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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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Generalized target behavior reductions and maintenance of effects following an augmented competing stimulus assessment sequenceCompeting stimulus assessments are one technology that aids in the development of treatment for automatically reinforced behavior. However, competing stimulus assessments do not always yield robust results. Stereotypic behaviors of different subtypes may require procedural modifications to successfully identify competing stimuli. The current investigation included functional analyses to determine whether participant responding aligned with proposed subtypes for such behaviors. Next, we implemented augmented competing-stimulus-assessment (A-CSA) procedures across target and generalization stimuli to determine whether (a) responding across either subtype was more likely to require intensive modifications and (b) the A-CSA procedures promoted generalized target behavior reduction within stimulus classes. Lastly, a treatment evaluation was conducted to determine the durability of these findings and the generalization of the reduced target behavior to other settings. The general applicability of the subtyping model remains unclear, but two participants demonstrated maintenance of competition effects.
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SELF-ASSEMBLING MULTIDOMAIN PROTEIN MICELLES FOR MOLECULAR IMAGING AND DRUG DELIVERYProteins are versatile biomacromolecules with strong self-assembly properties that play a vital role in virtually all forms of life. By taking advantage of these properties, it is possible to design biocompatible, biologically active materials that can be used for a range of biomedical purposes, such as molecular imaging as well as targeted drug delivery. Unlike many other material systems, proteins can be recombinantly expressed and purified with multiple functional domains encoded in a single gene, often eliminating the need for additional chemical conjugation steps. Here we describe the design and engineering of multidomain proteins containing at least one coiled-coil domain and one disordered elastin-like polypeptide domain per chain. These proteins spontaneously assemble into micelles in aqueous solution. By incorporating targeting peptides into the genetic sequence, we can additionally alter the pharmacokinetics and organ tropism of the resulting micelles. Chapter 1 provides a brief overview of the field of protein biomaterials, while Chapters 2-4 delve in the design and characterization of protein micelles with multiple functional domains. First, in Chapter 2, we devise a collagen-binding molecular imaging probe for the monitoring of metabolic associated steatohepatitis (MASH) disease progression. This probe, collagen type I-binding thermoresponsive assembled protein (Col1-TRAP), was first characterized in vitro before being used to study a mouse model of MASH. It was found to preferentially accumulate in the livers of mice with MASH compared to normal mice. Next, in Chapter 3, we investigate the effect of increasing the multiplicity of the coiled-coil domain on improving hydrophobic drug loading capacity and delivery efficiency. Increasing the number of repeats of the coiled-coil domain from 1 to 2 was found to increase the drug loading capacity by 1.7-fold while reducing micelle packing by 25%. This construct, targeted multidomain protein assembly (TMPA), was found to preferentially accumulate in tumor sites in mice implanted with glioblastoma xenografts. Finally, Chapter 4 focuses on the targeting of TMPA for specific drug delivery to HER2+ breast cancer by using the peptide P51. Targeted micelles loaded with doxorubicin displayed improved uptake into and cytotoxicity against breast cancer cells overexpressing the HER2 receptor, while showing no selectivity in triple-negative breast cancer cells. All micelle-drug formulations were found to be more effective than free drug alone, showing the utility of these protein materials.
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Brain, Environmental and Psychological Trauma: TBI and PTSD Markers, Mechanisms, and InteractionsTraumatic brain injury (TBI) and Post-traumatic stress disorder (PTSD) are significant public health concerns, particularly among individuals exposed to high-stress environments such as military combat. However, they can also occur anytime due to various head injuries and stress. This review examines the interplay between TBI and PTSD, highlighting their prevalence, symptoms, potential biomarkers, pathological mechanisms, and the interactions that occur with exposure to both conditions. Worldwide, an estimated 69 million individuals per year sustain TBI, while approximately 13 million people per year exhibit PTSD. Notably, PTSD is markedly higher among individuals with TBI, particularly in veterans, where an estimated 28% of patients with mild TBI also exhibit PTSD. Although each alone results in significant symptoms and pathology, the co-occurrence of PTSD and TBI exacerbates the situation due to overlapping symptoms and bidirectionally interacting pathological changes. The occurrence of both TBI and PTSD increased cognitive impairments, emotional dysregulation, and disability with reduced function and health. Here, I provide a synthesis of current literature and assess the relationships between TBI and PTSD. We draw upon clinical and preclinical data to provide this critical overview. TBI increases the risk of developing PTSD, and PTSD increases susceptibility to the consequences of TBI. This interaction is due primarily to several overlapping mechanisms, including disrupted fronto-limbic brain circuits, neuroinflammation, and dysregulation of the HPA axis and specific neurotransmitter systems. White matter and brain area changes affect neural connectivity and functioning. Stress systems, inflammation, neurotransmitter imbalances, and structural brain changes interact closely in both TBI and PTSD. For example, chronic stress dysregulates the HPA axis, amplifying neuroinflammation and altering cortisol levels, further impacting neurotransmitter systems like serotonin and dopamine. This biochemical cascade contributes to white matter degradation and reduced brain volume, especially in regions like the hippocampus and prefrontal cortex, worsening cognitive and emotional symptoms. These interconnected changes create a feedback loop that sustains dysfunction across neural networks, complicating recovery. These changes worsen cognitive and emotional symptoms and create a feedback loop that hinders recovery. Continued research is required to understand TBI and PTSD interactions better. Additional pathological mechanisms and targets for intervention using appropriately designed studies in experimental models and in the clinic. This “translational research” approach will help us discover future risk prevention, intervention, and rehabilitation strategies that can improve the quality of life for those impacted by these comorbid and disabling disorders.