Self-appropriation in nurse engagement: Facilitating the development of expert nurses using Benner and Lonergan.

Expert nurses, as described by the work of Patricia Benner, are at the peak of clinical nursing practice and vitally important in ensuring the best possible patient care and clinical outcomes. The development of Benner's theory and its relationship with the Dreyfus model of skill acquisition provides context for understanding the progression necessary for expert development. Contemporary healthcare challenges present implications to the development of advancing levels of nursing practice. Engagement has been identified as critical to achieving expert practice. I propose the incorporation of the philosophical framework of self-appropriation from Benard Lonergan as a strategy to develop internal engagement in nurses to facilitate expert practice. I outline the synergy between Benner's theory and the work of Lonergan, which provide overlap and opportunity to overcome barriers to developing expert nursing practice. In the challenging climate of healthcare, there is an obligation to promote engagement and facilitate expert nurse development, necessary for patient outcomes as well as clinical role models, preceptors, and leaders to guide future nurses.

Estrogen suppresses expression of the matrix metalloproteinase inhibitor reversion-inducing cysteine-rich protein with Kazal motifs (RECK) within the mouse uterus.

RECK (reversion-inducing cysteine-rich protein with Kazal motifs) is a membrane-anchored glycoprotein which regulates MMP2 and MMP9 activity and has been proposed to play a role in embryo implantation while misexpression of RECK has been associated with a variety of carcinomas. Unfortunately, understanding on the steroidal regulation of uterine RECK is lacking. To address this gap in our knowledge, we examined steroidal regulation and cellular expression of Reck mRNA and protein within the mouse uterus in vivo. Uterine Reck mRNA and protein were decreased by estrogen, while progesterone alone had no effect. The estrogen-induced down regulation could be partially blocked by progesterone. RECK was localized primarily to luminal and glandular epithelial cells and the level of expression was regulated in a similar fashion as in whole tissue by the steroids. Knock-down of endogenous RECK in human endometrial epithelial and stromal cells resulted in a significant increase in active MMP9 expression but not that of pro-MMP9 or MMP2. These studies demonstrate that RECK expression in the mouse uterus is steroidally regulated and that within endometrial epithelial and stromal cells, RECK regulates MMP9, but not MMP2 activity.

Steroidal regulation of uterine miRNAs is associated with modulation of the miRNA biogenesis components Exportin-5 and Dicer1.

MicroRNAs (miRNAs) are small, non-coding RNA molecules which post-transcriptionally regulate gene expression. We have previously demonstrated that within the uterus, miRNA expression is under steroidal control and that disruption of Dicer1, the enzyme which generates mature miRNAs, leads to abnormalities in the development and function of the female reproductive tract. Despite the apparent importance of miRNAs and the enzymes which lead to their generation, little to no information exists on the mechanisms which regulate the expression of this system in the female reproductive tract. The objective of the current study was to examine steroidal regulation of the miRNAs biogenesis enzymes, Drosha, Dgcr8, Exportin-5 and Dicer1 in the mouse uterus. The results of this study indicate that estrogen and progesterone significantly increased Exportin-5 mRNA expression while only progesterone increased Dicer1 expression. We conclude from these studies that the miRNA biogenesis components Drosha, Dgcr8, Exportin-5 and Dicer1 are expressed in the mouse uterus and that Exportin-5 and Dicer1 appear to be the major steroid regulated components in the miRNA biogenesis pathway. These observations suggest that in addition to steroids modulating miRNA expression at the level of transcription, they may also influence miRNA expression by regulating the expression of the miRNA biogenesis components necessary for their processing to the mature cytoplasmic form.

Estrogen induces distinct patterns of microRNA expression within the mouse uterus.

Control of estrogenic activity within the uterus is evident as unopposed estrogen action is associated with endometrial pathologies such as endometriosis and endometrial carcinoma. MicroRNAs (miRNAs) have emerged as important posttranscriptional regulators, which are postulated to fine-tune the actions of steroids in many systems including the uterus. The objective of the current study was to examine uterine expression of miRNAs in response to estrogen treatment within the mouse uterus using an ovariectomized, steroid-reconstituted mouse model. MicroRNA microarray analysis and subsequent quantitative real-time reverse transcriptase polymerase chain reaction (qRT-PCR) verification revealed that expression of mirn155, mirn429, and mirn451 was significantly increased by estrogen administration whereas mirn181b and mirn204 expression was significantly reduced. Pretreatment with the estrogen receptor (ER) antagonist ICI 182,780 confirmed that estrogen regulation was mediated via the classical ER pathway. This study demonstrates that estrogen regulates specific miRNAs within the murine uterus, which may participate in posttranscriptional regulation of estrogen-regulated genes.