Browsing by Author "Richard M. Fairbanks School of Public Health"

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    Ensuring a Strong Public Health Workforce for the 21st Century: Reflections on PH WINS 2017
    (Wolters Kluwer, 2019-03) Halverson, Paul K.; Richard M. Fairbanks School of Public Health
    The success of any organization can be attributed to one thing: its people. This is particularly true for local health departments (LHDs) and state health agencies (SHAs), as the public health workforce is fundamental to achieving organizational goals and improving the health outcomes of populations.
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    The Impact of Gain- and Loss-Framed Messages on Young Adults' Sexual Decision Making: An Experimental Study
    (Springer, 2017-02) Macapagal, Kathryn; Janssen, Erick; Matson, Margaret; Finn, Peter R.; Heiman, Julia R.; Richard M. Fairbanks School of Public Health
    Messages that frame a target behavior in terms of its benefits (gain frame) or costs (loss frame) have been widely and successfully used for health promotion and risk reduction. However, the impact of framed messages on decisions to have sex and sexual risk, as well as moderators of these effects, has remained largely unexplored. We used a computerized laboratory task to test the effects of framed messages about condom use on young adults' sexual decision making. Participants (N = 127) listened to both gain- and loss-framed messages and rated their intentions to have sex with partners who posed a high and low risk for sexually transmitted infections (STIs). The effects of message frame, partner risk, participant gender, ability to adopt the messages, and message presentation order on intentions to have sex were examined. Intentions to have sex with high-risk partners significantly decreased after the loss-framed message, but not after the gain-framed message, and intentions to have sex increased for participants who received the gain-framed message first. Yet, participants found it easier to adopt the gain-framed message. Results suggest that loss-framed messages may be particularly effective in reducing intentions to have sex with partners who might pose a higher risk for STIs, and that message presentation order may alter the relative effectiveness of gain- and loss-framed messages on sexual decision making. Future studies should examine the precise conditions under which gain- and loss-framed messages can promote healthy sexual behaviors and reduce sexual risk behaviors.
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    Polycyclic Aromatic Hydrocarbons and Pancreatic Cancer: An Analysis of the Blood Biomarker, r-1,t-2,3,c-4-Tetrahydroxy-1,2,3,4-tetrahydrophenanthrene and Selected Metabolism Gene SNPs
    (MDPI, 2024-02-28) Nguyen, Sierra; Carlson, Heather; Yoder, Andrea; Bamlet, William R.; Oberg, Ann L.; Petersen, Gloria M.; Carmella, Steven G.; Hecht, Stephen S.; Jansen, Rick J.; Richard M. Fairbanks School of Public Health
    Exposure to polycyclic aromatic hydrocarbons (PAHs), byproducts of incomplete combustion, and their effects on the development of cancer are still being evaluated. Recent studies have analyzed the relationship between PAHs and tobacco or dietary intake in the form of processed foods and smoked/well-done meats. This study aims to assess the association of a blood biomarker and metabolite of PAHs, r-1,t-2,3,c-4-tetrahydroxy-1,2,3,4-tetrahydrophenanthrene (PheT), dietary intake, selected metabolism SNPs, and pancreatic cancer. Demographics, food-frequency data, SNPs, treatment history, and levels of PheT in plasma were determined from 400 participants (202 cases and 198 controls) and evaluated based on pancreatic adenocarcinoma diagnosis. Demographic and dietary variables were selected based on previously published literature indicating association with pancreatic cancer. A multiple regression model combined the significant demographic and food items with SNPs. Final multivariate logistic regression significant factors (p-value < 0.05) associated with pancreatic cancer included: Type 2 Diabetes [OR = 6.26 (95% CI = 2.83, 14.46)], PheT [1.03 (1.02, 1.05)], very well-done red meat [0.90 (0.83, 0.96)], fruit/vegetable servings [1.35 (1.06, 1.73)], recessive (rs12203582) [4.11 (1.77, 9.91)], recessive (rs56679) [0.2 (0.06, 0.85)], overdominant (rs3784605) [3.14 (1.69, 6.01)], and overdominant (rs721430) [0.39 (0.19, 0.76)]. Of note, by design, the level of smoking did not differ between our cases and controls. This study does not provide strong evidence that PheT is a biomarker of pancreatic cancer susceptibility independent of dietary intake and select metabolism SNPs among a nonsmoking population.