Management of multiple frostbite casualties at a burn center: San Antonio, Texas, 12-20 February 2021.

BACKGROUND: Frostbite is an insidious disease that normally affects people of cold climates. Winter Storm Uri, which occurred from February 12-20, 2021, created unique metrological conditions for Texas. It caused prolonged sub-freezing temperatures and led to rolling blackouts, affecting 2.8 million Texans including 300,000 people in San Antonio. We report 13 frostbite patients admitted to one burn center during this event. OBJECTIVE: We aimed to determine the at-risk population for frostbite, to categorize their injury severity, and to describe their treatment. A secondary aim was to describe the rehabilitation management of these patients. METHODS: This is a single-center retrospective study. Each patient's injuries were assessed by a topographical grading system. Comparisons were made among those who were admitted to the intensive care unit (ICU), admitted to the progressive care unit (PCU), and treated as outpatients. RESULTS: Thirteen patients were identified. Ten (76.9 %) considered themselves homeless, and 9 (69.2 %) were directly exposed to the elements. The median delay between time of injury and presentation to a medical facility was 3 days (IQR 1-6). Only 3 patients presented to a medical facility within 24 h. Six (46 %) sustained grade 2 injuries, 2 (15 %) sustained grade 3 injuries, and 5 (38%) sustained grade 4 injuries. Only one patient met criteria to receive tissue plasminogen activator (tPA), which was discontinued due to hematochezia. Patients admitted to the ICU, when compared to patients admitted to the ward, had a longer length of stay (median 73 days v. 12 days, p = 0.0215), and required more amputations at below-the-knee or higher levels (3 v. 0, p-value 0.0442). CONCLUSION: In a region unaccustomed and perhaps unprepared to deal with winter storms, the population is particularly vulnerable to frostbite. Lack of awareness of frostbite injuries likely led to the delay in the presentation of patients, which prevented the timely use of tPA. Increasing public awareness may increase readiness.

Atypical caudate anatomy in children who stutter.

A temporal motor defect in speech preparation and/or planning may contribute to the development of stuttering. This defect may be linked to a dysfunctional cortical-subcortical network at the level of the striatum. To determine whether structural differences exist and whether group differences are associated with stuttering severity or manual laterality, the caudate was measured in 14 children who stutter (CWS) and in a control group of right-handed boys, ages 8-13 years. There was a statistically significant hemisphere by group effect for caudate volume. CWS had reduced right caudate volume and atypical leftward asymmetry compared to controls. Nine of the 13 CWS with atypical caudate asymmetry had atypical manual laterality. These anomalies may represent a vulnerability that perturbs speech planning/preparation and contributes to inefficiencies in action-perception coupling that may be an indicator of stuttering susceptibility. These results suggest that right-handed boys who stutter may have a defect in the feedforward cortico-striato-thalamo-cortical networks.

Nucleolar stress in Drosophila melanogaster: RNAi-mediated depletion of Nopp140.

Nucleolar stress results when ribosome biogenesis is disrupted. An excellent example is the human Treacher Collins syndrome in which the loss of the nucleolar chaperone, Treacle, leads to p53-dependent apoptosis in embryonic neural crest cells and ultimately to craniofacial birth defects. Here, we show that depletion of the related nucleolar phosphoprotein, Nopp140, in Drosophila melanogaster led to nucleolar stress and eventual lethality when multiple tissues were depleted of Nopp140. We used TEM, immuno-blot analysis and metabolic protein labeling to show the loss of ribosomes. Targeted loss of Nopp140 in larval wing discs caused Caspase-dependent apoptosis which eventually led to defects in the adult wings. These defects were not rescued by a p53 gene deletion, as the craniofacial defects were in the murine model of TCS, thus suggesting that apoptosis caused by nucleolar stress in Drosophila is induced by a p53-independent mechanism. Loss of Nopp140 in larval polyploid midgut cells induced premature autophagy as marked by the accumulation of mCherry-ATG8a into autophagic vesicles. We also found elevated phenoloxidase A3 levels in whole larval lysates and within the hemolymph of Nopp140-depleted larvae vs. hemolymph from parental genotype larvae. Phenoloxidase A3 enrichment was coincident with the appearance of melanotic tumors in the Nopp140-depleted larvae. The occurrence of apoptosis, autophagy and phenoloxidase A3 release to the hemolymph upon nucleolar stress correlated well with the demonstrated activation of Jun N-terminal kinase (JNK) in Nopp140-depleted larvae. We propose that JNK is a central stress response effector that is activated by nucleolar stress in Drosophila larvae.