Publications by authors named "S A Moyer"

The tumor suppressor gene is mutated early in most of the patients with triple-negative breast cancer (TNBC). The most frequent alterations are missense mutations that contribute to tumor aggressiveness. Here, we used an autochthonous somatic TNBC mouse model, in which mutant p53 can be toggled on and off genetically while leaving the tumor microenvironment intact and wild-type for p53 to identify physiological dependencies on mutant p53.

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Introduction: The purpose of this study was to explore the reliability and construct validity of the EPDS-US.

Methods: To enhance the perinatal mental health screen, we adapted the Edinburgh Postnatal Depression Screen (EPDS) for application in the United States, and evaluated reliability and construct validity of the EPDS-US in a sample of 100 postpartum individuals. We explored reliability by estimating internal consistency of the scale and evaluating concurrent validity with correlations to the Patient Health Questionnaire (PHQ-9) and the Generalized Anxiety Disorder Assessment (GAD-7); and construct validity using factor analysis and discriminant validity with correlations to the Perceived Stress Scale (PSS).

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Cryptococcosis studies often utilize the common C57BL/6J mouse model. Unfortunately, infection in these mice fails to replicate the basic course of human disease, particularly hampering immunological studies. This work demonstrates that SJL/J mice can recapitulate human infection better than other mouse strains.

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To present the development protocol of the Edinburgh Postnatal Depression Scale-United States (EPDS-US), an adapted version of the EPDS, that is inclusive and easy to understand for U.S. populations and incorporates a trauma-informed approach to perinatal mental health (PMH).

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The tumor suppressor gene is mutated early in the majority of patients with triple-negative breast cancer (TNBC). The most frequent alterations are missense mutations that contribute to tumor aggressiveness. We developed an autochthonous somatic K14-Cre driven TNBC mouse model with p53R172H and p53R245W mutations in which mutant p53 can be toggled on and off genetically while leaving the tumor microenvironment intact and wild-type for p53.

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