210 research outputs found

    Effect of fluoride on the calcification of allogenic bone implants in rats

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    Thesis (M.Sc.D.)--Boston University School of Graduate Dentistry, 1974. Periodontics.Bibliography included.In twenty-five (25) male adult rats which had decalcified allogenic bone implants placed in mid-fibular gaps and kept on a low-fluoride casein diet (1 ppm- fluoride), the addition of 25 p.p.m. fluoride to the drinking water did not show any direct detectable relationship to the mg % calcium in the ashed implants or in ashed adjacent tibial bone, nor in the percent ash content. Neither did the fluoride enhance or inhibit the success of the implants. For all implants did calcify and only one control mid-fibular gap closed on its own. It is our conclusion that fluoride at levels used in this experiment have no effect on calcification of allogenic bone implants

    The Economics of Hay Quality

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    Hay quality is often discussed when one considers the viability of cash hay operations. A great deal is known about how production impacts quality and how quality impacts animal performance. This knowledge certainly has economic implications, but the economics of hay quality has primarily been evaluated from the animal performance perspective. Analyzing the economics of hay quality from the cash hay producer’s prospective becomes more difficult due to data limitations. There are approximately 2.5 million acres of hay produced in Kentucky annually. The vast majority of this hay is grass type hay that is produced and fed on beef cattle operations. Higher quality hay production represents a much smaller portion of Kentucky’s hay industry, yet yields much greater value on a per acre basis. While a much larger share of this “upper end” hay production is sold off the farm, most is sold through private treaty, which means sale data is not available. Auction markets are becoming more commonly used in hay marketing and provide greater opportunity to analyze factors that impact hay value

    A Nodal Signaling Pathway Regulates the Laterality of Neuroanatomical Asymmetries in the Zebrafish Forebrain

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    AbstractAnimals show behavioral asymmetries that are mediated by differences between the left and right sides of the brain. We report that the laterality of asymmetric development of the diencephalic habenular nuclei and the photoreceptive pineal complex is regulated by the Nodal signaling pathway and by midline tissue. Analysis of zebrafish embryos with compromised Nodal signaling reveals an early role for this pathway in the repression of asymmetrically expressed genes in the diencephalon. Later signaling mediated by the EGF-CFC protein One-eyed pinhead and the forkhead transcription factor Schmalspur is required to overcome this repression. When expression of Nodal pathway genes is either absent or symmetrical, neuroanatomical asymmetries are still established but are randomized. This indicates that Nodal signaling is not required for asymmetric development per se but is essential to determine the laterality of the asymmetry

    Yearling Beef Cattle Grazing Diverse Summer Annual Swards

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    Utilizing summer annuals is often regarded as “a breakeven proposition at best” due to high establishment costs. This study investigated using botanical diversity to increase forage yield or animal performance to improve the economic feasibility of grazing summer annual forages in western Kentucky, USA. Sorghum-sudangrass (Sorghum bicolor x S. bicolor spp. drummondii)-based treatments included a monoculture, a three-species mixture (two grasses, one legume), and a 12-species mixture (five grasses, four legumes, two brassicas, and one forb). Angus-cross yearling beef calves (329, 366, and 297 kg in 2017, 2018, and 2019, respectively) grazed summer annuals in 2017-2019 for an average of 40 days each year without supplementation. Pastures were stocked when forage was approximately 1 m tall and calves were removed when forage was 2-2.5 m tall (seedheads present). In all years, forage dry matter yield was not different between treatments (p \u3e 0.85) and both mixtures were dominated by sorghum-sudangrass. In 2017 (p \u3c 0.03) and 2019 (p \u3c 0.03), calves grazing the 12-species mixture had lower average daily gains (ADG) than the monoculture and 3-species mixture, while there was no difference in 2018 (p \u3e 0.3). Average daily gains were suboptimal for stocker calves in all years (0.75, 0.01, 0.54 kg day-1 in 2017, 2018, and 2019). The extremely low ADG in 2018 was likely a result of stocking pastures late in the season when grasses were at physiological maturity. Additional species increased seed cost but did not contribute significantly to forage production and did not result in increased animal production. Unless greater forage yield or livestock gains are attained, planting mixtures may not provide any economic benefit. However, adjusting seeding rates to favor less dominant species may provide a more accurate representation of species diversity manipulation effects on forage and livestock production

    Adeno-Associated Virus-Mediated Rescue of the Cognitive Defects in a Mouse Model for Angelman Syndrome

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    Angelman syndrome (AS), a genetic disorder occurring in approximately one in every 15,000 births, is characterized by severe mental retardation, seizures, difficulty speaking and ataxia. The gene responsible for AS was discovered to be UBE3A and encodes for E6-AP, an ubiquitin ligase. A unique feature of this gene is that it undergoes maternal imprinting in a neuron-specific manner. In the majority of AS cases, there is a mutation or deletion in the maternally inherited UBE3A gene, although other cases are the result of uniparental disomy or mismethylation of the maternal gene. While most human disorders characterized by severe mental retardation involve abnormalities in brain structure, no gross anatomical changes are associated with AS. However, we have determined that abnormal calcium/calmodulin-dependent protein kinase II (CaMKII) regulation is seen in the maternal UBE3A deletion AS mouse model and is responsible for the major phenotypes. Specifically, there is an increased αCaMKII phosphorylation at the autophosphorylation sites Thr286 and Thr305/306, resulting in an overall decrease in CaMKII activity. CaMKII is not produced until after birth, indicating that the deficits associated with AS are not the result of developmental abnormalities. The present studies are focused on exploring the potential to rescue the learning and memory deficits in the adult AS mouse model through the use of an adeno-associated virus (AAV) vector to increase neuronal UBE3A expression. These studies show that increasing the levels of E6-AP in the brain using an exogenous vector can improve the cognitive deficits associated with AS. Specifically, the associative learning deficit was ameliorated in the treated AS mice compared to the control AS mice, indicating that therapeutic intervention may be possible in older AS patients

    The sixth international RASopathies symposium: Precision medicine—From promise to practice

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    The RASopathies are a group of genetic disorders that result from germline pathogenic variants affecting RAS‐mitogen activated protein kinase (MAPK) pathway genes. RASopathies share RAS/MAPK pathway dysregulation and share phenotypic manifestations affecting numerous organ systems, causing lifelong and at times life‐limiting medical complications. RASopathies may benefit from precision medicine approaches. For this reason, the Sixth International RASopathies Symposium focused on exploring precision medicine. This meeting brought together basic science researchers, clinicians, clinician scientists, patient advocates, and representatives from pharmaceutical companies and the National Institutes of Health. Novel RASopathy genes, variants, and animal models were discussed in the context of medication trials and drug development. Attempts to define and measure meaningful endpoints for treatment trials were discussed, as was drug availability to patients after trial completion

    Rapid selection of cyclic peptides that reduce alpha-synuclein toxicity in yeast and animal models

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    Phage display has demonstrated the utility of cyclic peptides as general protein ligands but cannot access proteins inside eukaryotic cells. Expanding a new chemical genetics tool, we describe the first expressed library of head-to-tail cyclic peptides in yeast (Saccharomyces cerevisiae). We applied the library to selections in a yeast model of alpha-synuclein toxicity that recapitulates much of the cellular pathology of Parkinson's disease. From a pool of 5 million transformants, we isolated two related cyclic peptide constructs that specifically reduced the toxicity of human alpha-synuclein. These expressed cyclic peptide constructs also prevented dopaminergic neuron loss in an established Caenorhabditis elegans Parkinson's model. This work highlights the speed and efficiency of using libraries of expressed cyclic peptides for forward chemical genetics in cellular models of human disease

    Sc65-Null Mice Provide Evidence for a Novel Endoplasmic Reticulum Complex Regulating Collagen Lysyl Hydroxylation

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    Collagen is a major component of the extracellular matrix and its integrity is essential for connective tissue and organ function. The importance of proteins involved in intracellular collagen post-translational modification, folding and transport was recently highlighted from studies on recessive forms of osteogenesis imperfecta (OI). Here we describe the critical role of SC65 (Synaptonemal Complex 65, P3H4), a leprecan-family member, as part of an endoplasmic reticulum (ER) complex with prolyl 3-hydroxylase 3. This complex affects the activity of lysyl-hydroxylase 1 potentially through interactions with the enzyme and/or cyclophilin B. Loss of Sc65 in the mouse results in instability of this complex, altered collagen lysine hydroxylation and cross-linking leading to connective tissue defects that include low bone mass and skin fragility. This is the first indication of a prolyl-hydroxylase complex in the ER controlling lysyl-hydroxylase activity during collagen synthesis

    Fundamental Neutron Physics: a White Paper on Progress and Prospects in the US

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    Fundamental neutron physics, combining precision measurements and theory, probes particle physics at short range with reach well beyond the highest energies probed by the LHC. Significant US efforts are underway that will probe BSM CP violation with orders of magnitude more sensitivity, provide new data on the Cabibbo anomaly, more precisely measure the neutron lifetime and decay, and explore hadronic parity violation. World-leading results from the US Fundamental Neutron Physics community since the last Long Range Plan, include the world's most precise measurement of the neutron lifetime from UCNτ\tau, the final results on the beta-asymmetry from UCNA and new results on hadronic parity violation from the NPDGamma and n-3{^3}He runs at the FNPB (Fundamental Neutron Physics Beamline), precision measurement of the radiative neutron decay mode and n-4{}^4He at NIST. US leadership and discovery potential are ensured by the development of new high-impact experiments including BL3, Nab, LANL nEDM and nEDM@SNS. On the theory side, the last few years have seen results for the neutron EDM from the QCD Ξ\theta term, a factor of two reduction in the uncertainty for inner radiative corrections in beta-decay which impacts CKM unitarity, and progress on {\it ab initio} calculations of nuclear structure for medium-mass and heavy nuclei which can eventually improve the connection between nuclear and nucleon EDMs. In order to maintain this exciting program and capitalize on past investments while also pursuing new ideas and building US leadership in new areas, the Fundamental Neutron Physics community has identified a number of priorities and opportunities for our sub-field covering the time-frame of the last Long Range Plan (LRP) under development. This white paper elaborates on these priorities.Comment: arXiv admin note: text overlap with arXiv:2304.0345
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