Power Grid Politics: Winter Storm Uri and Texas Governor Greg Abbott\u27s Image Repair Discourse

Winter storm Uri hit the state of Texas on February 14, 2021. Bringing record amounts of snow, ice, and prolonged sub-zero temperatures, the storm caused widespread power outages which led to hundreds of deaths, and created a complex rhetorical situation for Governor Greg Abbott. This article examines the image repair discourse engaged in by Abbott, and ultimately concludes that his use of blame-shifting, corrective action, and defeasibility strategies were ultimately effective, but to varying degrees based on each respective strategy. We argue herein that Abbott’s strategy of shifting the blame for the debacle to ERCOT was his most effective tactic, while his reliance on corrective action approaches (while necessary and expected by the audience) were only marginally persuasive. Abbott’s defeasibility strategy was undercut both by conflicting statements, and by the recent reality that Texas does, in fact, experience extreme weather events however rare. We also argue that severe weather events are likely to become more frequent in the future, and that Texas in particular will be uniquely impacted by these storms due to climate change. We conclude that the political fortunes of elected officials will increasingly depend on how they justify their response to these cataclysmic storms

Genetic differences in the aryl hydrocarbon receptor and CYP1A2 affect sensitivity to developmental polychlorinated biphenyl exposure in mice: relevance to studies of human neurological disorders

Polychlorinated biphenyls (PCBs) are persistent organic pollutants that remain a human health concern with newly discovered sources of contamination and ongoing bioaccumulation and biomagnification. Children exposed during early brain development are at highest risk of neurological deficits, but highly exposed adults reportedly have an increased risk of Parkinson\u27s disease. Our previous studies found allelic differences in the aryl hydrocarbon receptor and cytochrome P450 1A2 (CYP1A2) affect sensitivity to developmental PCB exposure, resulting in cognitive deficits and motor dysfunction. High-affinity Ahr b Cyp1a2(-/-) mice were most sensitive compared with poor-affinity Ahr d Cyp1a2(-/-) and wild-type Ahr b Cyp1a2(+/+) mice. Our follow-up studies assessed biochemical, histological, and gene expression changes to identify the brain regions and pathways affected. We also measured PCB and metabolite levels in tissues to determine if genotype altered toxicokinetics. We found evidence of AHR-mediated toxicity with reduced thymus and spleen weights and significantly reduced thyroxine at P14 in PCB-exposed pups. In the brain, the greatest changes were seen in the cerebellum where a foliation defect was over-represented in Cyp1a2(-/-) mice. In contrast, we found no difference in tyrosine hydroxylase immunostaining in the striatum. Gene expression patterns varied across the three genotypes, but there was clear evidence of AHR activation. Distribution of parent PCB congeners also varied by genotype with strikingly high levels of PCB 77 in poor-affinity Ahr d Cyp1a2(-/-) while Ahr b Cyp1a2(+/+) mice effectively sequestered coplanar PCBs in the liver. Together, our data suggest that the AHR pathway plays a role in developmental PCB neurotoxicity, but we found little evidence that developmental exposure is a risk factor for Parkinson\u27s disease