Factors affecting population density, group size and territory size of the European badger, Meles meles

This paper discusses the relationship between the distribution and biomass of the main prey of European badgers, Meles meles and the badgers group size, territory size and population density. The distribution of areas rich in earthworms, Lumbricus spp., is correlated with badger range size, whilst badger group size increases with the biomass of worms per badger territory and badger density increases with overall worm biomass. Regulation of badger density in an area is likely to take place through regulation of group size, in the absence of other factors such as persecution and lack of suitable sett-sites.     

Mendelian analysis of the organization of actin sequences in Physarum polycephalum

The genormic organization of the multiple actin DNA sequences in the lower eukaryote Physarum polycephalum was investigated by Mendelian mapping. Actin-homologous restriction endonuclease cleavage fragments detected by DNA blotting showed length polymorphisms when different strains were compared. These length polymorphisms were used as phenotypic markers for actin sequences in the genome. The meiotic assortment of the polymorphic restriction fragments was analysed, revealing four unlinked actin loci. The data for three-of the actin loci, ardB, C and D, are consistent with a single sequence or gene at each locus. The data for the other actin locus. ardA, is consistent with multiple linked actin sequences or genes.     

Cerebral Synaptic Transmission During Anoxia Is Protected by Creatine

Synaptic transmission in cerebral tissue fails very rapidly in the absence of oxygen; the metabolic basis for this is not known. We report here that the transmission failure in the guinea pig hippocampal slice can be delayed threefold by exposing the tissue to extracellular creatine (Cr) for 3 h. The improved survival is associated with an increase of tissue phosphocreatine (PCr) concentration. These data argue that the metabolic basis for synaptic transmission failure is a fall in tissue ATP concentrations. They also indicate a way to protect brain tissue against anoxic damage.     

Cell delivery systems: Toward the next generation of cell therapies for type 1 diabetes

Immunoprotection and oxygen supply are vital in implementing a cell therapy for type 1 diabetes (T1D). Without these features, the transplanted islet cell clusters will be rejected by the host immune system, and necrosis will occur due to hypoxia. The use of anti‐rejection drugs can help protect the transplanted cells from the immune system; yet, they also may have severe side effects. Cell delivery systems (CDS) have been developed for islet transplantation to avoid using immunosuppressants. CDS provide physical barriers to reduce the immune response and chemical coatings to reduce host fibrotic reaction. In some CDS, there is architecture to support vascularization, which enhances oxygen exchange. In this review, we discuss the current clinical and preclinical studies using CDS without immunosuppression as a cell therapy for T1D. We find that though CDS have been demonstrated for their ability to support immunoisolation of the grafted cells, their functionality has not been fully optimized. Current advanced methods in clinical trials demonstrate the systems are partly functional, physically complicated to implement or inefficient. However, modifications are being made to overcome these issues.     

Optimization of a series of quinazolinone-derived antagonists of CXCR3

The evaluation of the CXCR3 antagonist AMG 487 in clinic trials was complicated due to the formation of an active metabolite. In this Letter, we will discuss the further optimization of the quinazolinone series that led to the discovery of compounds devoid of the formation of the active metabolite that was seen with AMG 487. In addition, these compounds also feature increased potency and good pharmacokinetic properties. We will also discuss the efficacy of the lead compound 34 in a mouse model of cellular recruitment induced by bleomycin.     

A region of calpastatin domain L that reprimes cardiac L-type Ca2+ channels

Calpastatin, an endogenous inhibitor of calpain, is composed of domain L and four repetitive homologous domains 1-4. Domains 1-4 inhibit calpain, whereas domain L partially reprimes L-type Ca2+ channels for voltage-gated activation. In the present study, the effects on Ca2+ channel activity of four isoforms and a series of fragments of calpastatin domain L were investigated in guinea-pig ventricular myocytes with the patch-clamp method. With one exception, all the isoforms and fragment peptides that contained amino acid residues 54-64 of domain L reprimed the Ca2+ channels to comparable levels (9-15% of control activity) to those observed previously with a full-length form of calpastatin. These results suggest that the region containing amino acid residues 54-64 (EGKPKEHTEPK) is responsible for the Ca2+ channel repriming function of calpastatin domain L.     

The Effects of Chilling on the Fecundity and Life Span of Mass-reared Parasitoids (Hymenoptera: Braconidae) of the Mediterranean Fruit Fly, Ceratitis capitata (Wiedemann) (Diptera: Tephritidae)

Suppression of Mediterranean fruit fly (medfly), Ceratitis capitata (Wiedemann), populations may be achieved through the mass-rearing and augmentative aerial release of opiine braconid parasitoids. Typically, aerial release techniques require up to one hour of chilling of adult parasitoids at temperatures as low as 3.5°C prior to their dissemination. Such chilling potentially could affect the subsequent performance of the insects. Among three species of the genus Diachasmimorpha longicaudata (Ashmead), tryoni (Cameron), and krausii (Fullaway) there was little or no affect of chilling in the laboratory on female longevity, production of daughters, or offspring sex ratio. This is consistent with previous experiments that found chilling to have no discernable effect on the short-term mortality of D. tryoni or on its ability to take flight immediately after aerial release. While there was little effect of chilling on longevity and fecundity in a species from another opiine genus, Fopius arisanus (Sonan), exposure to low temperatures did result in a significantly more male-biased offspring sex ratio.     

Desulfovibrio vulgaris bacterioferritin uses H(2)O(2) as a co-substrate for iron oxidation and reveals DPS-like DNA protection and binding activities

β?-GPI (β?-glycoprotein I) is a plasma glycoprotein ascribed with an anti-angiogenic function; however, the biological role and molecular basis of its action in cell migration remain unknown. The aim of the present study was to assess the contribution of β?-GPI to HAEC (human aortic endothelial cell) migration and the details of its underlying mechanism. Using wound healing and Boyden chamber assays, we found that β?-GPI inhibited endothelial cell migration, which was restored by its neutralizing antibody. NF-κB (nuclear factor κB) inhibitors and lentiviral siRNA (small interfering RNA) silencing of NF-κB significantly attenuated the inhibitory effect of β?-GPI on cell migration. Moreover, β?-GPI was found to induce IκBα (inhibitor of NF-κB) phosphorylation and translocation of p65 and p50. We further demonstrated that mRNA and protein levels of eNOS [endothelial NO (nitric oxide) synthase] and NO production were all increased by β?-GPI and these effects were remarkably inhibited by NF-κB inhibitors and siRNAs of p65 and p50. Furthermore, β?-GPI-mediated inhibition of cell migration was reversed by eNOS inhibitors and eNOS siRNAs. The findings of the present study provide novel insight into the ability of β?-GPI to inhibit endothelial cell migration predominantly through the NF-κB/eNOS/NO signalling pathway, which indicates a potential direction for clinical therapy in vascular diseases.     

Towards genomic and proteomic studies of protein phosphorylation in plant-pathogen interactions

Phosphorylation is an effective method of post-translational protein modification but understanding its significance is hindered by its biological complexity. Many protein kinases and phosphatases have been identified that connect signal perception mechanisms to plant defence responses. Recent studies of mitogen-activated protein kinases, calcium-dependent protein kinases and other kinases and phosphatases have revealed some important mechanisms, but have also raised new questions. The regulation of any phosphorylation pathway is complex and dynamic. There are many protein kinases and phosphatases in the plant genome, which makes it hard to delineate the phosphorylation machinery fully. Genomics and proteomics have already identified new components and will continue to influence the study of phosphorylation profoundly in plant-pathogen interactions.     

Uniconazole-induced thermotolerance in soybean seedling root tissue

Soybean [Glycine max(L.) Merr. cv. A2] seeds were germinated in 0 or 1 mg 1¹ (3.4 uM) uniconazole, after which seedling roots were excised and exposed to 22 or 48°C for 90 min. Prior to the temperature treatments there were few ultrastructural differences between uniconazole-treated seedling roots and the controls. Following exposure to 48°C, electron micrographs revealed near complete loss of normal ultrastructure in control epidermal root cells, whereas cellular integrity was maintained in treated roots, indicating that uniconazole conferred tolerance to high temperature. Total electrolyte, sugar and K⁺ leakage were all greater from control roots than treated roots during exposure to 48°C. Proline content in the roots was unaffected by uniconazole at 22°C but was 25–30% greater in treated tissue than in controls following exposure to 48°C. Malondialdehyde content was unaffected by uniconazole at 22°C but was nearly 20% less in treated tissue than in controls following high temperature exposure. This indicates that uniconazole decreased high-temperature-induced lipid peroxidation. Uniconazole elevated several antiox-idant systems in the roots, including water-soluble sulfhydryl concentration and catalase, peroxidase and superoxide dismutase activities. These findings are consistent with the hypothesis that uniconazole-induced stress tolerance is due, at least in part, to enhanced antioxidant activity which reduces stress-related oxidative damage to cell membranes.