Series
Petit Institute Breakfast Club Seminar Series

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Event Series
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Associated Organization(s)

Publication Search Results

Now showing 1 - 10 of 30
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    The Spinal Cord: Parallel/Distributed Processor Regulating Limb Mechanics
    (Georgia Institute of Technology, 2014-10-14) Nichols, T. Richard
    The work in the Neurophysiology Laboratory is focused on mechanisms underlying motor coordination in mammalian systems. These mechanisms are to be found in the structure and dynamic properties of the musculoskeletal system as well as in the organization of neuronal circuits in the central nervous system. Our work concerns the interactions between the musculoskeletal system and spinal cord that give rise to normal and abnormal movement and posture, and in the manner in which central pattern-generating networks are modified for specific motor tasks. Their studies have applications in several movement disorders, including spinal cord injury. The experimental approaches span a number of levels, from mechanical studies of isolated muscle cells to kinematic measurements of natural behavior in quadrupeds.
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    RNA and Protein: A Match Made in the Hadean
    (Georgia Institute of Technology, 2014-09-09) Williams, Loren D.
    Biological systems record historical information, as seen in the growth rings of trees. On a molecular level, records are detailed and extensive, connecting us to the pre-history of biology (the origin of life). The most ancient macromolecules in biology are found in the ribosome, which is the RNA-protein complex responsible for the synthesis of all coded protein in living organisms. The catalytic core of the ribosome a deeply-frozen molecular fossil that is older than modern biology. The origins and early development of the ribosome, billions of years ago, remain firmly imprinted in the biochemistry of extant life. The ribosome tells us part of the story of the origin of life. The information contained within the ribosome guides our laboratory in experimentally recapitulating critical chemical and biochemical steps in the origin and early evolution of life.
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    Autonomous Mobile Robots for Personalized Caregiving
    (Georgia Institute of Technology, 2014-08-12) Kemp, Charles C.
    Mobile robots with autonomous capabilities have the potential to provide 24/7 personalized care, dramatically improving the quality of life of people with motor impairments. I will first provide an overview of opportunities for robots to provide beneficial physical assistance in the context of healthcare. I will then focus on my lab’s research to enable people with severe motor impairments to perform everyday tasks for themselves using mobile robots. In particular, I will focus on our work with Henry Evans, who has severe impairments due to a brain stem stroke. Through our research, Henry has been able to perform a number of tasks for himself for the first time in 10 years, such as pulling a blanket over himself, shaving himself, and operating mechanisms in his home. A key aspect of our work has been giving robots the ability to intelligently regulate the forces they apply while providing assistance.
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    Ancestry, Admixture and Selection in Colombian Genomes
    (Georgia Institute of Technology, 2014-04-08) Jordan, I. King
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    Osteoimmunology: Exploring the Role of the Immune System in Regulating Bone in Health and Disease
    (Georgia Institute of Technology, 2013-12-10) Pacifici, Roberto
    Our laboratory has pioneered the field of osteoimmunology. The laboratory is specialized in conducting in vivo studies in mice treated with PTH or subjected to ovariectomy. We use genetic models, retroviral transduction, bone marrow transplantation, T cell transfer and in vivo treatments with hormones, cytokines and antibodies. Typical end points include sophisticated flow cytometric analysis of bone marrow cells and microCT and histomorphometric analysis of bone structure. The lab is equipped with in vivo and in vitro microCT scanners. We have been the first to recognize that T cells play a pivotal role in the mechanism of action of estrogen and PTH in bone by regulating osteoclast and osteoblast development and function. We have shown that mice lacking T cells are protected against the bone loss induced by estrogen deficiency and hyperparathyroidism. We have has also shown that T cells regulate the number and function of mesenchymal stem cells. We are currently investigating the mechanism by which T cells mediate the expansion of hemopoietic stem cells caused by estrogen deficiency and PTH. Another main focus is to understand why “intermittent” PTH treatment causes bone anabolism while “continuous” PTH treatment causes bone loss. We hypothesize that the response to PTH depends on the effects of this hormone on T cell production of Wnt10b and TNF. A third project involves the use of intravital microscopy to study the effects of estrogen deficiency and PTH on the trafficking of T cells in the bone marrow.
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    Prediction and Design in Chemical Evolution
    (Georgia Institute of Technology, 2013-09-10) Grover, Martha A.
    Discrete atoms and molecules interact to form macromolecules and even larger mesoscale assemblies, ultimately yielding macroscopic structures and properties. A quantitative relationship between the nanoscale discrete interactions and the macroscale properties is required to design, optimize, and control such systems; yet in many applications, predictive models do not exist or are computationally intractable.
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    Regulation of Ryanodine Receptor Calcium Release Channels by Endogenous Effectors
    (Georgia Institute of Technology, 2013-07-09) Balog, Edward M.
    Fluctuations in the intracellular calcium (Ca2+) concentration are used to signal numerous cellular events. Impaired cellular Ca2+ regulation can lead to pathology and cell death, thus tight control of intracellular Ca2+ concentration is vital to the survival of all cells. This a particular challenge for cardiac and skeletal muscle cells as they use the controlled release of Ca2+ from the sarcoplasmic reticulum (SR) to initiate skeletal muscle contraction and the heartbeat. Ryanodine receptor (RyR) Ca2+ channels are the efflux pathway for the release of Ca2+ from the SR, however, these channels are not simple conduits for calcium efflux; rather they integrate cellular signals to finely tune Ca2+ release from intracellular stores. The critical role these channels play in muscle function is exemplified by the mutations in the channels that can lead to lethal cardiac arrhythmia or adverse reactions to anesthetics. Further these channel may contribute to muscle weakness associated with skeletal muscle fatigue and aging. A thorough understanding of RyR channel regulation by endogenous effectors is not only critical for our understanding of muscle function but may contribute to the development of therapeutic agents targeting these channels. I will discuss our work on two potential endogenous channel regulators, S-adenosyl-l-methionine (SAM) and calmodulin (CaM) and briefly describe some of our aging work. Physiological concentrations of SAM, the primary methyl group donor for enzyme-mediated methylation, activated the cardiac isoform of the RyR. This effect of SAM was unrelated to its role as a methyl group donor but rather was mediated by a RyR adenine nucleotide-binding site. Interestingly, SAM but not ATP activation was associated with a marked increase in the frequency of channel openings to a sub-conductance level. CaM is a small, ubiquitous protein that contains Ca2+-binding sites in each of its two lobes. Ca2+-free CaM activates the skeletal muscle RyR and Ca2+-bound CaM inhibits the channel. We have identified a CaM Ca2+-binding site required for the conversion of CaM from a RyR activator to a channel inhibitor. By manipulating the Ca2+ affinity of this site, we were able to modify the RyR activation profile. Future goals include defining the molecular characteristics required for adenine nucleotide activation of RyR channels and determining the role of CaM in voltage-activation of skeletal muscle.
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    Therapeutic Angiogenesis and Bone Regeneration with Natural and Synthetic Small Molecules
    (Georgia Institute of Technology, 2013-06-11) Botchwey, Edward A.
    Endothelial cells play significant roles in conditioning the environment in local tissues after injury by the production and secretion of angiocrine factors. At least two distinct subsets of leukocytes, CD45+ CD11b+ Ly6C+Gr1+CX3CR1lo inflammatory monocytes (IM) and CD45+CD11b+Ly6CGr1-CX3CR1hi anti-inflammatory monocytes (AM), respond differentially to these angiocrine factors and promote pathogen/debris clearance and angiogenesis/wound healing, respectively. Our laboratory is currently investigating how local sphingosine 1-phosphate receptor 3 (S1P3) agonism recruits AM to remodeling vessels. We employ micron and nanoscale biomaterials to deliver FTY720, a S1P1/3 agonist, to inflamed and ischemic tissues, to reduce in pro-inflammatory cytokine secretion and an increase in regenerative cytokine secretion. The altered balance of cytokine secretion results in a reduction in inflammatory monocyte recruitment and an increase in anti-inflammatory CX3CR1hi monocyte recruitment to a pro-regenerative perivascular niche. Increased S1P3 expression and activation on AM resulted in significantly enhanced SDF-1α chemotaxis over IM. AM recruitment also enhanced arteriolar diameter expansion and increased length density of the local vasculature: classic signs of vascular remodeling. This work establishes a role for S1P receptor signaling in the local conditioning of tissues by angiocrine factors that preferentially recruit regenerative monocytes that can enhance healing outcomes, bone tissue regeneration, and biomaterial implant functionality.