Drivers of low breeding success in the Lesser Spotted Woodpecker Dendrocopos minor in England: testing hypotheses for the decline

Capsule The breeding success of Lesser Spotted Woodpeckers Dendrocopos minor is now lower in England than previously reported and also lower than found in studies elsewhere in Europe.

Aims To quantify the breeding success and identify the causes of nest failure. To test the hypotheses that breeding success is related to aspects of food limitation and parental care, and inclement weather during the nesting period, or to interactions with Great Spotted Woodpeckers.

Methods Nests were monitored in three regions of England, recording survival and causes of failure. We measured aspects of food limitation and parental care, rainfall and Great Spotted Woodpecker interactions at nests, to explore whether there was any evidence that these factors were related to breeding success. We compared results to other studies from the UK and continental Europe.

Results Nest survival was 52%. The average number of chicks produced from successful nests was 2.8. Chick-stage daily nest survival was positively related to provisioning rates, indicating that food supply may be limiting. The most common cause of nest failure was presumed starvation of chicks after the disappearance of an adult. Some females ceased visiting nests, leaving provisioning solely to the male. This behaviour has been reported elsewhere in Europe, but in the present study males were unable to compensate fully by increasing their provisioning rates, leading to poor nest survival. Provisioning rates and chick-stage daily nest survival were negatively associated with rainfall. Nest predation by Great Spotted Woodpeckers occurred but was a less frequent cause of failure. Aggressive interactions were recorded between the two woodpecker species but these were unrelated to breeding parameters.

Conclusions Low breeding success is most probably related to food shortages in the breeding period. Simple population modelling using parameters from the present study and from published work shows that if the low productivity that we have observed is replicated throughout Britain, it would be sufficient to account for the observed population decline. However, the possibility that survival rates are also low cannot be ruled out.     

A genomewide search finds major susceptibility loci for gallbladder disease on chromosome 1 in Mexican Americans

Gallbladder disease (GBD) is one of the major digestive diseases. Its risk factors include age, sex, obesity, type 2 diabetes, and metabolic syndrome (MS). The prevalence of GBD is high in minority populations, such as Native and Mexican Americans. Ethnic differences, familial aggregation of GBD, and the identification of susceptibility loci for gallstone disease by use of animal models suggest genetic influences on GBD. However, the major susceptibility loci for GBD in human populations have not been identified. Using ultrasound-based information on GBD occurrence and a 10-cM gene map, we performed multipoint variance-components analysis to localize susceptibility loci for GBD. Phenotypic and genotypic data from 715 individuals in 39 low-income Mexican American families participating in the San Antonio Family Diabetes/Gallbladder Study were used. Two GBD phenotypes were defined for the analyses: (1) clinical or symptomatic GBD, the cases of cholecystectomies due to stones confirmed by ultrasound, and (2) total GBD, the clinical GBD cases plus the stone carriers newly diagnosed by ultrasound. With use of the National Cholesterol Education Program/Adult Treatment Panel III criteria, five MS risk factors were defined: increased waist circumference, hypertriglyceredemia, low high-density lipoprotein cholesterol, hypertension, and high fasting glucose. The MS risk-factor score (range 0-5) for a given individual was used as a single, composite covariate in the genetic analyses. After accounting for the effects of age, sex, and MS risk-factor score, we found stronger linkage signals for the symptomatic GBD phenotype. The highest LOD scores (3.7 and 3.5) occurred on chromosome 1p between markers D1S1597 and D1S407 (1p36.21) and near marker D1S255 (1p34.3), respectively. Other genetic locations (chromosomes 2p, 3q, 4p, 8p, 9p, 10p, and 16q) across the genome exhibited some evidence of linkage (LOD >or=1.2) to symptomatic GBD. Some of these chromosomal regions corresponded with the genetic locations of Lith loci, which influence gallstone formation in mouse models. In conclusion, we found significant evidence of major genetic determinants of symptomatic GBD on chromosome 1p in Mexican Americans.     

Mitochondrial defects and oxidative damage in patients with peripheral arterial disease

Abnormal mitochondrial function is present in patients with peripheral arterial disease and may contribute to its clinical manifestations. However, the specific biochemical mitochondrial defects and their association with increased oxidative stress have not been fully characterized. Gastrocnemius muscle was obtained from peripheral arterial disease patients (n = 25) and age-matched controls (n = 16) and mitochondrial parameters were measured. Complexes I through IV of the electron transport chain were individually evaluated to assess for isolated defects. Muscle was also evaluated for protein and lipid oxidative changes by measuring the levels of protein carbonyls, lipid hydroperoxides, and total 4-hydroxy-2-nonenal binding and for the activities of the antioxidant enzymes superoxide dismutase, catalase, and glutathione peroxidase. Mitochondrial electron transport chain complexes I, III, and IV in arterial disease patients demonstrated significant reductions in enzymatic activities and mitochondrial respiration compared to controls. Oxidative stress biomarker analysis demonstrated significantly increased levels of protein carbonyls, lipid hydroperoxides, and 4-hydroxy-2-nonenal compared to control muscle. Antioxidant enzyme activities were altered, with a significant decrease in superoxide dismutase activity and significant increases in catalase and glutathione peroxidase. Peripheral arterial disease is associated with abnormal mitochondrial function and evidence of significant oxidative stress.     

Monte Carlo Study of the Buckingham Exponential-six Fluid

Abstract

In this paper we report the results of extensive Monte Carlo simulations of a pure fluid of Buckingham modified exponential-six molecules. Data are presented for the configurational energy and pressure covering a wide range of temperatures and densities. These data are interpreted using the generalized van der Waals partition function with a novel separation into free volume and mean potential terms. We find, surprisingly, that the Buckingham fluid is described by a simple van der Waals-like equation of state provided that the b parameter is temperature dependent and chosen in a theoretically correct manner.     

Nitrogen budget of a shortgrass prairie ecosystem

Summary A N budget is presented for a shortgrass prairie ecosystem. The grassland was ungrazed by domestic herbivores. The quantities of N in various plant, animal, microorganism, and soil components of the ecosystem are estimated for the date when aboveground living biomass was at its maximum for the growing season of 1973. Annual transfers of N between the various compartments were also estimated.Of the total N, 99.5% was in organic forms. The relatively inert heteropolycondensate fraction of the organic matter in the soils contained 88.8% of the N. Living organisms contained 4.2% and dead but recognizable organisms or part thereof contained 6.5% of the total N. Belowground animals contained more than 10 times as much N as abovegroud animals, but combined, animals contained less than 0.1% of the total in the system. Living plant material contained 2.5% of the total N. Seventy-two percent of the living plant N was below ground. Microorganisms contained 1.4% of the total N.Total N uptake by plants from soil solution was 2.9 g·m^-2·yr^-1. Aerial portions of plants were allocated 1.9 N·m^-2·yr^-1 although apparently 26% of this amount came from internally recycled sources. The heteropolycondensate fraction of the soil contributed 0.7 g N·m^-2·yr^-1 to mineral forms, but these components of the system were assumed to be in steady state; thus an equal amount of mineral N was allocated back to the source. Mineralization of N from plant residues was sufficient to account for all of the N taken up by plants from soil solution. Soil animals immobilized about 0.4 g N·m^-2·yr^-1 while the amount shunted to aboveground animals was trivial.     

Absence of phylogenetic signal in the niche structure of meadow plant communities

A significant proportion of the global diversity of flowering plants has evolved in recent geological time, probably through adaptive radiation into new niches. However, rapid evolution is at odds with recent research which has suggested that plant ecological traits, including the beta- (or habitat) niche, evolve only slowly. We have quantified traits that determine within-habitat alpha diversity (alpha niches) in two communities in which species segregate on hydrological gradients. Molecular phylogenetic analysis of these data shows practically no evidence of a correlation between the ecological and evolutionary distances separating species, indicating that hydrological alpha niches are evolutionarily labile. We propose that contrasting patterns of evolutionary conservatism for alpha- and beta-niches is a general phenomenon necessitated by the hierarchical filtering of species during community assembly. This determines that species must have similar beta niches in order to occupy the same habitat, but different alpha niches in order to coexist.     

Selective loss of synaptic proteins in Alzheimer's disease: evidence for an increased severity with APOE varepsilon4

A pathological feature of Alzheimer's disease (AD) is an area-specific neuronal loss that may be caused by excitotoxicity-related synaptic dysfunction. Relative expression levels of synaptophysin, dynamin I, complexins I and II, N-cadherin, and alphaCaMKII were analysed in human brain tissue from AD cases and controls in hippocampus, and inferior temporal and occipital cortices. Synaptophysin and dynamin I are presynaptic terminal proteins not specific to any neurotransmitter system whereas complexin II, N-cadherin, and alphaCaMKII are specific for excitatory synapses. Complexin I is a presynaptic protein localised to inhibitory synapses. There were no significant differences in synaptophysin, dynamin I, N-cadherin, or alphaCaMKII protein levels between AD cases and controls. The complexin proteins were both markedly lower in AD cases than in controls (P < 0.01). Cases were also categorised by APOE genotype. Averaged across areas there was a 36% lowering of presynaptic proteins in AD cases carrying at least one epsilon4 allele compared with in AD cases lacking the epsilon4 allele. We infer that synaptic protein level is not indicative of neuronal loss, but the synaptic dysfunction may result from the marked relative loss of the complexins in AD, and lower levels of presynaptic proteins in AD cases with the APOE epsilon4 allele.     

Identification of potent pyrimidine inhibitors of phosphodiesterase 7 (PDE7) and their ability to inhibit T cell proliferation

A series of pyrimidine based inhibitors of PDE7 are discussed. The synthesis, structure–activity relationships (SAR) and selectivity against several other PDE family members as well as activity in T cells are presented. These compounds were found to have effects on T cell proliferation, however it is not clear whether the mechanism is related to PDE7 inhibition.     

Diffusion is capable of translating anisotropic apoptosis initiation into a homogeneous execution of cell death

Background  

Apoptosis is an essential cell death process throughout the entire life span of all metazoans and its deregulation in humans has been implicated in many proliferative and degenerative diseases. Mitochondrial outer membrane permeabilisation (MOMP) and activation of effector caspases are key processes during apoptosis signalling. MOMP can be subject to spatial coordination in human cancer cells, resulting in intracellular waves of cytochrome-c release. To investigate the consequences of these spatial anisotropies in mitochondrial permeabilisation on subsequent effector caspase activation, we devised a mathematical reaction-diffusion model building on a set of partial differential equations.