Our SOD wafers evidence a thermal resistance reduction of about 70% compared to conventional SOI materials, with heat source spatial extension in the micron range. (C) 2011 American Institute of Physics. [doi:10.1063/1.3643006]“
“The objective of this study was to quantify the effects of the Charolais-specific inactive myostatin allele on phenotypic
means and genetic parameters of heifer breeding traits. Records were registered from 1996 to 2006 in 282 herds dedicated to the on-farm French Charolais purebred progeny test. Data consisted of 36,867 female calf records, including 17,518 inseminated heifers that were bred by 186 genotyped sires, of which 43 were heterozygous and 6 were double muscled bulls. Six traits were analyzed under a univariate Fer-1 clinical trial animal model accounting for maternal effects and myostatin sire genotype: calving difficulty, birth and weaning weights, muscle and skeleton scores at weaning, and fertility of artificially inseminated heifers. The inactive myostatin allele had a large positive effect on weaned heifer muscle score, unfavorable effects on calving difficulty and skeleton score, and small effects on birth ALK inhibitor and weaning weight. This allele did not induce an adverse effect on heifer fertility. Univariate estimates of
polygenic variance parameters were almost unaffected by the estimation of the myostatin sire genotype, except for heifer morphology traits. Direct and maternal genetic variances and covariances were significantly reduced under a model accounting for the myostatin sire genotype effect on muscle score. The myostatin genotype explained 45% of the direct genetic variance and had a pleiotropic action across both direct and maternal effects on muscle score. Because the myostatin sire genotype had no significant effect on birth weight, the multitrait sire analysis concerned only the 5 other traits. Accounting for the myostatin sire genotype, estimates of polygenic correlation between skeleton score and muscle score, on the one hand, and calving difficulty on the other hand, were largely modified: from a negative
estimate R428 cost of -0.3 to 0.0 and from a positive estimate of 0.4 to 0.7, respectively.”
“Objective: The goal of this study was to verify the effects of treatment with melatonin and N-acetylserotonin on the pilocarpine-induced epilepsy model.
Methods: The animals were divided into four groups: (1) animals treated with saline (Saline); (2) animals that received pilocarpine and exhibited SE (SE); (3) animals that exhibited SE and were treated with N-acetylserotonin (30 minutes and 1, 2, 4, 6, 12, 24, 36, and 48 hours) alter SE onset (SE + NAS); (4) animals that exhibited SE and were treated with melatonin at the same time the SE + NAS group (SE + MEL). Behavioral (latency to first seizure, frequency of seizures, and mortality) and histological (Nissl and neo-Timm) parameters were analyzed.