Macon, GA, United States
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.

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Vitamin E-based amphiphilic copolymers are disclosed. Compositions containing vitamin E-based amphiphilic copolymers and/or nanocarriers are also disclosed. Methods of making vitamin E-based amphiphilic copolymers and/or nanocarriers and methods of using vitamin E-based amphiphilic copolymers and/or nanocarriers are also disclosed.


A method of transdermal delivery of a vaccine, comprising preparing microparticles of encapsulated vaccine by spray drying a mixture of the vaccine and at least one polymer, and injecting the microparticles transdermally using a microneedle delivery apparatus.


A transdermal delivery system of microneedles containing a bioactive material, comprising at least one layer of a support material; at least one biodegradable needle associated with the support material, each needle comprising at least one biodegradable polymer and at least one sugar, wherein each biodegradable needle is hollow and is adapted to retain a bioactive material.


Vitamin E-based amphiphilic copolymers are disclosed. Compositions containing vitamin E-based amphiphilic copolymers and/or nanocarriers are also disclosed. Methods of making vitamin E-based amphiphilic copolymers and/or nanocarriers and methods of using vitamin E-based amphiphilic copolymers and/or nanocarriers are also disclosed.


Lauterbach E.C.,Mercer University
Progress in Neuro-Psychopharmacology and Biological Psychiatry | Year: 2013

Recently, the genes p19 S-phase kinase-associated protein 1A (SKP1), huntingtin interacting protein-2 (UBE2K), aldehyde dehydrogenase family 1 subfamily A1 (ALDH1A1), 19 S proteasomal protein PSMC4, and heat shock 70-kDa protein 8 (HSPA8) have been found to predict the onset and progression of Parkinson's disease (PD). These findings prompted a review of the effects of commonly prescribed psychiatric medicines, drugs that are used in treating PD, on the expression of these genes. Findings in the published medical literature were reviewed and gene expression data in the Gene Expression Omnibus Profiles database were analyzed. The results indicate that fluoxetine upregulated the risk-attenuating genes Skp1a and Aldh1a1 and olanzapine downregulated risk-enhancing Hspa8 while also downregulating Aldh1a1. Less conclusive evidence suggested that fluoxetine might also downregulate Hspa8 and clozapine might downregulate risk-enhancing Ube2k, but that olanzapine might upregulate Ube2k. Together, the present findings suggest that these psychotropics may delay PD onset (fluoxetine, olanzapine, and perhaps clozapine) and progression (fluoxetine, clozapine, and perhaps olanzapine). These gene expression findings should be replicated by RT-PCR studies in humans and, if confirmed, these drugs should then be studied in animal models and PD patients. © 2012 Elsevier Inc.


Lauterbach E.C.,Mercer University
Progress in Neuro-Psychopharmacology and Biological Psychiatry | Year: 2012

Objectives: Psychotropic drugs are widely prescribed in Parkinson's disease (PD) without regard to their pathobiological effects, and these drugs affect the transcription of a large number of genes. Effects of these drugs on PD risk gene transcription were therefore surveyed. Methods: Results summarize a comprehensive survey of psychotropic effects on messenger ribonucleic acid (mRNA) expression evident in published data for 70 genes linked to PD risk. Results: Psychotropic drugs can meaningfully affect PD risk gene mRNA transcription, including antipsychotics (upregulate dopamine receptors D2 and D3 (DRD2, DRD3); downregulate low-density lipoprotein receptor-related protein 8 (LRP8), ubiquitin carboxyl-terminal esterase L1 (UCHL1, also known as PARK5)), haloperidol (upregulates DRD3, parkin (PRKN, also known as PARK2), DRD2; downregulates brain-derived neurotrophic factor (BDNF)), risperidone (upregulates monoamine oxidase B (MAOB), DRD2), olanzapine (upregulates transmembrane protein 163 (TMEM163), BDNF, glutathione S-transferase mu 1 (GSTM1), MAOB, DRD2, solute carrier organic anion transporter family, member 3A1 (SLCO3A1)), aripiprazole (upregulates DRD2), quetiapine, paliperidone, lurasidone, carbamazepine, and many antidepressants (upregulate BDNF), lithium and bupropion (downregulate BDNF), amitriptyline (upregulates DRD3, DRD2), imipramine (upregulates BDNF, DRD3, DRD2), desipramine (upregulates BDNF, DRD3), and fluoxetine (upregulates acid beta-glucosidase (GBA), coiled-coil domain containing 62 (CCDC62), BDNF, DRD3, UCHL1, unc-13 homolog B (UNC13B), and perhaps huntingtin interacting protein 1 related (HIP1R); downregulates microtubule-associated protein tau (MAPT), methylcrotonoyl-coenzyme A carboxylase I (MCCC1), GSTM1, 28. kDa calbindin 1 (CALB1)). Fluoxetine effects on BDNF and UCHL1 in GEO Profiles were statistically robust. Conclusions: This report provides an initial summary and framework to understand the potential impact of psychotropic drugs on PD-relevant genes. Antipsychotics and serotoninergic antidepressants may potentially attenuate PD risk, and lithium and bupropion may augment risk, through MAPT, GBA, CCDC62, HIP1R, BDNF, and DRD2 transcription, with MAPT, GBA, and CCDC62 being strongly associated with PD risk in recent meta-analyses. Limitations of these findings and a research agenda to better relate them to the nigrostriatum and PD are discussed. © 2012 Elsevier Inc.


Patent
Emory University, Mercer University and Union College at Schenectady | Date: 2015-07-08

This disclosure relates to solenopsin derivatives, pharmaceutical compositions, and therapeutic uses related thereto. In certain embodiments, the disclosure relates to compounds of the following formula:


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.


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.


Patent
Mercer University | Date: 2015-07-20

Listening lab kits are disclosed. Methods of making listening lab kits and methods of using listening lab kits are also disclosed.

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