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INTEGRATING ARTIFICIAL INTELLIGENCE IN THE INTELLIGENCE COMMUNITY: IDENTIFYING OBSTACLES AND WAYS TO MITIGATE THEM
Get PDFIn the age of rapid technological advancements, the Intelligence Community (IC) faces both immense opportunities and challenges arising from the development of artificial intelligence (AI) and digital technology. While AI is not a new concept, with its roots tracing back to 1956, its evolution has been characterized by sporadic leaps in technology followed by stagnant periods. This paper aims to analyze the opportunities and challenges presented by AI and digital innovation in the IC, evaluating the extent to which these technologies can support intelligence operations and augment the intelligence cycle.
As of 2023, AI has demonstrated immense potential in various fields, including machine learning(ML), neural networks, and robotics. The IC has been cognizant of these technological capabilities and has initiated numerous projects and plans since 2016, culminating in the release of a report by the National Security Commission on Artificial Intelligence(NSCAI) in 2021. Despite the IC’s efforts, the NSCAI concludes that the US is not sufficiently prepared to compete with rival nations such as China (National Security Commission on Artificial Intelligence, 2021).
In this paper, the NSCAI report will serve as a potential policy roadmap for assessing the Intelligence Community's approach to AI Implementation. Additionally, various official publications, including standards and guidelines from The Office of the Director of National Intelligence and its associated agencies, will be employed to further evaluate the strategic direction the IC may pursue
TELLING THE FIGHTER’S STORY: TALES OF ENDURANCE, GRIT, AND SURVIVAL
Get PDFThis anthology highlights the endurance, grit, and survival of people and nature adapting to and overcoming imperfect events and circumstances and describes medical, political, and social barriers that present opportunities for people to harness hope, push personal boundaries, and rise above challenging situations
Oral History of Ian Gilmore
No full textThis oral history about transgender experience in Baltimore was recorded as part of Vintage T, a public humanities project led by Monica Stevens, Jamie Grace Alexander, and Rahne Alexander and sponsored by Sistas of the “T” and the Winston Tabb Special Collections Research Center. Vintage T was launched in 2023 to document and archive the perspectives, strategies, and personal histories of trans individuals in Baltimore, thereby preserving valuable traditions within trans communities
The Potential for Hazardous Fuel Reduction Treatments to Produce Net Economic Benefits in California
Get PDFModern wildfire activity in California has been characterized by large uncontrolled fires and significant economic burden. From 2017-2021, wildfires have resulted in an estimated 34 billion on an initial $8.5 billion treatment cost- giving a benefit/cost ratio of 4x. Additionally, we found that fuel reduction treatments, rather than a reduction in emissions, are more influential on fire intensity potential projections. Lastly, while our findings suggest that large-scale hazardous fuel reduction treatments are more costly than fire suppression, there is evidence that fuel reduction treatments will ultimately result in a net economic benefit at the societal level
Oral History of Teresa Palomar
No full textThis oral history about transgender experience in Baltimore was recorded as part of Vintage T, a public humanities project led by Monica Stevens, Jamie Grace Alexander, and Rahne Alexander and sponsored by Sistas of the “T” and the Winston Tabb Special Collections Research Center. Vintage T was launched in 2023 to document and archive the perspectives, strategies, and personal histories of trans individuals in Baltimore, thereby preserving valuable traditions within trans communities
Assessing the Bankability of a Floating Offshore Wind Project on California’s Coast using a Financial Model
Get PDFThe purpose of this paper is to ascertain the “bankability” of a floating offshore wind project in California’s Morry Bay Wind Energy Area. This project will be considered “bankable” if it can achieve an 11% post-tax equity internal rate of return at a power purchase agreement price of $80 per Megawatt-hour.
The Literature Review covers California’s emphasis and support for offshore wind development, current floating offshore wind technologies, and potential challenges facing future projects.
A multi-step approach was used to qualitatively and quantitatively ascertain the required project assumptions to inform a financial model that would yield accurate results. The process of informing each assumption was nested in applying relevant literature on floating offshore wind to the specific site characteristics of Lease Area OCS-P0563. The assumptions were then used as inputs for the financial model to produce outputs for 4 scenarios that incorporated economic and supply chain conditions, while reviewing additional sensitivities regarding tax incentives. These outputs were used to determine the financial attractiveness of the project.
The results showed that a floating offshore wind project in Lease Area OCS-P0563 would not be “bankable” in any of the four scenarios analyzed and within the strike price and post-tax equity internal rate of return target. However, instances of political willingness to offer higher prices for offshore wind electricity, despite additional costs to consumers, suggests such a project could be financially attractive at higher power purchase agreement prices
VPS13D REGULATES MITOCHONDRIAL MORPHOLOGY AND PROMOTES PEROXISOME BIOGENESIS IN HUMAN CELLS
No full textThe VPS13 family is highly conserved among eukaryotes, from yeast to humans. There are four members of this family in mammals: VPS13A-D. Each gene has been near or completely definitely linked to distinct neurological disorders: Chorea-Acanthocytosis (VPS13A), Cohen Syndrome (VPS13B), Parkinson’s Disease (VPS13C), and Spinocerebellar Ataxia, autosomal recessive 4 (SCAR4). Until recently, their cellular functions were poorly understood and there remains much more to be elucidated. Recent research strongly suggests that yeast Vps13 and its orthologs could function as lipid transfer proteins at membrane contact sites (MCSs).
My thesis work strengthens the argument to designate VPS13D as a MCS lipid transfer protein. We generated VPS13A-D knockout (KO) HeLa cell lines for characterization. Of the individual KOs, only VPS13D had an apparent effect on organelle phenotypes. VPS13D-KO cells exhibit abnormal mitochondrial morphology. We also found that VPS13D loss induces a partial or total loss of peroxisomes. We support these findings by establishing non-homogenous VPS13D KO in other human cell types. This work also provides a clinical insight, as we found a similar (though less severe) peroxisomal phenotype in SCAR4 patient fibroblasts. Our data show that VPS13D specifically regulates peroxisome number through biogenesis.
In order to more precisely study the visual mitochondrial and peroxisomal phenotypes, I developed a method utilizing deep learning (DL) to generate two image classification models. These models provide an automated and less biased way to quantitate image-based phenotypes; in this case, the identification of peroxisomal loss by catalase (CAT) localization, and the rounded mitochondria phenotype distinct to VPS13D KO. This tool allows for accurate assaying of VPS13D’s role in both organelles, and even their linkage to each other
THREE-DIMENSIONAL GENOMIC ANALYSIS OF HUMAN PANCREATIC INTRAEPITHELIAL NEOPLASIA
No full textPancreatic ductal adenocarcinoma (PDAC) is a lethal disease with an 8% 5-year survival rate. PDAC arises from precursor lesions, the most common of which is pancreatic intraepithelial neoplasia (PanIN). Molecular analysis of human PanINs is critical to understand early pancreatic tumorigenesis, which could inform risk stratification, early detection, and cancer prevention approaches. Because PanINs are microscopic, it is challenging to determine their full extent and anatomic relationships using two dimensional histological sections. To determine the density and connectivity of PanINs, we utilized a novel machine learning algorithm (CODA) for three-dimensional (3D) reconstruction. Large blocks of grossly normal pancreas were harvested from 46 surgical pancreatectomy specimens, followed by formalin fixation, paraffin-embedding, serial sectioning, and hematoxylin and eosin (H&E) staining. 3D reconstruction using CODA revealed striking multifocality of PanINs within analyzed tissues, with 1,006 spatially separate PanINs being modeled. Next, to determine whether these multifocal PanINs arose as independent neoplasms or via intraductal spread of a single PanIN, we assessed their clonal relationships using somatic multi-region DNA next generation sequencing (NGS). To do so, eight of the aforementioned blocks were sectioned to allow for NGS, yielding 99 samples from the 37 anatomically distinct PanINs for genomic analysis. Each spatially unconnected PanIN was separately microdissected in five different regions to assess both intra- and inter-PanIN genetic heterogeneity. When sufficient DNA remained, whole exome sequencing and deep sequencing of KRAS was also performed. Nine PanINs shared no mutations with other PanINs in the same block, indicating independent clonal origin. Additionally, six PanINs shared only KRAS hotspot mutations with numerous other unshared mutations, indicating independent PanINs may share hotspot mutations by chance. Six spatially separate PanINs shared several somatic mutations with at least one other spatially unconnected PanIN, representing intraductal spread of PanINs. Furthermore, six PanINs harbored multiple KRAS mutations. The genetic origins of ten spatially separate PanINs could not be resolved due to a lack of discrete mutations on targeted sequencing. Our 3D genomic analysis of anatomically distinct PanINs demonstrates that the unexpectedly large number of PanINs in normal pancreas most often arise independently, providing new foundations for our understanding of early pancreatic tumorigenesis
Bi-level Proactive Transmission Planning Considering Transmission and Distribution Network Cost Recovery
No full textThis thesis studies, first, inefficient pricing of transmission and distribution grid assets in liberalized electricity markets to investigate how it influences market equilibria, and, second, how proactive grid planning, which anticipates the impact of inefficient pricing on the market, can correct distortions arising from inefficient pricing of transmission (charges designed to recover full transmission costs), distribution services (retail pricing based on average costs, and recovery of grid costs by volumetric charges), and prosumer generation (where "prosumers" are consumers who own distributed generation and can self-generate to avoid paying retail rates). Interactions and alternative inefficient pricing schemes, and between them and proactive transmission planning are not well understood, even though they have significant impacts on market efficiency.
I create alternative short- and long-run pricing models for generation, consumers, and prosumers, and incorporate them into novel proactive transmission models, solved as Mathematical Problems with Equilibrium Constraints through custom algorithms. I then show how nodal or zonal markets respond to alternative transmission cost recovery charges, retail pricing, and prosumer participation. Finally, I demonstrate how proactive transmission planners could design the grid to improve market efficiency while anticipating these responses.
This is the first study in the literature that explores interactions among market participants (generation, demand, and prosumers), alternative transmission and distribution charging systems, and proactive transmission planning under different short-run market designs. Key conclusions of my case studies include the following: both MW-mile charges and zonal pricing can cause significant efficiency loss by punishing efficient remote generation or by encouraging generation investment in network locations with high congestion, especially when planners naively disregard these inefficiencies. However, proactive planning that recognizes those distortions can correct much of them, reducing efficiency losses by 60-90%. Interestingly, adding MW-mile charges to a market with zonal spot markets can actually make systems more efficient by providing missing locational investment incentives to generation. Adding prosumers to the system can cause significant welfare losses by encouraging inefficient distributed resource investment, but proactive planning reduces those efficiency losses by 26% in my case study. But adding MW-mile charges to systems with prosumers instead reduces system efficiency, since they discriminate against bulk generation
BLOCKADE OF CXCR2 OVERCOMES NEUTROPHIL-MEDIATED RESISTANCE TO COMBINED ANTI-PD-1 AND MEK1/2 INHIBITON IN MURINE PANCREATIC DUCTAL ADENOCARCINOMA
No full textPancreatic ductal adenocarcinoma (PDAC), defined by an immunosuppressive desmoplastic tumor microenvironment (TME) orchestrated by oncogenic KRAS signaling, is notoriously resistant to both conventional therapies and immune-checkpoint blockade. We overcame this resistance through inhibition of the downstream KRAS effector MEK1/2 in combination with aPD-1 blockade. aPD-1+MEKi therapy routinely eradicated tumors in >80% of mice, with tumor-free survival and protection from tumor re-challenge extending as far as one-year post-treatment. Initial gene expression data showed a reduction in IL-8 homologs in aPD-1+MEKi tumors. Subsequent immunophenotyping data showed increased CXCR2(+) neutrophils in aPD-1+MEKi tumors compared to aPD-1+DMSO. Given the functional role of CXCR2 in IL-8-mediated NETosis, we compared tumors from aPD-1+MEKi sensitive (KPC_S) and resistant (KPC_R) KPC cell lines for NETosis signatures via multiplex IF. Within KPC_S groups, mean NET scores w/ SEM fell from 2.29 +/- 0.12 to 0.51 +/- 0.10 between aPD-1+DMSO and aPD-1+MEKi groups (p <= 0.0001). No difference was found within KPC_R treatment groups (2.10 +/- 0.11 vs 2.07 +/- 0.12, p = n.s.). Furthermore, 23.41 +/- 3.04% of ex vivo stimulated CD8(+) TILs from aPD-1+MEKi KPC_S tumors were IFNy(+) vs 9.09 +/- 2.02% in aPD-1+DMSO KPC_S and 6.55 +/- 1.38% in aPD-1+MEKi KPC_R cells (p = 0.016 and 0.011 respectively). We have demonstrated that resistance to aPD-1 blockade in PDAC can be annulled with combined MEK1/2 inhibition. The elimination of immunosuppressive NETs from sensitive KPC tumors but not resistant tumors suggests that MEKi works by modulating the TME rather than neutrophils directly