Effective leadership of healthcare professionals is critical for strengthening quality and integration of care. This study aimed to assess whether there exist an association between different leadership styles and healthcare quality measures. The search was performed in the Medline (National Library of Medicine, PubMed interface) and EMBASE databases for the time period 2004–2015. The research question that guided this review was posed as: “Is there any relationship between leadership style in healthcare settings and quality of care?” Eighteen articles were found relevant to our research question. Leadership styles were found to be strongly correlated with quality care and associated measures. Leadership was considered a core element for a well-coordinated and integrated provision of care, both from the patients and healthcare professionals.
22 September 2016 in Journal of Educational Evaluation for Health Professions
Purpose: The aim of this systematic review was to find best teaching strategies for teaching evidence-based practice (EBP) to undergraduate health students that have been adopted over the last years in healthcare institutions worldwide. Methods: The authors carried out a systematic, comprehensive bibliographic search using Medline database for the years 2005 to March 2015 (updated in March 2016). Search terms used were chosen from the USNLM Institutes of Health list of MeSH (Medical Subject Headings) and free text key terms were used as well. Selected articles were measured based on the inclusion criteria of this study and initially compared in terms of titles or abstracts. Finally, articles relevant to the subject of this review were retrieved in full text. Critical appraisal was done to determine the effects of strategy of teaching evidence-based medicine (EBM). Results: Twenty articles were included in the review. The majority of the studies sampled medical students (n=13) and only few conducted among nursing (n=2), pharmacy (n=2), physiotherapy/therapy (n=1), dentistry (n=1), or mixed disciplines (n=1) students. Studies evaluated a variety of educational interventions of varying duration, frequency and format (lectures, tutorials, workshops, conferences, journal clubs, and online sessions), or combination of these to teach EBP. We categorized interventions into single interventions covering a workshop, conference, lecture, journal club, or e-learning and multifaceted interventions where a combination of strategies had been assessed. Seven studies reported an overall increase to all EBP domains indicating a higher EBP competence and two studies focused on the searching databases skill. Conclusion: Followings were deduced from above analysis: multifaceted approach may be best suited when teaching EBM to health students; the use of technology to promote EBP through mobile devices, simulation, and the web is on the rise; and the duration of the interventions varying form some hours to even months was not related to the students’ EBP competence.
Tamoxifen is the treatment of choice in estrogen receptor alpha breast cancer patients that are eligible for adjuvant endocrine therapy. However, ∼50% of ERα‐positive tumors exhibit intrinsic or rapidly acquire resistance to endocrine treatment. Unfortunately, prediction of de novo resistance to endocrine therapy and/or assessment of relapse likelihood remain difficult. While several mechanisms regulating the acquisition and the maintenance of endocrine resistance have been reported, there are several aspects of this phenomenon that need to be further elucidated. Altered metabolic fate of tamoxifen within patients and emergence of tamoxifen‐resistant clones, driven by evolution of the disease phenotype during treatment, appear as the most compelling hypotheses so far. In addition, tamoxifen was reported to induce pluripotency in breast cancer cell lines, in vitro. In this context, we have performed a whole transcriptome analysis of an ERα‐positive (T47D) and a triple‐negative breast cancer cell line (MDA‐MB‐231), exposed to tamoxifen for a short time frame (hours), in order to identify how early pluripotency‐related effects of tamoxifen may occur. Our ultimate goal was to identify whether the transcriptional actions of tamoxifen related to induction of pluripotency are mediated through specific ER‐dependent or independent mechanisms. We report that even as early as 3 hours after the exposure of breast cancer cells to tamoxifen, a subset of ERα‐dependent genes associated with developmental processes and pluripotency are induced and this is accompanied by specific phenotypic changes (expression of pluripotency‐related proteins). Furthermore we report an association between the increased expression of pluripotency‐related genes in ERα‐positive breast cancer tissues samples and disease relapse after tamoxifen therapy. Finally we describe that in a small group of ERα‐positive breast cancer patients, with disease relapse after surgery and tamoxifen treatment, ALDH1A1 (a marker of pluripotency in epithelial cancers which is absent in normal breast tissue) is increased in relapsing tumors, with a concurrent modification of its intra‐cellular localization. Our data could be of value in the discrimination of patients susceptible to develop tamoxifen resistance and in the selection of optimized patient‐tailored therapies.
Recently an increased interest on Elk1 protein and its role in breast cancer evolution has been noted. This protein is an element of the Ets family of transcription factors and it has been involved in a number of important cell processes through the activation of different genes, in a number of normal tissues as well as in many malignancies. One hundred and seventy (n = 170) cases of operable breast cancer (invasive ductal, lobular and mixed type breast carcinomas) were randomly selected and investigated for the expression of pElk-1, Ki-67 and Cyclin D1 using immunohistochemistry. Our findings were correlated with tumors' clinicopathologic data and biologic profile. Activated Elk1 is positively associated with ER (p-value: 0.018) and also shows a positive association of with Cyclin D1 (p-value: <0.001). No relationship was noted between pElk1 and Ki67 (p-value: 0.213). Luminal A and B Her-2 negative breast cancer subtypes were showing greater pElk-1 immunoreactivity compared to Her-2 and Basal breast cancer subtypes, and also a higher staining intensity. No association of the molecule with other clinicopathologic characteristics (tumor size, stage, histological type or lymph node metastases) or disease adverse events (local recurrence, metastasis or death) was evidenced. Our findings offer a new perspective for the role of pElk-1 in breast neoplasia suggesting a direct relation of this molecule to tumor biology and a putative target of personalized breast cancer therapies, although its prognostic/discriminant role is not supported.