166 research outputs found

    Diverse Aging and Health Inequality by Race and Ethnicity

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    Although gerontologists have long embraced the concept of heterogeneity in theories and models of aging, recent research reveals the importance of racial and ethnic diversity on life course processes leading to health inequality. This article examines research on health inequality by race and ethnicity and identifies theoretical and methodological innovations that are transforming the study of health disparities. Drawing from cumulative inequality theory, we propose greater use of life course analysis, more attention to variability within racial and ethnic groups, and better integration of environmental context into the study of accumulation processes leading to health disparities

    Diverse Aging and Health Inequality by Race and Ethnicity

    Get PDF
    Although gerontologists have long embraced the concept of heterogeneity in theories and models of aging, recent research reveals the importance of racial and ethnic diversity on life course processes leading to health inequality. This article examines research on health inequality by race and ethnicity and identifies theoretical and methodological innovations that are transforming the study of health disparities. Drawing from cumulative inequality theory, we propose greater use of life course analysis, more attention to variability within racial and ethnic groups, and better integration of environmental context into the study of accumulation processes leading to health disparities

    Avoiding the Major Causes of Death: Does Childhood Misfortune Reduce the Likelihood of Being Disease Free in Later Life?

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    Objectives: Although previous research reveals the detrimental effects of early misfortune on the development of chronic diseases in later life, few studies have investigated its effects on remaining disease free. This study draws on cumulative inequality theory to investigate whether experiencing childhood misfortune reduces the likelihood of remaining disease free over time. Method: This study utilizes five waves of data from the Health and Retirement Study to test whether five domains of childhood misfortune predict being disease free at baseline (2004) and developing disease over time (2004–2012). Results: Respondents reporting risky parental behaviors during childhood were less likely to be disease free at baseline and had an increased risk of disease onset over time, the latter driven by having a guardian who smoked in combination with more pack-years smoked in adulthood. Furthermore, we find that adult resources, that is wealth, help to mitigate the noxious effects of other misfortunes, notably poor socioeconomic conditions. Discussion: Consistent with cumulative inequality theory, these findings reveal that experiencing multiple types of misfortune during childhood decreases the likelihood of remaining disease free in later life, but engaging in health behaviors, such as physical activity, can help to ameliorate some of the noxious effects of early misfortune

    Undetectable mannose binding lectin is associated with HRCT proven bronchiectasis in rheumatoid arthritis (RA)

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    Aim: The aim of this study was to ascertain whether mannose binding lectin deficiency is implicated in coexistent rheumatoid arthritis and bronchiectasis and to determine whether undetectable mannose binding lectin confers poorer long-term survival in coexistent rheumatoid arthritis and bronchiectasis or in rheumatoid arthritis in general. Materials and methods: A retrospective audit was conducted in a rheumatoid arthritis cohort in which mannose binding lectin had been measured by enzyme linked immunosorbent assay from 2007–11. Rheumatoid arthritis patients with physician diagnosed HRCT proven bronchiectasis were recruited during this time and compared to those with uncomplicated rheumatoid arthritis. Survival from disease onset was recorded in October 2018. Kaplan-Meier survival estimates were performed to assess mortality over time in the two groups. Log rank tests were used for equality of survivor functions. Results: The two groups were demographically comparable. A higher frequency of undetectable mannose binding lectin was observed in coexistent rheumatoid arthritis and bronchiectasis (37.5%) compared to uncomplicated rheumatoid arthritis, (8.9%, P = 0.005). Undetectable mannose binding lectin correlated with a strong trend toward poor survival in rheumatoid arthritis overall (P = 0.057). Cox regression analysis however, showed no difference in the hazard ratio for survival between the two groups when corrected for age, gender, prednisolone use ever, rheumatoid factor status and the full range of MBL concentrations. Conclusion: In summary, undetectable mannose binding lectin is associated with coexistent rheumatoid arthritis and bronchiectasis and correlates with poor survival in rheumatoid arthritis overall. These findings further implicate immunodeficiency in the genesis of bronchiectasis in rheumatoid arthriti

    Advancing the Entry-Level Practitioner: A Curricular Model of the Professional Occupational Therapy Doctoral Degree

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    The recent growth of entry-level occupational therapy doctoral (EL-OTD) programs has been met with mixed opinions from both occupational therapy educators and practitioners. These opinions occasionally have been accompanied by uncertainty about the specific curricular components that differentiate the EL-OTD from the entry-level master’s degree. In an effort to address this uncertainty, the purpose of this article is to present one example of an EL-OTD curricular model and describe its distinct educational components. This curricular model integrates recommendations for doctoral education originally proposed by Case-Smith et al. (2014) and is characterized by the following three components: 1) Advanced Coursework; 2) the Doctoral Capstone Project; and 3) the Doctoral Capstone Experience. We share the lessons learned after matriculating three cohorts of EL-OTD students and describe influences from the field of implementation science that have informed the development of our curriculum

    Kv7 channels are upregulated during striatal neuron development and promote maturation of human iPSC-derived neurons

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    Kv7 channels determine the resting membrane potential of neurons and regulate their excitability. Even though dysfunction of Kv7 channels has been linked to several debilitating childhood neuronal disorders, the ontogeny of the constituent genes, which encode Kv7 channels (KNCQ), and expression of their subunits have been largely unexplored. Here, we show that developmentally regulated expression of specific KCNQ mRNA and Kv7 channel subunits in mouse and human striatum is crucial to the functional maturation of mouse striatal neurons and human-induced pluripotent stem cell-derived neurons. This demonstrates their pivotal role in normal development and maturation, the knowledge of which can now be harnessed to synchronise and accelerate neuronal differentiation of stem cell-derived neurons, enhancing their utility for disease modelling and drug discovery

    Undetectable mannose binding lectin and corticosteroids increase serious infection risk in Rheumatoid Arthritis

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    Background: Infection is the leading cause of death in rheumatoid arthritis (RA). Corticosteroid (CS) use is a known and important risk factor for serious infections (SIs). Mannose binding lectin (MBL) is a genetically determined component of the innate immune system implicated in neonatal infections. Objective: Our aim was to determine whether MBL deficiency is a risk factor for SIs in RA and to compare it with CS use and also synthetic and biologic disease-modifying antirheumatic drug (DMARD) therapy. Methods: Data on 228 patients with RA were collected for up to 7 years (median = 5.9 years). Serum MBL concentrations were determined in all patients receiving synthetic (n = 96) or biologic (n = 132) DMARD therapy. Results: High rates of SIs were observed in RA irrespective of treatment (17%). Similar rates of SIs were observed in synthetic and biologic DMARD users. The rates of single and multiple Sis were similar, irrespective of the use of a biologic agent. Undetectable MBL (\u3c56 ng/mL) concentrations and maintenance prednisolone at 10 mg per day or higher were associated with an increased risk for an SI, with incident risk ratio of 4.67 (P = .001) and 4.70 (P \u3c .001), respectively. Conclusions: Undetectable MBL and prednisolone confer a high risk for an SI. The use of biologic DMARDs did not confer substantial SI risk in this observational study. MBL deficiency is hitherto an unrecognized risk factor for an SI in RA

    Isolation of a novel fusogenic orthoreovirus from Eucampsipoda africana bat flies in South Africa

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    We report on the isolation of a novel fusogenic orthoreovirus from bat flies (Eucampsipoda africana) associated with Egyptian fruit bats (Rousettus aegyptiacus) collected in South Africa. Complete sequences of the ten dsRNA genome segments of the virus, tentatively named Mahlapitsi virus (MAHLV), were determined. Phylogenetic analysis places this virus into a distinct clade with Baboon orthoreovirus, Bush viper reovirus and the bat-associated Broome virus. All genome segments of MAHLV contain a 5' terminal sequence (5'-GGUCA) that is unique to all currently described viruses of the genus. The smallest genome segment is bicistronic encoding for a 14 kDa protein similar to p14 membrane fusion protein of Bush viper reovirus and an 18 kDa protein similar to p16 non-structural protein of Baboon orthoreovirus. This is the first report on isolation of an orthoreovirus from an arthropod host associated with bats, and phylogenetic and sequence data suggests that MAHLV constitutes a new species within the Orthoreovirus genus.The project is jointly funded by the following grants awarded to: Janusz T. Paweska (CDC Global Disease Detection program, GDD 5U19 GH000571-05/96667), Wanda Markotter (South African National Research Foundation, Grant UID 91496 and 92524; Poliomyelitis Research Foundation, PRF Grant number 12/14) and Petrus Jansen van Vuren (South African National Research Foundation, Incentive Funding for Rated Researchers, Grant UID 85544).http://www.mdpi.com/journal/virusesam2016Microbiology and Plant Patholog
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