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Does urbanization explain differences in interactions between an insect herbivore and its natural enemies and mutualists?
Urbanization can alter the composition of arthropod communities. However, little is known about how urbanization affects ecological interactions. Using experimental colonies of the black bean aphid Aphis fabae Scopoli reared on Vicia faba L, we asked if patterns of predator-prey, host-parasitoid and ant-aphid mutualisms varied along an urbanization gradient across a large town in southern England. We recorded the presence of naturally occurring predators, parasitoid wasps and mutualistic ants together with aphid abundance. We examined how biotic (green areas and plant richness) and abiotic features (impervious surfaces and distance to town center) affected (1) aphid colony size, (2) the likelihood of finding predators, mutualistic ants and aphid mummies (indicating the presence of parasitoids), and (3) how the interplay among these factors affected patterns of parasitoid attack, predator abundance, mutualistic interactions and aphid abundance. The best model to predict aphid abundance was the number of mutualistic ants attending the colonies. Aphid predators responded negatively to both the proportion of impervious surfaces and to the number of mutualistic ants farming the colonies, and positively to aphid population size, whereas parasitized aphids were found in colonies with higher numbers of aphids and ants. The number of mutualistic ants attending was positively associated with aphid colony size and negatively with the number of aphid predators. Our findings suggest that for insect-natural enemy interactions, urbanization may affect some groups, while not influencing others, and that local effects (mutualists, host plant presence) will also be key determinants of how urban ecological communities are formed
Comparing permeability of matrix cover types for the marsh rice rat (Oryzomys palustris)
Multiple keratoacanthomas in a young woman: report of a case emphasizing medical management and a review of the spectrum of multiple keratoacanthomas
Friction, snake oil, and weird countries: Cybersecurity systems could deepen global inequality through regional blocking
EFFECTS OF MYCOPLASMAL UPPER-RESPIRATORY-TRACT DISEASE ON MOVEMENT AND THERMOREGULATORY BEHAVIOR OF GOPHER TORTOISES ( GOPHERUS POLYPHEMUS
HISTOLOGIC SPECTRUM OF CUTANEOUS INVOLVEMENT IN PATIENTS WITH MYELOGENOUS LEUKEMIA INCLUDING THE NEUTROPHILIC DERMATOSES
A randomized trial of vorinostat with treatment interruption after initiating antiretroviral therapy during acute HIV-1 infection
Objective and Design: A randomized, open-label pilot study in individuals treated with antiretroviral therapy (ART) since acute HIV infection (AHI) with a regimen including a histone deacetylase inhibitor to induce HIV from latency and control HIV replication during subsequent treatment interruption (TI). Methods: Fifteen participants who initiated ART at AHI were randomized to vorinostat/hydroxychloroquine/maraviroc (VHM) plus ART (n = 10) or ART alone (n = 5). The VHM arm received three 14-day vorinostat cycles within 10 weeks before TI. ART was resumed for plasma viral load (VL) > 1,000 HIV RNA copies/mL. Primary outcome was proportion of participants on VHM + ART versus ART only with VL < 50 copies/mL for 24 weeks after TI. Results: Fifteen participants on ART (median: 178 weeks: range 79-295) enrolled. Two on VHM + ART experienced serious adverse events. Fourteen participants underwent TI; all experienced VL rebound with no difference in time between arms: VHM + ART (n = 9) median: 4 weeks and ART only (n = 5) median: 5 weeks. VHM induced a 2.2-fold increase in VL (p = 0.008) by single-copy HIV RNA assay after the first cycle. Neopterin levels increased significantly following the first two cycles. After VHM treatment, the frequencies of peripheral blood mononuclear cells harboring total HIV DNA and cell-associated RNA were unchanged. All participants achieved VL suppression following ART re-initiation. Conclusions: Administration of VHM increased HIV VL in plasma, but this was not sustained. VHM did not impact time to viral rebound following TI and had no impact on the size of the HIV reservoir, suggesting that HIV reservoir elimination will require alternative treatment strategies
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