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Macon, GA, United States

Mercer University is a private, coeducational university with its main campus in Macon, Georgia, United States.Mercer enrolls more than 8,500 students in 12 colleges and schools: liberal arts, business, engineering, education, music, continuing and professional studies, law, theology, medicine, pharmacy, nursing, and health professions.Mercer has three campuses: the main campus in Macon, a graduate and professional education campus in Atlanta, and a four-year campus of the School of Medicine in Savannah. Mercer also has regional academic centers in Henry County, Douglas County, Eastman, and Newnan; the Walter F. George School of Law on its own campus in Macon; teaching hospitals in Macon, Savannah, and Columbus; a university press and a performing arts center, the Grand Opera House, in Macon; and the Mercer Engineering Research Center in Warner Robins. The Mercer University Health science Center encompasses Mercer's medical, pharmacy, nursing, and health professions programs in Macon, Atlanta, Savannah, and Columbus.In 2014, US News and World Report ranked Mercer the best value among comprehensive universities in the southern United States. The Princeton Review, which consistently ranks Mercer in the top 10% of colleges and universities in North America, wrote in 2014, "Mercer's exceptional reputation springs from its sound academic programs, excellent faculty, and modern facilities", and in 2005 called the main campus one of the five most beautiful in the United States. Mercer was cited by the Carnegie Foundation for the Advancement of Teaching for its community engagement, and was among the 113 institutions listed on the 2013 President's Higher Education Community Service Honor Roll with Distinction.Mercer has an NCAA Division I athletic program and fields teams in eight men's and ten women's sports; all university-sponsored sports compete in the Southern Conference except women's lacrosse and women's sand volleyball, which are not sponsored by the SoCon, and thus compete in the Atlantic Sun Conference. Wikipedia.


Blumental-Perry A.,Mercer University
Current Molecular Medicine | Year: 2012

Cigarette smoke (CS) is a risk factor for the development of chronic obstructive pulmonary disease (COPD). Oxidative stress is an immediate result of CS exposure and has the ability to modify cellular proteins. The endoplasmic reticulum (ER) is a compartment where early steps of synthesis and folding of membrane and secretory proteins takes place. Oxidative stress has been shown to interfere with protein folding in the ER and elicits the unfolded protein response (UPR). The UPR is a massive endoplasmic reticulum to the nucleus and the cellular kinase cascades signaling pathway. The UPR triggers a series of intracellular events that aim to help cells overcome the consequences of the stress or eliminate rogue cells by altering expression of genes involved in anti-oxidant defense, cell cycle progression, inflammation, and apoptosis. Recent data demonstrate that CS induces the UPR in vitro and in vivo. The timing of UPR induction in smokers and the mechanism of CS-induced UPR are areas of active investigation. The role of UPR in the protection of smoker's lungs from CS-induced oxidative stress, and its contribution to CS-induced apoptosis and inflammation, is beginning to emerge. This review discusses recent data about UPR in COPD and summarizes findings on UPR that have potential relevance to COPD. © 2012 Bentham Science Publishers.


VanDenBerg C.M.,Mercer University
Journal of Clinical Psychiatry | Year: 2012

Monoamine oxidase inhibitors (MAOIs) were once widely used as effective treatments for major depressive disorder, particularly for patients with atypical or treatment-resistant depression. Today, MAOIs have largely been replaced by newer antidepressants because of concerns over potential serious side effects due to their mechanism of action. Monoamine oxidase (MAO) is an enzyme that metabolizes serotonin, norepinephrine, and dopamine, the neurotransmitters that are most associated with depression; inhibiting MAO, therefore, makes more of these neurotransmitters available for synaptic action. However, MAO also metabolizes tyramine, a trace amine found in some foods that acts as a sympathomimetic. Allowing excess tyramine to accumulate via MAO inhibition can result in hypertensive crisis due to the release of norepinephrine; therefore, patients taking an MAOI have had to follow dietary restrictions to avoid tyramine-rich foods. Hypertensive crisis may also be precipitated by using MAOIs in conjunction with other drugs that have vasoconstrictive properties, that act as sympathomimetics, or that inhibit the reuptake of norepinephrine. Serotonin syndrome is another serious adverse effect that can potentially occur when using an MAOI with another drug that inhibits the reuptake of serotonin. In this article, the mechanism of action of MAOIs is reviewed, along with that of a newer MAOI formulation that lessens the need for dietary restrictions and has a greater safety and tolerability profile than the older oral formulations. © Copyright 2012 Physicians Postgraduate Press, Inc.


Cline S.D.,Mercer University
Biochimica et Biophysica Acta - Gene Regulatory Mechanisms | Year: 2012

How mitochondria process DNA damage and whether a change in the steady-state level of mitochondrial DNA damage (mtDNA) contributes to mitochondrial dysfunction are questions that fuel burgeoning areas of research into aging and disease pathogenesis. Over the past decade, researchers have identified and measured various forms of endogenous and environmental mtDNA damage and have elucidated mtDNA repair pathways. Interestingly, mitochondria do not appear to contain the full range of DNA repair mechanisms that operate in the nucleus, although mtDNA contains types of damage that are targets of each nuclear DNA repair pathway. The reduced repair capacity may, in part, explain the high mutation frequency of the mitochondrial chromosome. Since mtDNA replication is dependent on transcription, mtDNA damage may alter mitochondrial gene expression at three levels: by causing DNA polymerase γ nucleotide incorporation errors leading to mutations, by interfering with the priming of mtDNA replication by the mitochondrial RNA polymerase, or by inducing transcriptional mutagenesis or premature transcript termination. This review summarizes our current knowledge of mtDNA damage, its repair, and its effects on mtDNA integrity and gene expression. This article is part of a special issue entitled: Mitochondrial Gene Expression. © 2012 Elsevier B.V.


Mizisin A.P.,University of California at San Diego | Weerasuriya A.,Mercer University
Acta Neuropathologica | Year: 2011

The endoneurial microenvironment, delimited by the endothelium of endoneurial vessels and a multi-layered ensheathing perineurium, is a specialized milieu intérieur within which axons, associated Schwann cells and other resident cells of peripheral nerves function. The endothelium and perineurium restricts as well as regulates exchange of material between the endoneurial microenvironment and the surrounding extracellular space and thus is more appropriately described as a blood-nerve interface (BNI) rather than a blood-nerve barrier (BNB). Input to and output from the endoneurial microenvironment occurs via blood-nerve exchange and convective endoneurial fluid flow driven by a proximo-distal hydrostatic pressure gradient. The independent regulation of the endothelial and perineurial components of the BNI during development, aging and in response to trauma is consistent with homeostatic regulation of the endoneurial microenvironment. Pathophysiological alterations of the endoneurium in experimental allergic neuritis (EAN), and diabetic and lead neuropathy are considered to be perturbations of endoneurial homeostasis. The interactions of Schwann cells, axons, macrophages, and mast cells via cell-cell and cell-matrix signaling regulate the permeability of this interface. A greater knowledge of the dynamic nature of tight junctions and the factors that induce and/or modulate these key elements of the BNI will increase our understanding of peripheral nerve disorders as well as stimulate the development of therapeutic strategies to treat these disorders. © The Author(s) 2010.


Grant
Agency: Department of Defense | Branch: Defense Advanced Research Projects Agency | Program: STTR | Phase: Phase II | Award Amount: 999.35K | Year: 2015

Recent advances in mammalian artificial chromosome design and engineering offer an alternative to existing methodologies for cellular bioengineering and address unmet needs to bioengineer more complex functionalities into human cells for subsequent commercialization. In this ST13B-001 application we propose to demonstrate utility of a novel chromosome-based gene delivery vehicle that is amenable to large genetic payloads while avoiding insertional mutagenesis and maintaining stable, long-term, gene expression. A cornerstone to our proposal is the utilization of a distinctive mammalian artificial chromosome technology termed Artificial Chromosome Expression System (ACE System), an autonomous chromosome-based circuit-board designed to contain approximately 70 site-specific recombination acceptor sites that can carry single or multiple copies of genes or DNA elements of interest. In Phase I of this solicitation we delivered a 144Kbp BAC containing the MCT1 genomic locus onto the platform ACE that had previously been loaded with a 168Kbp BAC, resulting in 312Kbp of total DNA added. In addition to demonstrating the specificity of integration we confirmed the structural stability of the genomic DNAs. In Phase II we will expand this disruptive technology by engineering additional robust and complex functionalities into the ACE system toward the goal of cell-based therapeutics.

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