How New Caledonian crows solve novel foraging problems and what it means for cumulative culture.

New Caledonian crows make and use tools, and tool types vary over geographic landscapes. Social learning may explain the variation in tool design, but it is unknown to what degree social learning accounts for the maintenance of these designs. Indeed, little is known about the mechanisms these crows use to obtain information from others, despite the question's importance in understanding whether tool behavior is transmitted via social, genetic, or environmental means. For social transmission to account for tool-type variation, copying must utilize a mechanism that is action specific (e.g., pushing left vs. right) as well as context specific (e.g., pushing a particular object vs. any object). To determine whether crows can copy a demonstrator's actions as well as the contexts in which they occur, we conducted a diffusion experiment using a novel foraging task. We used a nontool task to eliminate any confounds introduced by individual differences in their prior tool experience. Two groups had demonstrators (trained in isolation on different options of a four-option task, including a two-action option) and one group did not. We found that crows socially learn about context: After observers see a demonstrator interact with the task, they are more likely to interact with the same parts of the task. In contrast, observers did not copy the demonstrator's specific actions. Our results suggest it is unlikely that observing tool-making behavior transmits tool types. We suggest it is possible that tool types are transmitted when crows copy the physical form of the tools they encounter.We are grateful to our funders: the SAGE Center for the Study of the Mind at the University of California Santa Barbara and the National Geographic Society/Waitt Grants Program (CJL), a Rutherford Discovery Fellowship from the Royal Society of New Zealand (AHT), the Marsden Fund (RG), and a BBSRC grant (WH; BB/I007997/1).This is the author accepted manuscript. The final version is available from Springer via http://dx.doi.org/10.3758/s13420-015-0194-

The Effect of Swimming Goggles on Intraocular Pressure and Blood Flow within the Optic Nerve Head

Purpose: Goggles are frequently worn in the sport of swimming and are designed to form a seal around the periorbital tissue orbit. The resultant pressure on the eye may have the potential to affect intraocular pressure and blood flow of the optic nerve head. This study evaluates the influence of wearing swimming goggles on intraocular pressure (IOP) and blood flow of the ocular nerve head (ONH) in normal subjects. Materials and Methods: Thirty healthy participants took part in this study. The IOP of each participant was measured using a Goldmann tonometer. Measurements were taken immediately before putting on swimming goggles, at 5, 10, 30, and 60 minutes after putting on swimming goggles, and then immediately after taking off the goggles. Blood flow of the ONH was measured using the Heidelberg retinal flowmeter. Results: The average IOP before, during and after wearing the swimming goggles were 11.88 ± 2.82 mmHg, 14.20 ± 2.81 mmHg and 11.78 ± 2.89 mmHg, respectively. The IOP increased immediately after putting on the goggles (p < 0.05) and then returned to normal values immediately after removal (p> 0.05). Blood flow of the ONH was 336.60 ± 89.07 Arbitrary Units (AU) before and 319.18 ± 96.02 AU after the goggles were worn (p < 0.05). Conclusion: A small but significant IOP elevation was observed immediately after the swimming goggles were put on. This elevated IOP was maintained while the goggles were kept on, and then returned to normal levels as soon as they were taken off. Blood flow of the ONH did not change significantly throughout the experiment. These facts should be considered for safety concerns, especially in advanced glaucoma patients

An ongoing case-control study to evaluate the NHS Bowel Cancer Screening Programme

© 2014 Massat et al.; licensee BioMed Central. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly credited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated

Multiple reassortment events in the evolutionary history of H1N1 influenza A virus since 1918

The H1N1 subtype of influenza A virus has caused substantial morbidity and mortality in humans, first documented in the global pandemic of 1918 and continuing to the present day. Despite this disease burden, the evolutionary history of the A/H1N1 virus is not well understood, particularly whether there is a virological basis for several notable epidemics of unusual severity in the 1940s and 1950s. Using a data set of 71 representative complete genome sequences sampled between 1918 and 2006, we show that segmental reassortment has played an important role in the genomic evolution of A/H1N1 since 1918. Specifically, we demonstrate that an A/H1N1 isolate from the 1947 epidemic acquired novel PB2 and HA genes through intra-subtype reassortment, which may explain the abrupt antigenic evolution of this virus. Similarly, the 1951 influenza epidemic may also have been associated with reassortant A/H1N1 viruses. Intra-subtype reassortment therefore appears to be a more important process in the evolution and epidemiology of H1N1 influenza A virus than previously realized

TALPID3/KIAA0586 Regulates Multiple Aspects of Neuromuscular Patterning During Gastrointestinal Development in Animal Models and Human

TALPID3/KIAA0586 is an evolutionary conserved protein, which plays an essential role in protein trafficking. Its role during gastrointestinal (GI) and enteric nervous system (ENS) development has not been studied previously. Here, we analyzed chicken, mouse and human embryonic GI tissues with TALPID3 mutations. The GI tract of TALPID3 chicken embryos was shortened and malformed. Histologically, the gut smooth muscle was mispatterned and enteric neural crest cells were scattered throughout the gut wall. Analysis of the Hedgehog pathway and gut extracellular matrix provided causative reasons for these defects. Interestingly, chicken intra-species grafting experiments and a conditional knockout mouse model showed that ENS formation did not require TALPID3, but was dependent on correct environmental cues. Surprisingly, the lack of TALPID3 in enteric neural crest cells (ENCC) affected smooth muscle and epithelial development in a non-cell-autonomous manner. Analysis of human gut fetal tissues with a KIAA0586 mutation showed strikingly similar findings compared to the animal models demonstrating conservation of TALPID3 and its necessary role in human GI tract development and patterning

Bat accelerated regions identify a bat forelimb specific enhancer in the HoxD locus

Author Summary: The limb is a classic example of vertebrate homology and is represented by a large range of morphological structures such as fins, legs and wings. The evolution of these structures could be driven by alterations in gene regulatory elements that have critical roles during development. To identify elements that may contribute to bat wing development, we characterized sequences that are conserved between vertebrates, but changed significantly in the bat lineage. We then overlapped these sequences with predicted developing limb enhancers as determined by ChIP-seq, finding 166 bat accelerated sequences (BARs). Five BARs that were tested for enhancer activity in mice all drove expression in the limb. Testing the mouse orthologous sequence showed that three had differences in their limb enhancer activity as compared to the bat sequence. Of these, BAR116 was of particular interest as it is located near the HoxD locus, an essential gene complex required for proper spatiotemporal patterning of the developing limb. The bat BAR116 sequence drove robust forelimb expression but the mouse BAR116 sequence did not show enhancer activity. These experiments correspond to analyses of HoxD gene expressions in developing bat limbs, which had strong forelimb versus weak hindlimb expression for Hoxd10 - 11 . Combined, our studies highlight specific genomic regions that could be important in shaping the morphological differences that led to the development of the bat wing

A critical role for endocytosis in Wnt signaling

BACKGROUND: The Wnt signaling pathway regulates many processes during embryonic development, including axis specification, organogenesis, angiogenesis, and stem cell proliferation. Wnt signaling has also been implicated in a number of cancers, bone density maintenance, and neurological conditions during adulthood. While numerous Wnts, their cognate receptors of the Frizzled and Arrow/LRP5/6 families and downstream pathway components have been identified, little is known about the initial events occurring directly after receptor activation. RESULTS: We show here that Wnt proteins are rapidly endocytosed by a clathrin- and dynamin-mediated process. While endocytosis has traditionally been considered a principal mechanism for receptor down-regulation and termination of signaling pathways, we demonstrate that interfering with clathrin-mediated endocytosis actually blocks Wnt signaling at the level of β-catenin accumulation and target gene expression. CONCLUSION: A necessary component of Wnt signaling occurs in a subcellular compartment distinct from the plasma membrane. Moreover, as internalized Wnts transit partially through the transferrin recycling pathway, it is possible that a "signaling endosome" serves as a nexus for activated Wnt pathway components

Amygdala circuitry mediating reversible and bidirectional control of anxiety

Anxiety—a sustained state of heightened apprehension in the absence of immediate threat—becomes severely debilitating in disease states. Anxiety disorders represent the most common of psychiatric diseases (28% lifetime prevalence) and contribute to the aetiology of major depression and substance abuse. Although it has been proposed that the amygdala, a brain region important for emotional processing, has a role in anxiety, the neural mechanisms that control anxiety remain unclear. Here we explore the neural circuits underlying anxiety-related behaviours by using optogenetics with two-photon microscopy, anxiety assays in freely moving mice, and electrophysiology. With the capability of optogenetics to control not only cell types but also specific connections between cells, we observed that temporally precise optogenetic stimulation of basolateral amygdala (BLA) terminals in the central nucleus of the amygdala (CeA)—achieved by viral transduction of the BLA with a codon-optimized channelrhodopsin followed by restricted illumination in the downstream CeA—exerted an acute, reversible anxiolytic effect. Conversely, selective optogenetic inhibition of the same projection with a third-generation halorhodopsin (eNpHR3.0) increased anxiety-related behaviours. Importantly, these effects were not observed with direct optogenetic control of BLA somata, possibly owing to recruitment of antagonistic downstream structures. Together, these results implicate specific BLA–CeA projections as critical circuit elements for acute anxiety control in the mammalian brain, and demonstrate the importance of optogenetically targeting defined projections, beyond simply targeting cell types, in the study of circuit function relevant to neuropsychiatric disease