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Recent neuroimaging and neuropsychological work has begun to shed light on how the brain responds to the viewing of facial expressions of emotion. However, one important category of facial expression that has not been studied on this level is the facial expression of pain. We investigated the neural response to pain expressions by performing functional magnetic resonance imaging (fMRI) as subjects viewed short video sequences showing faces expressing either moderate pain or, for comparison, no pain. In alternate blocks, the same subjects received both painful and non-painful thermal stimulation. Facial expressions of pain were found to engage cortical areas also engaged by the first-hand experience of pain, including anterior cingulate cortex and insula. The reported findings corroborate other work in which the neural response to witnessed pain has been examined from other perspectives. In addition, they lend support to the idea that common neural substrates are involved in representing one's own and others' affective states.

Sensorimotor gating, the ability to automatically filter sensory information, is deficient in a number of psychiatric disorders, yet little is known of the biochemical mechanisms underlying this critical neural process. Previously, we reported that mice expressing a constitutively active isoform of the G-protein subunit G α s (G α s * ) within forebrain neurons exhibit decreased gating, as measured by prepulse inhibition of acoustic startle (PPI). Here, to elucidate the biochemistry regulating sensorimotor gating and to identify novel therapeutic targets, we test the hypothesis that G α s * causes PPI deficits via brain region-specific changes in cyclic AMP (cAMP) signaling. As predicted from its ability to stimulate adenylyl cyclase, we find here that G α s * increases cAMP levels in the striatum. Suprisingly, however, G α s * mice exhibit reduced cAMP levels in the cortex and hippocampus because of increased cAMP phosphodiesterase (cPDE) activity. It is this decrease in cAMP that appears to mediate the effect of G α s * on PPI because Rp-cAMPS decreases PPI in C57BL/6J mice. Furthermore, the antipsychotic haloperidol increases both PPI and cAMP levels specifically in G α s * mice and the cPDE inhibitor rolipram also rescues PPI deficits of G α s * mice. Finally, to block potentially the pathway that leads to cPDE upregulation in G α s * mice, we coexpressed the R(AB) transgene (a dominant-negative regulatory subunit of protein kinase A (PKA)), which fully rescues the reductions in PPI and cAMP caused by G α s * . We conclude that expression of G α s * within forebrain neurons causes PPI deficits because of a PKA-dependent decrease in cAMP and suggest that cAMP PDE inhibitors may exhibit antipsychotic-like therapeutic effects.

We investigate the hypothesis that those subregions of the prefrontal cortex (PFC) found to support proactive interference resolution may also support delay-spanning distractor interference resolution. Ten subjects performed delayed-recognition tasks requiring working memory for faces or shoes during functional MRI scanning. During the 15-sec delay interval, task-irrelevant distractors were presented. These distractors were either all faces or all shoes and were thus either congruent or incongruent with the domain of items in the working memory task. Delayed-recognition performance was slower and less accurate during congruent than during incongruent trials. Our fMRI analyses revealed significant delay interval activity for face and shoe working memory tasks within both dorsal and ventral PFC. However, only ventral PFC activity was modulated by distractor category, with greater activity for congruent than for incongruent trials. Importantly, this congruency effect was only present for correct trials. In addition to PFC, activity within the fusiform face area was investigated. During face distraction, activity was greater for face relative to shoe working memory. As in ventrolateral PFC, this congruency effect was only present for correct trials. These results suggest that the ventrolateral PFC and fusiform face area may work together to support delay-spanning interference resolution.

Sensorimotor gating, the ability to automatically filter sensory information, is deficient in a number of psychiatric disorders, yet little is known of the biochemical mechanisms underlying this critical neural process. Previously, we reported that mice expressing a constitutively active isoform of the G-protein subunit Galphas (Galphas(*)) within forebrain neurons exhibit decreased gating, as measured by prepulse inhibition of acoustic startle (PPI). Here, to elucidate the biochemistry regulating sensorimotor gating and to identify novel therapeutic targets, we test the hypothesis that Galphas(*) causes PPI deficits via brain region-specific changes in cyclic AMP (cAMP) signaling. As predicted from its ability to stimulate adenylyl cyclase, we find here that Galphas(*) increases cAMP levels in the striatum. Suprisingly, however, Galphas(*) mice exhibit reduced cAMP levels in the cortex and hippocampus because of increased cAMP phosphodiesterase (cPDE) activity. It is this decrease in cAMP that appears to mediate the effect of Galphas(*) on PPI because Rp-cAMPS decreases PPI in C57BL/6J mice. Furthermore, the antipsychotic haloperidol increases both PPI and cAMP levels specifically in Galphas(*) mice and the cPDE inhibitor rolipram also rescues PPI deficits of Galphas(*) mice. Finally, to block potentially the pathway that leads to cPDE upregulation in Galphas(*) mice, we coexpressed the R(AB) transgene (a dominant-negative regulatory subunit of protein kinase A (PKA)), which fully rescues the reductions in PPI and cAMP caused by Galphas(*). We conclude that expression of Galphas(*) within forebrain neurons causes PPI deficits because of a PKA-dependent decrease in cAMP and suggest that cAMP PDE inhibitors may exhibit antipsychotic-like therapeutic effects.

Sensorimotor gating, the ability to automatically filter sensory information, is deficient in a number of psychiatric disorders, yet little is known of the biochemical mechanisms underlying this critical neural process. Previously, we reported that mice expressing a constitutively active isoform of the G-protein subunit Galphas (Galphas(*)) within forebrain neurons exhibit decreased gating, as measured by prepulse inhibition of acoustic startle (PPI). Here, to elucidate the biochemistry regulating sensorimotor gating and to identify novel therapeutic targets, we test the hypothesis that Galphas(*) causes PPI deficits via brain region-specific changes in cyclic AMP (cAMP) signaling. As predicted from its ability to stimulate adenylyl cyclase, we find here that Galphas(*) increases cAMP levels in the striatum. Suprisingly, however, Galphas(*) mice exhibit reduced cAMP levels in the cortex and hippocampus because of increased cAMP phosphodiesterase (cPDE) activity. It is this decrease in cAMP that appears to mediate the effect of Galphas(*) on PPI because Rp-cAMPS decreases PPI in C57BL/6J mice. Furthermore, the antipsychotic haloperidol increases both PPI and cAMP levels specifically in Galphas(*) mice and the cPDE inhibitor rolipram also rescues PPI deficits of Galphas(*) mice. Finally, to block potentially the pathway that leads to cPDE upregulation in Galphas(*) mice, we coexpressed the R(AB) transgene (a dominant-negative regulatory subunit of protein kinase A (PKA)), which fully rescues the reductions in PPI and cAMP caused by Galphas(*). We conclude that expression of Galphas(*) within forebrain neurons causes PPI deficits because of a PKA-dependent decrease in cAMP and suggest that cAMP PDE inhibitors may exhibit antipsychotic-like therapeutic effects.

The van-der-Waals material CrSBr stands out as a promising two-dimensional magnet. Here, we report on its detailed magnetic and structural characteristics. We evidence that it undergoes a transition to an A-type antiferromagnetic state below T N  ≈ 140 K with a pronounced two-dimensional character, preceded by ferromagnetic correlations within the monolayers. Furthermore, we unravel the low-temperature hidden-order within the long-range magnetically-ordered state. We find that it is associated to a slowing down of the magnetic fluctuations, accompanied by a continuous reorientation of the internal field. These take place upon cooling below T s  ≈ 100 K, until a spin freezing process occurs at T * ≈ 40 K. We argue this complex behavior to reflect a crossover driven by the in-plane uniaxial anisotropy, which is ultimately caused by its mixed-anion character. Our findings reinforce CrSBr as an important candidate for devices in the emergent field of two-dimensional magnetic materials. A 2D magnet CrSBr has attracted interest for applications in spintronics due to its high critical temperature and interesting magneto-electrical properties. Here the authors report a detailed study of its magnetic and structural phases and uncover a hidden magnetic order inside the magnetically-ordered phase.

For successful cross-pollination, most flowering plants rely on insects as pollinators and attract them by offering rewards, predominantly nectar and pollen. Bees–a highly important pollinator group—are especially dependent on pollen as their main source of essential nutrients, including proteins, lipids, and sterols. Fatty acids (FAs) in particular play a pivotal role as fundamental energy source, contributing to membrane structure integrity, cellular homeostasis, and cognitive processes. However, overconsumption of FAs can have detrimental effects on fitness and survival. Thus, bees need to precisely modulate FA intake. To better understand how Apis mellifera , the globally predominant managed pollinator, regulate FA intake, we conducted controlled feeding experiments with newly hatched honey bee workers by providing pollen with different FA concentrations. We additionally investigated the honey bee’s capacity to perceive individual FAs by means of chemotactile proboscis extension response (PER) conditioning. We tested both natural concentrations and concentrations exceeding those typically found in pollen. Given the dose-dependent importance of FAs observed in other bee species, we hypothesized that (i) a high FA concentration in pollen would reduce honey bee longevity, and (ii) honey bees are able to perceive individual FAs and differentiate between different FA concentrations via antennal sensation prior to consumption. Our study revealed that elevated FA concentrations in pollen resulted in reduced consumption rates and increased mortality in Apis mellifera . Workers can detect and discriminate between saturated and unsaturated FAs utilizing their antennae. Moreover, they were able to distinguish between individual FAs and also between different concentrations of the same FAs. Our results suggest a high sensitivity of A. mellifera towards both the concentration and composition of individual FAs, which greatly impacts their foraging decisions and fitness. These insights contribute to the growing evidence highlighting the importance of balanced nutrient ratios, in particular of FAs, for bees and other organisms.

A bstract We show how a method to construct canonical differential equations for multi-loop Feynman integrals recently introduced by some of the authors can be extended to cases where the associated geometry is of Calabi-Yau type and even beyond. This can be achieved by supplementing the method with information from the mixed Hodge structure of the underlying geometry. We apply these ideas to specific classes of integrals whose associated geometry is a one-parameter family of Calabi-Yau varieties, and we argue that the method can always be successfully applied to those cases. Moreover, we perform an in-depth study of the properties of the resulting canonical differential equations. In particular, we show that the resulting canonical basis is equivalent to the one obtained by an alternative method recently introduced in the literature. We apply our method to non-trivial and cutting-edge examples of Feynman integrals necessary for gravitational wave scattering, further showcasing its power and flexibility.

Evolving in sync with the computation revolution over the past 30 years, computational biology has emerged as a mature scientific field. While the field has made major contributions toward improving scientific knowledge and human health, individual computational biology practitioners at various institutions often languish in career development. As optimistic biologists passionate about the future of our field, we propose solutions for both eager and reluctant individual scientists, institutions, publishers, funding agencies, and educators to fully embrace computational biology. We believe that in order to pave the way for the next generation of discoveries, we need to improve recognition for computational biologists and better align pathways of career success with pathways of scientific progress. With 10 outlined steps, we call on all adjacent fields to move away from the traditional individual, single-discipline investigator research model and embrace multidisciplinary, data-driven, team science.