The effect of extended post-mortem ageing on the Warner–Brazler shear force of longissimus thoracis from beef heifers from two sire breeds, slaughtered at 20 or 25 mo of age

peer-reviewedwere examined. Spring-born Angus × Holstein-Friesian heifers (n = 48) and Belgian Blue × Holstein-Friesian heifers (n = 48) were slaughtered, within sire breed, at 20 or 25 mo of age. Approximately 48 h post-mortem, LT steaks (2.5 cm) were removed, and either stored at −20°C for chemical analysis or vacuum-packed, stored at 2°C for 7, 14 or 28 d post-mortem and then at −20°C pending Warner–Bratzler shear force (WBSF) analysis. Muscle from Angus-sired heifers had higher (P < 0.001) intramuscular fat (IMF) concentration, lower (P < 0.001) proportion of type IIX muscle fibres and higher (P < 0.001) proportion of type IIA and type I muscle fibres compared to muscle from Belgian Blue-sired heifers. Collagen characteristics did not differ between sire breeds. Later slaughter increased (P < 0.001) IMF concentration and decreased (P < 0.001) total and insoluble concentrations and collagen solubility. There were no interactions between the main effects for WBSF and no difference between sire breeds. Later slaughter and increasing the duration of ageing decreased (P < 0.05) WBSF. Based on threshold WBSF values in the literature, all samples would be considered tender (<39 N) after 7 d ageing. Untrained consumers are likely to detect the decrease in WBSF from 7 to 14 d ageing but not due to further ageing. Within the production system examined and based on WBSF data, extending LT ageing to 28 d is not necessary to ensure consumer satisfaction

Neural and Synaptic Defects in slytherin, a Zebrafish Model for Human Congenital Disorders of Glycosylation

Congenital disorder of glycosylation type IIc (CDG IIc) is characterized by mental retardation, slowed growth and severe immunodeficiency, attributed to the lack of fucosylated glycoproteins. While impaired Notch signaling has been implicated in some aspects of CDG IIc pathogenesis, the molecular and cellular mechanisms remain poorly understood. We have identified a zebrafish mutant slytherin (srn), which harbors a missense point mutation in GDP-mannose 4,6 dehydratase (GMDS), the rate-limiting enzyme in protein fucosylation, including that of Notch. Here we report that some of the mechanisms underlying the neural phenotypes in srn and in CGD IIc are Notch-dependent, while others are Notch-independent. We show, for the first time in a vertebrate in vivo, that defects in protein fucosylation leads to defects in neuronal differentiation, maintenance, axon branching, and synapse formation. Srn is thus a useful and important vertebrate model for human CDG IIc that has provided new insights into the neural phenotypes that are hallmarks of the human disorder and has also highlighted the role of protein fucosylation in neural development

Sheldon Spectrum and the Plankton Paradox: Two Sides of the Same Coin : A trait-based plankton size-spectrum model

The Sheldon spectrum describes a remarkable regularity in aquatic ecosystems: the biomass density as a function of logarithmic body mass is approximately constant over many orders of magnitude. While size-spectrum models have explained this phenomenon for assemblages of multicellular organisms, this paper introduces a species-resolved size-spectrum model to explain the phenomenon in unicellular plankton. A Sheldon spectrum spanning the cell-size range of unicellular plankton necessarily consists of a large number of coexisting species covering a wide range of characteristic sizes. The coexistence of many phytoplankton species feeding on a small number of resources is known as the Paradox of the Plankton. Our model resolves the paradox by showing that coexistence is facilitated by the allometric scaling of four physiological rates. Two of the allometries have empirical support, the remaining two emerge from predator-prey interactions exactly when the abundances follow a Sheldon spectrum. Our plankton model is a scale-invariant trait-based size-spectrum model: it describes the abundance of phyto- and zooplankton cells as a function of both size and species trait (the maximal size before cell division). It incorporates growth due to resource consumption and predation on smaller cells, death due to predation, and a flexible cell division process. We give analytic solutions at steady state for both the within-species size distributions and the relative abundances across species

Simple model systems: a challenge for Alzheimer's disease

The success of biomedical researches has led to improvement in human health and increased life expectancy. An unexpected consequence has been an increase of age-related diseases and, in particular, neurodegenerative diseases. These disorders are generally late onset and exhibit complex pathologies including memory loss, cognitive defects, movement disorders and death. Here, it is described as the use of simple animal models such as worms, fishes, flies, Ascidians and sea urchins, have facilitated the understanding of several biochemical mechanisms underlying Alzheimer's disease (AD), one of the most diffuse neurodegenerative pathologies. The discovery of specific genes and proteins associated with AD, and the development of new technologies for the production of transgenic animals, has helped researchers to overcome the lack of natural models. Moreover, simple model systems of AD have been utilized to obtain key information for evaluating potential therapeutic interventions and for testing efficacy of putative neuroprotective compounds

The legal framework for financial advertising:curbing behavioural exploitation

Policy makers and behavioural finance scholars express growing concern that marketing practices by financial institutions exploit retail investors’ behavioural biases. Investor protection regulation should thus address these marketing practices and include mechanisms curbing behavioural exploitation. That raises the question whether the marketing communications regime of the new Markets in Financial Instruments Directive can live up to this demand. This article develops a regulatory model that integrates behavioural finance insights into the new marketing communications regime. It then determines how regulatory authorities can apply this model when they interpret and apply specific regulatory requirements. It demonstrates how a regulatory authority or a court can translate empirical behavioural finance research findings into legal arguments when assessing whether marketing practices can significantly distort a model investor’s decision-making process. The article further establishes that the detailed requirements imposed on investment firms by the new Markets in Financial Instruments Directive are necessary in order to protect investors from behavioural exploitation. Finally, the article submits policy proposals that aim to protect investors more effectively from behavioural exploitation

A genome-wide genetic map of NB-LRR disease resistance loci in potato

Like all plants, potato has evolved a surveillance system consisting of a large array of genes encoding for immune receptors that confer resistance to pathogens and pests. The majority of these so-called resistance or R proteins belong to the super-family that harbour a nucleotide binding and a leucine-rich-repeat domain (NB-LRR). Here, sequence information of the conserved NB domain was used to investigate the genome-wide genetic distribution of the NB-LRR resistance gene loci in potato. We analysed the sequences of 288 unique BAC clones selected using filter hybridisation screening of a BAC library of the diploid potato clone RH89-039-16 (S. tuberosum ssp. tuberosum) and a physical map of this BAC library. This resulted in the identification of 738 partial and full-length NB-LRR sequences. Based on homology of these sequences with known resistance genes, 280 and 448 sequences were classified as TIR-NB-LRR (TNL) and CC-NB-LRR (CNL) sequences, respectively. Genetic mapping revealed the presence of 15 TNL and 32 CNL loci. Thirty-six are novel, while three TNL loci and eight CNL loci are syntenic with previously identified functional resistance genes. The genetic map was complemented with 68 universal CAPS markers and 82 disease resistance trait loci described in literature, providing an excellent template for genetic studies and applied research in potato

Dimethylsulphide production in the Southern Ocean using a nitrogen-based flow network model and field measurements from ACE-1

Dimethylsulphide (DMS) has been implicated in climate change as a possible negative feedback to global warming, and several Models have been developed that simulate the production of DMS in the marine environment. The focus of this study is to improve the nitrogen based Gabric Model, using field data collected during the Southern Hemisphere First Marine Aerosol Characterisation Experiment (ACE-1) in the Southern Ocean in 1995. Two Model Runs (Series A and B) were carried out with six simulations of varying biotic and abiotic inputs applied over the voyage transect (41-48°S), reflecting Model default values or field values from the experiment. The abiotic inputs were time-step, dissolved dimethylsulphoniopropionate (DMSP) and DMS, and the biotic nitrogen inputs were from phytoplankton, bacteria, zooflagellates, large protozoa, micro and mesozooplankton. The focus of the abiotic assessment was nutrient (nitrate) uptake and dissolved DMSP and DMS output. Model output of the biotic compartments was assessed for congruence with predicted ecological patterns of succession. Despite a limited data set the study provides a good insight into the utility of the Model, which functioned as a heuristic rather than predictive tool. In simulation 1 (Series A) where the only field value was nitrate, all latitudes from 41-48°S concurred with the ecological succession predicted by the Model authors and the successional pattern predicted by other researchers, with a double phytoplankton peak indicating remineralisation of nitrogen via the microbial loop. In many simulations the Model produced lower values of dissolved DMS than were measured, and production of DMS in the Model appears constrained. However, in simulation 5 (Series A) DMS model outputs were closest to the mean dissolved DMS levels reported on RV Discoverer. In this simulation, field values were used for phytoplankton, nitrate, dissolved DMSP and DMS, with bacterial abundance and micro and mesozooplankton increased over their Gabric default values. Also, the phytoplankton double peak occurred earlier, as did the peaks in bacteria, zooflagellates, and large protozoa. Simulations that deviated more significantly from the predicted successional patterns were characterised by single peaks in phytoplankton growth and delayed bacterial growth. Series C simulations at latitude 43°S, in an attempt to reduce phytoplankton predation by bacteria, increased DMS output reasonably successfully. However, significant recalibration of the Model is recommended in conjunction with field studies to gather vital background biological data - particularly in the areas of nutrient limitation, phytoplankton speciation, and the cellular content of the DMS precursor compound, DMSP