Publications by authors named "Vona Davis"

Introduction: Dissociative identity disorder (DID) is a treatable mental health condition that is associated with a range of psychobiological manifestations. However, historical controversy, modern day misunderstanding, and lack of professional education have prevented accurate treatment information from reaching most clinicians and patients. These obstacles also have slowed empirical efforts to improve treatment outcomes for people with DID.

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Objectives: Concerns about the cognitive adverse effects of electroconvulsive therapy (ECT) are common among recipients of the treatment despite its relatively small adverse effects on cognitive functioning. Interventions aimed at remediating or improving coping with cognitive adverse effects of ECT have not been developed. The Enhancing Cognitive Domains after ECT (ENCODE) program is a new group intervention aimed at teaching self-management strategies to cope with the cognitive challenges and associated anxiety that often accompanies ECT.

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Introduction: Publishing research is an important component of medical students' career development and becoming a more competitive residency applicant. Many medical schools offer structured programs to enable students to participate in research during their preclinical and clinical years, but the majority of student-mentor partnerships do not culminate in publication across a variety of institutions and medical specialties. The primary objective of this study is to determine if any factors associated with mentee-mentor partnerships are predictive of publication from two school-sponsored research programs at a single US medical school.

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Hyperspectral imaging (HSI) is a non-invasive optical imaging modality that shows the potential to aid pathologists in breast cancer diagnoses cases. In this study, breast cancer tissues from different patients were imaged by a hyperspectral system to detect spectral differences between normal and breast cancer tissues. Tissue samples mounted on slides were identified from 10 different patients.

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Little is known about how clinical oncology concepts are taught to PhD students or the most effective methods of doing so. In this study, electronic surveys were sent to faculty and students at PhD training programs, assessing their institution's methods of clinical oncology education and their perspective on optimal approaches to clinical oncology education. Only 40.

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Modern cancer therapy/care involves the integration of basic, clinical, and population-based research professionals using state-of-the-art science to achieve the best possible patient outcomes. A well-integrated team of basic, clinical, and population science professionals and educators working with a fully engaged group of creative junior investigators and trainees provides a structure to achieve these common goals. To this end, the structure provided by cancer-focused educational programs can create the integrated culture of academic medicine needed to reduce the burden of cancer on society.

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Obese postmenopausal women have an increased breast cancer risk, the principal mechanism for which is elevated estrogen production by adipose tissue; also, regardless of menstrual status and tumor estrogen dependence, obesity is associated with biologically aggressive breast cancers. Type 2 diabetes has a complex relationship with breast cancer risk and outcome; coexisting obesity may be a major factor, but insulin itself induces adipose aromatase activity and estrogen production and also directly stimulates breast cancer cell growth and invasion. Adipose tissue inflammation occurs frequently in obesity and type 2 diabetes, and proinflammatory cytokines and prostaglandin E2 produced by cyclooxygenase-2 in the associated infiltrating macrophages also induce elevated aromatase expression.

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Epidemiological studies provide strong evidence that obesity and the associated adipose tissue inflammation are risk factors for breast cancer; however, the molecular mechanisms are poorly understood. We evaluated the effect of a high-fat/high-calorie diet on mammary carcinogenesis in the immunocompetent MMTV-PyMT murine model. Four-week old female mice (20/group) were randomized to receive either a high-fat (HF; 60% kcal as fat) or a low-fat (LF; 16% kcal) diet for eight weeks.

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Purpose: Reducing vascular endothelial growth factor (VEGF) in adipose tissue alters adipose vascularity and metabolic homeostasis. We hypothesized that this would also affect metabolic responses during exercise-induced stress and that adipocyte-specific VEGF-deficient (adipoVEGF-/-) mice would have impaired endurance capacity.

Methods: Endurance exercise capacity in adipoVEGF-/- (n = 10) and littermate control (n = 11) mice was evaluated every 4 wk between 6 and 24 wk of age using a submaximal endurance run to exhaustion at 20 m·min(-1) at 10° incline.

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Purpose: Regular exercise and healthy eating are routinely recommended for breast cancer survivors, and past studies show benefits in quality of life and decreased inflammation. However, this has not been tested specifically in triple-negative breast cancer survivors. Increasing physical activity and losing body fat are thought to positively affect inflammatory biomarkers that have been associated with breast cancer.

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Risk perceptions are motivating factors for engaging in preventive health behaviors. Yet, almost one third of women attending a mobile mammography program targeted to rural and medically underserved Appalachian women respond "don't know" to their perceived 5-year risk of breast cancer. This study used cross-sectional data from women aged >40 years participating in Bonnie's Bus Mammography Screening and Preventive Care Survey from 2009 to 2011 to identify factors associated with "don't know" responses and accuracy of perceived risk according to constructs of the health belief model and sociodemographic characteristics.

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Breast cancer patients in rural Appalachia have a high prevalence of obesity and poverty, together with more triple-negative phenotypes. We reviewed clinical records for tumor receptor status and time to distant metastasis. Body mass index, tumor size, grade, nodal status, and receptor status were related to metastatic patterns.

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Inflammation of the adipose tissues occurs in association with obesity. This inflammatory process leads to the induction of cyclooxygenase-2 (COX-2) expression and a consequent elevation in prostaglandin (PG) production, which, together with proinflammatory cytokines, induce aromatase expression and estrogen synthesis. Infiltrating macrophages support the growth of breast epithelial cells and vascular endothelial cells by producing a milieu of cytokines and growth factors.

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Upper body obesity is a risk factor for postmenopausal breast cancer and is related to an aggressive tumor phenotype and a poor prognosis regardless of menopausal status. After the menopause, the major mechanism for the association with disease risk is elevated estrogen production by adipose tissue, due to a high level of aromatase activity: these hormone-dependent tumors express both estrogen and progesterone receptors. Other important biological factors of risk include leptin and adiponectin, adipokines with opposing endocrine and paracrine activities, and obesity-related hyperinsulinemia.

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Epidemiological studies have related hyperinsulinemia and type 2 diabetes to an increased breast cancer risk, an aggressive and metastatic phenotype, and a poor prognosis. Furthermore, diabetic retinopathy arises from pathological angiogenesis, which is also essential for breast cancer growth and metastasis. Insulin stimulates the proliferation of some human breast cancer cell lines in vitro by mechanisms that use both the phosphatidylinositol-3 kinase and the mitogen-activated protein kinase/Akt signaling pathways; it is also a cell survival (anti-apoptotic) agent and enhances tumor cell migration and invasive capacity.

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The objective was to review type 2 diabetes as a risk factor for breast cancer, its influence on tumor aggressiveness and prognosis, and the interactions with obesity. Consideration was given to the responsible biological mechanisms and how these relate to the potential of hypoglycemic agents, notably metformin, as breast cancer chemotherapeutic agents. Most epidemiological studies indicate that type 2 diabetes is a modest positive risk factor for postmenopausal, but not premenopausal, breast cancer; indeed before the menopause it may be associated with a reduced risk.

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The objectives of this study were to evaluate the characteristics (demographic, access to care, health-related behavioral, self and family medical history, psychosocial) of women age 40 years and above who participated in a mobile mammography screening program conducted throughout West Virginia (WV) to determine the factors influencing their self-reported adherence to mammography screening guidelines. Data were analyzed using the Andersen Behavioral Model of Healthcare Utilization framework to determine the factors associated with adherence to mammography screening guidelines in these women. Of the 686 women included in the analysis, 46.

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Obesity has a complex relationship to breast cancer risk that differs in premenopausal and postmenopausal women. Before the menopause, the level of adiposity is inversely related to risk, indicative of a protective effect, whereas in postmenopausal women, particularly the elderly, the association is a positive one, consistent with obesity being a risk factor. The importance of high estrogen production in adipose tissue, with consequent elevation of circulating biologically available estradiol, in the promotional effect of obesity on postmenopausal breast carcinogenesis is well established; the resulting tumors express both estrogen and progesterone receptors.

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In 2007, the American Cancer Society ranked West Virginia 43rd in breast cancer incidence rates for individual states. Despite our improvements in medical care, the advanced pathological characteristics of breast cancer at diagnosis receive little attention. Consequently, we compared the changing pattern of early breast cancer in several cohort studies conducted at regional medical centers in West Virginia.

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Pre-existing obesity and postoperative weight gain are related to a poor prognosis in breast cancer regardless of menopausal status. Delayed diagnosis may be one cause, but of more biological significance, especially in younger women, is the association of adiposity with estrogen receptor-negative tumors with a propensity for distant metastasis. After the menopause, the major mechanism for the relationship is the elevated estrogen synthesis by adipose tissue; these hormone-dependent tumors are estrogen receptor-positive.

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The prevalence of overweight and obesity is rapidly increasing world wide. Numerous epidemiological studies have shown that obesity is a risk factor for postmenopausal breast cancer and relapse. However, the biological factors that drive the growth and progression of these tumors and how obesity contributes to the tumor microenvironment are poorly understood.

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Objective: Socioeconomic deprivation is associated with an increased risk of breast cancer mortality. This article summarizes the relationships between socioeconomic status (SES) and breast cancer in white European women compared with racial and ethnic groups in the United States. Furthermore, we examine the association between obesity and breast cancer within socioeconomic disparities.

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Background: Our objective was to determine the clinicopathologic features of triple-negative (estrogen receptor, progesterone receptor, and human epidermal growth factor-2 receptor negative) breast cancer and their relationship to obesity in women drawn from a population with one of the highest obesity rates in the United States.

Methods: This retrospective study involved 620 White patients with invasive breast cancer in West Virginia. Hospital tumor registry, charts, and pathology records provided age at diagnosis, tumor histologic type, size, nodal status, and receptor status.

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