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Mosquito blood-feeding behavior is a key determinant of the epidemiology of dengue viruses (DENV), the most-prevalent mosquitoborne viruses. However, despite its importance, how DENV infection influences mosquito blood-feeding and, consequently, transmission remains unclear. Here, we developed a high-resolution, video-based assay to observe the blood-feeding behavior of Aedes aegypti mosquitoes on mice. We then applied multivariate analysis on the high-throughput, unbiased data generated from the assay to ordinate behavioral parameters into complex behaviors. We showed that DENV infection increases mosquito attraction to the host and hinders its biting efficiency, the latter resulting in the infected mosquitoes biting more to reach similar blood repletion as uninfected mosquitoes. To examine how increased biting influences DENV transmission to the host, we established an in vivo transmission model with immuno-competent mice and demonstrated that successive short probes result in multiple transmissions. Finally, to determine how DENV-induced alterations of host-seeking and biting behaviors influence dengue epidemiology, we integrated the behavioral data within a mathematical model. We calculated that the number of infected hosts per infected mosquito, as determined by the reproduction rate, tripled when mosquito behavior was influenced by DENV infection. Taken together, this multidisciplinary study details how DENV infection modulates mosquito blood-feeding behavior to increase vector capacity, proportionally aggravating DENV epidemiology. By elucidating the contribution of mosquito behavioral alterations on DENV transmission to the host, these results will inform epidemiological modeling to tailor improved interventions against dengue.

Studies of the fat-derived hormone leptin have provided key insights into the molecular and neural components of feeding behavior and body weight regulation. An important challenge lies in understanding how the rewarding properties of food interact with, and can override, physiological satiety signals and promote overeating. We used functional magnetic resonance imaging to measure brain responses in two human patients with congenital leptin deficiency who were shown images of food before and after 7 days of leptin replacement therapy. Leptin was found to modulate neural activation in key striatal regions, suggesting that the hormone acts on neural circuits governing food intake to diminish the perception of food reward while enhancing the response to satiety signals generated during food consumption.

Functional magnetic resonance imaging is used to examine brain areas whose activity correlates with subsequent feeding behaviour under different satiety states evoked by intravenous peptide YY 3–36 (PYY), administration. Under high PYY conditions, (mimicking the fed state) changes in orbitofrontal cortex activation better predicted subsequent feeding, whereas in low PYY conditions, hypothalamic activation predicted food intake. The ability to maintain adequate nutrient intake is critical for survival. Complex interrelated neuronal circuits have developed in the mammalian brain to regulate many aspects of feeding behaviour, from food-seeking to meal termination. The hypothalamus and brainstem are thought to be the principal homeostatic brain areas responsible for regulating body weight 1 , 2 . However, in the current ‘obesogenic’ human environment food intake is largely determined by non-homeostatic factors including cognition, emotion and reward, which are primarily processed in corticolimbic and higher cortical brain regions 3 . Although the pleasure of eating is modulated by satiety and food deprivation increases the reward value of food, there is currently no adequate neurobiological account of this interaction between homeostatic and higher centres in the regulation of food intake in humans 1 , 4 , 5 . Here we show, using functional magnetic resonance imaging, that peptide YY 3–36 (PYY), a physiological gut-derived satiety signal, modulates neural activity within both corticolimbic and higher-cortical areas as well as homeostatic brain regions. Under conditions of high plasma PYY concentrations, mimicking the fed state, changes in neural activity within the caudolateral orbital frontal cortex predict feeding behaviour independently of meal-related sensory experiences. In contrast, in conditions of low levels of PYY, hypothalamic activation predicts food intake. Thus, the presence of a postprandial satiety factor switches food intake regulation from a homeostatic to a hedonic, corticolimbic area. Our studies give insights into the neural networks in humans that respond to a specific satiety signal to regulate food intake. An increased understanding of how such homeostatic and higher brain functions are integrated may pave the way for the development of new treatment strategies for obesity.

\"Bestselling author and economist Ha-Joon Chang makes challenging economic ideas delicious by plating them alongside stories about food from around the world, using the diverse histories behind familiar food items to explore economic theory. For Chang, chocolate is a lifelong addiction, but more exciting are the insights it offers into postindustrial knowledge economies; and while okra makes Southern gumbo heart-meltingly smooth, it also speaks of capitalism's entangled relationship with freedom. Myth-busting, witty, and thought-provoking, Edible Economics serves up a feast of bold ideas about globalization, climate change, immigration, austerity, automation, and why carrots need not be orange. It shows that getting to grips with the economy is like learning a recipe: when we understand it, we can adapt and improve it--and better understand our world.\"--Front book jacket flap.

Environmental pollution by pharmaceuticals is increasingly recognized as a major threat to aquatic ecosystems worldwide. A variety of pharmaceuticals enter waterways by way of treated wastewater effluents and remain biochemically active in aquatic systems. Several ecotoxicological studies have been done, but generally, little is known about the ecological effects of pharmaceuticals. Here we show that a benzodiazepine anxiolytic drug (oxazepam) alters behavior and feeding rate of wild European perch (Perca fluviatilis) at concentrations encountered in effluent-influenced surface waters. Individuals exposed to water with dilute drug concentrations (1.8 micrograms liter -1 ) exhibited increased activity, reduced sociality, and higher feeding rate. As such, our results show that anxiolytic drugs in surface waters alter animal behaviors that are known to have ecological and evolutionary consequences.

Several different neuronal populations are involved in regulating energy homeostasis. Among these, agouti-related protein (AgRP) neurons are thought to promote feeding and weight gain; however, the evidence supporting this view is incomplete. Using designer receptors exclusively activated by designer drugs (DREADD) technology to provide specific and reversible regulation of neuronal activity in mice, we have demonstrated that acute activation of AgRP neurons rapidly and dramatically induces feeding, reduces energy expenditure, and ultimately increases fat stores. All these effects returned to baseline after stimulation was withdrawn. In contrast, inhibiting AgRP neuronal activity in hungry mice reduced food intake. Together, these findings demonstrate that AgRP neuron activity is both necessary and sufficient for feeding. Of interest, activating AgRP neurons potently increased motivation for feeding and also drove intense food-seeking behavior, demonstrating that AgRP neurons engage brain sites controlling multiple levels of feeding behavior. Due to its ease of use and suitability for both acute and chronic regulation, DREADD technology is ideally suited for investigating the neural circuits hypothesized to regulate energy balance.

Stress often affects eating behaviors, increasing caloric intake in some individuals and decreasing it in others. The determinants of feeding responses to stress are unknown, in part because this issue is rarely studied in rodents. We focused our efforts on the novelty-suppressed feeding (NSF) assay, which uses latency to eat as readout of anxiety-like behavior, but rarely assesses feeding per se. We explored how key variables in experimental paradigms – estrous and diurnal cyclicity, age and duration of social isolation, prandial state, diet palatability, and elevated body weight – influence stress-induced anxiety-like behavior and food intake in male and female C57BL/6J mice. Latency to eat in the novel environment is increased in both sexes across most of the conditions tested, while effects on caloric intake are variable. In the common NSF assay (i.e., lean mice in the light cycle), sex-specific effects of the length of social isolation, and not estrous cyclicity, are the main source of variability. Under conditions that are more physiologically relevant for humans (i.e., overweight mice in the active phase), the novel stress now elicits robust hyperphagia in both sexes . This novel model of stress eating can be used to identify underlying neuroendocrine and neuronal substrates. Moreover, these studies can serve as a framework to integrate cross-disciplinary studies of anxiety and feeding related behaviors in rodents. In times of heightened anxiety – say, during a global pandemic – many of us will reach for donuts or a particularly appetizing pizza for comfort. Others, however, will tend to shun food. What underlies these differences, and, in fact, the neural and hormonal pathways at play during stress eating (when people eat without being hungry due to emotional reasons), remain unclear. This is partly because scientists lack good animal models in which to study these behaviors. In particular, female rodents are usually excluded from studies under the assumption that their hormonal cycles will disrupt the results. Yet, women are overrepresented in studies on feeding habits. Modeling human behaviors using rodents is harder than it may appear. These animals are most active at night – yet most experiments are performed during the day. The same stressors also have different outcomes in males and females. François et al. therefore explored better ways to induce anxiety and evaluate feeding behavior in mice, hoping to reliably elicit stress eating. The starting point was a common type of experiments known as novelty-suppressed feeding. First, mice are kept alone in a cage for up to two weeks on a normal diet so that they are used to experimental conditions. Then they are deprived of food overnight, before being given free access to food in the morning in a new environment. This stressful experience normally causes mice to take longer to eat than in their home cage. In rodents, the delay is thought to reflect stress as it is reliably reversed by anti-anxiety compounds approved for human use. In the novelty-suppressed feeding assay, both male and female animals exhibit signs of anxiety, but how much females eat is variable. François et al. showed that this variability is not due to hormonal changes, but instead to how long female mice had been kept alone. Crucially, the test could be adapted so that mice would consistently exhibit behavior similar to human stress eating, whereby they eat more during the test without having fasted the night before. The changes included running the experiment at night, when the animals are normally most active, and using overweight mice (which captures the fact that, in humans, being overweight is associated with being prone to stress eating). Stress eating is an important clinical issue, hindering weigh loss in people with obesity. The new model developed by François et al. could be adopted by other laboratories, enabling better research into this behavior.