Urbanization Increases Pathogen Pressure on Feral and Managed Honey Bees

Given the role of infectious disease in global pollinator decline, there is a need to understand factors that shape pathogen susceptibility and transmission in bees. Here we ask how urbanization affects the immune response and pathogen load of feral and managed colonies of honey bees (Apis mellifera Linnaeus), the predominant economically important pollinator worldwide. Using quantitative real-time PCR, we measured expression of 4 immune genes and relative abundance of 10 honey bee pathogens. We also measured worker survival in a laboratory bioassay. We found that pathogen pressure on honey bees increased with urbanization and management, and the probability of worker survival declined 3-fold along our urbanization gradient. The effect of management on pathogens appears to be mediated by immunity, with feral bees expressing immune genes at nearly twice the levels of managed bees following an immune challenge. The effect of urbanization, however, was not linked with immunity; instead, urbanization may favor viability and transmission of some disease agents. Feral colonies, with lower disease burdens and stronger immune responses, may illuminate ways to improve honey bee management. The previously unexamined effects of urbanization on honey-bee disease are concerning, suggesting that urban areas may favor problematic diseases of pollinators.     

Heat-Shock Protein 70 Levels in Temperature-Stressed Mung Bean Shoots

Heat-shock protein 70 accumulation was induced by both increasesand decreases in temperature. An upward temperature shift ofabout 15C or a downward shift of about 10C was needed forthe response. In each case the accumulation was significantwithin 2 h and complete within about 6 h. Heat-shocked tissuecontained two new HSP70 isotypes not seen in the control tissueor in the cold-shocked tissue. Key words: Heat-shock protein, heat stress, cold stress, mung bean     

An ultrastructural stereological analysis of the myocardium in homoiothermal animals during cooling]

By methods of electron microscopy and stereology the ultrastructural cardiomyocyte reorganization of rats exposed to influence of low temperatures (exposure during 16 days at -7 degrees C) was studied. It was shown, that with this regime of cooling the disturbance of intracellular regeneration in cardiomyocytes occurred and the complex of morphological changes typical for the syndrome of regenerative-plastic deficiency was developed. The most essential changes were seen in myofibrils and mitochondria. According to the stereologic data a change in spatial reorganization of cardiomyocytes was connected largely with these organelles. With the increase in cooling duration an increase in the volume density of myofibrils and a decrease in this parameter for mitochondria were marked. As a result of these changes the mitochondria/myofibrils volume ratio was essentially decreased. As a whole, ultrastructural reorganization of cardiomyocytes under the influence of low temperatures on rats was characterized by a decrease in the ratio of the organelle volume to myofibrillar volume. The same quantitative reorganization was revealed in atrophied cardiomyocytes under the conditions of the decreased inflow of plastic substances to cells.     

Interaction of rabbit skeletal muscle glycogen synthase I with substrate analogs--oxo-UDP hydrazones]

Inhibition of rabbit skeletal muscle glycogen synthase I was studied by using several synthetic substrate analogs: dansylhydrazone of oxo-UDP, 3-hydroxy-2-naphthoylhydrazone of oxo-UDP, salicyloylhydrazone of oxo-UDP, 1-oxyl-2,2,5,5-tetramethylpyrrolidine-3-carbonylhydrazone of oxo-UDP, N'-(dansyl)hydrazinocarbonylhydrazone of oxo-UDP and N'-(fluorenylidene-9)-hydrazinocarbonylhydrazone of oxo-UDP. All these compounds (with the exception of the nitroxyl-containing hydrazone) were characterized by a nonlinear dependence of the reverse reaction rate on the analog concentration in Dixon coordinates. The parabolic type of inhibition was due to the fact that the analogs tested except for the nitroxyl-containing hydrazone were able to interact both with the active center of the enzyme and with the FMN-binding site. The inhibition constants for oxo-UDP hydrazones were calculated for the both centers; their comparison revealed that the affinity of the analogs for the FMN-binding site increased with an increase in the radical hydrophobicity. These data suggest that the site with a high binding affinity for FMN is hydrophobic in nature. Apparently, isoalloxasine-like compounds display the highest affinity for this site.     

Concomitant Information in Competing Risk Analysis

A competing risk model, accommodating both Type I censoring and random withdrawals, is expanded to incorporate concomitant information by allowing the parameters of the underlying distributions to be a linear function of two covariates. The model is developed for two competing risks, one following a Weibull distribution and the other a Rayleigh distribution, and random withdrawals following a Weibull distribution. A method is developed for testing the equality of the coefficients for a given covariate for each of the competing risks using MLE'.     

PCR-generated conspecific sodium channel gene probe for the house fly.

A segment of the house fly (Musca domestica) homologue of the para (paralytic) sodium channel gene of Drosophila melanogaster was isolated by using mixed sequence oligonucleotide primers in the polymerase chain reaction (PCR). The specificity of the procedure was demonstrated by genomic Southern analysis using the housefly PCR amplification product as a probe and by DNA sequence analysis. The latter showed structural homology to the para gene, but not to the corresponding region of DSC1, another D. melanogaster gene with structural similarity to vertebrate sodium channel genes.     

Essential roles of core starvation-stress response loci in carbon-starvation-inducible cross-resistance and hydrogen peroxide-inducible adaptive resistance to oxidative challenge in Salmonella typhimurium

The starvation-stress response (SSR) of Salmonella typhimurium encompasses the physiological changes that occur upon starvation for an essential nutrient, e.g. C-source. A subset of SSR genes, known as core SSR genes, are required for the long-term starvation survival of the bacteria. Four core SSR loci have been identified in S. typhimuriumrpoSstiAstiB, and stiC. Here we report that in S. typhimurium C-starvation induced a greater and more sustainable cross-resistance to oxidative challenge (15 mM hydrogen peroxide (H₂O₂) for 40 min) than either N- or P-starvation. Of the four core SSR loci, only rpoS and stiC mutants exhibited a defective C-starvation-inducible cross-resistance to H₂O₂ challenge. Interestingly, (unadapted) log-phase S. typhimurium rpoS and stiA mutants were very sensitive to oxidative challenge. Based on this, we determined if these core SSR loci were important for H₂O₂ resistance developed during a 60 min adaptive exposure to 60 μM H₂O₂ (adapted cells). Both unadapted and adapted rpoS and stiA mutants were hypersensitive to a H₂O₂ challenge. In addition, a stiB mutant exhibited normal adaptive resistance for the first 20 mins of H₂O₂ challenge but then rapidly lost viability, declining to a level of about 1.5% of the wild-type strain. The results of these experiments indicate that: (i) the rpoS and stiC loci are essential for the development of C-starvation-inducible cross-resistance to oxidative challenge, and (ii) the rpoSstiA, and, in a delayed effect, stiB loci are needed for H₂O₂-inducible adaptive resistance to oxidative challenge. Moreover, we found that both stiA and stiB are induced by a 60 μM H₂O₂ exposure, but only stiA was regulated (repressed) by (reduced form) OxyR.