Of hummingbirds and helicopters: Hovering costs, competitive ability, and foraging strategies

Wing morphology and flight kinematics profoundly influence foraging costs and the overall behavioral ecology of hummingbirds. By analogy with helicopters, previous energetic studies have applied the momentum theory of aircraft propellers to estimate hovering costs from wing disc loading (WDL), a parameter incorporating wingspan (or length) and body mass. Variation in WDL has been used to elucidate differences either among hummingbird species in nectar-foraging strategies (e.g., territoriality, traplining) and dominance relations or among gender-age categories within species. We first demonstrate that WDL, as typically calculated, is an unreliable predictor of hovering (induced power) costs; predictive power is increased when calculations use wing length instead of wingspan and when actual wing stroke amplitudes are incorporated. We next evaluate the hypotheses that foraging strategy and competitive ability are functions of WDL, using our data in combination with those of published sources. Variation in hummingbird behavior cannot be easily classified using WDL and instead is correlated with a diversity of morphological and physiological traits. Evaluating selection pressures on hummingbird wings will require moving beyond wing and body mass measurements to include the assessment of the aerodynamic forces, power requirements, and power reserves of hovering, forward flight, and maneuvering. However, the WDLhelicopter dynamics model has been instrumental in calling attention to the importance of comparative wing morphology and related aerodynamics for understanding the behavioral ecology of hummingbirds

Understanding disability glare: light scatter and retinal illuminance as predictors of sensitivity to contrast

The presence of a bright light in the visual field has two main effects on the retinal image: reduced contrast and increased retinal illuminance due to scattered light; the latter can, under some conditions, lead to an improvement in retinal sensitivity. The combined effect remains poorly understood, particularly at low light levels. A psychophysical flicker-cancellation test was used to measure the amount and angular distribution of scattered light in the eye for 40 observers. Contrast thresholds were measured using a functional contrast sensitivity test. Pupil-plane glare-source illuminances (i.e. 0, 1.35, 19.21 lm/m2), eccentricities (5°, 10°, 15°), and background luminances (1, 2.6, 26 cd/m2) were investigated. Visual performance was better than predicted, based on loss of retinal image contrast caused by scattered light, particularly in the mesopic range. Prediction accuracy improved significantly when the expected increase in retinal sensitivity in the presence of scattered light was also incorporated in the model

Adenosine receptors in GtoPdb v.2021.2

Adenosine receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on Adenosine Receptors [110]) are activated by the endogenous ligand adenosine (potentially inosine also at A3 receptors). Crystal structures for the antagonist-bound [153, 313, 221, 61], agonist-bound [375, 203, 204] and G protein-bound A2A adenosine receptors [49] have been described. The structures of an antagonist-bound A1 receptor [128] and an adenosine-bound A1 receptor-Gi complex [86] have been resolved by cryo-electronmicroscopy. Another structure of an antagonist-bound A1 receptor obtained with X-ray crystallography has also been reported [57]. caffeine is a nonselective antagonist for adenosine receptors, while istradefylline, a selective A2A receptor antagonist, is on the market for the treatment of Parkinson's disease

Adenosine receptors (version 2019.4) in the IUPHAR/BPS Guide to Pharmacology Database

Adenosine receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on Adenosine Receptors [103]) are activated by the endogenous ligand adenosine (potentially inosine also at A3 receptors). Crystal structures for the antagonist-bound [146, 305, 213, 55], agonist-bound [362, 196, 198] and G protein-bound A2A adenosine receptors [43] have been described. The structures of an antagonist-bound A1 receptor [123] and an adenosine-bound A1 receptor-Gi complex [80] have been resolved by cryo-electronmicroscopy. Another structure of an antagonist-bound A1 receptor obtained with X-ray crystallography has also been reported [51]

Adenosine receptors in GtoPdb v.2023.1

Adenosine receptors (nomenclature as agreed by the NC-IUPHAR Subcommittee on Adenosine Receptors [112]) are activated by the endogenous ligand adenosine (potentially inosine also at A3 receptors). Crystal structures for the antagonist-bound [155, 316, 224, 62], agonist-bound [379, 205, 206] and G protein-bound A2A adenosine receptors [49] have been described. The structures of an antagonist-bound A1 receptor [130] and an adenosine-bound A1 receptor-Gi complex [87] have been resolved by cryo-electronmicroscopy. Another structure of an antagonist-bound A1 receptor obtained with X-ray crystallography has also been reported [58]. The structure of the A2B receptor has also been elucidated [57]. caffeine is a nonselective antagonist for adenosine receptors, while istradefylline, a selective A2A receptor antagonist, is on the market for the treatment of Parkinson's disease

Structure of Herpes Simplex Virus Glycoprotein D Bound to the Human Receptor Nectin-1

Binding of herpes simplex virus (HSV) glycoprotein D (gD) to a cell surface receptor is required to trigger membrane fusion during entry into host cells. Nectin-1 is a cell adhesion molecule and the main HSV receptor in neurons and epithelial cells. We report the structure of gD bound to nectin-1 determined by x-ray crystallography to 4.0 Å resolution. The structure reveals that the nectin-1 binding site on gD differs from the binding site of the HVEM receptor. A surface on the first Ig-domain of nectin-1, which mediates homophilic interactions of Ig-like cell adhesion molecules, buries an area composed by residues from both the gD N- and C-terminal extensions. Phenylalanine 129, at the tip of the loop connecting β-strands F and G of nectin-1, protrudes into a groove on gD, which is otherwise occupied by C-terminal residues in the unliganded gD and by N-terminal residues in the gD/HVEM complex. Notably, mutation of Phe129 to alanine prevents nectin-1 binding to gD and HSV entry. Together these data are consistent with previous studies showing that gD disrupts the normal nectin-1 homophilic interactions. Furthermore, the structure of the complex supports a model in which gD-receptor binding triggers HSV entry through receptor-mediated displacement of the gD C-terminal region

ERRATUM: "DETERMINING TITAN'S SPIN STATE FROM CASSINI RADAR IMAGES" (2008, AJ, 135, 1669)

We previously reported an initial determination of Titan's rotational state from fits to overlapping radar images. We have since discovered a coding error in software used to make these fits, which led to systematic offsets of 1-2 km in recovered positions. While our principal results remain qualitatively unchanged, with this error corrected, the pole movement we previously reported (our weakest result) is now counterindicated. Our revised best fit is essentially the same as the "best-fit no pole wobble" result discussed at the top of the second column on page 1675. The determined pole location did not change significantly after the bug fix and thus we still conclude that the spin axis is not in the plane formed by Titan's orbit normal and the normal to the Laplace plane. Due to the correlations between pole wobble and spin rate (see Figure 3 on page 1672), the new best fit has a spin rate that differs from the synchronous value by an amount that is three times smaller than the value reported in the paper. The pole location changed by less than 0.01 deg (~500 m on the surface) and rate of increase in spin decreased by a factor of 2 from the previous fit. The new best-fit parameter values with 1σ error bars are: pole right ascension 39.4934 ± 0.0249 deg, pole declination 83.4368 ± 0.0024 deg, spin rate 22.57731 ± 0.00011 deg/day (0.00033 deg/day greater than synchronous spin rate), derivative of pole right ascension –6.52 ± 4.20 deg/century, derivative of pole declination –0.2212 ± 0.3567 deg/century, and derivative of spin rate 0.0247 ± 0.0050 deg/day/century. The corrected version of Table 3 (below) shows the residual systematic and random error of the several candidate models discussed in the paper. Fixing the bug reduced the residual systematic error of all the fitted models. The four models in which spin rate is allowed to vary from synchronous either due to a change in spin rate (Column 5, numbered from the left) or a change in its time derivative (Column 6) or both (Columns 7 and 8) have lower residual systematic errors and thus better represent the data than do the purely synchronous fit (Column 3). For this reason, an asynchronous spin rate is still supported by the data, although efforts (e.g., Mitchell 2009) to quantitatively interpret the asynchroneity should take our revised determination into account. On the other hand, as depicted by Columns 7 and 8, allowing the pole movement terms to vary from the predicted (IAU Titan) values results in no significant improvement in the fit, thus large short-term pole movement is not supported by the data. In fact, the best-fit values and error bars for the pole movement are consistent with the long-term pole trends that were predicted prior to the Cassini mission

Safety and Immunogenicity Study of Multiclade HIV-1 Adenoviral Vector Vaccine Alone or as Boost following a Multiclade HIV-1 DNA Vaccine in Africa

We conducted a double-blind, randomized, placebo-controlled Phase I study of a recombinant replication-defective adenovirus type 5 (rAd5) vector expressing HIV-1 Gag and Pol from subtype B and Env from subtypes A, B and C, given alone or as boost following a DNA plasmid vaccine expressing the same HIV-1 proteins plus Nef, in 114 healthy HIV-uninfected African adults.Volunteers were randomized to 4 groups receiving the rAd5 vaccine intramuscularly at dosage levels of 1×10(10) or 1×10(11) particle units (PU) either alone or as boost following 3 injections of the DNA vaccine given at 4 mg/dose intramuscularly by needle-free injection using Biojector® 2000. Safety and immunogenicity were evaluated for 12 months. Both vaccines were well-tolerated. Overall, 62% and 86% of vaccine recipients in the rAd5 alone and DNA prime - rAd5 boost groups, respectively, responded to the HIV-1 proteins by an interferon-gamma (IFN-γ) ELISPOT. The frequency of immune responses was independent of rAd5 dosage levels. The highest frequency of responses after rAd5 alone was detected at 6 weeks; after DNA prime - rAd5 boost, at 6 months (end of study). At baseline, neutralizing antibodies against Ad5 were present in 81% of volunteers; the distribution was similar across the 4 groups. Pre-existing immunity to Ad5 did not appear to have a significant impact on reactogenicity or immune response rates to HIV antigens by IFN-γ ELISPOT. Binding antibodies against Env were detected in up to 100% recipients of DNA prime - rAd5 boost. One volunteer acquired HIV infection after the study ended, two years after receipt of rAd5 alone.The HIV-1 rAd5 vaccine, either alone or as a boost following HIV-1 DNA vaccine, was well-tolerated and immunogenic in African adults. DNA priming increased the frequency and magnitude of cellular and humoral immune responses, but there was no effect of rAd5 dosage on immunogenicity endpoints.ClinicalTrials.gov NCT00124007