Comparison of Grain Sources (Barley, White Corn, and Yellow Corn) for Swine Diets and Their Effects on Meat Quality and Production Traits

Efficient pork production is a necessity for an economically viable swine industry. Number two yellow corn is considered the primary energy source for swine diets in the Midwest. Despite the low protein content, corn is considered one of the most economical feed stuffs available to the swine production system. Barley is a high fiber that has approximately 89% of the energy content of corn. While barley contains a higher protein and amino acid level than corn, animal performance is expected to be depressed due to the high fiber content. Because barley lacks the carotene content that yellow corn possesses, it has been hypothesized that barley-fed pigs will yield higher meat and fat quality that is desired by export markets. White corn was used in this trial to determine its contribution to meat quality and growth traits. An experiment was conducted to evaluate the effect of energy source on performance and carcass traits of pigs. Diet treatments (primary energy source) were: 1) yellow corn, 2) white corn, 3) 1/3 yellow corn, 2/3 white corn, 4) 2/3 yellow corn, 1/3 white corn, 5) barley. Pigs completing the trial were from two sires lines, Duroc (n=500) and Hamp x Duroc (n=499), that were mated to PIC 1055 females. Pigs were randomly allocated to pens based on genetic type and gender using a 2 x 2 x 5 factorial arrangement with two genetic types, two sexes (barrows and gilts) and five treatments. Animals fed these diets differing in energy source did not express a difference in average daily gain, average daily feed intake, feed-to-gain ratio, backfat depth or percent fat free lean. However, barley-fed pigs did have a smaller (p \u3c .05) loin muscle area than pigs fed corn-based diets. Diet did not have an effect on sensory panel traits for tenderness or chewiness and limited differences were observed for juiciness, flavor, and off-flavor. Percentage loin purge, and cooking loss did not differ among diets fed to the pigs with minimal difference noted for color values. Pigs fed barley diets did have lower iodine value content within the subcutaneous fat indicating that the fat is of firmer quality. Results of this trial suggest that barley does not have an advantage in meat quality traits when compared to traditional corn-based diets. Barley does however have a significant impact on the hardness of pork fat, but does not have a significant effect on subjective color values

Comparison of Grain Sources (Barley, White Corn, and Yellow Corn) for Swine Diets and Their Effect on Production and Carcass Traits

Energy sources differ in content, quality, and availability of nutrients. The objective of this study was to identify and compare differences in production and carcass traits in pigs fed different energy sources. While pigs fed a barley-based diet had a smaller loin muscle area, there was no difference among diets when comparing fat depth or percent fat-free lean. Barley based-diets and a diet containing one-third yellow corn and two-thirds white corn had a lower lean gain per day on test. There was no significant difference in average daily gain or feed-to-gain ratios

Altered Trabecular Bone Structure and Delayed Cartilage Degeneration in the Knees of Collagen VI Null Mice

Mutation or loss of collagen VI has been linked to a variety of musculoskeletal abnormalities, particularly muscular dystrophies, tissue ossification and/or fibrosis, and hip osteoarthritis. However, the role of collagen VI in bone and cartilage structure and function in the knee is unknown. In this study, we examined the role of collagen VI in the morphology and physical properties of bone and cartilage in the knee joint of Col6a1−/− mice by micro-computed tomography (microCT), histology, atomic force microscopy (AFM), and scanning microphotolysis (SCAMP). Col6a1−/− mice showed significant differences in trabecular bone structure, with lower bone volume, connectivity density, trabecular number, and trabecular thickness but higher structure model index and trabecular separation compared to Col6a1+/+ mice. Subchondral bone thickness and mineral content increased significantly with age in Col6a1+/+ mice, but not in Col6a1−/− mice. Col6a1−/− mice had lower cartilage degradation scores, but developed early, severe osteophytes compared to Col6a1+/+mice. In both groups, cartilage roughness increased with age, but neither the frictional coefficient nor compressive modulus of the cartilage changed with age or genotype, as measured by AFM. Cartilage diffusivity, measured via SCAMP, varied minimally with age or genotype. The absence of type VI collagen has profound effects on knee joint structure and morphometry, yet minimal influences on the physical properties of the cartilage. Together with previous studies showing accelerated hip osteoarthritis in Col6a1−/− mice, these findings suggest different roles for collagen VI at different sites in the body, consistent with clinical data

The Ionizing Radiation-Induced Bystander Effect: Evidence, Mechanism, and Significance

It has long been considered that the important biological effects of ionizing radiation are a direct consequence of unrepaired or misrepaired DNA damage occurring in the irradiated cells. It was presumed that no effect would occur in cells in the population that receive no direct radiation exposure. However, in vitro evidence generated over the past two decades has indicated that non-targeted cells in irradiated cell cultures also experience significant biochemical and phenotypic changes that are often similar to those observed in the targeted cells. Further, nontargeted tissues in partial body-irradiated rodents also experienced stressful effects, including oxidative and oncogenic effects. This phenomenon, termed the “bystander response,” has been postulated to impact both the estimation of health risks of exposure to low doses/low fluences of ionizing radiation and the induction of second primary cancers following radiotherapy. Several mechanisms involving secreted soluble factors, oxidative metabolism, gap-junction intercellular communication, and DNA repair, have been proposed to regulate radiation-induced bystander effects. The latter mechanisms are major mediators of the system responses to ionizing radiation exposure, and our knowledge of the biochemical and molecular events involved in these processes is reviewed in this chapter

Bi-allelic Loss-of-Function CACNA1B Mutations in Progressive Epilepsy-Dyskinesia.

The occurrence of non-epileptic hyperkinetic movements in the context of developmental epileptic encephalopathies is an increasingly recognized phenomenon. Identification of causative mutations provides an important insight into common pathogenic mechanisms that cause both seizures and abnormal motor control. We report bi-allelic loss-of-function CACNA1B variants in six children from three unrelated families whose affected members present with a complex and progressive neurological syndrome. All affected individuals presented with epileptic encephalopathy, severe neurodevelopmental delay (often with regression), and a hyperkinetic movement disorder. Additional neurological features included postnatal microcephaly and hypotonia. Five children died in childhood or adolescence (mean age of death: 9 years), mainly as a result of secondary respiratory complications. CACNA1B encodes the pore-forming subunit of the pre-synaptic neuronal voltage-gated calcium channel Cav2.2/N-type, crucial for SNARE-mediated neurotransmission, particularly in the early postnatal period. Bi-allelic loss-of-function variants in CACNA1B are predicted to cause disruption of Ca2+ influx, leading to impaired synaptic neurotransmission. The resultant effect on neuronal function is likely to be important in the development of involuntary movements and epilepsy. Overall, our findings provide further evidence for the key role of Cav2.2 in normal human neurodevelopment.MAK is funded by an NIHR Research Professorship and receives funding from the Wellcome Trust, Great Ormond Street Children's Hospital Charity, and Rosetrees Trust. E.M. received funding from the Rosetrees Trust (CD-A53) and Great Ormond Street Hospital Children's Charity. K.G. received funding from Temple Street Foundation. A.M. is funded by Great Ormond Street Hospital, the National Institute for Health Research (NIHR), and Biomedical Research Centre. F.L.R. and D.G. are funded by Cambridge Biomedical Research Centre. K.C. and A.S.J. are funded by NIHR Bioresource for Rare Diseases. The DDD Study presents independent research commissioned by the Health Innovation Challenge Fund (grant number HICF-1009-003), a parallel funding partnership between the Wellcome Trust and the Department of Health, and the Wellcome Trust Sanger Institute (grant number WT098051). We acknowledge support from the UK Department of Health via the NIHR comprehensive Biomedical Research Centre award to Guy's and St. Thomas' National Health Service (NHS) Foundation Trust in partnership with King's College London. This research was also supported by the NIHR Great Ormond Street Hospital Biomedical Research Centre. J.H.C. is in receipt of an NIHR Senior Investigator Award. The research team acknowledges the support of the NIHR through the Comprehensive Clinical Research Network. The views expressed are those of the author(s) and not necessarily those of the NHS, the NIHR, Department of Health, or Wellcome Trust. E.R.M. acknowledges support from NIHR Cambridge Biomedical Research Centre, an NIHR Senior Investigator Award, and the University of Cambridge has received salary support in respect of E.R.M. from the NHS in the East of England through the Clinical Academic Reserve. I.E.S. is supported by the National Health and Medical Research Council of Australia (Program Grant and Practitioner Fellowship)