Stress resiliency, psychological empowerment and conflict management styles among baccalaureate nursing students.

AIMS: This article is a report of a Neuman Systems Model-guided correlational study of the relations of stress resiliency, psychological empowerment, selected demographic characteristics (age, ethnicity, semester in school) and conflict management styles. BACKGROUND: Emerging evidence suggests that stress resiliency and psychological empowerment can strengthen student nurses in academic achievement and coping with stress. Little is known about conflict management styles of students and the relationship to empowerment, resiliency and the implications for managing workplace conflict. METHODS: A correlational study was conducted in Spring 2010 with 166 baccalaureate students. Most participants were female, single, Hispanic and 25 years old. The data collection instruments included the Stress Resiliency Profile, the Psychological Empowerment Instrument, the Conflict Mode Instrument and a demographic inventory. Descriptive and inferential correlational statistics were used to analyse the data. RESULTS: Students scored in the high range for focusing on their deficiencies in conflict situations; they scored above the 60th percentile for avoiding and accommodating behaviours and were less likely to use competing or collaborating strategies to manage conflict. Empowerment scores were significantly correlated with stress resiliency scores. Students with high scores on empowerment had high scores on the skill recognition subscale of the Stress Resiliency Profile suggesting more resilience; high scores on empowerment were related to high necessitating subscale scores of the Stress Resiliency Profile suggesting a predisposition to stress. CONCLUSIONS: Neuman Systems Model may provide guidance for educators to strengthen student nurses' management of stressors in the workplace.

A family history intervention: enhancing cardiovascular risk assessment.

This article describes the effect of individualized counseling using family history data and objective cardiovascular risk factors on intent to change and actual exercise behavior in a diverse sample of working adults. Using a longitudinal, quasi-experimental, crossover design, objective data (blood lipids, glucose, blood pressure, and body mass index) and subjective data (awareness of heart disease risk, depression, spirituality, and knowledge of family history) were collected from 91 (mostly female and with a mean age of 45 years) primary and secondary teachers in a southwestern city. The Transtheoretical Model of Change guided the study and measured intent to exercise. Objective risks in this sample mirrored national indices of risk for obesity and abnormal lipids. Although some participants increased their exercise, no significant differences were found between the groups in exercise behavior at 6 and 12 months. Using knowledge of family history to raise awareness and encourage lifestyle changes related to cardiovascular risk warrants further study.

Developmental reprogramming of IGF signaling and susceptibility to endometrial hyperplasia in the rat.

In rodents, a brief neonatal exposure of the developing reproductive tract to the xenoestrogen, diethylstilbestrol (DES) reprograms developing tissues to increase susceptibility to tumorigenesis in adult animals, including uterine adenocarcinoma. Progression from a normal endometrium to carcinoma occurs via the intermediate stage of endometrial hyperplasia. We previously reported that endometrial hyperplasia in postmenopausal women is linked to abnormal insulin-like growth factor-I (IGF-I) signaling. To identify early events involved in the development of hyperplasia in the endometrium, we examined expression and activation of IGF-I pathway components in endometrium of rats exposed to DES. By 5 months of age, 36/60 (60%) of rats exposed to DES on days 3-5 after birth developed endometrial hyperplasia compared to 0% of vehicle-treated controls. Consistent with activation of a mitogenic signaling pathway, Ki67-positive cells increased in DES-exposed endometrium despite compromised ovarian function and hypoestrogenic milieu characteristic of DES-exposed animals. The endometrium of DES-exposed rats overexpressed IGF-II and insulin receptor substrate-1 (IRS-1) and exhibited elevated Akt expression and activation (as judged by phosphorylation) and mTOR signaling (phosphorylation of S6) compared to vehicle-treated endometrium. In contrast to vehicle-treated endometrium, in which negative feedback to IRS-1 was observed (phosphorylation of S636/639), negative feedback to IRS-1 was absent in DES-exposed endometrium. These data support a central role for IGF-I signaling in the development of both human and rodent endometrial hyperplasia. Furthermore, both global activation of IGF-IR signaling and abrogation of negative feedback to IRS-1 appear to be reprogrammed by DES in endometrial hyperplasia, implicating for the first time loss of negative feedback to IRS-1 in development of a preneoplastic lesion.

Tamoxifen functions as a molecular agonist inducing cell cycle-associated genes in breast cancer cells.

Tamoxifen is a widely used breast cancer therapeutic and preventative agent. Although functioning as an estrogen antagonist at the cellular level, transcriptional profiling revealed that at the molecular level, tamoxifen functions largely as an agonist, virtually recapitulating the gene expression profile induced in breast cancer cells by estrogen. Remarkably, tamoxifen induces transcription factors and genes involved in promoting cell cycle progression including fos, myc, myb, cdc25a, cyclins E and A2, and stk15 with kinetics that paralleled that of cells cycling in response to estrogen, even though tamoxifen-treated cells are not transiting through the cell cycle. Induction of cell cycle-associated genes was specific for tamoxifen, and did not occur with raloxifene. However, cyclin D1 was a key estrogen-induced gene not expressed in response to tamoxifen or raloxifene but constitutively expressed in tamoxifen-resistant cells.

Treatment strategies for uterine leiomyoma: the role of hormonal modulation.

Uterine leiomyomas are the most common gynecological tumors and are a significant health concern for many women. Although the exact etiology of these tumors is unknown, epidemiological and experimental animal studies have established a role for ovarian hormones in the pathogenesis of this disease. Current treatment regimens for symptomatic tumors primarily require surgical intervention. However, a major emphasis of leiomyoma research involves understanding how hormones regulate tumor growth to target the hormonal dependence of these tumors with new therapeutic strategies. Gonadotropin-releasing hormone agonists that block hormone production and induce a hypoestrogenic milieu can be utilized as adjuvant therapy; however, these drugs do little to reduce tumor cellularity, and their negative impact on bone mineral density limits their use. Selective estrogen receptor modulators (SERMs) are nonsteroidal therapeutic agents that bind to the estrogen receptor and elicit tissue-specific estrogen agonist or antagonist effects. SERMs are effective in the treatment and prevention of breast cancer, and preclinical and clinical data suggest that these hormonal modulators may also be beneficial for the treatment of uterine leiomyomas. Continued efforts to understand the role of hormones in the development of this disease will allow the development of newer, less invasive treatment strategies, which will help minimize the negative impact of these tumors on women's health.

Enhancing resilience, empowerment, and conflict management among baccalaureate students: outcomes of a pilot study.

To manage interpersonal conflict, nursing students need evidence-based interventions to strengthen stress resiliency, psychological empowerment, and conflict management skills. A pilot 1-group, pre-post-design, 2-semester intervention used simulated experiences to enhance these skills with 60 undergraduate nursing students. Findings suggest that integration of conflict resolution skills throughout the curriculum, with repeated opportunities to practice using a variety of styles of conflict management in relation to situational factors, may be beneficial to prepare students for the challenges of today's healthcare environment.

Interaction between genetic susceptibility and early-life environmental exposure determines tumor-suppressor-gene penetrance.

Gene-environment interactions are important determinants of cancer risk. Traditionally, gene-environment interactions are thought to contribute to tumor-suppressor-gene penetrance by facilitating or inhibiting the acquisition of additional somatic mutations required for tumorigenesis. Here, we demonstrate that a distinctive type of gene-environment interaction can occur during development to enhance the penetrance of a tumor-suppressor-gene defect in the adult. Using rats carrying a germ-line defect in the tuberous sclerosis complex 2 (Tsc-2) tumor-suppressor gene predisposed to uterine leiomyomas, we show that an early-life exposure to diethylstilbestrol during development of the uterus increased tumor-suppressor-gene penetrance from 65% to >90% and tumor multiplicity and size in genetically predisposed animals, but it failed to induce tumors in wild-type rats. This exposure was shown to impart a hormonal imprint on the developing uterine myometrium, causing an increase in expression of estrogen-responsive genes before the onset of tumors. Loss of function of the normal Tsc-2 allele remained the rate-limiting event for tumorigenesis; however, tumors that developed in exposed animals displayed an enhanced proliferative response to steroid hormones relative to tumors that developed in unexposed animals. These data suggest that exposure to environmental factors during development can permanently reprogram normal physiological tissue responses and thus lead to increased tumor-suppressor-gene penetrance in genetically susceptible individuals.