Because I Am Human: Centering Black Women with Dis/abilities in Transition Planning from High School to College

Indiana University-Purdue University Indianapolis (IUPUI)There is a dearth of literature about post-secondary transition experiences of Black women with dis/abilities (BWD). In this qualitative study, I explore transition experiences of five post-secondary BWD from high school to college in order to privilege her chronicles and narratives as knowledge. In addition, two urban public high school transition coordinators (TC) participated in the study. Three inquiries guided my dissertation: (1) features of educational experiences narrated by BWD, (2) features of transition services provided to students with dis/abilities, including roles of and approaches as described by the TCs, and (3) how BWD narratives may be leveraged to critique and extend transition services as the TCs described them. I engaged in three semi-structured interviews with six of the seven participants (one interview with the seventh). I drew from Disability Studies/Disability Studies in Education (DSE), Critical Race Theory, and Womanist/Black Feminist Theory and their shared tenets of voice and counternarratives and concepts of social construction and falsification of consciousness to analyze the narratives of BWD participants. I drew from the DS/DSE tenet of interlocking systems of oppression, DisCrit tenet three, race and ability, and constructs of Inputs and Outcomes in work on Modeling Transition Education to analyze the TCs’ narratives and in connection to the narratives of the BWD. Across both sets of participants, three themes in the form of Truths emerged; they were terrible and sticky experiences of racial/dis/ability oppression for the BWDs and, imposing of whiteness and normalization within the transition education practices described by the TCs. For the BWD, those terrible and sticky truths took three forms: (a) Pathologization; (b) Disablement; and (c) Exclusion. Another type of truth in the BWD’s narratives, however, was Subverted Truths: (re)defined identities and radical love, (re)placed competence and knowledge, and (revalued sisterhood and community, the ways of pushing back and resisting the Truths and their effects. I discuss implications for BWD post-secondary transition-planning-and-programming theory, research, policy, practice, praxis, and spirituality

Radical (re)naming through a tapestry of autoethographic voices: Finding healing through dis/ability theorizing

In this article, we engaged in a multi-layered collective autoethnography about disability, ableism, and identity within the context of schools and society by exploring the relationship between Curriculum Studies and Dis/ability Studies in Education. While excerpts of our individual narratives are embedded in the article, our final piece weaves together our individual reflections to illustrate that there is no single experience of dis/ability; however, there are themes about dis/ability and resistance to ableism that can be gleaned from hearing a multiplicity of voices within a context of intersectionality for radical individual, social and (inter)disciplinary transformation

Ablation of PGC-1β Results in Defective Mitochondrial Activity, Thermogenesis, Hepatic Function, and Cardiac Performance

The transcriptional coactivator peroxisome proliferator-activated receptor-gamma coactivator-1β (PGC-1β) has been implicated in important metabolic processes. A mouse lacking PGC-1β (PGC1βKO) was generated and phenotyped using physiological, molecular, and bioinformatic approaches. PGC1βKO mice are generally viable and metabolically healthy. Using systems biology, we identified a general defect in the expression of genes involved in mitochondrial function and, specifically, the electron transport chain. This defect correlated with reduced mitochondrial volume fraction in soleus muscle and heart, but not brown adipose tissue (BAT). Under ambient temperature conditions, PGC-1β ablation was partially compensated by up-regulation of PGC-1α in BAT and white adipose tissue (WAT) that lead to increased thermogenesis, reduced body weight, and reduced fat mass. Despite their decreased fat mass, PGC1βKO mice had hypertrophic adipocytes in WAT. The thermogenic role of PGC-1β was identified in thermoneutral and cold-adapted conditions by inadequate responses to norepinephrine injection. Furthermore, PGC1βKO hearts showed a blunted chronotropic response to dobutamine stimulation, and isolated soleus muscle fibres from PGC1βKO mice have impaired mitochondrial function. Lack of PGC-1β also impaired hepatic lipid metabolism in response to acute high fat dietary loads, resulting in hepatic steatosis and reduced lipoprotein-associated triglyceride and cholesterol content. Altogether, our data suggest that PGC-1β plays a general role in controlling basal mitochondrial function and also participates in tissue-specific adaptive responses during metabolic stress

Canagliflozin and renal outcomes in type 2 diabetes and nephropathy

BACKGROUND Type 2 diabetes mellitus is the leading cause of kidney failure worldwide, but few effective long-term treatments are available. In cardiovascular trials of inhibitors of sodium–glucose cotransporter 2 (SGLT2), exploratory results have suggested that such drugs may improve renal outcomes in patients with type 2 diabetes. METHODS In this double-blind, randomized trial, we assigned patients with type 2 diabetes and albuminuric chronic kidney disease to receive canagliflozin, an oral SGLT2 inhibitor, at a dose of 100 mg daily or placebo. All the patients had an estimated glomerular filtration rate (GFR) of 30 to <90 ml per minute per 1.73 m2 of body-surface area and albuminuria (ratio of albumin [mg] to creatinine [g], >300 to 5000) and were treated with renin–angiotensin system blockade. The primary outcome was a composite of end-stage kidney disease (dialysis, transplantation, or a sustained estimated GFR of <15 ml per minute per 1.73 m2), a doubling of the serum creatinine level, or death from renal or cardiovascular causes. Prespecified secondary outcomes were tested hierarchically. RESULTS The trial was stopped early after a planned interim analysis on the recommendation of the data and safety monitoring committee. At that time, 4401 patients had undergone randomization, with a median follow-up of 2.62 years. The relative risk of the primary outcome was 30% lower in the canagliflozin group than in the placebo group, with event rates of 43.2 and 61.2 per 1000 patient-years, respectively (hazard ratio, 0.70; 95% confidence interval [CI], 0.59 to 0.82; P=0.00001). The relative risk of the renal-specific composite of end-stage kidney disease, a doubling of the creatinine level, or death from renal causes was lower by 34% (hazard ratio, 0.66; 95% CI, 0.53 to 0.81; P<0.001), and the relative risk of end-stage kidney disease was lower by 32% (hazard ratio, 0.68; 95% CI, 0.54 to 0.86; P=0.002). The canagliflozin group also had a lower risk of cardiovascular death, myocardial infarction, or stroke (hazard ratio, 0.80; 95% CI, 0.67 to 0.95; P=0.01) and hospitalization for heart failure (hazard ratio, 0.61; 95% CI, 0.47 to 0.80; P<0.001). There were no significant differences in rates of amputation or fracture. CONCLUSIONS In patients with type 2 diabetes and kidney disease, the risk of kidney failure and cardiovascular events was lower in the canagliflozin group than in the placebo group at a median follow-up of 2.62 years

Averting biodiversity collapse in tropical forest protected areas

The rapid disruption of tropical forests probably imperils global biodiversity more than any other contemporary phenomenon¹⁻³. With deforestation advancing quickly, protected areas are increasingly becoming final refuges for threatened species and natural ecosystem processes. However, many protected areas in the tropics are themselves vulnerable to human encroachment and other environmental stresses⁴⁻⁹. As pressures mount, it is vital to know whether existing reserves can sustain their biodiversity. A critical constraint in addressing this question has been that data describing a broad array of biodiversity groups have been unavailable for a sufficiently large and representative sample of reserves. Here we present a uniquely comprehensive data set on changes over the past 20 to 30 years in 31 functional groups of species and 21 potential drivers of environmental change, for 60 protected areas stratified across the world’s major tropical regions. Our analysis reveals great variation in reserve ‘health’: about half of all reserves have been effective or performed passably, but the rest are experiencing an erosion of biodiversity that is often alarmingly widespread taxonomically and functionally. Habitat disruption, hunting and forest-product exploitation were the strongest predictors of declining reserve health. Crucially, environmental changes immediately outside reserves seemed nearly as important as those inside in determining their ecological fate, with changes inside reserves strongly mirroring those occurring around them. These findings suggest that tropical protected areas are often intimately linked ecologically to their surrounding habitats, and that a failure to stem broad-scale loss and degradation of such habitats could sharply increase the likelihood of serious biodiversity declines.Keywords: Ecology, Environmental scienc

Entre réforme sociale et mouvement national

Cet ouvrage est dédié à la mémoire d’Avriel Butovsk