We tested the hypothesis that underrepresented students in active-learning classrooms experience narrower achievement gaps than underrepresented students in traditional lecturing classrooms, averaged across all science, technology, engineering, and mathematics (STEM) fields and courses. We conducted a comprehensive search for both published and unpublished studies that compared the performance of underrepresented students to their overrepresented classmates in active-learning and traditional-lecturing treatments. This search resulted in data on student examination scores from 15 studies (9,238 total students) and data on student failure rates from 26 studies (44,606 total students). Bayesian regression analyses showed that on average, active learning reduced achievement gaps in examination scores by 33% and narrowed gaps in passing rates by 45%. The reported proportion of time that students spend on in-class activities was important, as only classes that implemented high-intensity active learning narrowed achievement gaps. Sensitivity analyses showed that the conclusions are robust to sampling bias and other issues. To explain the extensive variation in efficacy observed among studies, we propose the heads-and-hearts hypothesis, which holds that meaningful reductions in achievement gaps only occur when course designs combine deliberate practice with inclusive teaching. Our results support calls to replace traditional lecturing with evidence-based, active-learning course designs across the STEM disciplines and suggest that innovations in instructional strategies can increase equity in higher education.

The ability to sense and respond to stressful conditions is essential to maintain organismal homeostasis. It has long been recognized that stress response factors that improve survival in changing conditions can also influence longevity. In this review, we discuss different strategies used by animals in response to decreased O2 (hypoxia) to maintain O2 homeostasis, and consider interactions between hypoxia responses, nutritional status, and H2S signaling. O2 is an essential environmental nutrient for almost all metazoans as it plays a fundamental role in development and cellular metabolism. However, the physiological response(s) to hypoxia depend greatly on the amount of O2 available. Animals must sense declining O2 availability to coordinate fundamental metabolic and signaling pathways. It is not surprising that factors involved in the response to hypoxia are also involved in responding to other key environmental signals, particularly food availability. Recent studies in mammals have also shown that the small gaseous signaling molecule hydrogen sulfide (H2S) protects against cellular damage and death in hypoxia. These results suggest that H2S signaling also integrates with hypoxia response(s). Many of the signaling pathways that mediate the effects of hypoxia, food deprivation, and H2S signaling have also been implicated in the control of lifespan. Understanding how these pathways are coordinated therefore has the potential to reveal new cellular and organismal homeostatic mechanisms that contribute to longevity assurance in animals.

Low oxygen conditions (hypoxia) can impair essential physiological processes and cause cellular damage and death. We have shown that specific hypoxic conditions disrupt protein homeostasis in C . elegans , leading to protein aggregation and proteotoxicity. Here, we show that nutritional cues regulate this effect of hypoxia on proteostasis. Animals fasted prior to hypoxic exposure develop dramatically fewer polyglutamine protein aggregates compared to their fed counterparts, indicating that the effect of hypoxia is abrogated. Fasting also reduced the hypoxia-induced exaggeration of proteostasis defects in animals that express Aβ 1–42 and in animals with a temperature-sensitive mutation in dyn-1 , suggesting that this effect was not specific to polyglutamine proteins. Our data also demonstrate that the nutritional environment experienced at the onset of hypoxia dictates at least some aspects of the physiological response to hypoxia. We further demonstrate that the insulin/IGF-like signaling pathway plays a role in mediating the protective effects of fasting in hypoxia. Animals with mutations in daf-2 , the C . elegans insulin-like receptor, display wild-type levels of hypoxia-induced protein aggregation upon exposure to hypoxia when fed, but are not protected by fasting. DAF-2 acts independently of the FOXO transcription factor, DAF-16, to mediate the protective effects of fasting. These results suggest a non-canonical role for the insulin/IGF-like signaling pathway in coordinating the effects of hypoxia and nutritional state on proteostasis.

Low oxygen conditions (hypoxia) can impair essential physiological processes and cause cellular 1 damage and death. We have shown that specific hypoxic conditions disrupt protein 2 homeostasis in C. elegans, leading to protein aggregation and proteotoxicity. Here, we show 3 that nutritional cues regulate this effect of hypoxia on proteostasis. Animals fasted prior to 4 hypoxic exposure develop dramatically fewer protein aggregates compared to their fed 5 counterparts, indicating that the effect of hypoxia is abrogated. Fasting is effective at protecting 6 against hypoxia-induced proteostasis defects in multiple developmental stages, tissues, and in 7 different models of misfolded or aggregation prone proteins. Our data also demonstrate that 8 the effect of fasting is induced and reversed quite rapidly, suggesting that the nutritional 9 environment experienced at the onset of hypoxia dictates at least some aspects of the 10 physiological response to hypoxia. We further demonstrate that the insulin/IGF-like signaling 11 pathway plays a role in mediating the protective effects of fasting in hypoxia. Animals with 12 mutations in daf-2, the C. elegans insulin-like receptor, display wild-type levels of hypoxia-13induced protein aggregation upon exposure to hypoxia when fed, but are not protected by 14fasting. However, we found that DAF-2 acts independently of the FOXO transcription factor, 15DAF-16, to mediate the protective effects of fasting. These results suggest a non-canonical role 16for the insulin/IGF-like signaling pathway in coordinating the effects of hypoxia and nutritional 17 state on proteostasis. 18 Author SummaryWhen blood flow to various parts of the body becomes restricted, those tissues suffer from a 19 lack of oxygen, a condition called hypoxia. Hypoxia can cause cellular damage and death, such 20as is observed as a result of stroke and cardiovascular disease. We have found that in the model 21 organism C. elegans (a roundworm) specific concentrations of hypoxia cause aggregation of 22 polyglutamine proteins -the same kind of proteins that are found in an aggregated state in the 23 neurodegenerative disorder Huntington's disease. Here, we show that that worms can be 24 protected from hypoxia-induced protein aggregation if they are fasted (removed from their 25 food source) prior to experiencing hypoxia. Furthermore, we show that the insulin receptor is 26 required for this protection. The insulin receptor is responsible for detecting insulin, a hormone 27 that is released after feeding. Worms with a nonfunctional version of the insulin receptor 28 displayed hypoxia-induced protein aggregation despite being fasted before the hypoxic 29 exposure. Our results highlight a new role for the insulin signaling pathway in coordinating the 30 effects of both hypoxia and nutritional state on protein aggregation. 31 4 Introduction 32