RSS 1.0Welcome 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.
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Physical inactivity and sedentary behavior negatively impact postural balance and gaitBackground: The benefits of physical activity (PA) do not depend on the PA level, but also on sedentary behavior (SB). An interaction between PA and SB (i.e., PA-SB interplay) is important to determine one’s health status. This study explored the effect of PA-SB interplay on balance and gait in healthy young adults.Methods: Healthy young adults (n = 133, 18-35 yrs) were placed in four PA-SB interplay groups using the American College of Sports Medicine PA guidelines (i.e., sedentary active [>6hr/day, >150min/week], sedentary inactive [>6hr/day, <150min/week], physically active [<6hr/day, >150min/week] and physically inactive [<6hr/day, <150min/week]). Participants’ balance and gait were assessed with inertial measurement units placed on seven bodily sites. Significance level was set at p < 0.1. Results: Sway acceleration RMS during eyes closed on stable surface in the balance test showed a statistically significant difference among the PA-SB interplay groups (p = 0.055) which was found between sedentary active and physically inactive (p = 0.066). Anticipatory postural adjustment (APA) duration during gait showed a statistically significant difference among the PA-SB interplay groups (p = 0.010) which was found between sedentary inactive and physically active (p = 0.019) and between sedentary active and physically active (p = 0.026). Conclusion: PA-SB interplay influences static (sway acceleration RMS) and dynamic balance (APA duration) of healthy young adults. Findings suggest that somatosensory processing during balance and gait initiation are significantly impacted by PA-SB interplay. Future studies should explore PA-SB interplay on balance and gait in elderly and diseased populations.
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Predicting Customer Churn in the Telecom Sector Using Machine LearningTelecom companies spend a lot to acquire new customers, making it crucial to retain these customers and ensure they continue using their plans. Churn refers to customers leaving their current service provider for another one. Once companies secure a long-term customer, they can profit significantly from them. Therefore, customer churn is a major concern for a company’s revenue and business growth, especially in the competitive telecommunications industry. By analyzing customer behavior and the services they use, companies can predict churn. This predictive capability allows them to minimize losses and enhance their business performance.
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Nanotherapeutics for Immune Modulation in SepsisDue to its complexity and heterogeneity, managing immune dysregulation in sepsis poses a significant clinical challenge. Thus, there is great demand to both improve our understanding of mediators of immune dysregulation in sepsis and develop nuanced therapeutic approaches to provide precise immune modulation for sepsis treatment. This thesis first investigates the novel phenomenon of cytokine charge disparity as a potential regulator of cytokine function. Then, two novel telodendrimer immune modulation approaches are presented as a personalized medicine strategy for sepsis. Through extensive database and literature review, we have established cytokine charge disparity as a potential mechanism for immune regulation. Using our versatile telodendrimers (TDs), we then optimized and validated our TD nanotrap approach for effective and selective targeting of plasma cytokines. Our lead selective TD nanotraps displayed charge selective cytokine targeting and our lead pan-affinitive TD nanotrap demonstrated superior cytokine removal efficacy compared to commercial resin control. Additionally, pan-affinitive TD nanotrap maintained efficacy across a wide range patient immune status, indicating promising therapeutic potential to reduce mortality risk associated with overwhelming cytokine profiles. To further expand our immune modulation tool set for sepsis treatment, we optimized our TD nanodrug for delivery of dimethyl itaconate (ITA) to control both hyperinflammation and pyroptosis. Encapsulating ITA into TD nanoparticles (ITA:TDNPs) resulted in a sustained-release profile and improved biocompatibility compared to free ITA. ITA:TDNPs more effectively inhibited both LPS- and LTA-induced inflammation and pyroptosis in macrophages compared to ITA or TDNP alone. Finally, ITA:TDNPs demonstrated superior therapeutic efficacy in both an IV LPS and polymicrobial cecal slurry sepsis model compared to individual therapies. Collectively, we have uncovered a novel phenomenon of cytokine charge disparity and validated it as a potential mechanism to regulate cytokine activity, as well as established it as targeting mechanism for effective immune modulation via charge selective TD nanotrap. We further developed an immune modulating TD nanodrug for ITA delivery to control both hyperinflammation and immune cell pyroptosis in sepsis. Through precise targeting of immune dysregulation in sepsis using a systematic multimodal TD therapeutic approach for personalized medicine, we may successfully improve patient outcomes in this devastating disease.
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Mechanism of Mitochondria-Induced Muscle Atrophy During AgingMitochondrial dysfunction is strongly associated with aging-related degenerative diseases including muscle atrophy. However, whether bioenergetic defects are the sole drivers of mitochondria-induced muscle atrophy remains unknown. The Chen lab discovered that various forms of mitochondrial damage can disrupt protein import, leading to the toxic accumulation of unimported mitochondrial precursors in the cytosol. This causes a stress termed mitochondrial Precursor Over-accumulation Stress (mPOS). A mouse model of mPOS was developed in which the mitochondrial inner membrane protein, ANT1, was overexpressed to saturate the protein import machinery. Ant1Tg/+ mice were found to have a severe muscle wasting phenotype. The overarching goal of this dissertation is to investigate the mechanism by which mPOS drives muscle wasting and its implications for normative muscle aging. The findings presented in this thesis led to three conclusions. First, we identified a novel mitochondria-to-lysosomal proteostatic axis through which mPOS induces lysosomal damage. Lysosomal damage subsequently causes the release proteolytic enzymes, which leads to excessive protein degradation and subsequent progressive muscle atrophy. Importantly, we found that this pathway operates independently of mitochondrial respiratory complex activity and reactive oxygen species (ROS) production. Second, we demonstrated the presence of mPOS in physiologically aged muscle. Sarcopenic muscle exhibited phenotypes similar to those found in Ant1Tg/+ mice, evidenced by overlapping transcriptional and proteomic profiles, and lysosomal damage. These findings indicate that mitochondria-induced changes to autophagic activity may play a central role in the pathogenesis of sarcopenia. However, considering the overall protein content of muscle is elevated during aging, we propose that reduced protein quality, rather than absolute protein content, drives sarcopenia. We therefore termed this phenomenon Muscle Atrophy Independent of Protein Content (MAIPC). Finally, we explored additional cellular factors that affect proteostasis and muscle mass maintenance. We found that the GCN2 kinase, a well-established activator of the Integrated Stress Response (ISR), plays a role in protecting myofibers from mPOS-induced stress and muscle wasting in Ant1Tg/+ muscle. Interestingly, we found that this effect is ISR-independent. The data presented in this dissertation provide valuable insights into the mechanistic role of mitochondrial dysfunction in both normative aging and chronic muscle wasting conditions. Our findings conclude that mitochondria-induced muscle atrophy is induced by mechanisms that extend beyond bioenergetic defects. By characterizing these alternative pathways, this work opens new avenues for therapeutic strategies targeting mitochondrial stress in chronic muscle wasting conditions.
