Ella
Shanks
Sponsor: Jens Hilscher, Ph.D. Ag & Resource Economics The transformative potential of artificial intelligence (AI) is undeniable, yet its influence on asset pricing remains a complex puzzle. In this research, I introduce a novel measure of AI-related risk: a long-short factor constructed from NVIDIA's (NVDA) beta. This approach isolates exposure to the market's perception of AI risk, disentangling it from broader market influences and offering a clearer picture of how industries with varying AI sensitivity are priced. Crucially, by leveraging NVDA's beta rather than raw returns, I mitigate the attenuation bias that can distort the true relationship between AI risk and industry returns, providing a more robust and accurate assessment of how the market perceives and prices AI risk. My findings reveal a significant and economically meaningful relationship between this AI risk factor and industry returns, demonstrating distinct return patterns for industries with differing AI exposure. These results reveal the financial relevance of AI risk and contribute to a deeper understanding of how this transformative technology is shaping asset pricing, offering valuable insights for investors and policymakers seeking to capitalize on the opportunities and mitigate the risks of the AI-driven market. Investigating Transformation Growth Factor β (TGF-β) as a Therapeutic Target for Protecting Brain Function in a Rat Model of Acute Organophosphate Intoxication
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Ella Shanks
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Acute intoxication with organophosphate (OP) cholinesterase inhibitors, which include pesticides and nerve agents, can trigger life-threatening seizures. While current standard-of-care (SOC) increases survival rate, it does not protect against the development of acquired epilepsy and cognitive decline. Therefore, there is an urgent need for more effective therapeutic strategies. We are investigating TGF-β as a potential therapeutic target using a rat model of acute intoxication with the OP diisopropylfluorophosphate (DFP). Adult male and female rats were administered DFP or vehicle (VEH, phosphate-buffered saline), followed by SOC. At 1, 3, 7, and 14 days post-exposure (DPE), rats were euthanized, and levels of TGF-β were quantified in brain tissue by quantitative PCR (qPCR) and western blotting. qPCR revealed a fourfold increase in TGF-β mRNA at 1 DPE and a fivefold increase at 7 DPE in the hippocampus and cortex. Western blot analysis detected total SMAD2/3 protein, a downstream signaling molecule activated by TGF-β, in all samples, but revealed increased levels of phosphorylated SMAD2/3 (pSMAD2/3) in brains of DFP rats compared to VEH controls. Our findings indicate that TGF-β signaling is triggered by acute OP-exposure, supporting the validity of investigating TGF-β as a therapeutic target. This work was supported by NIH (U54 NS127758). Dimerization of Protein Kinase D1 in Vivo: Investigating the Role of the ULD Domain Aryan Sharma
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UC Davis / VM: Molecular Bio Sciences / 2025
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Ella Shanks