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.

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Recent Submissions

  • PublicationOpen Access
    Evaluating the Potential for Mutualisms to Enhance Restoration Success in Urban Salt Marshes
    (2021-12-15) Whaley, Thomas; Dr. Mark Lesser
    Efforts to restore degraded ecosystems often focus on the effects of single species on ecosystem processes while neglecting the influence of species interactions. Understanding these interactions can expedite the restoration process and prevent unforeseen negative outcomes. Spartina alterniflora (Saltmarsh Cordgrass) and Geukensia demissa (Atlantic Ribbed Mussel) play a foundational role in wetland biogeochemical processes and community structure in coastal marshes throughout the Eastern United States. The relationship between Spartina and Geukensia is widely considered to be a textbook example of a facultative mutualism. Spartina provide structure that promotes Geukensia settlement and shading that protects Geukensia from overheating and desiccation. Geukensia promote the growth of Spartina by transferring nutrients from the water column to sediments. Both species influence biogeochemical processes by altering oxygen and carbon availability in sediments. However, some studies in constructed and urban marshes have indicated that this interaction may be context-dependent, responding to environmental factors such as sedimentation and ambient nutrient availability. We performed a systematic review and meta-analysis to quantify trends in the strength and effects of this mutualism. We looked at how the two species affected biomass and growth of their mutualist, and we quantified the effects of both species on nitrogen-cycling processes. Mutualistic effects are significantly stronger in non-urban than urban systems, and in natural relative to recently constructed wetlands. The effect of the two species on the marsh nitrogen cycle remains relatively the same regardless of context. To determine the ability of Geukensia to recruit to a restored urban Spartina marsh, we examined patterns in the abundance and size distributions of Geukensia population data at two sites within Jamaica Bay (New York, NY), an urban site with significant human impact, over the period of 2005-2012. Elders East was the site of a 40-acre restoration in 2006, and JoCo was monitored as an unmodified reference site. Geukensia abundance and size increased at Elders East beginning two years after restoration, indicating that restored marshes provide suitable habitat for Geukensia. Initial colonization occurred along marsh edges and creek banks. Geukensia abundance declined at JoCo, possibly due to loss of edge habitat in the unrestored marsh. We performed a mussel addition experiment to investigate how the mutualism behaves under different sedimentation conditions. Our sediment depleted site was Elders East in Jamaica Bay, while our sediment replete site was Randall’s Island, an island in NYC’s Harlem River that was also the subject of a Spartina marsh restoration in 2006. We found that Geukensia presence did not significantly influence Spartina growth characteristics or soil organic content in these systems. There were greater differences between sites than between treatment types, but the site differences were still non-significant in most cases. The variability in the outcomes of the Spartina-Geukensia mutualism suggests that care must be taken when incorporating species interactions into habitat management programs.
  • PublicationOpen Access
    Vimentin Cytoskeleton Collapses in Response to the Small Molecule Inhibitor of FH2 Domains (SMIFH2)-Induced Electrophilic Stress
    (2026-01) Capella, Benjamin; Christopher Turner
    Elevated levels of vimentin are detectable in cancerous tissue from malignant neoplasms as well as fibrotic tissue. Vimentin constitutes one of the polymer-based components of the cytoskeleton that regulates cellular morphology and promotes effective and efficient cellular migration and motility. These aspects of cellular behavior contribute to the homeostatic repair of tissue, as evidenced by the trafficking of immune cells and fibroblasts to the lesion site, as well as the progression of pathological conditions, as demonstrated by the invasion of tumor cells through the stromal matrix. Within the cell, the vimentin cytoskeletal network serves as a viscoelastic, load-bearing scaffold that surrounds the nucleus and radiates throughout the cell. Through direct and/or indirect interactions, the vimentin cytoskeleton bidirectionally communicates with the actin and microtubule cytoskeletal networks. To date, the formin family of actin-modifying proteins have not been implicated as mediators of crosstalk between the actin and vimentin cytoskeletal networks. However, recent work in our lab has demonstrated that treatment with the small-molecule inhibitor of formin homology 2 domains (SMIFH2) disrupts vimentin organization and collapses the network to the perinuclear region of the cell. However, this inhibitor has also been found to affect other proteins and cellular pathways independent of formin function. Therefore, potentially uncovering a connection between formins and the vimentin cytoskeleton or discovering the off-target, formin-independent, mechanism that SMIFH2 collapses the vimentin network warrants interest as a necessary research direction in order to expand the area of vimentin-related biomedical research. The work presented in Chapter 2 of this dissertation presents sufficient evidence that the disruptive effect SMIFH2 induces on the vimentin cytoskeleton is the result of the inhibitor's electrophilic characteristic and not formin-dependent inhibition. Importantly, we have shown that formin depletion, actin cytoskeleton disruption, or potential off-target inhibition of actomyosin contractility do not disrupt the vimentin cytoskeleton in a manner similar to SMIFH2 treatment. SMIFH2 exerts its electrophilic effect directly onto vimentin and interferes with network dynamics. These findings, as well as the general discussion in Chapter 3, address whether formins regulate vimentin organization, but also highlight the need to further refine and develop more specific cellular manipulations in order to limit unintended, off-target effects of drugs and therapeutics.
  • PublicationOpen Access
    Is It Too Much to Request a Formal Neurology Consultation After Thoracic Endovascular Aortic Aneurysm Repair?
    (2020-09-06) Awad, Hamdy; Alcodray, Gabriel; Kelani, Hesham; Essandoh, Michael
  • PublicationOpen Access
    Elevated Expression of MiR-17 in Microglia of Alzheimer's Disease Patients Abrogates Autophagy-Mediated Amyloid-β Degradation.
    (2021-07-27) Estfanous, Shady; Daily, Kylene P; Eltobgy, Mostafa; Deems, Nicholas P; Anne, Midhun N K; Krause, Kathrin; Badr, Asmaa; Hamilton, Kaitlin; Carafice, Cierra; Hegazi, Ahmad; Abu Khweek, Arwa; Kelani, Hesham; Nimjee, Shahid; Awad, Hamdy; Zhang, Xiaoli; Cormet-Boyaka, Estelle; Haffez, Hesham; Soror, Sameh; Mikhail, Adel; Nuovo, Gerard; Barrientos, Ruth M; Gavrilin, Mikhail A; Amer, Amal O
    Autophagy is a proposed route of amyloid-β (Aβ) clearance by microglia that is halted in Alzheimer's Disease (AD), though mechanisms underlying this dysfunction remain elusive. Here, primary microglia from adult AD (5xFAD) mice were utilized to demonstrate that 5xFAD microglia fail to degrade Aβ and express low levels of autophagy cargo receptor NBR1. In 5xFAD mouse brains, we show for the first time that AD microglia express elevated levels of microRNA cluster Mirc1/Mir17-92a, which is known to downregulate autophagy proteins. By hybridization in post-mortem AD human tissue sections, we observed that the Mirc1/Mir17-92a cluster member is also elevated in human AD microglia, specifically in the vicinity of Aβ deposits, compared to non-disease controls. We show that NBR1 expression is negatively correlated with expression of in human AD microglia via immunohistopathologic staining in human AD brain tissue sections. We demonstrate in healthy microglia that autophagy cargo receptor NBR1 is required for Aβ degradation. Inhibiting elevated in 5xFAD mouse microglia improves Aβ degradation, autophagy, and NBR1 puncta formation and improves NBR1 expression . These findings offer a mechanism behind dysfunctional autophagy in AD microglia which may be useful for therapeutic interventions aiming to improve autophagy function in AD.
  • PublicationOpen Access
    Mouse Model of Spinal Cord Hypoperfusion with Immediate Paralysis Caused by Endovascular Repair of Thoracic Aortic Aneurysm.
    (2023-04-01) Kelani, Hesham; Corps, Kara; Mikula, Sarah; Fisher, Lesley C; Shalaan, Mahmoud T; Sturgill, Sarah; Ziolo, Mark T; Abdel-Rasoul, Mahmoud; Basso, D Michele; Awad, Hamdy
    BACKGROUND: A clinically relevant mouse model of thoracic endovascular aortic repair-induced ischemic spinal cord injury has been lacking since the procedure was first employed in 1991. The hypothesis was that ligation of mouse intercostal arteries would simulate thoracic endovascular aortic repair-induced ischemic spinal cord injury and behavioral deficit. The aim was to create a mouse model of thoracic endovascular aortic repair-induced spinal cord hypoperfusion by ligating five pairs of mouse intercostal vessels. METHODS: Mice were divided into sham (n = 53) and ligation (n = 60) groups. The procedures called for double ligation of three pairs and single ligation of two pairs of thoracic intercostal arteries in adult C57BL/6 mice. A laser Doppler probe was used in vivo on the spinal cords and intercostal arteries to document the extent of arterial ligation and spinal cord hypoperfusion. The Basso Mouse Scale for Locomotion, histological studies, and electron microscopy demonstrated postligation locomotive and histopathological changes. RESULTS: Ligation induced a significant and instantaneous drop in blood flow in the intercostal arteries (% change; mean = -63.81; 95% CI, -72.28 to -55.34) and the thoracic spinal cord (% change; mean = -68.55; 95% CI, -80.23 to -56.87). Paralysis onset was immediate and of varying degree, with behavioral deficit stratified into three groups: 9.4% exhibited severe paralysis, 37.5% moderate paralysis, and 53.1% mild paralysis at day 1 (n = 32; P < 0.001). Mild and moderate paralysis was transient, gradually improving over time. Severe paralysis showed no improvement and exhibited a higher mortality rate (83%; n = 15 of 18) compared to moderately (33%; n = 6 of 18) and mildly (24%; n = 6 of 25) paralyzed mice (P < 0.001). The overall ligation group survival rate (84%; n = 46 of 55) was significantly lower than the sham group (100%; n = 48 of 48) with P = 0.003. CONCLUSIONS: The mouse model generates reproducible spinal cord hypoperfusion and accompanying histopathological ischemic spinal cord damage. The resulting anatomical changes and variable behavioral deficits mimic the variability in radiological and clinical findings in human patients.
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