ScholarWorks@UMassAmherst

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Graduate students: Directions for submissions can be found in this guide. Please email scholarworks@library.umass.edu if you have any questions.

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Please see our ScholarWorks guide for more information about submitting your work to ScholarWorks.

Featured Items

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Data Do's and Don'ts: A Primer on Indigenous Data Sovereignty

Anderson, Jane; Smith, Vanessa

2026

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A Mighty Event: Eight Lessons Learned by Bringing People Together Through Music to Support Our Mission

White, Caroline J.; Fill, Kim D.

On the evening of November 7, 2025, the University Libraries at the University of Massachusetts Amherst held its annual Fall Reception, attended by an audience of 300. “An Evening with Folk New England: A Tribute to Eric von Schmidt” represented both a return to the longstanding tradition of an event held to showcase the Libraries while thanking our donors for all they make possible and an exceptionally successful and memorable version of that event. Celebrating the partnership of Folk New England and the Libraries' Robert S. Cox Special Collections and University Archives Research Center, the event generated so much interest that it was ultimately moved to a larger venue, and the move impacted all aspects of the event. Although the planning team cannot count on replicating the event or its impact in the near future, the team took away many lessons from the planning and pivoting, as well as from the event itself.

2026-03-19

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Regional Invasive Species & Climate Change Research to Practice Paper: Rock you like a hurricane: The perfect storm for an invasion

Putnam, Aly B.; Al-Shayeb, Sofia M. A.; Buonaiuto, Daniel M.; Daniel, Wesley; Geiger, Megan Lynn; Lieurance, Deah; Parsons, Elliott W.; Pfingsten, Ian; Williams-Soriano, John Paul; Evans, Annette E.

Hurricanes (also called typhoons or cyclones) and other rare weather occurrences are increasing in intensity and frequency with global climate change. These extreme weather events can drastically alter ecosystems in ways that directly or indirectly facilitate the introduction, establishment, spread, and impacts of invasive species. For example, high winds or flood waters during hurricanes can disperse invasives and displace native species. Impacts could also occur after the main storm event; invasive species can invade during relief efforts or establish more easily in disturbed habitats [1,2]. Various possible mechanisms link hurricanes and invasive species (Figure 1). To identify shared challenges as well as region-specific dynamics and possible impacts, we highlight case studies from the Southeast, Pacific Islands, Caribbean, and Northeast regions of the United States (Table 1). By synthesizing examples across diverse ecological and management contexts, this summary can help practitioners anticipate common mechanisms of spread and consider strategies that could be implemented before and after hurricane events to manage vulnerable species, habitats, and ecosystems.

2026

Recent Submissions

  • PublicationOpen Access
    The Use of Fusiform Rays as a Basis for Distinguishing the Woods of P. sylvestris and P. resinosa
    (1987-05) Zarifian, Sharon Ann
    Because the woods of Scots pine (Pinus sylvestris) and red pine (P. resinosa) have been considered inseparable from one another, a search was made for distinguishing anatomical features. Tangential sections of 44 samples of each species were examined microscopically, with special attention to measurements of uniseriate and fusiform rays. Observations and measurements were evaluated using discriminant analysis. The most discriminating features were the significantly greater fusiform ray height (in microns) and the height (in microns) of the longer of the two uniseriate extensions of fusiform rays in P. sylvestris. Using both features together gives the strongest basis for separating the two species, although occasional specimens cannot be positively identified.
  • PublicationEmbargo
    TISSUE ENGINEERING AND REGENERATIVE MEDICINE APPLICATIONS OF PULSED ELECTRIC FIELDS
    (2026-02) Raghuraman Rajagopalan, Neeraj
    Ultrashort direct current electrical pulses, also called pulsed electric fields (PEF), can permeabilize the cell membrane in a process termed electroporation. Currently, PEF is used in patients for killing cells by compromising their membrane function and for drug delivery to tumors, as well as gene transfection in the lab. A unique feature of PEF technology is that the biological response from cells requires a miniscule injection of energy. Due to this working mechanism, there is limited heating of the tissue being treated resulting in preservation of extracellular matrix proteins and anatomic structures. This aspect of PEF treatment creates interesting opportunities in tissue engineering and regenerative medicine. Here, we developed and applied PEF technology on three distinct topic areas. The first aim explored in-vivo and ex-vivo decellularization of tissues using PEF, for use as graft material. We showed that PEF treated tissues can produce acellular scaffolds with superior preservation of ECM proteins compared to chemical processing, supporting tissue regeneration and tested the technique’s in vivo feasibility and safety for preparing intra-surgical graft material for bladder reconstruction. In the second aim, PEF was used to stimulate endothelial cells by modulation of the actin cytoskeleton. PEF treated endothelial cells secreted copious amounts of growth factors, enhanced cell migration and angiogenic sprouting with potential for use in promoting healing and normalization of aberrant endothelial cells in various disease conditions. In the third aim, we demonstrated that by leveraging the inherent variations in electrical properties of tissue and its interactions with PEF parameters such as pulse width, electric field strength and frequency, that selective ablation of tissue compartments may be feasible. Overall, PEF is a promising technique that is relatively easy to translate to clinic for tissue engineering and regenerative medicine applications.
  • PublicationEmbargo
    Structural and functional insights into the disordered region of CaMKII with implications in autoinhibition and neurological diseases
    (2026-02) Nguyen, Viet Chi Bao
    Ca2+/calmodulin-dependent protein kinase II (CaMKII) is a family of Ser/Thr-protein kinases that are important for Ca2+ regulation, whose mutations can result in neurodevelopmental disorder, cardiovascular and muscular defects, and infertility. Despite the rich understanding of CaMKII biological roles in Ca2+-sensitive cells, the mechanisms by which CaMKII can be regulated by and specifically respond to Ca2+ signals in these excitable cells remain elusive, partly due to the high diversification of CaMKII proteoforms and limited information on CaMKII structural regulations. In this dissertation, projects have been developed to address several areas of CaMKII research with an ultimate goal of identifying factors regulating the autoinhibited state of CaMKII. In the first chapter, I present a review on the progress of understanding CaMKII functions through dissecting the available CaMKII structures. Chapter 2 focuses on the regulatory roles of the linker region of CaMKII, which is intrinsically disordered and highly variable due to alternative splicing. This chapter contains evidence for a domain-swap conformation of CaMKII dimers, which facilitate a linker-mediated allosteric regulation on Ca2+/CaM sensitivity of CaMKII holoenzyme. The specificity in the linker sequence carrying out the regulation emphasizes the importance of diversification in CaMKII proteoforms to fine-tuning CaMKII response to different Ca2+ signaling in different cell types. Chapter 3 focuses on the roles of T286 and T305/306 in regulating CaMKII holoenzyme stoichiometry and stability. These sites have only been studied in the context of kinase activity, and with less focus on CaMKII holoenzyme stoichiometry. The results show that biochemical properties of T286 and T305/306 affect CaMKII holoenzyme structure and activation properties. I also reveal that CaMKII form clusters upon activation that is dependent solely on the regulatory segment and the hub domain, clarifying on the role of the kinase domain in regulating CaMKII holoenzyme cluster formation. In chapter 4, I developed a protocol to identify CaMKII interactors in primary neurons, implicating CaMKII in numerous pathways in the postsynaptic density, mitochondrial biology, and translational regulation. Overall, the results shown here enrich our understanding of CaMKII autoinhibition regulation and activation properties that can justify for the rich interactome that CaMKII possesses to carry out its functions.
  • PublicationEmbargo
    Uncovering the mechanism of CaMKII degradation
    (2026-02) Heikal, Rehab
    Ca2+calmodulin dependent protein kinase II (CaMKII) is an oligomeric kinase that plays a central role in synaptic plasticity, learning, and memory. It is one of the most concentrated proteins in the postsynaptic density (PSD), where its activity and positioning are tightly coupled to synaptic signaling. CaMKII is crucial for NMDA receptor (NMDAR)-dependent long-term potentiation (LTP): its recruitment to synapses through NMDAR binding is required for LTP induction, while sustained activation supports local translation of CaMKII at synapses, thereby maintaining long-term synaptic function. These mechanisms of activation, and its essential role in learning and memory, particularly in the induction and maintenance of LTP has been extensively studied. However, how the abundance of CaMKII is regulated remains a mystery. This thesis aims to understand the mechanism of CaMKII regulation, its degradation mechanisms, and the pathogenesis of CaMKII-related disorders. Using genome wide CRISPR screening coupled with global protein stability profiling, we found that the E3 ubiquitin (Ub) ligase UBE3A mediates the degradation of CaMKII. We employed a combination of biochemical and cellular experiments and found that UBE3A preferentially ubiquitinates the active form of CaMKII and a pathogenic mutant that causes intellectual disabilities, suggesting that these two forms share the same degradation pathway. We next performed structural and biochemical assays to identify the domains of CaMKII that are specifically recognized by UBE3A. Our results revealed that CaMKII kinase domain is both necessary and sufficient for UBE3A-mediated ubiquitination. This discovery highlights a critical regulatory interface and opens new directions for dissecting the molecular interplay between UBE3A, CaMKII, and their implications in neurodevelopmental disorders. Together, uncovering the fundamental process governing CaMKII degradation will enhance our understanding of the UPS’s role in synaptic function and pave the way for potential therapeutic interventions targeting CaMKII related disorders.
  • PublicationEmbargo
    HEALTH RISKS OF FOODBORNE SILICON DIOXIDE NANOPARTICLES: SYSTEMIC AND REPRODUCTIVE ADVERSE EFFECTS MEDIATED BY GUT MICROBIOTA AND THE GUT–ORGAN AXIS
    (2026-02) Du, Hengjun
    Silicon dioxide (SiO₂) is one of the most widely used food additives, commonly employed as an anticaking and flow agent. Although synthetic amorphous silica is generally regarded as safe, growing evidence suggests that its nanoscale fractions may exhibit distinct biological activities. However, the systemic health consequences of chronic dietary exposure to foodborne SiO₂ NPs (NPs), particularly under metabolically vulnerable conditions and across biological sex, remain poorly understood. This dissertation aimed to systematically evaluate the metabolic and reproductive toxicity of dietary SiO₂ NPs and to elucidate the gut microbiota–mediated mechanisms underlying their biological effects. Using a combination of lean and diet-induced obese mouse models of both sexes, this work investigated the absorption, tissue distribution, and toxicological outcomes of chronic dietary exposure to SiO₂ NPs in comparison with food-grade synthetic amorphous silica (E551). Comprehensive phenotypic, molecular, and multi-omics approaches were employed, including metabolic profiling, histopathology, gene expression analysis, targeted bile acid metabolomics, short-chain fatty acid quantification, and gut microbiota characterization. Chronic SiO₂ NPs exposure induced systemic and organ-specific toxicities that were not reflected by overt changes in body weight or food intake. Obesity emerged as a major sensitizing factor, amplifying intestinal inflammation, hepatic lipid accumulation, mitochondrial dysfunction, and glucose intolerance. Pronounced sex-dependent effects were observed, with female mice exhibiting heightened metabolic susceptibility, including altered body weight trajectories, impaired glucose homeostasis, and increased tissue silica accumulation, whereas male mice displayed marked reproductive toxicity characterized by impaired spermatogenesis, reduced sperm quality, and disruption of steroidogenic and cell cycle–related pathways. Mechanistically, this dissertation identifies the gut microbiota as a central mediator of SiO₂ NP-induced systemic toxicity. Dietary SiO₂ NPs disrupted gut microbial community structure and reduced microbial diversity in a sex-dependent manner. Functionally, SiO₂ NP exposure selectively depleted butyrate-producing bacteria, particularly Clostridium XIVa, leading to impaired short-chain fatty acid production. Concurrently, SiO₂ NPs profoundly remodeled the intestinal bile acid pool, characterized by enrichment of taurine-conjugated primary bile acids and suppression of secondary bile acid formation, indicative of compromised microbiota-dependent bile acid biotransformation. Importantly, bile acid remodeling engaged host enterohepatic signaling pathways. Altered intestinal bile acid composition was associated with enhanced activation of the intestinal FXR–FGF15 axis and suppression of hepatic bile acid synthesis via downregulation of Cyp7a1, revealing a gut-origin endocrine mechanism linking microbial dysbiosis to hepatic metabolic regulation. Across all endpoints, SiO₂ NPs consistently exerted stronger biological effects than food-grade E551, highlighting the critical role of nanoscale physicochemical properties in determining biological impact. Collectively, this dissertation demonstrates that chronic dietary exposure to foodborne SiO₂ NPs disrupts gut microbial homeostasis and gut–organ communication, leading to systemic metabolic and reproductive toxicity in a sex- and metabolic state–dependent manner. These findings challenge the assumption of biological inertness of foodborne nanomaterials and underscore the necessity of incorporating host metabolic status, sex differences, and gut microbiota–mediated mechanisms into future food additive safety assessment.
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