Influence of heterosis and plane of nutrition on rate and economy of gains, digestion and carcass composition of pigs

This report includes much of the material presented by senior author as a dissertation for the Doctor of Philosophy degree in August, 1951--P. [3].Digitized 2007 AES.Includes bibliographical references (pages 41-42)

Effects of Late Castration and Zeranol on Growth Rate, Feed Efficiency, and Carcass and Meat Traits of Bovine Males

It is generally recognized that intact bovine males gain weight faster and require less feed per unit of gain than castrate bovine males. Further, carcasses from intact bovine males have a higher percentage of retail or edible product, but meat from intact males is generally evaluated slightly lower on palatability characteristics, particularly tenderness, than carcasses from castrate bovine males. It has been suggested that much of the advantage of intact vs castrate for rate of gain, efficiency of gain, and composition of gain may be expressed by an age of about 1 year and the disadvantages, including aggressive male behavior, that result in reduced rate and efficiency of gain, begin at about 1 year of age (at or immediately after puberty). Thus, there was need to determine the effects of castration at about 1 year on rate of gain, efficiency of gain, composition of gain, meat characteristics, and behavioral characteristics. Reports have shown that, when the anabolic agent zeranol [6-(6,10-dyhydroxyundecyl)-B-resorcyclic acid-d-lactone] is implanted in intact male calves at or before weaning, rate of gain is increased and rate of testicular growth is decreased. These experiments were conducted to determine the effects of castration and zeranol implants at 13 months of age on rate of gain, efficiency of gain, behavioral characteristics, and carcass and meat traits of bovine males

Effects of Managing Heifers to Calve First at Two \u3ci\u3evs\u3c/i\u3e Three Years of Age on Longevity and Lifetime Production of Beef Cows

Resources used by cow herds for beef production vary greatly. To optimize reproduction and other production characteristics in the cow herd, breeding and management should be matched with the feed resources available for production. One management decision is whether to develop replacement females to calve first as 2-year-olds or as 3-year-olds. When feed resources are limited or expensive relative to other costs and value of output, it may be economical to delay the first calving until 3 years of age. When feed resources are adequate to support rapid growth and development of heifers and thus to reduce age at puberty to 14 months of age or less, then calving at 2 years of age may be optimum. another management decision is whether or not cows should be culled the first time they are open, or held over for another opportunity to breed (in lieu of keeping an additional replacement heifer). This study was conducted to evaluate effects of 2-year-old vs 3-year-old first calf management on longevity and lifetime production of cows and on current economics of beef production

Effects of Heterosis on Longevity in Beef Cattle

Longevity can be important to the economic efficiency of beef production. The longer cows remain productive in a herd, the fewer the number of replacement heifers needed and the greater the calf output per cow maintained. In this way, more heifers can be sold for feeding and slaughter, and the cost of growing out replacement females to a productive age is reduced. Less culling of infertile cows also increases output per cow exposed. This study was conducted to determine effects of heterosis on longevity and associated factors in crosses of the Hereford, Angus, and Shorthorn breeds

Control of center of mass motion during walking correlates with gait and balance in people with incomplete spinal cord injury

BackgroundThere is evidence that ambulatory people with incomplete spinal cord injury (iSCI) have an impaired ability to control lateral motion of their whole-body center of mass (COM) during walking. This impairment is believed to contribute to functional deficits in gait and balance, however that relationship is unclear. Thus, this cross-sectional study examines the relationship between the ability to control lateral COM motion during walking and functional measures of gait and balance in people with iSCI.MethodsWe assessed the ability to control lateral COM motion during walking and conducted clinical gait and balance outcome measures on 20 ambulatory adults with chronic iSCI (C1-T10 injury, American Spinal Injury Association Impairment Scale C or D). To assess their ability to control lateral COM motion, participants performed three treadmill walking trials. During each trial, real-time lateral COM position and a target lane were projected on the treadmill. Participants were instructed to keep their lateral COM position within the lane. If successful, an automated control algorithm progressively reduced the lane width, making the task more challenging. If unsuccessful, the lane width increased. The adaptive lane width was designed to challenge each participant’s maximum capacity to control lateral COM motion during walking. To quantify control of lateral COM motion, we calculated lateral COM excursion during each gait cycle and then identified the minimum lateral COM excursion occurring during five consecutive gait cycles. Our clinical outcome measures were Berg Balance Scale (BBS), Timed Up and Go test (TUG), 10-Meter Walk Test (10MWT) and Functional Gait Assessment (FGA). We used a Spearman correlation analysis (ρ) to examine the relationship between minimum lateral COM excursion and clinical measures.ResultsMinimum lateral COM excursion had significant moderate correlations with BBS (ρ = −0.54, p = 0.014), TUG (ρ = 0.59, p = 0.007), FGA (ρ = −0.59, p = 0.007), 10MWT-preferred (ρ = −0.59, p = 0.006) and 10MWT-fast (ρ = −0.68, p = 0.001).ConclusionControl of lateral COM motion during walking is associated with a wide range of clinical gait and balance measures in people with iSCI. This finding suggests the ability to control lateral COM motion during walking could be a contributing factor to gait and balance in people with iSCI

Enhancement of dye regeneration kinetics in dichromophoric porphyrin-carbazole triphenylamine dyes influenced by more exposed radical cation orbitals

Reduction kinetics of oxidized dyes absorbed on semiconductor surfaces and immersed in redox active electrolytes has been mainly modeled based on the free energy difference between the oxidation potential of the dye and the redox potential of the electrolyte. Only a few mechanisms have been demonstrated to enhance the kinetics by other means. In this work, the rate constant of the reduction of oxidized porphyrin dye is enhanced by attaching non-conjugated carbazole triphenylamine moiety using iodine/triiodide and tris(2,2′-bispyridinium)cobalt II/III electrolytes. These results are obtained using transient absorption spectroscopy by selectively probing the regeneration kinetics at the porphyrin radical cation and the carbazole triphenylamine radical cation absorption wavelengths. The enhancement in the reduction kinetics is not attributed to changes in the driving force, but to the more exposed dye cation radical orbitals of the dichromophoric dye. The results are important for the development of high efficiency photo-electrochemical devices with minimalized energy loss at electron transfer interfaces

Characterisation of the Cullin-3 mutation that causes a severe form of familial hypertension and hyperkalaemia

Deletion of exon 9 from Cullin‐3 (CUL3, residues 403–459: CUL3Δ403–459) causes pseudohypoaldosteronism type IIE (PHA2E), a severe form of familial hyperkalaemia and hypertension (FHHt). CUL3 binds the RING protein RBX1 and various substrate adaptors to form Cullin‐RING‐ubiquitin‐ligase complexes. Bound to KLHL3, CUL3‐RBX1 ubiquitylates WNK kinases, promoting their ubiquitin‐mediated proteasomal degradation. Since WNK kinases activate Na/Cl co‐transporters to promote salt retention, CUL3 regulates blood pressure. Mutations in both KLHL3 and WNK kinases cause PHA2 by disrupting Cullin‐RING‐ligase formation. We report here that the PHA2E mutant, CUL3Δ403–459, is severely compromised in its ability to ubiquitylate WNKs, possibly due to altered structural flexibility. Instead, CUL3Δ403–459 auto‐ubiquitylates and loses interaction with two important Cullin regulators: the COP9‐signalosome and CAND1. A novel knock‐in mouse model of CUL3WT/Δ403–459 closely recapitulates the human PHA2E phenotype. These mice also show changes in the arterial pulse waveform, suggesting a vascular contribution to their hypertension not reported in previous FHHt models. These findings may explain the severity of the FHHt phenotype caused by CUL3 mutations compared to those reported in KLHL3 or WNK kinases