89 research outputs found

    Playing to our Strengths: An Academic/Health Department Collaboration to Facilitate Public Protections Against Tuberculosis

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    Background: Economic modeling and analysis can facilitate evidence-based policy and practice. Such analyses may exceed the technical capacity and mission of public health agencies, yet may be critical to sustain health protections such as tuberculosis (TB) control. The net effect of TB prevention is incompletely understood, hampering objective value judgments of national TB elimination policies. This may promote inefficiencies and threaten individual and public health protections. We describe how a HRSA-funded Texas Public Health Training Center (TPHTC) coordinated specialized analytical skills with the needs of a state public health department to create a user-friendly tool to inform planning and resource allocation; and to identify risks, benefits, opportunities, and value in the context of Texas’ Department of State Health Services (TDSHS) TB control programs. Methods: Key informants within TDSHS and faculty from the University of North Texas Health Science Center (UNTHSC) and its associated TPHTC collaborated to develop a combined health, cost, and outcome model to answer questions of interest to TDSHS. The model incorporates standard techniques, TB specific logic and data, and Texas specific population, epidemiologic, and programmatic data into a Microsoft Excel platform. Outcome measures include 2013 USD costs from a public agency perspective and health losses denominated in Quality Adjusted Life Years (QALYs) (but not assigned a dollar value). Outcomes represent the 10-year accrued net present value (NPV) of variable costs associated with each incident TB case. The model used only publicly available, non-confidential data. Results: Under current public TB prevention and control practices we estimate public spending for acute medical care and health losses for Texas’ 1325 TB cases in 2011 will exceed a NPV 100,000,000and4800QALYsby2022;societalcostswouldlikelybemuchhigher.PublicTBcontrolisrelativelycosteffectiveandpreserves3.7QALYs/caseavertedat100,000,000 and 4800 QALYs by 2022; societal costs would likely be much higher. Public TB control is relatively cost effective and preserves 3.7 QALYs/case averted at 54,000/QALY. Implications: Partnerships between academic institutions and public health departments offer the potential to produce the economic analyses needed for judicious use of public resources. We used accessible methods, data, and technology to create a model to analyze the relative value of public TB control in Texas as well as to identify potential efficiencies within activities. Our analysis suggests public efforts against latent TB infection effectively and efficiently mitigate some of the substantial health and cost impact of TB to Texas. Most of TB’s burden remains, however, and more careful targeting of prevention by risk promises rich rewards

    Personal and Societal Health Quality Lost to Tuberculosis

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    Background: In developed countries, tuberculosis is considered a disease with little loss of Quality-Adjusted Life Years (QALYs). Tuberculosis treatment is predominantly ambulatory and death from tuberculosis is rare. Research has shown that there are chronic pulmonary sequelae in a majority of patients who have completed treatment for pulmonary tuberculosis (PTB). This and other health effects of tuberculosis have not been considered in QALY calculations. Consequently both the burden of tuberculosis on the individual and the value of tuberculosis prevention to society are underestimated. We estimated QALYs lost to pulmonary TB patients from all known sources, and estimated health loss to prevalent TB disease. Methodology/Principal Findings: We calculated values for health during illness and treatment, pulmonary impairment after tuberculosis (PIAT), death rates, years-of-life-lost to death, and normal population health. We then compared the lifetime expected QALYs for a cohort of tuberculosis patients with that expected for comparison populations with latent tuberculosis infection and without tuberculosis infection. Persons with culture-confirmed tuberculosis accrued fewer lifetime QALYs than those without tuberculosis. Acute tuberculosis morbidity cost 0.046 QALYs (4% of total) per individual. Chronic morbidity accounted for an average of 0.96 QALYs (78% of total). Mortality accounted for 0.22 QALYs lost (18% of total). The net benefit to society of averting one case of PTB was about 1.4 QALYs. Conclusions/Significance: Tuberculosis, a preventable disease, results in QALYs lost owing to illness, impairment, and death. The majority of QALYs lost from tuberculosis resulted from impairment after microbiologic cure. Successful TB prevention efforts yield more health quality than previously thought and should be given high priority by health policy makers. (Refer to Abstracto S1 for Spanish language abstract

    Pulmonary impairment after tuberculosis and its contribution to TB burden

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    <p>Abstract</p> <p>Background</p> <p>The health impacts of pulmonary impairment after tuberculosis (TB) treatment have not been included in assessments of TB burden. Therefore, previous global and national TB burden estimates do not reflect the full consequences of surviving TB. We assessed the burden of TB including pulmonary impairment after tuberculosis in Tarrant County, Texas using Disability-adjusted Life Years (DALYs).</p> <p>Methods</p> <p>TB burden was calculated for all culture-confirmed TB patients treated at Tarrant County Public Health between January 2005 and December 2006 using identical methods and life tables as the Global Burden of Disease Study. Years of life-lost were calculated as the difference between life expectancy using standardized life tables and age-at-death from TB. Years lived-with-disability were calculated from age and gender-specific TB disease incidence using published disability weights. Non-fatal health impacts of TB were divided into years lived-with-disability-acute and years lived-with-disability-chronic. Years lived-with-disability-acute was defined as TB burden resulting from illness prior to completion of treatment including the burden from treatment-related side effects. Years lived-with-disability-chronic was defined as TB burden from disability resulting from pulmonary impairment after tuberculosis.</p> <p>Results</p> <p>There were 224 TB cases in the time period, of these 177 were culture confirmed. These 177 subjects lost a total of 1189 DALYs. Of these 1189 DALYs 23% were from years of life-lost, 2% were from years lived-with-disability-acute and 75% were from years lived-with-disability-chronic.</p> <p>Conclusions</p> <p>Our findings demonstrate that the disease burden from TB is greater than previously estimated. Pulmonary impairment after tuberculosis was responsible for the majority of the burden. These data demonstrate that successful TB control efforts may reduce the health burden more than previously recognized.</p

    Personal and Societal Health Quality Lost to Tuberculosis

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    BACKGROUND: In developed countries, tuberculosis is considered a disease with little loss of Quality-Adjusted Life Years (QALYs). Tuberculosis treatment is predominantly ambulatory and death from tuberculosis is rare. Research has shown that there are chronic pulmonary sequelae in a majority of patients who have completed treatment for pulmonary tuberculosis (PTB). This and other health effects of tuberculosis have not been considered in QALY calculations. Consequently both the burden of tuberculosis on the individual and the value of tuberculosis prevention to society are underestimated. We estimated QALYs lost to pulmonary TB patients from all known sources, and estimated health loss to prevalent TB disease. METHODOLOGY/PRINCIPAL FINDINGS: We calculated values for health during illness and treatment, pulmonary impairment after tuberculosis (PIAT), death rates, years-of-life-lost to death, and normal population health. We then compared the lifetime expected QALYs for a cohort of tuberculosis patients with that expected for comparison populations with latent tuberculosis infection and without tuberculosis infection. Persons with culture-confirmed tuberculosis accrued fewer lifetime QALYs than those without tuberculosis. Acute tuberculosis morbidity cost 0.046 QALYs (4% of total) per individual. Chronic morbidity accounted for an average of 0.96 QALYs (78% of total). Mortality accounted for 0.22 QALYs lost (18% of total). The net benefit to society of averting one case of PTB was about 1.4 QALYs. CONCLUSIONS/SIGNIFICANCE: Tuberculosis, a preventable disease, results in QALYs lost owing to illness, impairment, and death. The majority of QALYs lost from tuberculosis resulted from impairment after microbiologic cure. Successful TB prevention efforts yield more health quality than previously thought and should be given high priority by health policy makers. (Refer to Abstracto S1 for Spanish language abstract)

    A social-ecological-technological systems framework for urban ecosystem services

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    As rates of urbanization and climatic change soar, decision-makers are increasingly challenged to provide innovative solutions that simultaneously address climate-change impacts and risks and inclusively ensure quality of life for urban residents. Cities have turned to nature-based solutions to help address these challenges. Nature-based solutions, through the provision of ecosystem services, can yield numerous benefits for people and address multiple challenges simultaneously. Yet, efforts to mainstream nature-based solutions are impaired by the complexity of the interacting social, ecological, and technological dimensions of urban systems. This complexity must be understood and managed to ensure ecosystem-service provisioning is effective, equitable, and resilient. Here, we provide a social-ecological-technological system (SETS) framework that builds on decades of urban ecosystem services research to better understand four core challenges associated with urban nature-based solutions: multi-functionality, systemic valuation, scale mismatch of ecosystem services, and inequity and injustice. The framework illustrates the importance of coordinating natural, technological, and socio-economic systems when designing, planning, and managing urban nature-based solutions to enable optimal social-ecological outcomes

    A social-ecological-technological systems framework for urban ecosystem services

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    As rates of urbanization and climatic change soar, decision-makers are increasingly challenged to provide innovative solutions that simultaneously address climate change impacts and risks and inclusively ensure quality of life for urban residents. Cities have turned to nature-based solutions to help address these challenges. Nature-based solutions, through the provision of ecosystem services, can yield numerous benefits for people and address multiple challenges simultaneously. Yet, efforts to mainstream nature-based solutions are impaired by the complexity of the interacting social, ecological, and technological dimensions of urban systems. This complexity must be understood and managed to ensure ecosystem-service provisioning is effective, equitable, and resilient. Here, we provide a social-ecological-technological system (SETS) framework that builds on decades of urban ecosystem services research to better understand four core challenges associated with urban nature-based solutions: multi-functionality, systemic valuation, scale mismatch of ecosystem services, and inequity and injustice. The framework illustrates the importance of coordinating natural, technological, and socio-economic systems when designing, planning, and managing urban nature-based solutions to enable optimal social-ecological outcomes

    Non-hispanic whites have higher risk for pulmonary impairment from pulmonary tuberculosis

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    <p>Abstract</p> <p>Background</p> <p>Disparities in outcomes associated with race and ethnicity are well documented for many diseases and patient populations. Tuberculosis (TB) disproportionately affects economically disadvantaged, racial and ethnic minority populations. Pulmonary impairment after tuberculosis (PIAT) contributes heavily to the societal burden of TB. Individual impacts associated with PIAT may vary by race/ethnicity or socioeconomic status.</p> <p>Methods</p> <p>We analyzed the pulmonary function of 320 prospectively identified patients with pulmonary tuberculosis who had completed at least 20 weeks standard anti-TB regimes by directly observed therapy. We compared frequency and severity of spirometry-defined PIAT in groups stratified by demographics, pulmonary risk factors, and race/ethnicity, and examined clinical correlates to pulmonary function deficits.</p> <p>Results</p> <p>Pulmonary impairment after tuberculosis was identified in 71% of non-Hispanic Whites, 58% of non-Hispanic Blacks, 49% of Asians and 32% of Hispanics (<it>p </it>< 0.001). Predictors for PIAT varied between race/ethnicity. PIAT was evenly distributed across all levels of socioeconomic status suggesting that PIAT and socioeconomic status are not related. PIAT and its severity were significantly associated with abnormal chest x-ray, <it>p </it>< 0.0001. There was no association between race/ethnicity and time to beginning TB treatment, <it>p </it>= 0.978.</p> <p>Conclusions</p> <p>Despite controlling for cigarette smoking, socioeconomic status and time to beginning TB treatment, non-Hispanic White race/ethnicity remained an independent predictor for disproportionately frequent and severe pulmonary impairment after tuberculosis relative to other race/ethnic groups. Since race/ethnicity was self reported and that race is not a biological construct: these findings must be interpreted with caution. However, because race/ethnicity is a proxy for several other unmeasured host, pathogen or environment factors that may contribute to disparate health outcomes, these results are meant to suggest hypotheses for further research.</p

    Addressing disparities in maternal health care in Pakistan: gender, class and exclusion

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    Background: After more than two decades of the Safe Motherhood Initiative and Millennium Development Goals aimed at reducing maternal mortality, women continue to die in childbirth at unacceptably high rates in Pakistan. While an extensive literature describes various programmatic strategies, it neglects the rigorous analysis of the reasons these strategies have been unsuccessful, especially for women living at the economic and social margins of society. A critical gap in current knowledge is a detailed understanding of the root causes of disparities in maternal health care, and in particular, how gender and class influence policy formulation and the design and delivery of maternal health care services. Taking Pakistan as a case study, this research builds upon two distinct yet interlinked conceptual approaches to understanding the phenomenon of inequity in access to maternal health care: social exclusion and health systems as social institutions. Methods/Design: This four year project consists of two interrelated modules that focus on two distinct groups of participants: (1) poor, disadvantaged women and men and (2) policy makers, program managers and health service providers. Module one will employ critical ethnography to understand the key axes of social exclusion as related to gender, class and zaat and how they affect women’s experiences of using maternal health care. Through health care setting observations, interviews and document review, Module two will assess policy design and delivery of maternal health services. Discussion: This research will provide theoretical advances to enhance understanding of the power dynamics of gender and class that may underlie poor women’s marginalization from health care systems in Pakistan. It will also provide empirical evidence to support formulation of maternal health care policies and health care system practices aimed at reducing disparities in maternal health care in Pakistan. Lastly, it will enhance inter-disciplinary research capacity in the emerging field of social exclusion and maternal health and help reduce social inequities and achieve the Millennium Development Goal No. 5

    Psychological stress in adolescent and adult mice increases neuroinflammation and attenuates the response to LPS challenge

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    <p>Abstract</p> <p>Background</p> <p>There is ample evidence that psychological stress adversely affects many diseases. Recent evidence has shown that intense stressors can increase inflammation within the brain, a known mediator of many diseases. However, long-term outcomes of chronic psychological stressors that elicit a neuroinflammatory response remain unknown.</p> <p>Methods</p> <p>To address this, we have modified previously described models of rat/mouse predatory stress (PS) to increase the intensity of the interaction. We postulated that these modifications would enhance the predator-prey experience and increase neuroinflammation and behavioral dysfunction in prey animals. In addition, another group of mice were subjected to a modified version of chronic unpredictable stress (CUS), an often-used model of chronic stress that utilizes a combination of stressors that include physical, psychological, chemical, and other. The CUS model has been shown to exacerbate a number of inflammatory-related diseases via an unknown mechanism. Using these two models we sought to determine: 1) whether chronic PS or CUS modulated the inflammatory response as a proposed mechanism by which behavioral deficits might be mediated, and 2) whether chronic exposure to a pure psychological stressor (PS) leads to deficits similar to those produced by a CUS model containing psychological and physical stressors. Finally, to determine whether acute PS has neuroinflammatory consequences, adult mice were examined at various time-points after PS for changes in inflammation.</p> <p>Results</p> <p>Adolescent mice subjected to chronic PS had increased basal expression of inflammation within the midbrain. CUS and chronic PS mice also had an impaired inflammatory response to a subsequent lipopolysaccharide challenge and PS mice displayed increased anxiety- and depressive-like behaviors following chronic stress. Finally, adult mice subjected to acute predatory stress had increased gene expression of inflammatory factors.</p> <p>Conclusion</p> <p>Our results demonstrate that predatory stress, an ethologically relevant stressor, can elicit changes in neuroinflammation and behavior. The predatory stress model may be useful in elucidating mechanisms by which psychological stress modulates diseases with an inflammatory component.</p

    The AURORA Study: A Longitudinal, Multimodal Library of Brain Biology and Function after Traumatic Stress Exposure

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    Adverse posttraumatic neuropsychiatric sequelae (APNS) are common among civilian trauma survivors and military veterans. These APNS, as traditionally classified, include posttraumatic stress, postconcussion syndrome, depression, and regional or widespread pain. Traditional classifications have come to hamper scientific progress because they artificially fragment APNS into siloed, syndromic diagnoses unmoored to discrete components of brain functioning and studied in isolation. These limitations in classification and ontology slow the discovery of pathophysiologic mechanisms, biobehavioral markers, risk prediction tools, and preventive/treatment interventions. Progress in overcoming these limitations has been challenging because such progress would require studies that both evaluate a broad spectrum of posttraumatic sequelae (to overcome fragmentation) and also perform in-depth biobehavioral evaluation (to index sequelae to domains of brain function). This article summarizes the methods of the Advancing Understanding of RecOvery afteR traumA (AURORA) Study. AURORA conducts a large-scale (n = 5000 target sample) in-depth assessment of APNS development using a state-of-the-art battery of self-report, neurocognitive, physiologic, digital phenotyping, psychophysical, neuroimaging, and genomic assessments, beginning in the early aftermath of trauma and continuing for 1 year. The goals of AURORA are to achieve improved phenotypes, prediction tools, and understanding of molecular mechanisms to inform the future development and testing of preventive and treatment interventions
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