.
Physiology and Behavior | Year: 2014

Obesity-induced changes in the metabolic and endocrine milieu elicit deficits in neuroplasticity, including increased risk for development of neuropsychiatric disorders such as depressive illness. We previously demonstrated that downregulation of hypothalamic insulin receptors (hypo-IRAS) elicits a phenotype that is consistent with features of the metabolic syndrome (MetS) and that rats with this phenotype exhibit deficits in neuronal plasticity, including depressive-like behaviors such as anhedonia. Since food restriction paradigms effectively inhibit obesity-induced neuroplasticity deficits, the aim of the current study was to determine whether food restriction could reverse obesity-induced anhedonia in hypo-IRAS rats. Compared to hypo-IRAS rats provided ad lib food access, food restriction paradigms that were initiated either prior to increases in body weight or following development of the MetS/obesity phenotype effectively restored sucrose intake in hypo-IRAS rats. Moreover, food restriction paradigms were able to prevent and reverse the changes in the endocrine/metabolic/inflammatory milieu observed in hypo-IRAS, such as increases in plasma leptin and triglyceride levels and increases in pro-inflammatory cytokines such as IL-1α, IL-6 and C-reactive protein (CRP). Collectively, these results demonstrate that obesity-induced anhedonia is a reversible process and identify some potential mechanistic mediators that may be responsible for co-morbid depression in obesity. © 2014.


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 .


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


Sido J.M.,University of South Carolina | Yang X.,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 Leukocyte Biology | Year: 2015

MDSCs are potent immunosuppressive cells that are induced during inflammatory responses, as well as by cancers, to evade the anti-tumor immunity. We recently demonstrated that marijuana cannabinoids are potent inducers of MDSCs. In the current study, we investigated the epigenetic mechanisms through which THC, an exogenous cannabinoid, induces MDSCs and compared such MDSCs with the na¨ıve MDSCs found in BM of BL6 (WT) mice. Administration of THC into WT mice caused increased methylation at the promoter region of DNMT3a and DNMT3b in THC-induced MDSCs, which correlated with reduced expression of DNMT3a and DNMT3b. Furthermore, promoter region methylation was decreased at Arg1 and STAT3 in THC-induced MDSCs, and consequently, such MDSCs expressed higher levels of Arg1 and STAT 3. In addition, THC-induced MDSCs secreted elevated levels of S100A8, a calcium-binding protein associated with accumulation of MDSCs in cancer models. Neutralization of S100A8 by use of anti-S100A8 (8H150) in vivo reduced the ability of THC to trigger MDSCs. Interestingly, the elevated S100A8 expression also promoted the suppressive function of MDSCs. Together, the current study demonstrates that THC mediates epigenetic changes to promoteMDSC differentiation and function and that S100A8 plays a critical role in this process. © Society for Leukocyte Biology.


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.


Busbee P.B.,University of South Carolina | Nagarkatti M.,University of South Carolina | Nagarkatti M.,Dorn Veterans Affairs Medical Center | Nagarkatti P.S.,University of South Carolina
PLoS ONE | Year: 2015

Staphylococcal enterotoxin B (SEB) is a potent superantigen capable of inducing inflammation characterized by robust immune cell activation and proinflammatory cytokine release. Exposure to SEB can result in food poisoning as well as fatal conditions such as toxic shock syndrome. In the current study, we investigated the effect of natural indoles including in-dole-3-carbinol (I3C) and 3,3′-diindolylmethane (DIM) on SEB-mediated liver injury. Injection of SEB into D-galactosamine-sensitized female C57BL/6 mice resulted in liver injury as indicated by an increase in enzyme aspartate transaminase (AST) levels, induction of inflammatory cytokines, and massive infiltration of immune cells into the liver. Administration of I3C and DIM (40mg/kg), by intraperitonal injection, attenuated SEB-induced acute liver injury, as evidenced by decrease in AST levels, inflammatory cytokines and cellular infiltration in the liver. I3C and DIM triggered apoptosis in SEB-activated T cells primarily through activation of the intrinsic mitochondrial pathway. In addition, inhibitor studies involving caspases revealed that I3C and DIM-mediated apoptosis in these activated cells was dependent on caspase-2 but independent of caspase-8, 9 and 3. In addition, I3C and DIM caused a decrease in Bcl-2 expression. Both compounds also down-regulated miR-31, which directly targets caspase-2 and influences apoptosis in SEB-activated cells. Our data demonstrate for the first time that indoles can effectively suppress acute hepatic inflammation caused by SEB and that this may be mediated by decreased expression of miR-31 and consequent caspase-2-dependent apoptosis in T cells. © 2015 Busbee et al.


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.

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