Open Access Pilot Awards

Permanent URI for this collectionhttps://hdl.handle.net/10675.2/625013

The Augusta University Faculty Senate (AUFS) launched a pilot program in fall 2023 to finance article and monograph processing fees (APCs) for faculty members who wish to publish their research in eligible open-access, peer-reviewed journals. The Office of the Provost supports the program in collaboration with the AUFS, the University Libraries, and the Office of the Senior VP for Research. The program is being administered through the University Libraries. The program aims to increase the visibility and accessibility of Augusta University's research and scholarship by supporting faculty members in publishing their work in open-access journals. It also works towards creating greater equality of access to information, highlighting student success activities, and contributing towards the Carnegie Community Engagement Classification aspirational imperative. Each college and school was eligible for up to four awards until December 31, 2023, after which the approved requests will be awarded on a first-come, first-serve basis.

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Recent Submissions

Now showing 1 - 8 of 8
  • ItemOpen Access
    Changes in Body Weight and Lifestyle Behaviors among U.S. Adults following the Introduction of COVID-19 Lockdown: Evidence from the Behavioral Risk Factor Surveillance System
    (Wiley, 2021-11-22) Qiu, Qihua; Davis, Will; Sung, Jaesang; Augusta University
    The COVID-19 pandemic and its associated policies may impact body weight in a variety of ways. Using data from the 2018-2020 waves of the Behavioral Risk Factor Surveillance System (BRFSS), we estimate the COVID-19 pandemic’s effect on Body Mass Index and the probability of obesity for adults in the United States. Using a difference-in-differences framework which relies on the plausibly exogenous timing of COVID-19 lockdown as an indicator of when individuals’ lives were first affected by the pandemic, we find statistically significant associations between the introduction of initial lockdown and body weight gain. Event study results suggest that adults experience a temporary decrease in body weight following the first month of lockdown and an increase in body weight as time since initial lockdown increases. We find larger effects for men but more persistent effects for women, as well as greater and more persistent effects for non-white adults, less-educated adults, and adults living in more densely populated states. Analyzing potential mechanisms driving the observed increase in body weight, we find evidence of potential changes in diets and sedentary behaviors following initial lockdown based on increased Google search intensity for terms related to food delivery, high calorie foods, and video streaming platforms.
  • ItemOpen Access
    The protective role of CD73 in periodontitis: preventing hyper-inflammatory fibroblasts and driving osteoclast energy metabolism
    (Frontiers, 2023-12-13) Morandini, Ana Carolina; Ramos-Junior, Erivan S; Dawson, Shantiece; Ryan, Weston; Clinebell, Braden; Serrano- Lopez, Rogelio; Russell, Marsha; Brumbaugh, Rylee; Zhong, Roger; Fernandes, Jussara Goncalves; Shaddox, Luciana M.; Cutler, Christopher W.; Augusta University
    Periodontitis is an immune-mediated inflammatory disease affecting almost half of the adult population and is the leading cause of tooth loss in the United States. The role of extracellular nucleotide signaling including nucleotide metabolizing enzyme CD73 adds an important layer of interaction of purine mediators capable of orchestrating inflammatory outcomes. CD73 is able to catabolize 5′-adenosine monophosphate into adenosine at the extracellular level, playing a critical role in regulating many processes under physiological and pathological conditions. Here, we explored the role of CD73 in ligature-induced periodontitis in vivo comparing wild-type C57Bl/6J and CD73-deficient mice.
  • ItemOpen Access
    Identification of small molecules that suppress cell invasion and metastasis promoted by WASF3 activation
    (Science Direct, 2023-10) Silva, Jeane; Omar, Nivin; Sittaramane, Vinoth; Cowell, John K.; Augusta University
    The WASF3 gene promotes cancer cell invasion and metastasis, and genetic inactivation leads to suppression of metastasis. To identify small molecules that might interfere with WASF3 function, we performed an in silico docking study to the regulatory pocket of WASF3 using the National Cancer Institute (NCI) diversity set VI small molecule library. Compounds that showed the maximum likelihood of interaction with WASF3 were screened for their effect on cell movement in breast and prostate cancer cells, a well-established predictor of invasion and metastasis. Three hit compounds were identified that affected cell movement, and the same compounds also suppressed cell migration and invasion in vitro in both MDA-MB-231 breast cancer cells and Du145 prostate cancer cells. Using a zebrafish metastasis assay, one of these compounds, NSC670283, showed significant suppression of metastasis in vivo while not affecting cell proliferation. NSC670283 showed a consistent effect on suppression of invasion and metastasis, and cellular temperature shift assays provided support for physical interaction with WASF3. In addition, suppression of cell movement and invasion was accompanied by a decrease in actin filament polymerization. The data in this study suggest that these small molecules inhibit cancer cell invasion and metastasis, and to our knowledge, it is the first identification of a small molecule that can potentially inhibit WASF3-directed metastasis, laying the foundation for medicinal chemistry approaches to enhance the potency of the identified compounds.
  • ItemOpen Access
    Crisis Leadership and Moral Rhetoric After a Foreign Attack on the Homeland: Zelenskyy, Bush, and Churchill
    (Sage Journals, 2024-03) Murray, Gregg R.; Sandlin, Grantham; Tatalovich, Raymond; Augusta University
    What kind of moral rhetoric do national leaders use after their homelands are attacked by foreign forces? Informed by crisis leadership literature, this study uses Moral Foundations Theory (MFT) to examine the rhetoric of three leaders of nations before and after attacks by foreign forces: Ukrainian President Zelenskyy and the 2022 Russian invasion, U.S. President Bush and the September 11, 2001, terrorist attacks, and British Prime Minister Churchill and the 1940–41 German bombing campaign. The word-based automated content analysis shows that following the attacks the leaders substantially shifted their moral rhetoric. They also employed similar moral rhetoric, mainly by using Harm rhetoric, presumably to condemn the destruction and loss of life suffered by their nations. All three also emphasized Loyalty rhetoric, presumably as a call to nationalism, and Authority rhetoric, presumably to rally followership. Otherwise, they gave little attention to Degradation rhetoric, which presumably would demonize the enemy. This study is one of very few to evaluate political elite rhetoric during crises. It is also one of a small number to assess political elite rhetoric through the lens of MFT. It demonstrates that MFT can be a useful tool for understanding political elite rhetoric and crisis management across heterogeneous contexts.
  • ItemOpen Access
    Multiplex analysis of inflammatory proteins associated with risk of coronary artery disease in type‐1 diabetes patients
    (Wiley, 2023-08-21) Beatty, Carol; Richardson, Katherine P.; Tran, Paul M.H.; Satter, khaled B.; Hopkins, Diane; Melissa, Gardiner; Sharma, Ashok; Purohit, Sharad; Augusta University
    Background: Chronic uncontrolled hyperglycemia, a precursor to chronic low‐grade inflammation, is a leading cause of coronary artery disease (CAD) due to plaque buildup in type‐1 diabetes (T1D) patients. We evaluated levels of 22 inflammatory markers in cross‐sectional serum samples from 1222 subjects to evaluate their potential as risk factors for CAD in T1D patients. Hypothesis: Circulating levels of markers of inflammation may be the risk factors for incident CAD. Methods: The T1D subjects were divided into two groups: those without CAD (n = 1107) and with CAD (n = 115). Serum levels of proteins were assayed using multiplex immunoassays on a Luminex Platform. Differences between the two groups were made by univariate analysis. Multivariate logistic regression was used to ascertain the potential of proteins as risk factors for CAD. Influence of age, duration of diabetes, sex, hypertension, and dyslipidemia was determined in a stepwise manner. Serum levels of 22 proteins were combined into a composite score using Ridge regression for risk‐based stratification. Results: Mean levels of CRP, IGFBP1, IGFBP2, insulin‐like growth factors binding protein‐6 (IGFBP6), MMP1, SAA, sTNFRI, and sTNFRII were elevated in CAD patients (n = 115) compared to T1D patients without CAD (nCAD, n = 1107). After adjusting for age, duration of diabetes, sex, hypertension, and dyslipidemia, higher levels of sTNFRI (odds ratio [OR] = 2.18, 1.1 × 10−3), sTNFRII (OR = 1.52, 1 × 10−2), and IGFBP6 (OR = 3.62,1.8 × 10−3) were significantly associated with CAD. The composite score based on Ridge regression, was able to stratify CAD patients into low, medium, and high‐risk groups. Conclusions: The results show activation of the TNF pathway in CAD patients. Evaluating these markers in serum can be a potential tool for identifying high‐risk T1D patients for intensive anti‐inflammatory therapeutic interventions.
  • ItemOpen Access
    Production of a p65fl/fl/LysMCre mouse model with dysfunctional NF-kappaB signaling in bone marrow-derived macrophages
    (Sage Journals) Bradford, jennifer W; Korkaya, Ahment K; Fischer, Jeffrey; Peppers, Anthony; Crosson, Sean; Rayamajhi, Manira; Miao, Edward A; Baldwin Jr, Albert S; Augusta University
    Here, we describe the production and characterization of a novel p65fl/fl/LysMCre mouse model, which lacks canonical nuclear factor-kappaB member RelA/p65 (indicated as p65 hereafter) in bone marrow-derived macrophages. Cultured bone marrow-derived macrophages that lack p65 protein reveal NF-κB signaling deficiencies, a reduction in phagocytic ability, and reduced ability to produce nitrites. Despite abnormal bone marrow-derived macrophage function, p65fl/fl/LysMCre mice do not exhibit differences in naïve systemic immune profiles or colony forming units and time to death following Salmonella infection as compared to controls. Additionally, p65fl/fl/LysMCre mice, especially females, display splenomegaly, but no other obvious physical or behavioral differences as compared to control animals. As bone marrow-derived macrophages from this transgenic model are almost completely devoid of canonical nuclear factor-kappaB pathway member p65, this model has the potential for being very useful in investigating bone marrow-derived macrophage NF-kappaB signaling in diverse biological and biomedical studies.
  • ItemOpen Access
    Decolonizing Botany: Indonesia, UNESCO, and the Making of a Global Science
    (2023-10-11) Goss, Andrew; Augusta University
    Decolonization created new opportunities for international scientific research collaboration. In Indonesia this began in the late 1940s, as Indonesian scientists and officials sought to remake the formerly colonial botanical gardens in the city of Bogor into an international research center. Indonesia sponsored the Flora Malesiana project, a flora of all of island Southeast Asia. This project was formally centered in Bogor, Indonesia, with participation from tropical botanists from around the world. The international orientation of Indonesian science led to the establishment of one of UNESCO’s Field Science Co-operation Offices in Jakarta, and to a period of close collaboration between Indonesian botanists and UNESCO. This paper examines the importance of UNESCO’s Humid Tropics research program, which initially provided further opportunities for Indonesian botanists to participate in international scientific networks. The paper concludes by showing that the Humid Tropics program led to the slow erosion of Indonesian agency and authority over tropical botany, and the assertion of Western control and management over tropical botany research.
  • ItemOpen Access
    Calbindin 2-specific deletion of arginase 2 preserves visual function after optic nerve crush
    (Cell Death & Disease, 2023-10) Zaidi, Syed A.H.; Xu, Zhimin; Lemtalsi, Tahira; Sandow, Porsche; Athota, Sruthi; Liu, Fang; Haigh, Stephen; Huo, Yuqing; Narayanan, S. Priya; Fulton, David J.R.; Rojas, Modesto A.; Fouda, Abdelrahman Y.; Caldwell, Robert W.; Caldwell, Ruth B.
    We previously found that global deletion of the mitochondrial enzyme arginase 2 (A2) limits optic nerve crush (ONC)-induced neuronal death. Herein, we examined the cell-specific role of A2 in this pathology by studies using wild type (WT), neuronal-specific calbindin 2 A2 KO (Calb2cre/+ A2 f/f), myeloid-specific A2 KO (LysMcre/+ A2f/f), endothelial-specific A2 KO (Cdh5cre/+ A2f/f), and floxed controls. We also examined the impact of A2 overexpression on mitochondrial function in retinal neuronal R28 cells. Immunolabeling showed increased A2 expression in ganglion cell layer (GCL) neurons of WT mice within 6 h-post injury and inner retinal neurons after 7 days. Calb2 A2 KO mice showed improved neuronal survival, decreased TUNEL-positive neurons, and improved retinal function compared to floxed littermates. Neuronal loss was unchanged by A2 deletion in myeloid or endothelial cells. We also found increased expression of neurotrophins (BDNF, FGF2) and improved survival signaling (pAKT, pERK1/2) in Calb2 A2 KO retinas within 24-hour post-ONC along with suppression of inflammatory mediators (IL1β, TNFα, IL6, and iNOS) and apoptotic markers (cleavage of caspase3 and PARP). ONC increased GFAP and Iba1 immunostaining in floxed controls, and Calb2 A2 KO dampened this effect. Overexpression of A2 in R28 cells increased Drp1 expression, and decreased mitochondrial respiration, whereas ABH-induced inhibition of A2 decreased Drp1 expression and improved mitochondrial respiration. Finally, A2 overexpression or excitotoxic treatment with glutamate significantly impaired mitochondrial function in R28 cells as shown by significant reductions in basal respiration, maximal respiration, and ATP production. Further, glutamate treatment of A2 overexpressing cells did not induce further deterioration in their mitochondrial function, indicating that A2 overexpression or glutamate insult induce comparable alterations in mitochondrial function. Our data indicate that neuronal A2 expression is neurotoxic after injury, and A2 deletion in Calb2 expressing neurons limits ONC-induced retinal neurodegeneration and improves visual function.