Informing the Creation of a Financial Literacy Tool for Cal Poly Students

This research project examines the wants, needs, and desires of Cal Poly students to inform the creation of a financial literacy tool (tentatively named “MoneySmart”) to be created by another student. The methodologies used to gauge these metrics were a literature review and questionnaire. The literature review aids in understanding research regarding the current state of student financial literacy in the United States, including student attitudes toward the topic. Subsequent findings were used to create the questionnaire, which inquired about students’ financial stress, confidence in their abilities to manage their personal finances, specific interests for the design and contents of a financial literacy training tool, and demographics. Key findings showed that on average, Cal Poly students experience just below moderate levels of stress with regard to finances just below moderately often, they have received a moderate-to-low amount of financial literacy education, and they have moderate-to-low levels of confidence in their knowledge of personal finances. Furthermore, no significant preference was found between learning about the topics of budgeting, loans/debt management, credit, or taxes, but a notable portion of students were interested in learning about stocks and other investments. Finally, students were drawn to the idea of a financial literacy training tool that is interactive, engaging, portrays relatable transactions, and is high resolution. They were less drawn to the tool being student-made, having an endorsement from Cal Poly, including quizzes throughout, and offering a digital certificate upon completion

AMP-activated protein kinase regulation of myeloid antigen presenting cell activity.

Inflammatory and metabolic processes are critical to the survival of multicellular organisms. Inflammation and metabolism are closely linked, and many pathologies are associated with dysregulation of both of these processes, including obesity, cancer, diabetes, and atherosclerosis. Understanding the mechanistic links of inflammation and metabolism are critical for the development of treatments of metabolic and inflammatory diseases. AMP-activated protein kinase, AMPK, is a serine/threonine kinase that regulates energy homeostasis and metabolic stress in eukaryotes. When cellular ATP is low, AMPK is activated and turns off ATP-consuming anabolic pathways and turns on ATP-generating catabolic pathways. Previous work from our laboratory, as well as by others, has provided evidence that AMPKa1 acts as a negative regulator of TLR-induced inflammatory function. The goal of this dissertation was to investigate the role of AMPKa1 in myeloid antigen presenting cell activity. Herein we demonstrate that AMPKa1-deficient macrophages and dendritic cells (DCs) exhibit heightened inflammatory function and an enhanced capacity for antigen presentation favoring the promotion of Th1 and Th17 responses. Macrophages and DCs generated from AMPKa1-deficient mice produced higher levels of proinflammatory cytokines and decreased production of the anti-inflammatory cytokine IL-10 in response to both TLR and CD40 stimulation as compared to AMPKa1+/+ cells. In assays of antigen presentation, AMPKa1 deficiency in both the myeloid APC and T cell populations contributed to enhanced IL-17 and IFN? production. Focusing on the CD154-CD40 interaction, we found that CD40 stimulation resulted in increased phosphorylation of ERK1/2, p38, and NF-?B p65 and decreased activation of the antiinflammatory Akt - GSK3ß - CREB pathway in DCs deficient for AMPKa1. AMPKa1 serves to attenuate LPS and CD40-mediated proinflammatory activity of myeloid APC and AMPKa1 activity in both APC and T cells antagonizes the development of proinflammatory T cell responses during antigen presentation. Additionally, we sought to investigate the influence of macrophage-expressed AMPKa1 on tumor-macrophage interactions and macrophage polarization in the tumor microenvironment. Our studies show that macrophage-expressed AMPKa1 polarizes tumor-infiltrating macrophages (TIMs) to an anti-inflammatory phenotype and contributes to tumor growth. To evaluate the role of myeloid cell-expressed AMPKa1 in tumor growth and metastasis, we used an AMPKa1 Cre-lox transgenic mouse model. AMPKa1flox/flox LysM-Cre+ (described subsequently as MacAMPKa1 KO) mice had reduced Lewis lung carcinoma (LLC) tumor growth and metastasis compared to AMPKa1flox/- LysM-Cre- (WT) mice. Additionally, TIMs isolated from MacAMPKa1 KO mice exhibited higher production of proinflammatory cytokines and matrix metalloproteinases (MMPs). Furthermore, TIMs isolated from MacAMPKa1 KO mice had higher phosphorylation of p65 NF-?B and reduced phosphorylation of Akt and CREB. Overall, deficiency of myeloid AMPKa1 results in higher proinflammatory activity of TIMs and decreased tumor growth. Our studies herein demonstrate that AMPKa1 counter-regulates myeloid cell TLR- and CD154-induced inflammatory activity and antagonizes the development of proinflammatory effector T cell responses. Furthermore, myeloid-expressed AMPKa1 contributes to the polarization of TIMs to an anti-inflammatory phenotype and leads to increased tumor growth and metastasis. These studies demonstrate that AMPKa1 is an important link to inflammation and metabolism and is a valuable potential target for the treatment of inflammatory and metabolic diseases. Additionally, these studies provide evidence that activation of AMPKa1 in cancer therapy may contribute to increased tumor growth through polarization of TIMs to an anti-inflammatory phenotype, a valuable observation given that many AMPK activators are being studied as cancer therapeutics

THE EFFECTS OF HEALTH ON HEALTH INSURANCE STATUS IN FRAGILE FAMILIES

We use data from the Fragile Families and Child Wellbeing study to estimate the effects of poor infant health, pre-pregnancy health conditions of the mother, and the father’s health status on health insurance status of urban, mostly unmarried, mothers and their one-year-old children. Virtually all births were covered by health insurance, but one year later about one third of mothers and over 10 percent of children were uninsured. We separately examine births that were covered by public insurance and those that were covered by private insurance. The child’s health status had no effect, for the most part, on whether the mother or child became uninsured. For publicly insured births, a maternal physical health condition made it less likely that both the mother and child became uninsured, while maternal mental illness made it more likely that both the mother and child lost insurance coverage. For privately insured births, the father’s suboptimal physical health made it more likely that the mother, but not the child, became uninsured.

The Effects of Health on Health Insurance Status in Fragile Families

We use data from the Fragile Families and Child Wellbeing study to estimate the effects of poor infant health, pre-pregnancy health conditions of the mother, and the father's health status on health insurance status of urban, mostly unmarried, mothers and their one-year-old children. Virtually all births were covered by health insurance, but one year later about one third of mothers and over 10 percent of children were uninsured. We separately examine births that were covered by public insurance and those that were covered by private insurance. The child's health status had no effect, for the most part, on whether the mother or child became uninsured. For publicly insured births, a maternal physical health condition made it less likely that both the mother and child became uninsured, while maternal mental illness made it more likely that both the mother and child lost insurance coverage. For privately insured births, the father's suboptimal physical health made it more likely that the mother, but not the child, became uninsured.

FOXA1 mutations in hormone-dependent cancers.

The forkhead protein, FOXA1, is a critical interacting partner of the nuclear hormone receptors, oestrogen receptor-α (ER) and androgen receptor (AR), which are major drivers of the two most common cancers, namely breast and prostate cancer. Over the past few years, progress has been made in our understanding of how FOXA1 influences nuclear receptor function, with both common and distinct roles in the regulation of ER or AR. Recently, another level of regulation has been described, with the discovery that FOXA1 is mutated in 1.8% of breast and 3-5% prostate cancers. In addition, a subset of both cancer types exhibit amplification of the genomic region encompassing the FOXA1 gene. Furthermore, there is evidence of somatic changes that influence the DNA sequence under FOXA1 binding regions, which may indirectly influence FOXA1-mediated regulation of ER and AR activity. These recent observations provide insight into the heterogeneity observed in ER and AR driven cancers

Infographics: An Innovative Tool to Capture Consumers Attention

Using infographics as educational tools has emerged as a strategy to reach consumers in today\u27s information-saturated environment. Through the use of engaging and informative graphics, educators can deliver meaningful messages tailored to targeted audiences. Varying types of effectively designed infographics can be used to capture the attention of consumers by: telling a story, clarifying complex information with evidence-based information or research findings, using innovative design, and reaching targeted audiences in easily accessible places. Combining innovative infographic design and targeted dissemination strategies, Extension educators can capture consumers\u27 attention and deliver clear messages to improve communication with consumers

Preserving North Carolina's Last Textile Landscape: The Case for Henry River Mill Village

This paper investigates the history and architecture of the functionally obsolete and abandoned Henry River Mill Village and offers a preservation strategy for the site. This thesis contributes to the historical narrative of the textile industry and the landscapes that emerged from this industry in the state of North Carolina between 1880 and 1915. Based on research via primary and secondary sources, a site visit, interviews with historians, planners, non-profits and local and state leaders over a year-long period, it became apparent that traditional preservation strategies for Henry River were not appropriate and/or viable options. The preservation strategy offered is for the site to function as a cultural resource set in a public park, with the extant and ruinous architecture stabilized and interpreted, with the exception of the company store which should be rehabilitated and renovated. The site will function as a connector to the region and state's greenway and blueway corridors. To conclude, preservation in this form, as a "ghost town," represents the state's textile heritage in the purest form because its ruinous state does not conceal the post-industrial condition of the departed textile industry. Refurbished historic sites are not realistic representations of the condition of the recent past. Henry River Mill Village could serve as the first and only representation of an intact, post-industrial textile landscape in North Carolina

Genetic networks in Parkinson's and Alzheimer's disease

Parkinson\u27s disease (PD) and Alzheimer\u27s disease (AD) are the most common neurodegenerative diseases and there is increasing evidence that they share common physiological and pathological links. Here we have conducted the largest network analysis of PD and AD based on their gene expressions in blood to date. We identified modules that were not preserved between disease and healthy control (HC) networks, and important hub genes and transcription factors (TFs) in these modules. We highlighted that the PD module not preserved in HCs was associated with insulin resistance, and HDAC6 was identified as a hub gene in this module which may have the role of influencing tau phosphorylation and autophagic flux in neurodegenerative disease. The AD module associated with regulation of lipolysis in adipocytes and neuroactive ligand-receptor interaction was not preserved in healthy and mild cognitive impairment networks and the key hubs TRPC5 and BRAP identified as potential targets for therapeutic treatments of AD. Our study demonstrated that PD and AD share common disrupted genetics and identified novel pathways, hub genes and TFs that may be new areas for mechanistic study and important targets in both diseases

A microfluidic-multiwell platform for rapid phase mapping of surfactant solutions

Measurement of the phase behavior and (meta)stability of liquid formulations, including surfactant solutions, is required for the understanding of mixture thermodynamics, as well as their practical utilization. We report a microfluidic platform with a stepped temperature profile, imposed by a dual Peltier module, connected to an automated multiwell plate injector and optical setup, for rapid solution phase mapping. The measurement protocol is defined by the temperature step ΔT ≡ T1 − T2 (≲100 ○C), volumetric flow rate Q ≡ ΔV/Δt (≲50 μl/min), which implicitly set the thermal gradient ΔT/Δt (≃0.1–50 ○C/min), and measurement time (which must exceed the intrinsic timescale of the relevant phase transformation). Furthermore, U-shaped microchannels can assess the reversibility of such transformations, yielding a facile measurement of the metastable zone width of the phase diagram. By contrast with traditional approaches, the platform precisely controls the cooling and heating rates by tuning the flow rate, and the absolute temperature excursion by the hot and cold thermal profile, which remain stationary during operation, thus allowing the sequential and reproducible screening of large sample arrays. As a model system, we examined the transition from the micellar (L1) to the liquid crystalline lamellar phase (Lα), upon cooling, of aqueous solutions of sodium linear alkylbenzene sulfonate, a biodegradable anionic surfactant extensively employed in industry. Our findings are validated with quiescent optical microscopy and small angle neutron scattering data