Welcome to the SUNY Open Access Repository
The SUNY Open Access Repository (SOAR) is a centrally managed online digital repository that stores, indexes, and makes available scholarly and creative works of SUNY faculty, students, and staff across SUNY campuses. SOAR serves as an open access platform for those SUNY campuses that do not have their own open access repository environments.
Access to SUNY campus communities in SOAR are available below under SUNY sectors and also listed alphabetically under the Campus Communities in SOAR on the navigation bar on the left.
Additional information includes
- Approved SUNY Campus Open Access Policies (clicking on this link will take you out of SOAR)
- Links to additional SUNY repositories
- SOAR guidelines
Communities in SUNY Open Access Repository
Select a community to browse its collections.
Recently Added
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Ocean CleanupEcologist and marine/fishery biologist Simon Reddy states, "the weight of ocean plastics will exceed the combined weight of all fish in the seas by 2050" (2018). The matter of climate change and surrounding concerns are often brought up but continuously brushed off by individuals and countries alike. However, after digging deeper into this subject, it quickly becomes apparent how serious this is. This essay explores the severity of plastic pollution in the oceans, explains what the Great Pacific Garbage Patch is, how this issue is impacting both people and animals, and possible solutions, specifically the work being done by the Ocean Cleanup.
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Older Adults, Retirement Income, and LifestyleAlthough the retirement period comes at the end of one's laborious working life, there is no certainty that one can live comfortably during these years. To support oneself during retirement, one must accrue enough income and benefits to last until death. Retirement can only be pursued with a sufficient amount of income. One must understand the fundamentals of retirement income to understand retirement as a whole. This literature review will explore how retirement income impacts an older adult's retirement lifestyle. Key topics of this question include the influence of individual characteristics, like gender, ethnicity, and immigrant status, on the type of retirement income received. Social forces, such as type of pension reform, geographic location, and economic events, will be investigated for their impact on an older adult's retirement income. The direct influence of retirement income on health will also be explored to fully understand the role retirement income plays in an older adult's life. Using online databases, these sources were analyzed and included based on their thorough discussion of retirement income and how detailed they are in their explanation of what happened to an older adult when types of retirement income were provided.
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Computational Approaches to Understanding the Role of Fibroblast-Myocyte Interactions in Cardiac ArrhythmogenesisThe adult heart is composed of a dense network of cardiomyocytes surrounded by nonmyocytes, the most abundant of which are cardiac fibroblasts. Several cardiac diseases, such as myocardial infarction or dilated cardiomyopathy, are associated with an increased density of fibroblasts, that is, fibrosis. Fibroblasts play a significant role in the development of electrical and mechanical dysfunction of the heart; however the underlying mechanisms are only partially understood. One widely studied mechanism suggests that fibroblasts produce excess extracellular matrix, resulting in collagenous septa. These collagenous septa slow propagation, cause zig-zag conduction paths, and decouple cardiomyocytes resulting in a substrate for arrhythmia. Another emerging mechanism suggests that fibroblasts promote arrhythmogenesis through direct electrical interactions with cardiomyocytes via gap junctions. Due to the challenges of investigating fibroblast-myocyte coupling in native cardiac tissue, computational modeling and in vitro experiments have facilitated the investigation into the mechanisms underlying fibroblast-mediated changes in cardiomyocyte action potential morphology, conduction velocity, spontaneous excitability, and vulnerability to reentry. In this paper, we summarize the major findings of the existing computational studies investigating the implications of fibroblast-myocyte interactions in the normal and diseased heart. We then present investigations from our group into the potential role of voltage-dependent gap junctions in fibroblast-myocyte interactions.
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Cell-Specific Cardiac Electrophysiology ModelsThe traditional cardiac model-building paradigm involves constructing a composite model using data collected from many cells. Equations are derived for each relevant cellular component (e.g., ion channel, exchanger) independently. After the equations for all components are combined to form the composite model, a subset of parameters is tuned, often arbitrarily and by hand, until the model output matches a target objective, such as an action potential. Unfortunately, such models often fail to accurately simulate behavior that is dynamically dissimilar (e.g., arrhythmia) to the simple target objective to which the model was fit. In this study, we develop a new approach in which data are collected via a series of complex electrophysiology protocols from single cardiac myocytes and then used to tune model parameters via a parallel fitting method known as a genetic algorithm (GA). The dynamical complexity of the electrophysiological data, which can only be fit by an automated method such as a GA, leads to more accurately parameterized models that can simulate rich cardiac dynamics. The feasibility of the method is first validated computationally, after which it is used to develop models of isolated guinea pig ventricular myocytes that simulate the electrophysiological dynamics significantly better than does a standard guinea pig model. In addition to improving model fidelity generally, this approach can be used to generate a cell-specific model. By so doing, the approach may be useful in applications ranging from studying the implications of cell-to-cell variability to the prediction of intersubject differences in response to pharmacological treatment.
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Illuminating Myocyte-Fibroblast Homotypic and Heterotypic Gap Junction Dynamics Using Dynamic ClampFibroblasts play a significant role in the development of electrical and mechanical dysfunction of the heart; however, the underlying mechanisms are only partially understood. One widely studied mechanism suggests that fibroblasts produce excess extracellular matrix, resulting in collagenous septa that slow propagation, cause zig-zag conduction paths, and decouple cardiomyocytes, resulting in a substrate for cardiac arrhythmia. An emerging mechanism suggests that fibroblasts promote arrhythmogenesis through direct electrical interactions with cardiomyocytes via gap junction (GJ) channels. In the heart, three major connexin (Cx) isoforms, Cx40, Cx43, and Cx45, form GJ channels in cell-type-specific combinations. Because each Cx is characterized by a unique time- and transjunctional voltage-dependent profile, we investigated whether the electrophysiological contributions of fibroblasts would vary with the specific composition of the myocyte-fibroblast (M-F) GJ channel. Due to the challenges of systematically modifying Cxs in vitro, we coupled native cardiomyocytes with in silico fibroblast and GJ channel electrophysiology models using the dynamic-clamp technique. We found that there is a reduction in the early peak of the junctional current during the upstroke of the action potential (AP) due to GJ channel gating. However, effects on the cardiomyocyte AP morphology were similar regardless of the specific type of GJ channel (homotypic Cx43 and Cx45, and heterotypic Cx43/Cx45 and Cx45/Cx43). To illuminate effects at the tissue level, we performed multiscale simulations of M-F coupling. First, we developed a cell-specific model of our dynamic-clamp experiments and investigated changes in the underlying membrane currents during M-F coupling. Second, we performed two-dimensional tissue sheet simulations of cardiac fibrosis and incorporated GJ channels in a cell type-specific manner. We determined that although GJ channel gating reduces junctional current, it does not significantly alter conduction velocity during cardiac fibrosis relative to static GJ coupling. These findings shed more light on the complex electrophysiological interplay between cardiac fibroblasts and myocytes.