Predicting plant invasions under climate change: are species distribution models validated by field trials?

Climate change may facilitate alien species invasion into new areas, particularly for species from warm native ranges introduced into areas currently marginal for temperature. Although conclusions from modelling approaches and experimental studies are generally similar, combining the two approaches has rarely occurred. The aim of this study was to validate species distribution models by conducting field trials in sites of differing suitability as predicted by the models, thus increasing confidence in their ability to assess invasion risk. Three recently naturalized alien plants in New Zealand were used as study species (Archontophoenix cunninghamiana, Psidium guajava and Schefflera actinophylla): they originate from warm native ranges, are woody bird‐dispersed species and of concern as potential weeds. Seedlings were grown in six sites across the country, differing both in climate and suitability (as predicted by the species distribution models). Seedling growth and survival were recorded over two summers and one or two winter seasons, and temperature and precipitation were monitored hourly at each site. Additionally, alien seedling performances were compared to those of closely related native species (Rhopalostylis sapida, Lophomyrtus bullata and Schefflera digitata). Furthermore, half of the seedlings were sprayed with pesticide, to investigate whether enemy release may influence performance. The results showed large differences in growth and survival of the alien species among the six sites. In the more suitable sites, performance was frequently higher compared to the native species. Leaf damage from invertebrate herbivory was low for both alien and native seedlings, with little evidence that the alien species should have an advantage over the native species because of enemy release. Correlations between performance in the field and predicted suitability of species distribution models were generally high. The projected increase in minimum temperature and reduced frosts with climate change may provide more suitable habitats and enable the spread of these species.     

In vivo functions of integrins: lessons from null mutations in mice.

The integrin family (Hynes, R.O., 1992. Integrins: versatility, modulation, and signaling in cell adhesion. Cell 69, 11-25) is composed of at least 24 heterodimers formed from eight beta subunits and 18 alpha subunits. Thus far, mice expressing null mutations of seven of the eight beta subunits and 13 of the 18 known alpha subunits have been generated, With only a few exceptions, the phenotypes of each of the knockout lines are quite distinct. Studies utilizing integrin knockout mice and cells derived from these mice have provided considerable and sometimes surprising insights into unique functions of individual members of this family.     

Dose-dependent inhibition of cold air-induced bronchoconstriction by atropine

We undertook a study to demonstrate whether inhalation of atropine could inhibit cold air-induced bronchoconstriction in a dose-dependent fashion. In seven subjects with asthma we assessed the effects of placebo and of various doses of inhaled atropine (0.13-2.08 mg) on a base-line specific airway resistance (sRaw) and on the increase in sRaw produced by 5 min of voluntary eucapnic hyperventilation with subfreezing air at -17 degrees C. We also assessed the effect of the lowest doses of atropine on the increase in sRaw produced by five breaths of 1.0% metacholine. Atropine in doses of 0.13 or 0.26 mg caused a maximal reduction in base-line sRaw and completely inhibited the effect of 1.0% methacholine on sRaw, but it did not inhibit the bronchomotor response to cold air. Higher doses of atropine did inhibit the effect of cold air on sRaw in a dose-dependent fashion. The dose of atropine required to inhibit this effect of cold air varied with the increase in sRaw produced by cold air after placebo. These results suggest that cold air causes bronchoconstriction through vagal pathways and that higher doses of antimuscarinic agents are required to inhibit vagally mediated bronchoconstriction than those required to reduce base-line airway tone or to inhibit the effects of a large dose of an inhaled muscarinic agonist.     

A value added manure management system using the black soldier fly

A manure management system for laying hens using the black soldier fly, Hermetia illucens (L.) converted manure to a 42% protein, 35% fat feedstuff, reduced manure accumulation by at least 50% and eliminated house fly breeding. No extra facility or added energy was required. Mature larvae self-harvested producing a feedstuff as they attempted to pupate. Optimal feedstuff to manure dry matter yield was 7·8%. This insect occurs worldwide in tropical and warm-temperature regions and can digest many biological wastes.     

Disulfiram-based disulfides as narrow-spectrum antibacterial agents

Sixteen disulfides derived from disulfiram (Antabuse?) were evaluated as antibacterial agents. Derivatives with hydrocarbon chains of seven and eight carbons in length exhibited antibacterial activity against Gram-positive Staphylococcus, Streptococcus, Enterococcus, Bacillus, and Listeria spp. A comparison of the cytotoxicity and microsomal stability with disulfiram further revealed that the eight carbon chain analog was of lower toxicity to human hepatocytes and has a longer metabolic half-life. In the final analysis, this investigation concluded that the S-octylthio derivative is a more effective growth inhibitor of Gram-positive bacteria than disulfiram and exhibits more favorable cytotoxic and metabolic parameters over disulfiram.     

Temporal occurrence of third-stage larvae of Elaeophora schneideri in Tabanus lineola hinellus on South Island, South Carolina

The occurrence of third-stage larvae of the arterial worm (Elaeophora schneideri) in populations of the horse fly, Tabanus lineola hinellus, was studied on South Island, Georgetown County, South Carolina. Over the period from mid-April to mid-October 1982, horse flies had a bimodal pattern of abundance with peak populations in June and September. During individual bimonthly horse fly collections, the prevalence of infection of T. l. hinellus ranged from 0 to 1.23%. Prevalence of infected horse flies was biphasic with peaks in mid-May (1.23%) and mid-August (1.22%), 2 to 4 wk prior to peaks in horse fly populations. The intensity of infection of T. l. hinellus increased as time progressed and was highest in late summer. This increase resulted in greater recovery of infective larvae during August-September (mean intensity = 25) than in May-June (mean intensity = 4). Both prevalence and intensity of infection of T. l. hinellus were low compared to primary intermediate hosts of E. schneideri in the western U.S.     

Tumor necrosis factor inhibits a polymorphonuclear leukocyte-dependent airway edema in guinea pigs

Intravenously administered endotoxin inhibits the polymorphonuclear leukocyte (PMN)-dependent airway edema produced in guinea pigs exposed to toluene diisocyanate (TDI). Tumor necrosis factor (TNF) is produced in vivo by peripheral blood monocytes and tissue macrophages stimulated with endotoxin and has been shown to activate PMN's and vascular endothelial cells. To determine whether the inhibition of airway edema is mediated by TNF, guinea pigs were treated with intravenous saline or 75,000 U/kg recombinant human TNF 1.5 h before exposure to air or 3 ppm TDI for 1 h. Animals were then injected intravenously with 50 mg/kg Evans blue dye as a marker of protein extravasation. Saline-treated animals exposed to TDI had a significant increase in tracheal Evans blue dye extravasation (85 +/- 6.5 micrograms dye/g trachea, mean +/- SE) compared with saline-treated animals exposed to air (31.3 +/- 2.5, P less than 0.001). The tracheal extravasation of Evans blue dye was significantly inhibited (P less than 0.05) in TDI-exposed animals treated with TNF (64.7 +/- 7.5). Neither heat-inactivated TNF (104.9 +/- 9.5) nor TNF neutralized with a monoclonal antibody against TNF (99.7 +/- 17.9) inhibited TDI-induced airway edema. In addition, treatment with 15,000 U/kg (99.9 +/- 21.3) or 150,000 U/kg (103.2 +/- 17.6) interleukin 1, a monokine also produced in response to endotoxin, did not prevent airway edema. These results suggest that TNF released in response to endotoxin mediates endotoxin's inhibition of a PMN-dependent airway edema.