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Strategy Two: Research Initiation Award

  • Objective

    The activities of the Research Initiation Award (RIA) strategy will help to realize the second objective of the TRANSFORM grant which is to increase the number of Gannon female faculty achieving advancement in rank. The research initiation award will provide resources for early- or mid- career, female STEM faculty as they pursue research initiatives that are likely to support promotion.

    Champions

    • Weslene Tallmadge, Ph.D., Department of Chemistry, Associate Professor and Chair
    • Sreela Sasi, Ph.D., Department of Computer and Information Science, Professor

    Description

    The Research Initiation Award (RIA) provides release time and funds to female, assistant or associate professors to conduct research projects that will enhance their ability to compete successfully for external funding and achieve advancement in rank.  One award will be granted in each of the years 2012, 2013, 2014 and 2015.  The successful applicant will be awarded a total grant of $7,500 and three credits of release time each semester for the two year period of the award.  The RIA provides funds for adjunct faculty to cover the 3 credits of release time.  The awardees are summarized in the following table.

    Year  Awardees Department
    2015 Lisa Nogai, Ph.D. Chemistry
    2014 Quyen Aoh, Ph.D. Biology
    2013      Lin Zhao, Ph.D. Electrical and Computer Engineering
    2012 Sarah Ewing, Ph.D. Biology

    ELIGIBILITY

    The award application is available to full-time, tenure-track, female faculty at the associate or assistant level with appointments in Biology, Chemistry, Computer & Information Science, Electrical & Computer Engineering, Environmental Science, Mathematics, Mechanical Engineering, Physics, Psychology and Software Engineering.

    SELECTION CRITERIA

    Successful proposals will define a  project for which preliminary data can be obtained within a two year period; provide a self-contained account of what will be done; demonstrate the likelihood of a significant contribution to the field; and show strong potential to result in publication and presentations.  One award will be granted in each of years 2-5 of the Gannon NSF PAID funding (i.e., a total of four awards during the five year period).

    REVIEW PROCESS

    Proposals are reviewed by an ad-hoc committee appointed by the Gannon University NSF PAID Steering Committee. The review committee will be composed of senior faculty across multiple disciplines. The Steering Committee makes the final determination based on award recommendations of the review committee. Decisions will be made in early April.

    REPORTING

    Award recipients are required to report on the outcomes of their research. Progress reports should include details about research work, new grant proposals submitted, presentations, papers, collaborations, and other related scholarship.

            Progress reports:

    •  One-year Interim Report
    • Two-year Report
    •  Year 5 of PAID grant (May 5, 2016)       

    PROPOSAL FORMAT

    The main body of the proposal must be no more than 2 pages including any pictures, graphs and tables.   An additional page may be used for a bibliography.  The proposal should include the following:

    1. Statement of Research Objectives
    2. Background and Significance  
    3. Methodology
    4. Anticipated Results / Dissemination

     Budget 

    The budget should be no more than one page and should include a list of costs and a narrative justification.   Funds may be requested for capital equipment, supplies, support of a graduate research assistant during any part of the year, summer undergraduate assistant salary, research expendables, and other expenses as justified.

    Both the department chair and the Dean must sign a statement indicating that the three credits of release time each semester for two years will be granted to the award recipient.

    Curriculum Vitae

    Attach a two page CV which includes select papers and publications from the past 5 years.

    An electronic version of the proposal is due to Weslene Tallmadge, Department of Chemistry. You will receive an email confirmation acknowledging receipt of your proposal. 

    References

    The strategy draws on the success of the following ADVANCE programs:

  • Awardees

    2015 Lisa Nogay, Ph.D. Chemistry

    Assistant Professor Department of Chemistry
    Title: Optical Sensors Based on Carbon Nanotube Fluorescence

    Statement of Research Objectives

    The purpose of this study is to construct an optical sensor based on fluorescence from single-walled carbon nanotubes (SWNTs). Nanoscale materials like SWNTs display outstanding sensitivity to analytes in sensing devices, owing to the fact that all carbon atoms in the particle are situated on the surface. However, this same characteristic can be detrimental because any damage that disrupts the SWNT sidewall alters its optical behavior and can interfere with selectivity to a particular analyte. To optimize the performance of SWNTs in optical sensors, we identify the following core objectives.

    • Objective 1: To introduce defect sites in SWNTs systematically using ultrasonic processing.
    • Objective 2: To quantify the average number of defect sites per SWNT for each sample in our library.
    • Objective 3: To correlate SWNT defect density and fluorescence performance.
    • Objective 4: To generate an SWNT sensing device with nanolithography based on our optimized protocol.

    Background and Significance

    An SWNT can be envisioned as a hexagonal grid of carbon atoms rolled into a narrow cylinder (Fig. 1). All nanotube synthesis methods generate mixtures of SWNTs that have different diameters, lengths, chiralities and electronic properties. Semiconducting varieties of SWNTs display size-tunable fluorescence, possess exceptional photostability and exhibit higher luminescence quantum yields than most other near-infrared emitters. Such qualities are highly sought-after for biological sensing and optoelectronic applications. However, numerous sidewall defects are generated during nanotube synthesis and subsequently when they are encapsulated in wrapping agents, a processing step needed to prevent interactions between neighboring nanotubes during optical measurements. SWNTs have been isolated successfully for optical measurements and even sorted according to structure, yet the necessary processing techniques remain harsh and the sorting methods complex. The current study is significant because we have an incomplete understanding of the relationship between sidewall defects and SWNT optical properties, which has limited their incorporation into fluorescence-based devices. Surprisingly absent from the literature is a systematic study showing how the luminescence properties of SWNTs are altered by structural defects generated during ultrasonic processing.

    Anticipated Results and Dissemination

    Initially, we expect that as samples are processed for longer times and at higher power levels, both the absorbance and fluorescence intensities will increase until we observe a critical defect density at which SWNTs suddenly do not fluoresce. If successful, this research would firmly define the link between SWNT optical properties and structural defects, leading to development of improved standard samples and enabling straightforward comparison of results between different laboratories. Our measurements will make it possible to perceive how SWNTs, especially with an improved control over structural imperfections, might finally be incorporated into commercially relevant products like near-infrared biological labels and optical sensors.

    2014 Quyen Aoh, Ph.D. Biology

    Assistant Professor, Department of Biology
    Title: The Role of Trafficking from the trans-Golgi Network and Endosomes in Cell Survival

    Research Objectives

    Membrane traffic, the movement of proteins between subcellular compartments, is vital to cell survival and is often dysregulated in human diseases such as cancer, cardiovascular disease, and diabetes. Many of these diseases are also characterized by fundamental changes in metabolism; however, it unclear how these changes regulate and alter membrane traffic. In this proposal, we will use the small budding yeast Saccharomyces cerevisiae to examine how membrane traffic from the trans-Golgi network and endosomes (TGN-E) helps to ensure cell survival during metabolic stress induced by nitrogen and aminoacid starvation. Using a combination of genetic and biochemical methods, we will (1) test if ablating traffic from the TGN-E affects cell survival, (2) determine if TGN-E trafficking is required to deliver dispensable proteins,  and (3) examine how amino acid sensing signaling pathways alter TGN-E traffic during nitrogen and amino acid starvation. Because the metabolism of yeast can mimic both normal and cancerous cells, our studies will provide important insight into mechanisms that ensure normal cell survival and that cancer cells may manipulate to outcompete other cells.

    Background and Significance

    A distinguishing feature of eukaryotic organisms is the compartmentalization of the cell into smaller membrane-bound organelles. These organelles sequester specific and fundamental cellular functions such as protein synthesis and degradation, detoxification, and lipid production. The ability to move and transport proteins and other cargo between organelles, collectively called membrane traffic, is essential for organelle function. Trafficking at the TGN-E is important for delivering and regulating the localization of proteins that function at the cell surface. These include nutrient transporters, such as the insulin regulated glucose transporter GLUT4 implicated in Type II diabetes and signaling receptors implicated in cancers, such as the epidermal growth factor receptor. TGN-E trafficking also regulates the delivery of proteins to the lysosome, a primarily a degradative compartment, that prevents tumorigenic signaling and is vital for survival following acute cellular starvation (Leto and Saltiel, 2012; Shachar et al., 2011; Woodman, 2009).

    Cell survival is dependent on homeostasis, the ability to maintain a constant internal environment despite changes in the surrounding environment. This includes maintaining a steady supply of nitrogen and amino acids, which are required for DNA, protein, and vitamin synthesis. Cells generally maintain low intracellular reserves of nitrogen and amino acids; therefore, the cell imports a large amount of nitrogen and amino acids from the extracellular environment.  Acute changes to the environment, such as amino acid starvation, lead to immediate cellular stress. An immediate survival response to replenish the cell’s supply of free amino acids is mounted by altering the traffic of dispensable proteins to lysosome/vacuole for degradation. The internalization and degradation of plasma membrane proteins has been shown to be a source of dispensable proteins (Jones et al., 2012). However, the TGN-E is a major hub of newly synthesized proteins and diverting traffic from TGN-E to the vacuole may significantly contribute to this supply. The focus of this proposal will be to examine the role of the TGN-E in delivering dispensable proteins following nitrogen and amino acid starvation.

    The various steps in trafficking cargo, from sorting and packaging cargo into transport vesicles and then directing vesicles to their target destination involves a number of proteins and protein complexes. Dysfunctions in or the inability to regulate trafficking proteins at the TGN-E is associated with many types of diseases and disorders including cancer, diabetes, and neurodegeneration (Bryant et al., 2002; Liang et al., 2008; Tian and Abel, 2001; Woodman, 2009). In yeast, a number of proteins, called adaptors, are responsible for sorting and packaging cargo into transport vesicles at the TGN-E. These include the clathrin adaptors (Gga2, Ent5, Ent3, and AP-1), the AP-3 complex, and Ent4 (Aoh et al., 2011; Costaguta et al., 2006; Deng et al., 2009). Ablation of these adaptors often leads to a growth defect, suggesting they are important for cell survival. We will directly test if ablation of these adaptors affects survival during acute nitrogen and amino acid starvation.

    I will utilize the yeast Saccharomyces cerevisiae to examine TGN-E trafficking. Many trafficking pathways are similar in yeast and metazoans, such that human proteins can frequently complement for the loss of yeast proteins and vice versa. Indeed, studies in yeast laid the foundation for our understanding of trafficking. Yeast offer many technical advantages that will be essential for dissecting the role of TGN-E trafficking in cell survival. In addition to standard biochemical methodologies, the ease of genetic manipulation makes mutant construction simple. The ability to examine genetic interactions using high- throughput genetic and biochemical screening assays using commercially available mutant libraries will be a powerful tool to understand how signaling can affect TGN-E traffic.

    2013 Lin Zhao, Ph.D. Electrical and Computer Engineering

    Lin Zhao, Department of  Electrical and Computer Engineering, Associate Professor, http://www.gannon.edu/FacultyProfiles.aspx?profile=zhao001
    Title: Doubly-Fed-Induction-Generator Modeling and Control for Wind Energy Harvesting

    Statement of Research Objectives and Background and Significance

    USA Department of Energy (DOE) has initiated "20 percent wind energy by 2030" in response to the energy crisis and finding alternative/renewable energy resources. For large scale wind farms, variable-speed generators (including DFIG) are widely used due to their better controllability and low maintenance cost. However, issues and challenges are still present in the research areas of the modeling, analysis and control of DFIG. The proposed project is to develop accurate dynamic models of DFIG and a HiTL system of DFIG. Upon completion of the project, variant operation and control techniques of the DFIG wind turbine will be able to be simulated with the virtual model in real time. The developed HiTL system will act as a down-sized wind farm in a lab environment to test the feasibility and controllability of different types of control strategies and fault-ride-thorough techniques.

    The overall objectives of this proposal are to:

    • Develop a hardware-in-the-loop (HiTL) system of the doubly-fed-induction-generator (DFIG) in order to investigate different types of control strategies and fault-ride-through techniques for large scale wind farm operation
    • Gain research experience and publication for external funding competition and advancement in rank
    • Encourage female engineering students' participation in research activities

    The significance of the proposed research has three folds:

    1. Significant impact on DFIG research. The expected research outcomes will mimic and predict the dynamic operation of DFIG during wind energy harvesting and provide guidelines to avoid the fault case. The HiTL down-sized wind farm in the lab environment will provide an economic testing workbench to emulate different scenarios with optimum control strategies to ensure stable electricity generation and transmission. This concept will be among the first of its kind.
    2. Significant impact on my professional development and expertise. This provides me with much needed opportunity to establish a vital research area which is expected to lead to external funding application and advancement in rank.
    3. Significant impact on student's research and engaging female students in research. Technical skills in DFIG & electric drives in general have high demanding from industry. My research activities will provide students (especially female students) with research experience much needed by industry. 

    2012 Sarah Ewing, Ph.D. Biology

    Sarah Ewing, Department of Biology, Assistant Professor, http://www.gannon.edu/FacultyProfiles.aspx?profile=ewing003
    Title: Effect of Manganese on Dopamine Metabolism and Dopaminergic Cell Toxicity

    Statement of Research Objectives and Background and Significance

    Parkinson’s disease (PD) is a progressive neurodegenerative disorder pathologically characterized by loss of dopamine-producing neurons in the substantia nigra pars compacta (SNpc) of the brain (1-3). Loss of dopamine production and signaling is responsible for many symptoms associated with the disease including resting tremor, rigidity, bradykinesia and postural instability (1-3). Despite vast efforts, the causes of PD and specific death of dopamine-producing neurons in the SNpc are still poorly understood (1-3). Many theories have been proposed to explain the etiology of PD including one called the “catecholamine/catecholaldehyde hypothesis” (1, 3-4). This hypothesis suggests dopamine and its metabolism are toxic because of production and accumulation of toxic metabolites, specifically, 3, 4–dihydroxylphenylacetaldehyde (DOPAL). DOPAL accumulation occurs particularly in response to mitochondrial dysfunction and oxidative stress, which inhibits further degradation to the less toxic metabolite, 3, 4-dihydroxyphenylglycolaldehyde (DOPAC) (1, 2, 4-7). Evidence has also led scientists to look for an environmental role in PD. Rural living, farming as an occupation, drinking well water, and pesticide exposure have all been associated with an increase in one’s susceptibility for developing sporadic PD (2). Exposure to high levels of manganese through mining, welding or exposure to pesticides containing manganese (Maneb) also results in a Parkinsonism-like disease (8-10). Many of these environmental agents including manganese elicit their effects in dopaminergic cells by blocking mitochondrial function and inducing oxidative stress (1, 2, 11-14).

    The overall objective of this proposal is to investigate the effects of manganese on dopamine (DA) metabolism and toxicity in dopaminergic cells. Specifically, we hypothesize manganese has the ability to 1) elicit increased levels of DOPAL in dopaminergic cells and 2) increase dopaminergic cell toxicity when combined with elevated levels of DA or DOPAL compared to treatment with DA and/or DOPAL alone.

    To address these hypotheses I propose the following specific aims:

    1. To determine whether or not manganese disrupts the levels of dopamine metabolites in cultured dopaminergic cells over time in a dose dependent manner.
    2. To determine whether or not manganese increases dopaminergic cell toxicity over time in response to excess 1) dopamine (DA) 2) DOPAL or 3) DOPAL quinone.

    The results of this study will provide the first evidence linking manganese to DOPAL levels in dopaminergic cells and further elucidate the effects of manganese on DA-induced toxicity in these cells. These findings could therefore contribute to our overall understanding of the mechanism through which manganese elicits neuronal cell toxicity and a potential means through which manganese may contribute to the etiology of Parkinson’s disease.