Foraging Behavior of Swainson\u27s Thrushes (Catharus ustulatus) During Spring Migration through Arkansas

Foraging behavior of Swainson’s Thrushes on spring migration was studied in western Arkansas in the spring of 2013 and 2014. Observations were made in two forested field sites, one of them urban and the other suburban. The former had a significantly higher woody stem area (cm2) than the latter. For each foraging observation, the following three parameters were noted: Foraging Stratum (Ground, Shrub, Sapling, Sub canopy, and Canopy); Foraging Substrate (Ground/Litter, Herb, Foliage, Bark, and Air); and Foraging Maneuver (Glean, Probe, Dive/Glean, Hover, Jump Hover, and Hawking). We tested the hypotheses that these foraging variables differed significantly between the urban and suburban sites, and between the two years. These hypotheses were rejected for all three parameters. The consolidated data from both the sites and years revealed that a significantly higher proportion (67%) of the observations were on the Ground stratum, compared to the Shrub (13.7%) and Sapling strata (13%). Similarly, a significantly higher proportion (66%) of the foraging substrate used was Ground/Litter, followed by Foliage (16.7%) and Bark (15.8%). Gleaning was the most common foraging maneuver used (71.5%), and was significantly higher than Probing (12.3%) and Dive Gleaning (8.4%)

Phenylbutyric Acid Rescues Endoplasmic Reticulum Stress-Induced Suppression of APP Proteolysis and Prevents Apoptosis in Neuronal Cells

BACKGROUND: The familial and sporadic forms of Alzheimer's disease (AD) have an identical pathology with a severe disparity in the time of onset [1]. The pathological similarity suggests that epigenetic processes may phenocopy the Familial Alzheimer's disease (FAD) mutations within sporadic AD. Numerous groups have demonstrated that FAD mutations in presenilin result in 'loss of function' of gamma-secretase mediated APP cleavage [2], [3], [4], [5]. Accordingly, ER stress is prominent within the pathologically impacted brain regions in AD patients [6] and is reported to inhibit APP trafficking through the secretory pathway [7], [8]. As the maturation of APP and the cleaving secretases requires trafficking through the secretory pathway [9], [10], [11], we hypothesized that ER stress may block trafficking requisite for normal levels of APP cleavage and that the small molecular chaperone 4-phenylbutyrate (PBA) may rescue the proteolytic deficit. METHODOLOGY/PRINCIPAL FINDINGS: The APP-Gal4VP16/Gal4-reporter screen was stably incorporated into neuroblastoma cells in order to assay gamma-secretase mediated APP proteolysis under normal and pharmacologically induced ER stress conditions. Three unrelated pharmacological agents (tunicamycin, thapsigargin and brefeldin A) all repressed APP proteolysis in parallel with activation of unfolded protein response (UPR) signaling-a biochemical marker of ER stress. Co-treatment of the gamma-secretase reporter cells with PBA blocked the repressive effects of tunicamycin and thapsigargin upon APP proteolysis, UPR activation, and apoptosis. In unstressed cells, PBA stimulated gamma-secretase mediated cleavage of APP by 8-10 fold, in the absence of any significant effects upon amyloid production, by promoting APP trafficking through the secretory pathway and the stimulation of the non-pathogenic alpha/gamma-cleavage. CONCLUSIONS/SIGNIFICANCE: ER stress represses gamma-secretase mediated APP proteolysis, which replicates some of the proteolytic deficits associated with the FAD mutations. The small molecular chaperone PBA can reverse ER stress induced effects upon APP proteolysis, trafficking and cellular viability. Pharmaceutical agents, such as PBA, that stimulate alpha/gamma-cleavage of APP by modifying intracellular trafficking should be explored as AD therapeutics

P2X7 is an archaic scavenger receptor recognizing apoptotic neuroblasts in early human neurogenesis

The expression and function of P2X7 receptors in adult CNS have been widely studied, however, the roles of these purinergic receptors in human neural development has largely focused on the effects of receptor activation. Previous studies of embryonic and adult rodent neural precursors suggest adenosine triphosphate (ATP), the physiological agonist for P2X receptors, can act as a potent modifier of proliferation, migration and differentiation, mediated via intracellular calcium ([Ca2+]i) signaling. The P2X7 receptor has a ubiquitous distribution in the body but is most abundant on macrophages and microglia where its activation by ATP leads to secretion of proinflammatory cytokines. However, extracellular ATP concentrations in the CNS are usually at sub-micromolar levels suggesting that ATP-induced activation of the P2X7 receptor will not occur under physiological circumstances in the CNS. Another possible role for P2X7 receptors has been suggested by recent work on macrophages and neural precursor cells. In these studies the P2X7 receptor was shown to act as a scavenger receptor i.e. a receptor present on a phagocytotic cell which detects molecules present on the surface of apoptotic cells and facilitates phagocytosis of the apoptotic cell. In a recent study of human neural precursor cells (hNPCs) and neuroblasts isolated from human fetal telencephalons at 16-19 WG, our group showed that both P2X7Rhigh/DCXlow hNPCs and P2X7Rhigh/DCXhigh neuroblasts were capable of phagocytic engulfment of a range of targets including latex beads, apoptotic ReN cells and apoptotic neuroblasts. We found that these neuroblasts and their precursor cells expressed functional P2X7 receptors on their cell surface. Although expression of P2X7 is widespread in the cells of the neuroblast, it is those DCX+ neuroblasts with the highest expression of P2X7 which are actively phagocytic towards an autologous apoptotic neighbour or other phagocytic targets, including latex beads and apoptotic ReNcells. Pre-incubation of P2X7high neuroblasts with ATP or oxidized ATP inhibited phagocytosis of targets by these cells. Moreover siRNA knockdown of P2X7R also inhibited phagocytosis of the apoptotic targets. This review considers this major new role for the P2X7 receptor in early human neurogenesis

The Role of the P2X7 Receptor in Infectious Diseases

ATP is an extracellular signal for the immune system, particularly during an inflammatory response. It is sensed by the P2X7 receptor, the expression of which is upregulated by pro-inflammatory cytokines. Activation of the P2X7 receptor opens a cation-specific channel that alters the ionic environment of the cell, activating several pathways, including (i) the inflammasome, leading to production of IL-1β and IL-18; (ii) the stress-activated protein kinase pathway, resulting in apoptosis; (iii) the mitogen-activated protein kinase pathway, leading to generation of reactive oxygen and nitrogen intermediates; and (iv) phospholipase D, stimulating phagosome-lysosome fusion. The P2X7 receptor can initiate host mechanisms to remove pathogens, most particularly those that parasitise macrophages. At the same time, the P2X7 receptor may be subverted by pathogens to modulate host responses. Moreover, recent genetic studies have demonstrated significant associations between susceptibility or resistance to parasites and bacteria, and loss-of-function or gain-of-function polymorphisms in the P2X7 receptor, underscoring its importance in infectious disease

Lack of a functioning P2X7 receptor leads to increased susceptibility to toxoplasmic ileitis

Background: Oral infection of C57BL/6J mice with the protozoan parasite Toxoplasma gondii leads to a lethal inflammatory ileitis. Principal Findings: Mice lacking the purinergic receptor P2X7R are acutely susceptible to toxoplasmic ileitis, losing significantly more weight than C57BL/6J mice and exhibiting much greater intestinal inflammatory pathology in response to infection with only 10 cysts of T. gondii. This suscep-tibility is not dependent on the ability of P2X7R-deficient mice to control the parasite, which they accomplish just as efficiently as C57BL/6J mice. Rather, susceptibility is associated with elevated ileal concentrations of pro-inflammatory cytokines, reactive nitrogen interme-diates and altered regulation of elements of NFκB activation in P2X7R-deficient mice. Conclusions: Our data support the thesis that P2X7R, a well-documented activator of pro-inflammatory cytokine production, also plays an important role in the regulation of intestinal inflammation

Identification of leukocyte surface P2X7 as a biomarker associated with Alzheimer\u27s disease

Alzheimer\u27s disease (AD) has shown altered immune responses in the periphery. We studied P2X7 (a proinflammatory receptor and a scavenger receptor) and two integrins, CD11b and CD11c, on the surface of circulating leukocytes and analysed their associations with Aβ-PET, brain atrophy, neuropsychological assessments, and cerebrospinal fluid (CSF) biomarkers. Total 287 age-matched, sex-balanced participants were recruited in a discovery cohort and two validation cohorts through the AIBL study and studied using tri-colour flow cytometry. Our results demonstrated reduced expressions of P2X7, CD11b, and CD11c on leukocytes, particularly monocytes, in Aβ +ve cases compared with Aβ -ve controls. P2X7 and integrin downregulation was observed at pre-clinical stage of AD and stayed low throughout disease course. We further constructed a polygenic risk score (PRS) model based on 12 P2RX7 risk alleles to assess the genetic impact on P2X7 function in AIBL and ADNI cohorts. No significant association was identified between the P2RX7 gene and AD, indicating that P2X7 downregulation in AD is likely caused by environmental changes rather than genetic factors. In conclusion, the downregulation of P2X7 and integrins at pre-clinical stage of AD indicates altered pro-inflammatory responses, phagocytic functions, and migrating capabilities of circulating monocytes in early AD pathogenesis. Our study not only improves our understanding of peripheral immune involvement in early stage of AD but also provides more insights into novel biomarker development, diagnosis, and prognosis of AD

Synthesis and Characterization of Cobalt(II) N,N′‑Diphenylazodioxide Complexes

Removal of chloride from CoCl2 with TlPF6 in acetonitrile, followed by addition of excess nitrosobenzene, yielded the eight-coordinate cobalt(II) complex salt [Co{Ph(O)NN(O)- Ph}4](PF6)2, shown by single-crystal X-ray analysis to have a distorted tetragonal geometry. The analogous treatment of the bipyridyl complex Co(bpy)Cl2 yielded the mixed-ligand cobalt(II) complex salt [Co(bpy){Ph(O)NN(O)Ph}2](PF6)2, whose singlecrystal X-ray structure displays a trigonal prismatic geometry, similar to that of the iron(II) cation in the previously known complex salt [Fe{Ph(O)NN(O)Ph}3](FeCl4)2. The use of TlPF6 to generate solvated metal complex cations from chloride salts or chlorido complexes, followed by the addition of nitrosobenzene, is shown to be a useful synthetic strategy for the preparation of azodioxide complex cations with the noncoordinating, diamagnetic PF6 − counteranion. Coordination number appears to be more important than d electron count in determining the geometry and metal−ligand bond distances of diphenylazodioxide complexes

Panoramic SETI: on-sky results from prototype telescopes and instrumental design

The Panoramic SETI (Search for Extraterrestrial Intelligence) experiment (PANOSETI) aims to detect and quantify optical transients from nanosecond to second precision over a large field-of-view (∼4,450 square-degrees). To meet these challenging timing and wide-field requirements, the PANOSETI experiment will use two assemblies of ∼45 telescopes to reject spurious signals by coincidence detection, each one comprising custom-made fast photon-counting hardware combined with (f/1.32) focusing optics. Preliminary on-sky results from pairs of PANOSETI prototype telescopes (100 sq.deg.) are presented in terms of instrument performance and false alarm rates. We found that a separation of >1 km between telescopes surveying the same field-of-view significantly reduces the number of false positives due to nearby sources (e.g., Cherenkov showers) in comparison to a side- by-side configuration of telescopes. Design considerations on the all-sky PANOSETI instrument and expected field-of-views are reported

Lessons Learned from the First 10 Years of the Oaks and Prairies Joint Venture’s Grassland Restoration Incentive Program (GRIP)

The Oaks and Prairies Joint Venture (OPJV) was formed in 2008 as a public-private partnership of agencies and organizations working across jurisdictional boundaries in portions of Texas and Oklahoma, USA. The OPJV’s major focus is reversing declines of bird populations by supporting strategic habitat conservation (biological planning, conservation design, conservation delivery, mission-based monitoring, and assumption-driven research) for northern bobwhite (Colinus virginianus), grasslandobligate species, and their respective habitats. Our objective for this paper is to document and share a decade of lessons learned in developing a partnership-based native grassland conservation program to meet grassland bird conservation targets. We share lessons learned about how to manage partnership-based, large-scale habitat incentive programs to better target project locations and habitat practice types. To establish initial shared purpose, OPJV partners drew from population and habitat objectives in various state, national, and international bird conservation plans, stepped down to ecoregion levels, to establish the OPJV Grassland Bird Conservation Business Plan. The plan has 4 strategies directly contributing to the achievement of OPJV grassland bird biological objectives that are directly supported by OPJV staff or resources (or both). The overall objective for 2015–2025 was 619,978 ha (1,532,000 acres) improved within 40 focal counties, representing 1/3 of all counties in the OPJV. Our main strategy was to provide financial incentives through the OPJV Grassland Restoration Incentive Program (GRIP) to private landowners for conducting beneficial grassland bird habitat management practices. Since inception in 2013, GRIP has treated over 44,515 ha (110,000 acres) on private lands in Texas and Oklahoma, with the goal of maintaining highquality grassland bird habitat on treated hectares for ≥5 years. In 2017, OPJV partners working with USDA Natural Resources Conservation Service, began a 5-year, $6.1 million partnership to provide additional technical and financial assistance to private landowners interested in grassland conservation through the Regional Conservation Partnership Program (RCPP). A project scoring system was designed to strategically encourage individual projects to include prescribed fire—one of the lowest cost practices per hectare—as a recurring practice to maintain program-achieved grassland improvements. Post-inception of the RCPP, the area treated with prescribed fire increased from approximately 809 ha (2,000 acres)/year to 3,237 ha (8,000 acres)/ year, while maintaining average annual hectares of all other beneficial practices. Beginning in 2013, bird point count surveys were conducted annually to monitor northern bobwhite and grassland bird populations, including a subset of points under the National Bobwhite Conservation Initiative (NBCI) Coordinated Implementation Plan. To date, nearly 25,000 individual point counts have been performed in Texas (n = 20,111) and Oklahoma (n = 4,558). Working together, OPJV partners have made significant progress toward meeting grassland bird habitat and population objectives, while tracking progress and improving methods. However, there is still considerable work ahead