Non-human animal studies demonstrate relationships between stress and selective intake of palatable food. In humans, exposure to laboratory stressors and self-reported stress are associated with greater food intake. Large studies have yet to examine chronic stress exposure and eating behavior. The current study assessed the relationship between stress (perceived and chronic), drive to eat, and reported food frequency intake (nutritious food vs. palatable non-nutritious food) in women ranging from normal weight to obese (N = 457). Greater reported stress, both exposure and perception, was associated with indices of greater drive to eat— including feelings of disinhibited eating, binge eating, hunger, and more ineffective attempts to control eating (rigid restraint; r’s from .11 to .36, p ’s < .05). These data suggest that stress exposure may lead to a stronger drive to eat and may be one factor promoting excessive weight gain. Relationships between stress and eating behavior are of importance to public health given the concurrent increase in reported stress and obesity rates.

Dysfunction of the RNA-binding protein, TDP-43, is strongly implicated as a causative event in many neurodegenerative diseases including amyotrophic lateral sclerosis (ALS). TDP-43 is normally found in the nucleus and pathological hallmarks of ALS include the presence of cytoplasmic protein aggregates containing TDP-43 and an associated loss of TDP-43 from the nucleus. Loss of nuclear TDP-43 likely contributes to neurodegeneration. Using Drosophila melanogaster to model TDP-43 loss of function, we show that reduced levels of the voltage-gated calcium channel, cacophony, mediate some of the physiological effects of TDP-43 loss. Null mutations in the Drosophila orthologue of TDP-43, named TBPH, resulted in defective larval locomotion and reduced levels of cacophony protein in whole animals and at the neuromuscular junction. Restoring the levels of cacophony in all neurons or selectively in motor neurons rescued these locomotion defects. Using TBPH immunoprecipitation, we showed that TBPH associates with cacophony transcript, indicating that it is likely to be a direct target for TBPH. Loss of TBPH leads to reduced levels of cacophony transcript, possibly due to increased degradation. In addition, TBPH also appears to regulate the inclusion of some alternatively spliced exons of cacophony. If similar effects of cacophony or related calcium channels are found in human ALS patients, these could be targets for the development of pharmacological therapies for ALS.

SUMMARYConventional soluble guanylyl cyclases form α/β heterodimers that are activated by nitric oxide (NO). Recently, atypical members of the soluble guanylyl cyclase family have been described that include the ratβ2 subunit and MsGC-β3 from Manduca sexta. Predictions from the Drosophila melanogaster genome identify three atypical guanylyl cyclase subunits: Gyc-88E (formerly CG4154), Gyc-89Da (formerly CG14885) and Gyc-89Db (formerly CG14886). Preliminary data showed that transient expression of Gyc-88E in heterologous cells generated enzyme activity in the absence of additional subunits that was slightly stimulated by the NO donor sodium nitroprusside (SNP) but not the NO donor DEA-NONOate or the NO-independent activator YC-1. Gyc-89Db was inactive when expressed alone but when co-expressed with Gyc-88E enhanced the basal and SNP-stimulated activity of Gyc-88E, suggesting that they may form heterodimers in vivo. Here,we describe the localization of Gyc-88E and Gyc-89Db and show that they are expressed in the embryonic and larval central nervous systems and are colocalized in several peripheral neurons that innervate trachea, basiconical sensilla and the sensory cones in the posterior segments of the embryo. We also show that there are two splice variants of Gyc-88E that differ by seven amino acids, although no differences in biochemical properties could be determined. We have also extended our analysis of the NO activation of Gyc-88E and Gyc-89Db, showing that several structurally unrelated NO donors activate Gyc-88E when expressed alone or when co-expressed with Gyc-89Db.

Interest in artificial intelligence (AI) research has grown rapidly over the past few years, in part thanks to the numerous successes of modern machine learning techniques such as deep learning, the availability of large datasets and improvements in computing power. AI is proving to be increasingly applicable to healthcare and there is a growing list of tasks where algorithms have matched or surpassed physician performance. Despite the successes there remain significant concerns and challenges surrounding algorithm opacity, trust and patient data security. Notwithstanding these challenges, AI technologies will likely become increasingly integrated into emergency medicine in the coming years. This perspective presents an overview of current AI research relevant to emergency medicine.

Background and Purpose-We sought to examine the frequency, predictors, and effects of nontreatment with antithrombotic and antihypertensive therapies 3 months after ischemic stroke. Methods-The population-based South London Community Stroke Register prospectively collected data on first-in-alifetime strokes between 1995 and 1997. Among patients registered with ischemic stroke, treatment status with antithrombotic and antihypertensive therapies was examined 3 months after the event. Results-In a cohort of 457 patients with ischemic stroke, 393 (86.0%) were considered appropriate for antiplatelet medication, 32 (7.0%) for anticoagulant medication, and 254 (55.9%) for antihypertensive medication. The rates of nontreatment observed 3 months after the event were 24.4% for antiplatelet, 59.4% for anticoagulant, and 29.5% for antihypertensive medication. Independent risk factors for nontreatment with antithrombotic therapies (antiplatelets and anticoagulants) were the subtype of stroke (nonlacunar infarct: ORϭ1.60, 95% CI 1.07 to 2.54), stroke severity measured by the Glasgow Coma Scale (GCS) score (GCS Յ13: OR 2.08, 95% CI 1.18 to 3.66) and the Barthel Index (BI) score 5 days after the event (BI Յ10: OR 1.85, 95% CI 1.17 to 2.93). For antihypertensive therapies the stroke subtype (OR 2.46, 95% CI 1.33 to 4.54), GCS score (OR 2.97, 95% CI 1.35 to 6.53), BI score (OR 2.33, 95% CI 1.27 to 4.29), and ethnicity (Caucasian: OR 2.43, 95% CI 1.15 to 5.14) were independently associated with nontreatment. Cox regression modeling showed no significant association between the treatment status and recurrence-free 3-year survival rates after controlling for severity and subtype of stroke. Conclusions-Secondary prevention for a common disease such as stroke appears to be inadequate in the study area.Healthcare professionals need to consider antithrombotic and antihypertensive therapies for all stroke patients. (Stroke. 2000;31:469-475.)