213 research outputs found

    The Color of Sound

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    A Survey of Horse Training in New England

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    New England no longer has a significant horse training industry. It has many small operations with no obvious and overlapping training philosophies or practices. Show and competition programs are intense and competitive at regional, national and even international levels leading to the observation that techniques employed are equally strategic and tediously designed in order to encourage the exemplary results in the show ring. This study aimed to examine the methods, routines, and strategies that are used by top tier trainers in the New England region of the United States. This information was collected both in survey form and in interview form, to maximize collection and indications of how each particular trainer, breeder, or owner was most easily contacted. The data was then compiled, analyzed for trends, outliers, and other points of interest with the end goal of giving a basic but thorough view of the methods and strategies used by trainers of prestige in the New England area. Results of this study will hold relevance both to those interested in this luxury hobby and to economy minded individuals, as horses are still a substantial percentage of livestock in the New England area. Future studies in the New England area could target a larger group of trainers and stables, while future studies could also be performed in other regions of the United States

    CENP-A is phosphorylated by Aurora B kinase and plays an unexpected role in completion of cytokinesis

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    Aurora B is a mitotic protein kinase that phosphorylates histone H3, behaves as a chromosomal passenger protein, and functions in cytokinesis. We investigated a role for Aurora B with respect to human centromere protein A (CENP-A), a centromeric histone H3 homologue. Aurora B concentrates at centromeres in early G2, associates with histone H3 and centromeres at the times when histone H3 and CENP-A are phosphorylated, and phosphorylates histone H3 and CENP-A in vitro at a similar target serine residue. Dominant negative phosphorylation site mutants of CENP-A result in a delay at the terminal stage of cytokinesis (cell separation). The only molecular defects detected in analysis of 22 chromosomal, spindle, and regulatory proteins were disruptions in localization of inner centromere protein (INCENP), Aurora B, and a putative partner phosphatase, PP1γ1. Our data support a model where CENP-A phosphorylation is involved in regulating Aurora B, INCENP, and PP1γ1 targeting within the cell. These experiments identify an unexpected role for the kinetochore in regulation of cytokinesis

    Active establishment of centromeric CENP-A chromatin by RSF complex

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    Centromeres are chromosomal structures required for equal DNA segregation to daughter cells, comprising specialized nucleosomes containing centromere protein A (CENP-A) histone, which provide the basis for centromeric chromatin assembly. Discovery of centromere protein components is progressing, but knowledge related to their establishment and maintenance remains limited. Previously, using anti-CENP-A native chromatin immunoprecipitation, we isolated the interphase–centromere complex (ICEN). Among ICEN components, subunits of the remodeling and spacing factor (RSF) complex, Rsf-1 and SNF2h proteins, were found. This paper describes the relationship of the RSF complex to centromere structure and function, demonstrating its requirement for maintenance of CENP-A at the centromeric core chromatin in HeLa cells. The RSF complex interacted with CENP-A chromatin in mid-G1. Rsf-1 depletion induced loss of centromeric CENP-A, and purified RSF complex reconstituted and spaced CENP-A nucleosomes in vitro. From these data, we propose the RSF complex as a new factor actively supporting the assembly of CENP-A chromatin

    Domain Specific Self-Efficacy Mediates the Impact of Pain Catastrophizing on Pain and Disability in Overweight and Obese Osteoarthritis Patients

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    This study examined whether self-efficacy mediated the relationship between pain catastrophizing and pain and disability. Participants were 192 individuals diagnosed with osteoarthritis (OA) of the knees who were overweight or obese. Multiple mediator analyses were conducted to simultaneously test self-efficacy for pain control, physical function, and emotional symptoms as mediators while controlling for demographic and medical status variables. Higher pain catastrophizing was associated with lower self-efficacy in all three domains (ps< .05). Self-efficacy for pain control fully mediated the relationship between pain catastrophizing and pain (Beta=.08, Sobel test Z=1.97, p<.05). The relationship between pain catastrophizing and physical disability was fully mediated by self-efficacy for physical function (Beta=.06, Sobel test Z=1.95, p=.05). Self-efficacy for emotional symptoms partially mediated the relationship between pain catastrophizing and psychological disability (Beta=. 12, Sobel test Z=2.92, p<.05). These results indicate that higher pain catastrophizing contributed to greater pain and disability via lower domain-specific self-efficacy. Efforts to reduce pain and improve functioning in OA patients should consider addressing pain catastrophizing and domain specific selfefficacy. Pain catastrophizing may be addressed through cognitive therapy techniques and selfefficacy may be enhanced through practice of relevant skills and personal accomplishments. Perspective- This paper found that higher pain catastrophizing contributed to great pain and disability via domain specific self-efficacy. These results suggest that treatment efforts to reduce pain and improve functioning in OA patients who are overweight or obese should consider addressing both pain catastrophizing and self-efficacy. Originally published Journal of Pain, Vol. 9, No. 10, Oct 200

    A Rapid FACS-Based Strategy to Isolate Human Gene Knockin and Knockout Clones

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    Gene targeting protocols for mammalian cells remain inefficient and labor intensive. Here we describe FASTarget, a rapid, fluorescent cell sorting based strategy to isolate rare gene targeting events in human somatic cells. A fluorescent protein is used as a means for direct selection of targeted clones obviating the need for selection and outgrowth of drug resistant clones. Importantly, the use of a promoter-less, ATG-less construct greatly facilitates the recovery of correctly targeted cells. Using this method we report successful gene targeting in up to 94% of recovered human somatic cell clones. We create functional EYFP-tagged knockin clones in both transformed and non-transformed human somatic cell lines providing a valuable tool for mammalian cell biology. We further demonstrate the use of this technology to create gene knockouts. Using this generally applicable strategy we can recover gene targeted clones within approximately one month from DNA construct delivery to obtaining targeted monoclonal cell lines
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