MFA09 (MFA 2009)

Catalogue of a culminating student exhibition held at the Mildred Lane Kemper Art Museum in 2009. Content includes A new paradigm / Carmon Colangelo -- Evolving practices / Patricia Olynyk -- Stephanie Barenz -- Carolyn Dawn Bendel -- Jacob Cruzen -- Rachel Ann Dennis -- Bryan Eaton -- Maya Escobar -- Meredith Foster -- Morgan Gehris -- Gina Grafos -- Stephen Hoskins -- Amelia Jones -- Hye Young Kim -- Anne Lindberg -- Goran Maric -- Kelda Martensen -- Erica L. Millspaugh -- Carianne Noga -- Joel Parker -- Rebecca C. Potts -- Shannon Randol -- Elaine Rickles -- Michael Kenneth Smith -- Dan Solberg -- Natalie Toney -- Glenn Tramantano -- Kathryn Trout -- J. Taylor Wallace.https://openscholarship.wustl.edu/books/1006/thumbnail.jp

Epigenetic regulation of caloric restriction in aging

The molecular mechanisms of aging are the subject of much research and have facilitated potential interventions to delay aging and aging-related degenerative diseases in humans. The aging process is frequently affected by environmental factors, and caloric restriction is by far the most effective and established environmental manipulation for extending lifespan in various animal models. However, the precise mechanisms by which caloric restriction affects lifespan are still not clear. Epigenetic mechanisms have recently been recognized as major contributors to nutrition-related longevity and aging control. Two primary epigenetic codes, DNA methylation and histone modification, are believed to dynamically influence chromatin structure, resulting in expression changes of relevant genes. In this review, we assess the current advances in epigenetic regulation in response to caloric restriction and how this affects cellular senescence, aging and potential extension of a healthy lifespan in humans. Enhanced understanding of the important role of epigenetics in the control of the aging process through caloric restriction may lead to clinical advances in the prevention and therapy of human aging-associated diseases

Chondroitinase improves anatomical and functional outcomes after primate spinal cord injury.

Inhibitory extracellular matrices form around mature neurons as perineuronal nets containing chondroitin sulfate proteoglycans that limit axonal sprouting after CNS injury. The enzyme chondroitinase (Chase) degrades inhibitory chondroitin sulfate proteoglycans and improves axonal sprouting and functional recovery after spinal cord injury in rodents. We evaluated the effects of Chase in rhesus monkeys that had undergone C7 spinal cord hemisection. Four weeks after hemisection, we administered multiple intraparenchymal Chase injections below the lesion, targeting spinal cord circuits that control hand function. Hand function improved significantly in Chase-treated monkeys relative to vehicle-injected controls. Moreover, Chase significantly increased corticospinal axon growth and the number of synapses formed by corticospinal terminals in gray matter caudal to the lesion. No detrimental effects were detected. This approach appears to merit clinical translation in spinal cord injury.This work was supported by the National Institutes of Health (NIH, grant no. NS042291 to M.H.T.) and Acorda Therapeutics. Core infrastructure support for the primate spinal cord research facility was provided by the Veterans Administration (Gordon Mansfield Spinal Cord Injury Collaborative Consortium grant nos. IP50RX001045 and RR&D B7332R to M.H.T. and grant no. RR&D 1I01RX002245 to A.R.F.). The California National Primate Research Center is funded by the NIH (grant no. NCRR P51 OD011107-56). Funding was also provided by the Craig H. Neilsen Foundation (M.H.T.), the Bernard and Anne Spitzer Charitable Trust (M.H.T.), the Dr. Miriam and Sheldon G. Adelson Medical Research Foundation (M.H.T.), the British Medical Research Council (J.W.F.) and the Christopher & Dana Reeve Foundation (J.W.F.)

Chondroitinase improves anatomical and functional outcomes after primate spinal cord injury.

Inhibitory extracellular matrices form around mature neurons as perineuronal nets containing chondroitin sulfate proteoglycans that limit axonal sprouting after CNS injury. The enzyme chondroitinase (Chase) degrades inhibitory chondroitin sulfate proteoglycans and improves axonal sprouting and functional recovery after spinal cord injury in rodents. We evaluated the effects of Chase in rhesus monkeys that had undergone C7 spinal cord hemisection. Four weeks after hemisection, we administered multiple intraparenchymal Chase injections below the lesion, targeting spinal cord circuits that control hand function. Hand function improved significantly in Chase-treated monkeys relative to vehicle-injected controls. Moreover, Chase significantly increased corticospinal axon growth and the number of synapses formed by corticospinal terminals in gray matter caudal to the lesion. No detrimental effects were detected. This approach appears to merit clinical translation in spinal cord injury