Search

Uranium mining for the production of nuclear technologies has left visible scars across the United States and perpetuated legacies of extraction that extend beyond material consumption to the exploitation of people and the environment. Influenced by important ongoing conversations in the environmental and energy humanities, posthumanism, and decolonial studies, I analyze how uranium extraction has been conceived of as an "event" within a colonial temporal framework. A critical examination of how religious worldviews have informed the ways that time is conceptualized and understood shifts thinking about extraction away from colonial temporalities and helps reimagine extraction through a decolonial perspective as temporally distributed, enmeshed, and complex. This reframing is imperative to foster an understanding that the radioactive byproducts of uranium created through the nuclear production process are globally dispersed, will persist across generations, and will have transgenerational implications for human and non-human organisms and the health and viability of ecologic systems. [ABSTRACT FROM AUTHOR]

Rationale: New pulmonary rehabilitation models can improve access to this effective but underused treatment for people with chronic respiratory disease; however, cost-effectiveness has not been determined. Objectives: To compare the cost-effectiveness of telerehabilitation, including videoconferencing and synchronous supervision, with standard center-based pulmonary rehabilitation. Methods: Prospective economic analyses were undertaken from a societal perspective alongside a randomized controlled equivalence trial in which adults with stable chronic respiratory disease undertook an 8-week outpatient center-based program or telerehabilitation. Clinical assessment for effectiveness (Chronic Respiratory Disease Questionnaire dyspnea domain score) was undertaken at baseline, after pulmonary rehabilitation, and at 12-month follow-up. Individual-level administrative and self-report healthcare cost data were collected over 12 months after the program (Australian dollars, 2020). Results: There were no between-group differences for effectiveness (Chronic Respiratory Disease Questionnaire dyspnea domain mean difference, −0.2 [standard error, 1.0]; P = 0.61) or total costs ($565 [5,452]; P = 0.92) over 12 months. On the cost-effectiveness plane, 97.4% of estimates fell between the equivalence margins for effectiveness. Application of a range of values for cost margin demonstrated a 95% probability that telerehabilitation was equivalent to center-based pulmonary rehabilitation when the threshold was $11,000. The results were robust to approach and sensitivity and subgroup analyses. The internal rate of return was 134% over 5 years. Program completion (regardless of model) was associated with a significant reduction in total costs in the following 12 months (β, −$17,960; 95% confidence interval, −29,967 to −5,952). Conclusions: This study supports delivery of telerehabilitation as a cost-effective alternative model of pulmonary rehabilitation for people with chronic respiratory disease. Clinical trial registered with the Australian and New Zealand Clinical Trials Register (ACTRN12616000360415). [ABSTRACT FROM AUTHOR]

Insulin and insulin-like growth factor 1 (IGF-1) are metabolic hormones with known effects on CD4+ T cells through insulin receptor (IR) and IGF-1 receptor (IGF-1R) signaling. Here, we describe specific and distinct roles for these hormones and receptors. We have found that IGF-1R, but not IR, expression is increased following CD4+ T cell activation or following differentiation toward Th17 cells. Although both insulin and IGF-1 increase the metabolism of CD4+ T cells, insulin has a more potent effect. However, IGF-1 has a unique role and acts specifically on Th17 cells to increase IL-17 production and Th17 cell metabolism. Furthermore, IGF-1 decreases mitochondrial membrane potential and mitochondrial reactive oxygen species (mROS) in Th17 cells, providing a cytoprotective effect. Interestingly, both IR and IGF-1R are required for this effect of IGF-1 on mitochondria, which suggests that the hybrid IR/IGF-1R may be required for mediating the effect of IGF-1 on mitochondrial membrane potential and mROS production. [ABSTRACT FROM AUTHOR]

Even as attention is drawn to the increasing number of individuals who experience health inequalities in the United States, little is known about the health inequalities experienced by individuals with intellectual and developmental disabilities. Current disability research mainly focuses on physical disabilities. This article discusses the health disparities experienced by individuals with intellectual and developmental disabilities. The authors conducted focus groups with parents/guardians, self-advocates, and community support professionals and key informant interviews with health care professionals to assess the needs of this less frequently documented population. Results from this study indicate that individuals with intellectual and developmental disabilities face health care disparities and inequities in four areas: access, knowledge, communication, and quality.

Introduction [CD4.sup.+] T lymphocytes are critical to mediating or suppressing normal immunity as well as inflammatory or autoimmune diseases. Antigen exposure initially leads to T cell activation, inducing rapid growth [...], Activation of [CD4.sup.+] T cells results in rapid proliferation and differentiation into effector and regulatory subsets. [CD4.sup.+] effector T cell (Teff) (Th1 and Th17) and Treg subsets are metabolically distinct, yet the specific metabolic differences that modify T cell populations are uncertain. Here, we evaluated [CD4.sup.+] T cell populations in murine models and determined that inflammatory Teffs maintain high expression of glycolytic genes and rely on high glycolytic rates, while Tregs are oxidative and require mitochondrial electron transport to proliferate, differentiate, and survive. Metabolic profiling revealed that pyruvate dehydrogenase (PDH) is a key bifurcation point between T cell glycolytic and oxidative metabolism. PDH function is inhibited by PDH kinases (PDHKs). PDHK1 was expressed in Th17 cells, but not Th1 cells, and at low levels in Tregs, and inhibition or knockdown of PDHK1 selectively suppressed Th17 cells and increased Tregs. This alteration in the [CD4.sup.+] T cell populations was mediated in part through ROS, as N-acetyl cysteine (NAC) treatment restored Th17 cell generation. Moreover, inhibition of PDHK1 modulated immunity and protected animals against experimental autoimmune encephalomyelitis, decreasing Th17 cells and increasing Tregs. Together, these data show that [CD4.sup.+] subsets utilize and require distinct metabolic programs that can be targeted to control specific T cell populations in autoimmune and inflammatory diseases.