Time filter

Source Type

Temple, TX, United States

Mancini M.A.,Saint Louis University | Linhorst D.M.,Saint Louis University | Menditto A.A.,Fulton State Hospital | Coleman J.,Central Texas Veterans Healthcare System
Journal of Behavioral Health Services and Research | Year: 2013

This study evaluated a statewide demonstration project to implement a group-based intervention called Procovery in selected inpatient and community mental health centers. Procovery is a facilitated mutual support group designed to build hope and a sense of social inclusion by raising consciousness and helping people develop an understanding of the ways one can move toward recovery in their own lives. This evaluation sought to determine both consumer outcomes and perceptions of the program and implementation efforts held by consumers and the facilitators of the intervention. A multidimensional approach was used, including a quasi-experimental design with consumers, questionnaires and focus groups with the intervention facilitators, and individual interviews with administrators. The Procovery model was shown to have a positive impact on consumers' recoveries and was viewed favorably by consumers, facilitators, and administrators. Several barriers to effective implementation were identified. These findings and their implications for future practice and research are discussed.© 2013 National Council for Community Behavioral Healthcare.

McMillin M.,Texas A&M University | McMillin M.,Digestive Disease Research Center | Frampton G.,Texas A&M University | Frampton G.,Digestive Disease Research Center | And 9 more authors.
Journal of Neuroinflammation | Year: 2014

Background: Acute liver failure leads to systemic complications with one of the most dangerous being a decline in neurological function, termed hepatic encephalopathy. Neurological dysfunction is exacerbated by an increase of toxic metabolites in the brain that lead to neuroinflammation. Following various liver diseases, hepatic and circulating chemokines, such as chemokine ligand 2 (CCL2), are elevated, though their effects on the brain following acute liver injury and subsequent hepatic encephalopathy are unknown. CCL2 is known to activate microglia in other neuropathies, leading to a proinflammatory response. However, the effects of CCL2 on microglia activation and the pathogenesis of hepatic encephalopathy following acute liver injury remain to be determined. Methods: Hepatic encephalopathy was induced in mice via injection of azoxymethane (AOM) in the presence or absence of INCB 3284 dimesylate (INCB), a chemokine receptor 2 inhibitor, or C 021 dihydrochloride (C021), a chemokine receptor 4 inhibitor. Mice were monitored for neurological decline and time to coma (loss of all reflexes) was recorded. Tissue was collected at coma and used for real-time PCR, immunoblots, ELISA, or immunostaining analyses to assess the activation of microglia and consequences on pro-inflammatory cytokine expression. Results: Following AOM administration, microglia activation was significantly increased in AOM-treated mice compared to controls. Concentrations of CCL2 in the liver, serum, and cortex were significantly elevated in AOM-treated mice compared to controls. Systemic administration of INCB or C021 reduced liver damage as assessed by serum liver enzyme biochemistry. Administration of INCB or C021 significantly improved the neurological outcomes of AOM-treated mice, reduced microglia activation, reduced phosphorylation of ERK1/2, and alleviated AOM-induced cytokine upregulation. Conclusions: These findings suggest that CCL2 is elevated systemically following acute liver injury and that CCL2 is involved in both the microglia activation and neurological decline associated with hepatic encephalopathy. Methods used to modulate CCL2 levels and/or reduce CCR2/CCR4 activity may be potential therapeutic targets for the management of hepatic encephalopathy due to acute liver injury. © 2014 McMillin et al.; licensee BioMed Central Ltd.

Jinadatha C.,Central Texas Veterans Healthcare System | Jinadatha C.,Texas A&M University | Simmons S.,Xenex Disinfection Services | Dale C.,Xenex Disinfection Services | And 6 more authors.
American Journal of Infection Control | Year: 2015

The doffing of personal protective equipment (PPE) after contamination with pathogens such as Ebola poses a risk to health care workers. Pulsed xenon ultraviolet (PX-UV) disinfection has been used to disinfect surfaces in hospital settings. This study examined the impact of PX-UV disinfection on an Ebola surrogate virus on glass carriers and PPE material to examine the potential benefits of using PX-UV to decontaminate PPE while worn, thereby reducing the pathogen load prior to doffing. Ultraviolet (UV) safety and coverage tests were also conducted. PX-UV exposure resulted in a significant reduction in viral load on glass carriers and PPE materials. Occupational Safety and Health Administrationedefined UV exposure limits were not exceeded during PPE disinfection. Predoffing disinfection with PX-UV has potential as an additive measure to the doffing practice guidelines. The PX-UV disinfection should not be considered sterilization; all PPE should still be considered contaminated and doffed and disposed of according to established protocols. Copyright © 2015 by the Association for Professionals in Infection Control and Epidemiology, Inc. Published by Elsevier Inc. All rights reserved.

McMillin M.,Central Texas Veterans Healthcare System | McMillin M.,Texas A&M University | Frampton G.,Central Texas Veterans Healthcare System | Frampton G.,Texas A&M University | And 10 more authors.
Journal of Neurochemistry | Year: 2015

Hepatic encephalopathy (HE) is a serious neurological complication of acute and chronic liver failure. Expression of the neurosteroid/bile acid receptor Takeda G protein-coupled receptor 5 (TGR5) has been demonstrated in the brain and is thought to be neuroprotective. However, it is unknown how TGR5 signaling can influence the progression and associated neuroinflammation of HE. HE was induced in C57Bl/6 mice via intraperitoneal injection of azoxymethane (AOM) and tissue was collected throughout disease progression. TGR5 expression was elevated in the frontal cortex following AOM injection in mice. The cellular localization of TGR5 was found in both neurons and microglia in the cortex of C57Bl/6 mice. Central infusion of the TGR5 agonist, betulinic acid, prior to AOM injection delayed neurological decline, increased cortical cyclic adenosine monophosphate concentrations, reduced microglia activation and proliferation, and reduced proinflammatory cytokine production. Betulinic acid treatment in vitro reduced the neuronal expression of chemokine ligand 2, a chemokine previously demonstrated to contribute to HE pathogenesis. Lastly, treatment of the microglia cell line EOC-20 with conditioned media from betulinic acid-treated primary neurons decreased phagocytic activity and cytokine production. Together, these data identify that activation of TGR5, which is up-regulated during HE, alleviates neuroinflammation and improves outcomes of AOM-treated mice through neuron and microglia paracrine signaling. © 2015 International Society for Neurochemistry.

Pugh M.J.V.,Veterans Evidence Based Research Dissemination Implementation Center | Pugh M.J.V.,University of Texas Health Science Center at San Antonio | Marcum Z.A.,University of Pittsburgh | Copeland L.A.,Central Texas Veterans Healthcare System | And 16 more authors.
Drugs and Aging | Year: 2013

Background: Clinical validation studies of the Healthcare Effectiveness Data and Information Set (HEDIS®) measures of inappropriate prescribing in the elderly are limited. Objectives: The objective of this study was to examine associations of new exposure to high-risk medication in the elderly (HRME) and drug-disease interaction (Rx-DIS) with mortality, hospital admission, and emergency care. Methods: A retrospective database study was conducted examining new use of HRME and Rx-DIS in fiscal year 2006 (Oct 2005-Sep 2006; FY06), with index date being the date of first HRME/Rx-DIS exposure, or first day of FY07 if no HRME/Rx-DIS exposure. Outcomes were assessed 1 year after the index date. The participants were veterans who were ≥65 years old in FY06 and received Veterans Health Administration (VA) care in FY05-06. A history of falls/hip fracture, chronic renal failure, and/or dementia per diagnosis codes defined the Rx-DIS subsample. The variables included a number of new unique HRME drug exposures and new unique Rx-DIS drug exposure (0, 1, >1) in FY06, and outcomes (i.e., 1-year mortality, hospital admission, and emergency care) up to 1 year after exposure. Descriptive statistics summarized variables for the overall HRME cohort and the Rx-DIS subset. Multivariable statistical analyses using generalized estimating equations (GEE) models with a logit link accounted for nesting of patients within facilities. For these latter analyses, we controlled for demographic characteristics, chronic disease states, and indicators of disease burden the previous year (e.g., number of prescriptions, emergency/hospital care). Results: Among the 1,807,404 veterans who met inclusion criteria, 5.2 % had new HRME exposure. Of the 256,388 in the Rx-DIS cohort, 3.6 % had new Rx-DIS exposure. Multivariable analyses found that HRME was significantly associated with mortality [1: adjusted odds ratio (AOR) = 1.62, 95 % CI 1.56-1.68; >1: AOR = 1.80, 95 % CI 1.45-2.23], hospital admission (1: AOR = 2.31, 95 % CI 2.22-2.40; >1: AOR = 3.44, 95 % CI 3.06-3.87), and emergency care (1: AOR = 2.59, 95 % CI 2.49-2.70; >1: AOR = 4.18, 95 % CI 3.71-4.71). Rx-DIS exposure was significantly associated with mortality (1: AOR = 1.60, 95 % CI 1.51-1.71; >1: AOR = 2.00, 95 % CI 1.38-2.91), hospital admission for one exposure (1: AOR = 1.12, 95 % CI 1.03-1.27; >1: AOR = 1.18, 95 % CI 0.71-1.95), and emergency care for two or more exposures (1: AOR = 1.06, 95 % CI 0.97-1.15; >1: AOR = 2.0, 95 % CI 1.35-3.10). Conclusions: Analyses support the link between HRME/Rx-DIS exposure and clinically significant outcomes in older veterans. Now is the time to begin incorporating input from both patients who receive these medications and providers who prescribe to develop approaches to reduce exposure to these agents. © 2013 Springer International Publishing Switzerland (outside the USA).

Discover hidden collaborations