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Henry Fork, VA, United States

Randolph–Macon College is a private, co-educational liberal arts college located in Ashland, Virginia, United States, near the capital city of Richmond. Founded in 1830, the school has an enrollment of more than 1,300 students. The college offers bachelor's degrees in 38 major disciplines in the liberal arts, including political science, business, psychology, biology, international studies, and computer science, as well as 34 minors, including education. Randolph–Macon College is a member of the Annapolis Group of colleges in the United States, as well as the Virginia Foundation for Independent Colleges. Wikipedia.


Clabough E.B.D.,Randolph-Macon College
Yale Journal of Biology and Medicine | Year: 2013

Huntington's disease (HD†) is an autosomal dominant genetic disorder that specifically causes neurodegeneration of striatal neurons, resulting in a triad of symptoms that includes emotional, cognitive, and motor disturbances. The HD mutation causes a polyglutamine repeat expansion within the N-terminal of the huntingtin (Htt) protein. This expansion causes aggregate formation within the cytosol and nucleus due to the presence of misfolded mutant Htt, as well as altered interactions with Htt's multiple binding partners, and changes in post-translational Htt modifications. The present review charts efforts toward a therapy that delays age of onset or slows symptom progression in patients affected by HD, as there is currently no effective treatment. Although silencing Htt expression appears promising as a disease modifying treatment, it should be attempted with caution in light of Htt's essential roles in neural maintenance and development. Other therapeutic targets include those that boost aggregate dissolution, target excitotoxicity and metabolic issues, and supplement growth factors. © 2013.


Riddell I.A.,University of Cambridge | Smulders M.M.J.,University of Cambridge | Clegg J.K.,University of Cambridge | Clegg J.K.,University of Queensland | And 4 more authors.
Nature Chemistry | Year: 2012

Biochemical systems are adaptable, capable of reconstitution at all levels to achieve the functions associated with life. Synthetic chemical systems are more limited in their ability to reorganize to achieve new functions; they can reconfigure to bind an added substrate (template effect) or one binding event may modulate a receptor's affinity for a second substrate (allosteric effect). Here we describe a synthetic chemical system that is capable of structural reconstitution on receipt of one anionic signal (perchlorate) to create a tight binding pocket for another anion (chloride). The complex, barrel-like structure of the chloride receptor is templated by five perchlorate anions. This second-order templation phenomenon allows chemical networks to be envisaged that express more complex responses to chemical signals than is currently feasible. © 2012 Macmillan Publishers Limited. All rights reserved.


Unilateral naris occlusion has long been the method of choice for effecting stimulus deprivation in studies of olfactory plasticity. A significant body of literature speaks to the myriad consequences of this manipulation on the ipsilateral olfactory pathway. Early experiments emphasized naris occlusion's deleterious and age-critical effects. More recent studies have focused on life-long vulnerability, particularly on neurogenesis, and compensatory responses to deprivation. Despite the abundance of empirical data, a theoretical framework in which to understand the many sequelae of naris occlusion on olfaction has been elusive. This paper focuses on recent data, new theories, and underappreciated caveats related to the use of this technique in studies of olfactory plasticity. Copyright © 2012 David M. Coppola.


Gan Q.,University of Cambridge | Ronson T.K.,University of Cambridge | Vosburg D.A.,Harvey Mudd College | Thoburn J.D.,Randolph-Macon College | Nitschke J.R.,University of Cambridge
Journal of the American Chemical Society | Year: 2015

In order to design artificial chemical systems that are capable of achieving complex functions, it is useful to design synthetic receptors that mimic their biological counterparts. Biological functions are underpinned by properties that include specific binding with high affinity and selectivity, cooperativity, and release triggered by external stimuli. Here we show that a metal-organic receptor constructed through subcomponent self-assembly can selectively and cooperatively load and release oxocarbon anions. The flexible coordination spheres of its cadmium(II) centers allow the receptor to dynamically adjust its structure upon exchanging four triflate or triflimide counterions for two oxocarbon anions, resulting in strong cooperativity and very tight binding, with an apparent association constant for C5O5 2- of 5 × 1010 M-1. Substituting the cadmium(II) ions for copper(I) by switching solvent prompted a structural reorganization and release of the oxocarbon anions. Its cooperative behavior allows the receptor to carry a greater payload than would be possible in a noncooperative analogue. © 2015 American Chemical Society.


Rao R.R.,Roswell Park Cancer Institute | Li Q.,Roswell Park Cancer Institute | Bupp M.,Randolph-Macon College | Shrikant P.,Roswell Park Cancer Institute
Immunity | Year: 2012

The evolutionary conserved Foxo transcription factors are important regulators of quiescence and longevity. Although, Foxo1 is known to be important in regulating CD8 + T cell trafficking and homeostasis, its role in functional differentiation of antigen-stimulated CD8 + T cells is unclear. Herein, we demonstrate that inactivation of Foxo1 was essential for instructing T-bet transcription factor-mediated effector differentiation of CD8 + T cells. The Foxo1 inactivation was dependent on mTORC1 kinase, given that blockade of mTORC1 abrogated mTORC2-mediated Akt (Ser473) kinase phosphorylation, resulting in Foxo1-dependent switch from T-bet to Eomesodermin transcription factor activation and increase in memory precursors. Silencing Foxo1 ablated interleukin-12- and rapamycin-enhanced CD8 + T cell memory responses and restored T-bet-mediated effector functions. These results demonstrate an essential role of Foxo1 in actively repressing effector or terminal differentiation processes to promote memory CD8 + T cell development and identify the functionally diverse mechanisms utilized by Foxo1 to promote quiescence and longevity. © 2012 Elsevier Inc..

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