Multinuclear solid state NMR studies of α-tricalcium phosphate and silicon substituted α-tricalcium phosphate

a-tricalcium phosphate (a-TCP, Ca3(PO4)2) demonstrates both bioactive and resorbable characteristics. Substitution of SiO4 4- for PO4 3- in a-TCP (Si-a-TCP) is found to stabilize the structure at lower temperatures and improve mechanical (and possibly bioactive) properties. The mechanism of electroneutrality in the Si-a-TCP structure is not fully understood, though is thought to take place through the creation of O2- vacancies or through excess Ca2+. This study addresses some structural properties of a-TCP using 31P MAS NMR at intermediate B0 fields (11.7 T) and 43Ca DOR NMR at multiple fields (20.0 T, 14.1 T, 11.7 T), and via correlation of the measured 31P and 43Ca isotropic chemical shifts (Oiso) against calculated values obtained with GIPAW DFT methods using the CASTEP code. These results show that the structure has high short range order and clearly support the monoclinic P21/a (12 P site/18 Ca site) model. In contrast, solid state 31P MAS and 43Ca DOR NMR studies of Si-a-TCP demonstrate that significant disorder broadening is characteristic of these data, however the corresponding 29Si MAS NMR data affords reasonably resolved resonances, a low intensity Q2 resonance at 0iso {84.5 ppm, and multiple resonances in the range 0iso - {70 -{75 ppm, despite this shift range normally associated with Q0 speciation, 29Si refocused-INADEQUATE data shows that Q1 resonances can also exist in this region. 31P-29Si HETCOR data from these systems suggests that, despite the intrinsic disorder, explicit PO43- framework species can be associated with the different Q0/Q1 Si species, and while there is some dispersion of the silicon throughout the structure it is predominantly associated with a small number of P sites. DFT calculations for the Si-a-TCP system suggest that the more favourable mechanism for charge balance is Ca2+ excess, despite this, the 29Si NMR data is in greater agreement with the DFT calculations for the O2- mechanism, whereby two adjoining cation-anion-columns in the structure are bridged together by a Q1 unit , 29Si NMR data also suggests the existence of Ca2SiO4 and Ca3Si3O9 existing as solid solutions within the a-TCP structure

At What Rate Do Farmers Substitute Manure For Commercial Fertilizers?

Water quality has implications for the health of our ecosystem and the welfare of our population. Agriculture is one of the major contributors of non-point source pollution that contaminates our nation's water supplies. Understanding how farmers substitute manure for commercial fertilizers allows us to better understand the level of nitrogen that enters the soil and can seep into our waterways. In this paper, we explore the factors that help determine farmers' substitution rates between the two types of fertilizers. Location, crop type, and time all could play important roles. We analyze USDA farm level survey data for both crop and livestock farms covering the years 1996 to 2002 to create substitution rate estimates used on corn, soybean, and wheat fields. While the substitution rates we found did not appear to change over the time frame examined, we did find that crop type and location significantly affected the rates that farmers use. Additionally, and perhaps most importantly, the substitution rates we did find did not conform to the "perfect substitution" between N coming from commercial sources and manure used in much of the literature. This means that previous studies could have underestimated the potential level of pollution of our water by our nations' farms.Farm Management,

Dreaming Of Home Sweet Home

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Rose of Washington Square

https://digitalcommons.library.umaine.edu/mmb-vp/6140/thumbnail.jp

At The End Of The Road

Contains advertisements and/or short musical examples of pieces being sold by publisher.https://digitalcommons.library.umaine.edu/mmb-vp/6784/thumbnail.jp

Indiana

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You Can\u27t Run Around With A Lot Of Little Girls : If You Want TO Run Around With Me

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Chin - Chin Chinaman

https://digitalcommons.library.umaine.edu/mmb-vp/3544/thumbnail.jp

Huntington's disease: the case for genetic modifiers

For almost three decades, Huntington's disease has been a prototype for the application of genetic strategies to human disease. HD, the Huntington's disease gene, was the first autosomal defect mapped using only DNA markers, a finding in 1983 that helped to spur similar studies in many other disorders and contributed to the concept of the human genome project. The search for the genetic defect itself pioneered many mapping and gene-finding technologies, and culminated in the identification of the HD gene, its mutation and its novel protein product in 1993. Since that time, extensive investigations into the pathogenic mechanism have utilized the knowledge of the disease gene and its defect but, with notable exceptions, have rarely relied for guidance on the genetic findings in human patients to interpret the relevance of findings in non-human model systems. However, the human patient still has much to teach us through a detailed analysis of genotype and phenotype. Such studies have implicated the existence of genetic modifiers - genes whose natural polymorphic variation contributes to altering the development of Huntington's disease symptoms. The search for these modifiers, much as the search for the HD gene did in the past, offers to open new entrées into the process of Huntington's disease pathogenesis by unlocking the biochemical changes that occur many years before diagnosis, and thereby providing validated target proteins and pathways for development of rational therapeutic interventions