Evidence of non-additive genetic effects on predicted carcass composition

The document attached has been archived with permission from the World Congress on Genetics Applied to Livestock Production.Genetic effects on pre- and post-weaning body weight and developmental traits of Jersey and Limousin cross cattle has been reported (Afolayan et al., 2001). As in this earlier study which indicated the importance of epistasis at older ages, maternal effects (Meyer, 1992) and heterotic effects (Pitchford et al., 1993) have also been found on post-weaning growth traits of some breed of beef cattle. Genetic improvement programs in beef cattle could be enhanced through understanding of the genetic effects on live animal traits at various ages. However, the value of beef cattle lies better in their ability to efficiently produce a carcass composed of optimal proportions of muscle, bone and fat at market weight (Tatum et al., 1986). In essence, the knowledge of the genetic effects on different carcass components is of more importance to the breeders/producers of livestock. This study, therefore, examines the estimates of four genetic effects on predicted carcass traits using live-animal measurements

Orbiting passive microwave sensor simulation applied to soil moisture estimation

A sensor/scene simulation program was developed and used to determine the effects of scene heterogeneity, resolution, frequency, look angle, and surface and temperature relations on the performance of a spaceborne passive microwave system designed to estimate soil water information. The ground scene is based on classified LANDSAT images which provide realistic ground classes, as well as geometries. It was determined that the average sensitivity of antenna temperature to soil moisture improves as the antenna footprint size increased. Also, the precision (or variability) of the sensitivity changes as a function of resolution

Breed variation and genetic parameters for growth and body development in diverse beef cattle genotypes

Conformation scores can account for more than 20% of cattle price variation at Australian livestock sales. However, there are limited available references which define genetic factors relating objective live developmental traits to carcass composition. Weaning and post-weaning weight, height, length, girth, muscle (ratio of stifle to hip width) and fat depth of 1202 progeny from mature Hereford cows (637) mated to seven sire breeds (Jersey, Wagyu, Angus, Hereford, South Devon, Limousin and Belgian Blue) were examined for growth and development across ages. Crossbred Wagyu and Jersey were both lighter in weight and smaller in size (height, length and girth) than purebred Hereford and crossbred Angus, South Devon, Limousin and Belgian Blue. Within the five larger crossbreds, there were significant changes in relative weight from weaning to 600 days. Sire breeds differed in fat depth, with Angus being the fattest (9% on average fatter than Hereford and Wagyu), and Jersey 5% less fat than Hereford, followed by South Devon and Limousin (19% lower than Hereford) and Belgian Blue (39% lower than Hereford). Direct heritability ranged from 19 to 42% and was higher than the proportion of total phenotypic variance accounted for by maternal effects (which ranged from 0 to 17%) for most body measurement traits except for weight (38 v. 18%) and girth (36 v. 9%) traits at weaning, an indication of maternal effect on some body conformation traits at early ages. Muscularity (19 to 44%) and fat depth (26 to 43%) were moderately to highly heritable across ages. There were large differences for growth and the objective measures of body development between crossbreds with a degree of overlap among the progeny of the seven sire breeds. The variation between genetic (positive) and environmental (negative) correlations for dry versus wet season average daily gains in weight and fat, suggested the potential use of live-animal conformation traits for within breed selection of genetically superior animal in these traits across seasons.R. A. Afolayan, W. S. Pitchford, M. P. B. Deland and W. A. McKierna

Hexatic-Herringbone Coupling at the Hexatic Transition in Smectic Liquid Crystals: 4-ϵ\epsilon Renormalization Group Calculations Revisited

Simple symmetry considerations would suggest that the transition from the smectic-A phase to the long-range bond orientationally ordered hexatic smectic-B phase should belong to the XY universality class. However, a number of experimental studies have constantly reported over the past twenty years "novel" critical behavior with non-XY critical exponents for this transition. Bruinsma and Aeppli argued in Physical Review Letters {\bf 48}, 1625 (1982), using a $4-\epsilon$ renormalization-group calculation, that short-range molecular herringbone correlations coupled to the hexatic ordering drive this transition first order via thermal fluctuations, and that the critical behavior observed in real systems is controlled by a `nearby' tricritical point. We have revisited the model of Bruinsma and Aeppli and present here the results of our study. We have found two nontrivial strongly-coupled herringbone-hexatic fixed points apparently missed by those authors. Yet, those two new nontrivial fixed-points are unstable, and we obtain the same final conclusion as the one reached by Bruinsma and Aeppli, namely that of a fluctuation-driven first order transition. We also discuss the effect of local two-fold distortion of the bond order as a possible missing order parameter in the Hamiltonian.Comment: 1 B/W eps figure included. Submitted to Physical Review E. Contact: [email protected]

A pleurocidin analogue with greater conformational flexibility, enhanced antimicrobial potency and in vivo therapeutic efficacy.

Antimicrobial peptides (AMPs) are a potential alternative to classical antibiotics that are yet to achieve a therapeutic breakthrough for treatment of systemic infections. The antibacterial potency of pleurocidin, an AMP from Winter Flounder, is linked to its ability to cross bacterial plasma membranes and seek intracellular targets while also causing membrane damage. Here we describe modification strategies that generate pleurocidin analogues with substantially improved, broad spectrum, antibacterial properties, which are effective in murine models of bacterial lung infection. Increasing peptide-lipid intermolecular hydrogen bonding capabilities enhances conformational flexibility, associated with membrane translocation, but also membrane damage and potency, most notably against Gram-positive bacteria. This negates their ability to metabolically adapt to the AMP threat. An analogue comprising D-amino acids was well tolerated at an intravenous dose of 15 mg/kg and similarly effective as vancomycin in reducing EMRSA-15 lung CFU. This highlights the therapeutic potential of systemically delivered, bactericidal AMPs

Optimal liability sharing and court errors: an exploratory analysis

We focus in this paper on the effects of court errors on the optimal sharing of liability between firms and financiers, as an environmental policy instrument. Using a structural model of the interactions between firms, financial institutions, governments and courts we show, through numerical simulations, the distortions in liability sharing between firms and financiers that the imperfect implementation of government policies implies. We consider in particular the role played by the efficiency of the courts in avoiding Type I (finding an innocent firm guilty of inappropriate care) and Type II (finding a guilty firm innocent of inappropriate care) errors. This role is considered in a context where liability sharing is already distorted (when compared with first best values) due not only to the courts' own imperfect assessment of safety care levels exerted by firm but also to the presence of moral hazard and adverse selection in financial contracting, as well as of noncongruence of objectives between firms and financiers on the one hand and social welfare maximization on the other. Our results indicate that an increase in the efficiency of the court system in avoiding errors raises safety care levels, thereby reducing the probability of accident, and allowing the social welfare maximizing government to impose a lower liability [higher] share for firms [financiers] as well as a lower standard level of care

Insulin Resistance Impairs Circulating Angiogenic Progenitor Cell Function and Delays Endothelial Regeneration

OBJECTIVE Circulating angiogenic progenitor cells (APCs) participate in endothelial repair after arterial injury. Type 2 diabetes is associated with fewer circulating APCs, APC dysfunction, and impaired endothelial repair. We set out to determine whether insulin resistance adversely affects APCs and endothelial regeneration. RESEARCH DESIGN AND METHODS We quantified APCs and assessed APC mobilization and function in mice hemizygous for knockout of the insulin receptor (IRKO) and wild-type (WT) littermate controls. Endothelial regeneration after femoral artery wire injury was also quantified after APC transfusion. RESULTS IRKO mice, although glucose tolerant, had fewer circulating Sca-1+/Flk-1+ APCs than WT mice. Culture of mononuclear cells demonstrated that IRKO mice had fewer APCs in peripheral blood, but not in bone marrow or spleen, suggestive of a mobilization defect. Defective vascular endothelial growth factor–stimulated APC mobilization was confirmed in IRKO mice, consistent with reduced endothelial nitric oxide synthase (eNOS) expression in bone marrow and impaired vascular eNOS activity. Paracrine angiogenic activity of APCs from IRKO mice was impaired compared with those from WT animals. Endothelial regeneration of the femoral artery after denuding wire injury was delayed in IRKO mice compared with WT. Transfusion of mononuclear cells from WT mice normalized the impaired endothelial regeneration in IRKO mice. Transfusion of c-kit+ bone marrow cells from WT mice also restored endothelial regeneration in IRKO mice. However, transfusion of c-kit+ cells from IRKO mice was less effective at improving endothelial repair. CONCLUSIONS Insulin resistance impairs APC function and delays endothelial regeneration after arterial injury. These findings support the hypothesis that insulin resistance per se is sufficient to jeopardize endogenous vascular repair. Defective endothelial repair may be normalized by transfusion of APCs from insulin-sensitive animals but not from insulin-resistant animals