Prey preferences of six species of Carabidae (Coleoptera) and one Lycosidae (Araneae) commonly found in UK arable crop fields

Abstract: Laboratory experiments were used to determine the feeding preferences of six carabid beetles and one lycosid spider on aphid and collembolan prey. The first investigation used only five species of carabid Pterostichus melanarius Illiger, Pterostichus madidus F., Harpalus rufipes DeGeer, Nebria brevicollis F. and Carabus violaceus L., which had been caught most commonly in pitfall traps in the headland region of arable crop fields. When offered Brevicoryne brassicae L., Sitobion avenae F., Metopolophium dirhodum Walker and Rhopalosiphum padi L. as prey items, the species consistently consumed in high numbers was M. dirhodum . In subsequent experiments four carabids Pterostichus cupreus L., P. melanarius, P. madidus. H. rufipes and a lycosid spider Trochosa ruricola DeGeer whose distribution was shown by pitfall trapping to extend throughout the arable crop, were the chosen predators. These predators were offered a choice between M. dirhodum and entomobryid collembolans (a recognised alternative prey item) to gauge their preference between the two prey types. Both male and female P. cupreus and P. melanarius showed a significant preference for the aphid prey, while there was no significant preference displayed by the other species. The effect of temperature on the voracity of these five predators fed on M. dirhodum was investigated. There were significant differences in the number of aphids consumed by the species and sexes at the different temperatures. Regression analysis on the mean numbers of aphids eaten by each sex of the five predators, showed that in the majority of cases there was a significant increase in predation with increasing temperature. In considering the dietary preferences illustrated by these experiments, it appeared that P. cupreus and P. melanarius offered the greatest potential in controlling aphids on arable crops.     

Purification and characterization of Dolichos lablab lectin

The mannose/glucose-binding Dolichos lablab lectin (designated DLL) has been purified from seeds of Dolichos lablab (hyacinth bean) to electrophoretic homogeneity by affinity chromatography on an ovalbumin- Sepharose 4B column. The purified lectin gave a single symmetric protein peak with an apparent molecular mass of 67 kDa on gel filtration chromatography, and five bands ranging from 10 kDa to 22 kDa upon SDS-PAGE. N-Terminal sequence analysis of these bands revealed subunit heterogeneity due to posttranslational proteolytic truncation at different sites mostly at the carboxyl terminus. The carbohydrate binding properties of the purified lectin were investigated by three different approaches: hemagglutination inhibition assay, quantitative precipitation inhibition assay, and ELISA. On the basis of these studies, it is concluded that the Dolichos lablab lectin has neither an extended carbohydrate combining site, nor a hydrophobic binding site adjacent to it. The carbohydrate combining site of DLL appears to most effectively accommodate a nonreducing terminal alpha-d-mannosyl unit, and to be complementary to the C-3, C-4, and C-6 equatorial hydroxyl groups of alpha-d-mannopyranosyl and alpha-d-glucopyranosyl residues. DLL strongly precipitates murine IgM but not IgG, and the recent finding that this lectin interacts specifically with NIH 3T3 fibroblasts transfected with the Flt3 tyrosine kinase receptor and preserves human cord blood stem cells and progenitors in a quiescent state for prolonged periods in culture, make this lectin a valuable tool in biomedical research.      

Metabolic perturbations of postnatal growth restriction and hyperoxia-induced pulmonary hypertension in a bronchopulmonary dysplasia model

Introduction

Neonatal pulmonary hypertension (PH) is a common manifestation of bronchopulmonary dysplasia (BPD) and contributes to increased morbidity and mortality of preterm birth. Postnatal growth restriction (PNGR) and hyperoxia are independent contributors to PH development, as indicated by our previous work in a rat model of BPD.

Objective

To explore the metabolic consequences of induction of PH with hyperoxia and PNGR in a rat model of BPD.

Methods

Sprague–Dawley rat pups (n?=?4/group) underwent three modes of PH induction: (1) growth restriction-induced by larger litter size; (2) hyperoxia-induced by 75% oxygen exposure; (3) combined growth restriction and hyperoxia. Primary metabolism, complex lipids, biogenic amines, and lipid mediators were characterized in plasma and lung tissue using GC- and LC-MS technologies.

Results

Specific to hyperoxic induction, pulmonary metabolomics suggested increased reactive oxygen species (ROS) generation as indicated by: (1) increased indicators of β-oxidation and mitochondrial respiration; (2) changes in ROS-sensitive pathway activity and metabolites including the polyol pathway and xanthine oxidase pathways, and reduced glutathione; (3) decreased plasmalogens. Unlike the lung, circulating metabolite changes were induction mode-specific or additive in the combined modes (e.g. 1) growth-restriction reduced phosphatidylcholine; (2) hyperoxia increased oxylipins and trimethylamine-N-oxide (TMAO); (3) additive effects on 3-hydroxybutyric acid and arginine.

Conclusion

The present study highlights the variety of metabolic changes that occur due to PNGR- and hyperoxia-induced PH, identifying numerous metabolites and pathways influenced by treatment-specific or combined effects. The rat model used in this study presents a robust means of uncovering the mechanisms that contribute to the pathology of PH.

     

The p75 neurotrophin receptor

The pan neurotrophin receptor (p75(NTR)) is best known for mediating neural cell death during development as well as in the adult following injury, the latter making it a target for the treatment of neurodegenerative disease. Although p75(NTR) has been studied for over 30 years, a number of recent discoveries have changed our understanding of its regulation. Here we provide a brief overview of the p75(NTR) protein, its post-translational modifications, and the phenotype of p75(NTR)-deficient mice as a starting point for researchers unfamiliar with this complex receptor. The accepted mechanisms underlying the ability of p75(NTR) to regulate cell death as well as a number of other neural functions, most notably neuronal differentiation, neurite outgrowth and synaptic plasticity, are also summarised.     

Ecological consequences of genetic diversity

Understanding the ecological consequences of biodiversity is a fundamental challenge. Research on a key component of biodiversity, genetic diversity, has traditionally focused on its importance in evolutionary processes, but classical studies in evolutionary biology, agronomy and conservation biology indicate that genetic diversity might also have important ecological effects. Our review of the literature reveals significant effects of genetic diversity on ecological processes such as primary productivity, population recovery from disturbance, interspecific competition, community structure, and fluxes of energy and nutrients. Thus, genetic diversity can have important ecological consequences at the population, community and ecosystem levels, and in some cases the effects are comparable in magnitude to the effects of species diversity. However, it is not clear how widely these results apply in nature, as studies to date have been biased towards manipulations of plant clonal diversity, and little is known about the relative importance of genetic diversity vs. other factors that influence ecological processes of interest. Future studies should focus not only on documenting the presence of genetic diversity effects but also on identifying underlying mechanisms and predicting when such effects are likely to occur in nature.     

Neutrophils exhibit distinct phenotypes toward chitosans with different degrees of deacetylation: implications for cartilage repair

Introduction  

Osteoarthritis is characterized by the progressive destruction of cartilage in the articular joints. Novel therapies that promote resurfacing of exposed bone in focal areas are of interest in osteoarthritis because they may delay the progression of this disabling disease in patients who develop focal lesions. Recently, the addition of 80% deacetylated chitosan to cartilage microfractures was shown to promote the regeneration of hyaline cartilage. The molecular mechanisms by which chitosan promotes cartilage regeneration remain unknown. Because neutrophils are transiently recruited to the microfracture site, the effect of 80% deacetylated chitosan on the function of neutrophils was investigated. Most studies on neutrophils use preparations of chitosan with an uncertain degree of deacetylation. For therapeutic purposes, it is of interest to determine whether the degree of deacetylation influences the response of neutrophils to chitosan. The effect of 95% deacetylated chitosan on the function of neutrophils was therefore also investigated and compared with that of 80% deacetylated chitosan.