Predators and Prickly Paradigms: Nesting Ecology of Bobwhites and Scaled Quail in West Texas

Sporadic recruitment appears to be the impetus for the irruptive population patterns observed along the western edge of northern bobwhite (Colinus virginianus) range. We investigated hen survival, nest selection strategies, and reproductive success of sympatric northern bobwhites and scaled quail (Callipepla squamata) in west Texas. Radio-marked bobwhites, along with a smaller sample of sympatric scaled quail, were monitored during the spring and summer of 1994 and 1995. Predation was the major source of mortality, with mammals and raptors responsible for about 60 and 30 percent of the mortalities observed, respectively. We used TrailMaster camera systems to document the presence and behavior of various nest predators. Raccoons (Procyon lotor) appear to be the dominant nest predator in this area, accounting for over 80 percent of the nests destroyed. Photographic surveillance of artificial nests provides some clues for making objective assessments of predators involved in nest depredations. The amount and kinds of egg shell evidence at a nest site varied with egg size (chicken vs quail). We found egg shell evidence at 83 percent of nests using chicken eggs, but only at 3 percent of nests using quail eggs. We predict that snakes are overrated in their importance as a nest predator, when such diagnoses are based solely on the absence of physical evidence (i.e., no egg shells). Our results suggest that pricklypear (Opuntia spp.) was a key nesting microhabitat. Overall, 12 of 21 bobwhite and 8 of 12 scaled quail nests were located in pricklypear. Subsequent investigations revealed that nests situated in pricklypear were afforded higher survival, especially in more arid sites with less traditional nesting cover (e.g., Schizachyrium scoparium). Initial results with intensive, short-term mammal removal suggest that nest survival can be increased for about $0.35 per hectare

The medial habenula: still neglected

The habenula is a small, bilateral brain structure located at the dorsal end of the diencephalon. This structure sends projections to the dopaminergic striatum and receives inputs from the limbic forebrain, making the habenula a unique modulator of cross-talk between these brain regions. Despite strong interest in the habenula during the seventies and eighties (Herkenham and Nauta, 1977; Beckstead, 1979; Beckstead et al., 1979; Herkenham and Nauta, 1979; Caldecott-Hazard et al., 1988), interest waned due to lack of a clearly identifiable functional role. Following Matsumoto and Hikosaka's seminal work on the lateral habenula as a predictor of negative reward in monkeys, the habenula has undergone a resurgence of scientific interest. Matsumoto and Hikosaka demonstrated an increase in habenular neuron firing when monkeys did not receive an expected juice reward (Matsumoto and Hikosaka, 2007). Studies have shown that increased habenular activity inactivates dopaminergic cells in the Rostromedial Tegmental Nucleus (RMTg) through GABAergic mechanisms (Jhou et al., 2009a,b). Additional studies link habenular activity to the regulation of serotonin and norepinephrine, suggesting the habenula modulates multiple brain systems (Strecker and Rosengren, 1989; Amat et al., 2001). These discoveries ushered in a series of new studies that have refocused attention on the lateral habenula and the importance of this small brain structure (Bianco and Wilson, 2009; Jhou et al., 2009a; Matsumoto and Hikosaka, 2009; Sartorius et al., 2010; Savitz et al., 2011). Recently, Geisler and Trimble reviewed this renewed interest in: The Lateral Habenula: No Longer Neglected (Geisler and Trimble, 2008). While the lateral habenula (LHb) has been extensively studied, the anatomically and histochemically distinct medial habenula (MHb) remains largely understudied. This short review argues that the MHb is functionally important and should be studied more aggressively

The Effect of Topical Fluoride on Dental Caries Experience in Adult Females of a Military Population

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/66668/2/10.1177_00220345550340011801.pd

Precise Estimates of the Physical Parameters for the Exoplanet System HD-17156 Enabled by HST FGS Transit and Asteroseismic Observations

We present observations of three distinct transits of HD 17156b obtained with the Fine Guidance Sensors (FGS) on board the Hubble Space Telescope} (HST). We analyzed both the transit photometry and previously published radial velocities to find the planet-star radius ratio R_p/R_s = 0.07454 +/- 0.00035, inclination i=86.49 +0.24/-0.20 deg, and scaled semi-major axis a/R = 23.19 +0.32/-0.27. This last value translates directly to a mean stellar density determination of 0.522 +0.021/-0.018 g cm^-3. Analysis of asteroseismology observations by the companion paper of Gilliland et al. (2009) provides a consistent but significantly refined measurement of the stellar mean density. We compare stellar isochrones to this density estimate and find M_s = 1.275 +/- 0.018 M_sun and a stellar age of $3.37 +0.20/-0.47 Gyr. Using this estimate of M_s and incorporating the density constraint from asteroseismology, we model both the photometry and published radial velocities to estimate the planet radius R_p= 1.0870 +/- 0.0066 Jupiter radii and the stellar radius R_s = 1.5007 +/- 0.0076 R_sun. The planet radius is larger than that found in previous studies and consistent with theoretical models of a solar-composition gas giant of the same mass and equilibrium temperature. For the three transits, we determine the times of mid-transit to a precision of 6.2 s, 7.6 s, and 6.9 s, and the transit times for HD 17156 do not show any significant departures from a constant period. The joint analysis of transit photometry and asteroseismology presages similar studies that will be enabled by the NASA Kepler Mission.Comment: Accepted for publication to Ap

Starting, building and sustaining a program of research in emergency medicine in Canada

Objective: To develop pragmatic recommendations for starting, building and sustaining a program of research in emergency medicine (EM) in Canada at sites with limited infrastructure and/or prior research experience. Methods: At the direction of the Canadian Association of Emergency Physicians (CAEP) academic section, we assembled an expert panel of 10 EM researchers with experience building programs of research. Using a modified Delphi approach, our panel developed initial recommendations for (1) starting, (2) building, and (3) sustaining a program of research in EM. These recommendations were peer-reviewed by emergency physicians and researchers from each of the panelist’s home institutions and tested for face and construct validity, as well as ease of comprehension. The recommendations were then iteratively revised based on feedback and suggestions from peer review and amended again after being presented at the 2020 CAEP academic symposium. Results: Our panel created 15 pragmatic recommendations for those intending to start (formal research training, find mentors, local support, develop a niche, start small), build (funding, build a team, collaborate, publish, expect failure) and sustain (become a mentor, obtain leadership roles, lead national studies, gain influence, prioritize wellness) a program of EM research in centers without an established research culture. Additionally, we suggest four recommendations for department leads aiming to foster a program of research within their departments. Conclusion: These recommendations serve as guidance for centres wanting to establish a program of research in EM

Auriculocondylar syndrome 2 results from the dominant-negative action of PLCB4 variants.

Auriculocondylar syndrome 2 (ARCND2) is a rare autosomal dominant craniofacial malformation syndrome linked to multiple genetic variants in the coding sequence of phospholipase C β4 (PLCB4). PLCB4 is a direct signaling effector of the endothelin receptor type A (EDNRA)-Gq/11 pathway, which establishes the identity of neural crest cells (NCCs) that form lower jaw and middle ear structures. However, the functional consequences of PLCB4 variants on EDNRA signaling is not known. Here, we show, using multiple signaling reporter assays, that known PLCB4 variants resulting from missense mutations exert a dominant-negative interference over EDNRA signaling. In addition, using CRISPR/Cas9, we find that F0 mouse embryos modeling one PLCB4 variant have facial defects recapitulating those observed in hypomorphic Ednra mouse models, including a bone that we identify as an atavistic change in the posterior palate/oral cavity. Remarkably, we have identified a similar osseous phenotype in a child with ARCND2. Our results identify the disease mechanism of ARCND2, demonstrate that the PLCB4 variants cause craniofacial differences and illustrate how minor changes in signaling within NCCs may have driven evolutionary changes in jaw structure and function. This article has an associated First Person interview with the first author of the paper

UBC-Nepal expedition: The use of oral antioxidants does not alter cerebrovascular function at sea-level or high-altitude

Hypoxia is associated with an increased systemic and cerebral formation of free radicals and associated reactants that may be linked to impaired cerebral vascular function a neurological sequela. To what extent oral antioxidants prophylaxis impacts cerebrovascular function in humans throughout the course of acclimatization to the hypoxia of terrestrial high-altitude has not been examined. Thus, the purpose of the current study was to examine the influence of orally ingested antioxidants at clinically relevant doses (vitamin C, E, and alpha-lipoic acid) on cerebrovascular regulation at sea-level (344 m; n = 12; female n = 2 participants), and at high altitude (5050 m; n = 9; female n = 2), in a randomized, placebo-controlled, and double-blinded crossover design. Hypercapnic and hypoxic cerebrovascular reactivity tests of the internal carotid (ICA)] were conducted at sea-level, while global and regional cerebral blood flow [i.e. ICA and vertebral artery (VA)] were assessed after 10–12 days following arrival at 5050 m. At sea-level, acute administration of antioxidants did not alter cerebral hypoxic cerebrovascular reactivity (pre vs. post: 1.5 ± 0.7 vs. 1.2 ± 0.8 %∆CBF/-%∆SpO2; P = 0.96), or cerebral hypercapnic cerebrovascular reactivity (pre vs. post: 5.7 ± 2.0 vs. 5.8 ± 1.9 %∆CBF/∆mmHg; P = 0.33). Furthermore, global cerebral blood flow (P = 0.43), as well as cerebral vascular conductance (ICA P = 0.08; VA P = 0.32), were unaltered at 5050 m following antioxidant administration. In conclusion, these data show that an oral antioxidant cocktail known to attenuate systemic oxidative stress failed to alter cerebrovascular function at sea-level and cerebral blood flow during acclimatization to high-altitude

Stress debriefing and patterns of recovery following a natural disaster

Stress debriefing has been used extensively following traumatic events; however, there is little evidence of its effectiveness. This paper reports the effects of stress debriefing on the rate of recovery of 195 helpers (e.g., emergency service personnel and disaster workers) following an earthquake in Newcastle, Australia (62 debriefed helpers and 133 who were not debriefed). Post-trauma stress reactions (Impact of Event Scale) and general psychological morbidity (General Health Questionnaire: GHQ-12) were assessed on four occasions over the first 2 years postearthquake. There was no evidence of an improved rate of recovery among those helpers who were debriefed, even when level of exposure and helping-related stress were taken into account. More rigorous investigation of the effectiveness of stress debriefing and its role in posttrauma recovery is urgently required

Deficiency of the zinc finger protein ZFP106 causes motor and sensory neurodegeneration

Acknowledgements We are indebted to Jim Humphries, JennyCorrigan, LizDarley, Elizabeth Joynson, Natalie Walters, Sara Wells and the whole necropsy, histology, genotyping and MLC ward 6 teams at MRC Harwell for excellent technical assistance. We thank the staff of the WTSI Illumina Bespoke Team for the RNA-seq data, the Sanger Mouse Genetics Project for the initial mouse characterization and Dr David Adams for critical reading of the manuscript. We also thank KOMP for the mouse embryonic stem cells carrying the knockout first promoter-less allele (tm1a(KOMP)Wtsi) within Zfp016. Conflict of Interest statement. None declared. Funding This work was funded by the UK Medical Research Council (MRC) to A.A.-A. and a Motor Neurone Disease Association (MNDA) project grant to A.A.-A. and EMCF. D.L.H.B. is a Wellcome Trust Senior Clinical Scientist Fellow and P.F. is a MRC/MNDA Lady Edith Wolfson Clinician Scientist Fellow. Funding to pay the Open Access publication charges for this article was provided by the MRC grant number: MC_UP_A390_1106.Peer reviewedPublisher PD

Shear-Mediated Dilation of the Internal Carotid Artery Occurs Independent of Hypercapnia.

Evidence for shear stress as a regulator of carotid artery dilation in response to increased arterial carbon dioxide was recently demonstrated in humans during sustained elevations in CO2 (hypercapnia); however, the relative contributions of CO2 and shear stress to this response remains unclear. We examined the hypothesis that, following a 30-second transient increase in arterial CO2 tension and consequent increase in internal carotid artery shear stress, internal carotid artery diameter would increase, indicating shear-mediated dilation, in the absence of concurrent hypercapnia. In 27 healthy participants the partial pressures of end-tidal O2 and CO2, ventilation (pneumotachography), blood pressure (finger-photoplethysmography), heart-rate (electrocardiogram), internal carotid artery flow, diameter and shear stress (high resolution duplex ultrasound) and middle cerebral artery blood velocity (transcranial Doppler) were measured during 4-minute steady state and transient 30-second hypercapnic tests (both +9mmHg CO2). Internal carotid artery dilation was lower in the transient, compared to the steady state hypercapnia (3.3±1.9% vs. 5.3±2.9%, respectively; P<0.03). Increases in internal carotid artery shear stress preceded increases in diameter in both the transient (time: 16.8±13.2s vs. 59.4±60.3s; P<0.01) and steady state (time: 18.2±14.2s vs. 110.3±79.6s; P<0.01) tests. Internal carotid artery dilation was positively correlated with shear rate area under the curve in the transient (r(2)=0.44; P<0.01), but not steady state (r(2)=0.02; P=0.53) trial. Collectively, these results suggest that hypercapnia induces shear-mediated dilation of the internal carotid artery in humans. This study further promotes the application and development of hypercapnia as a clinical strategy for the assessment of cerebrovascular vasodilatory function and health in humans