Clinical decision making: validation of the nursing anxiety and self-confidence with clinical decision making scale (NASC-CDM ©) into Spanish and comparative cross-sectional study in nursing students.

BACKGROUND: Decision making is a pivotal component of nursing education worldwide. This study aimed to accomplish objectives: (1) Cross-cultural adaptation and psychometric validation of the Nursing Anxiety and Self-Confidence with Clinical Decision Making (NASC-CDM©) scale from English to Spanish; (2) Comparison of nursing student groups by academic years; and (3) Analysis of the impact of work experience on decision making. METHODS: Cross-sectional comparative study. A convenience sample comprising 301 nursing students was included. Cultural adaptation and validation involved a rigorous process encompassing translation, back-translation, expert consultation, pilot testing, and psychometric evaluation of reliability and statistical validity. The NASC-CDM© scale consists of two subscales: self-confidence and anxiety, and 3 dimensions: D1 (Using resources to gather information and listening fully), D2 (Using information to see the big picture), and D3 (Knowing and acting). To assess variations in self-confidence and anxiety among students, the study employed the following tests: Analysis of Variance tests, homogeneity of variance, and Levene's correction with Tukey's post hoc analysis. RESULTS: Validation showed high internal consistency reliability for both scales: Cronbach's α = 0.920 and Guttman's λ2 = 0.923 (M = 111.32, SD = 17.07) for self-confidence, and α = 0.940 and λ2 = 0.942 (M = 80.44, SD = 21.67) for anxiety; and comparative fit index (CFI) of: 0.981 for self-confidence and 0.997 for anxiety. The results revealed a significant and gradual increase in students' self-confidence (p =.049) as they progressed through the courses, particularly in D2 and D3. Conversely, anxiety was high in the 1st year (M = 81.71, SD = 18.90) and increased in the 3rd year (M = 86.32, SD = 26.38), and significantly decreased only in D3. Work experience positively influenced self-confidence in D2 and D3 but had no effect on anxiety. CONCLUSION: The Spanish version (NASC-CDM-S©) was confirmed as a valid, sensitive, and reliable instrument, maintaining structural equivalence with the original English version. While the students' self-confidence increased throughout their training, their levels of anxiety varied. Nevertheless, these findings underscored shortcomings in assessing and identifying patient problems.

Antitumor Effects of Ral-GTPases Downregulation in Glioblastoma.

Glioblastoma (GBM) is the most common tumor in the central nervous system in adults. This neoplasia shows a high capacity of growth and spreading to the surrounding brain tissue, hindering its complete surgical resection. Therefore, the finding of new antitumor therapies for GBM treatment is a priority. We have previously described that cyclin D1-CDK4 promotes GBM dissemination through the activation of the small GTPases RalA and RalB. In this paper, we show that RalB GTPase is upregulated in primary GBM cells. We found that the downregulation of Ral GTPases, mainly RalB, prevents the proliferation of primary GBM cells and triggers a senescence-like response. Moreover, downregulation of RalA and RalB reduces the viability of GBM cells growing as tumorspheres, suggesting a possible role of these GTPases in the survival of GBM stem cells. By using mouse subcutaneous xenografts, we have corroborated the role of RalB in GBM growth in vivo. Finally, we have observed that the knockdown of RalB also inhibits cell growth in temozolomide-resistant GBM cells. Overall, our work shows that GBM cells are especially sensitive to Ral-GTPase availability. Therefore, we propose that the inactivation of Ral-GTPases may be a reliable therapeutic approach to prevent GBM progression and recurrence.

The perception of training and professional development according to nursing students as health workers during COVID-19: A qualitative study.

AIM: To explore the perception of education and professional development of final-year nursing students who carried out health relief tasks during the COVID-19 pandemic. BACKGROUND: The COVID-19 pandemic has led to a global health emergency. This situation has exacerbated the need for additional healthcare employees, forcing the Spanish government to incorporate volunteer nursing students as auxiliary health staff. DESIGN: A qualitative study framed in the constructivist paradigm. METHODS: Twenty-two students of nursing were recruited. A purposeful sampling was implemented until reaching saturation. A semi-structured interview as a conversational technique was used to collect information based on three dimensions: academic curriculum, disciplinary professional development, and patient care. Subsequently, a content analysis of the information was carried out. Three phases were followed in the data analysis process: theoretical, descriptive-analytical, and interpretive. The COREQ checklist was used to evaluate the study. RESULTS: The most important results are linked to the students' professional and academic preparation, how the nurses handled the pandemic situation and the characteristics of the COVID-19 patients. CONCLUSIONS: Students require training in order to offer holistic care to patients, adapted to the context. Participants highlight the importance of professional values and recognise a high level of competence and autonomy in nurses.

Experiences, emotional responses, and coping skills of nursing students as auxiliary health workers during the peak COVID-19 pandemic: A qualitative study.

The COVID-19 crisis in Spain has exacerbated the shortage of nursing staff to respond to increasing healthcare demands. For this reason, nursing students were requested to collaborate voluntarily as auxiliary health staff. This emergency has led to mental health problems in health professionals, hence the relevance of coping techniques. The objectives of this study were to explore the experiences and emotional responses of final-year nursing students who volunteered to carry out healthcare relief tasks during the peak of the COVID-19 pandemic, and to identify the coping strategies they adopted to deal with this situation. A qualitative study was conducted in the constructivist paradigm. Purposive sampling was used, and twenty-two students participated in semi-structured interviews, which were then content-analysed. The study is reported using the COREQ checklist. Five themes emerged in the 'Experiences and emotional response' dimension (context, patients, emotions and feelings, risk of contagion, and personal satisfaction), and three themes emerged in the 'Coping strategies' dimension strategies in the work environment, in daily life and personal life. Although the students expressed negative emotions due to the highly complex context and lack of professional experience, they evaluated the experience positively in terms of learning and usefulness. Most notably, the students employed adaptive coping strategies to deal with the pandemic.

Cytoplasmic cyclin D1 regulates glioblastoma dissemination.

Glioblastoma (GBM) is a highly invasive brain neoplasia with an elevated recurrence rate after surgical resection. The cyclin D1 (Ccnd1)/Cdk4-retinoblastoma 1 (RB1) axis is frequently altered in GBM, leading to overproliferation by RB1 deletion or by Ccnd1-Cdk4 overactivation. High levels of Ccnd1-Cdk4 also promote GBM cell invasion by mechanisms that are not so well understood. The purpose of this work is to elucidate the in vivo role of cytoplasmic Ccnd1-Cdk4 activity in the dissemination of GBM. We show that Ccnd1 activates the invasion of primary human GBM cells through cytoplasmic RB1-independent mechanisms. By using GBM mouse models, we observed that evaded GBM cells showed cytoplasmic Ccnd1 colocalizing with regulators of cell invasion such as RalA and paxillin. Our genetic data strongly suggest that, in GBM cells, the Ccnd1-Cdk4 complex is acting upstream of those regulators. Accordingly, expression of Ccnd1 induces focal adhesion kinase, RalA and Rac1 activities. Finally, in vivo experiments demonstrated increased GBM dissemination after expression of membrane-targeted Ccnd1. We conclude that Ccnd1-Cdk4 activity promotes GBM dissemination through cytoplasmic and RB1-independent mechanisms. Therefore, inhibition of Ccnd1-Cdk4 activity may be useful to hinder the dissemination of recurrent GBM. © 2019 Pathological Society of Great Britain and Ireland. Published by John Wiley & Sons, Ltd.

Regulation of small GTPase activity by G1 cyclins.

Together with a cyclin-dependent kinase (CDK) partner G1 cyclins control cell cycle entry by phosphorylating a number of nuclear targets and releasing a transcriptional program at the end of G1 phase. Yeast G1 cyclins also operate on cytoplasmic targets involved in the polarization of the cytoskeleton and vesicle trafficking. These processes are mainly controlled by the small GTPase Cdc42, and G1 cyclins regulate the activity of this and other small GTPases through the modulation of their regulators and effectors. This regulation is key for different developmental outcomes in unicellular organisms. In mammalian cells cytoplasmic G1 cyclin D1 has been shown to promote the activity of Rac1 and Ral GTPases and to block RhoA. Regulation of these small GTPases by G1 cyclins may constitute a mechanism to coordinate proliferation with cell migration and morphogenesis, important processes not only during normal development and organogenesis but also for tumor formation and metastasis. Here we briefly review the evidence supporting a role of G1 cyclins and CDKs as regulators of the activity of small GTPases, emphasizing their functional relevance both in budding yeast and in mammalian cells.

Cytoplasmic cyclin D1 regulates cell invasion and metastasis through the phosphorylation of paxillin.

Cyclin D1 (Ccnd1) together with its binding partner Cdk4 act as a transcriptional regulator to control cell proliferation and migration, and abnormal Ccnd1·Cdk4 expression promotes tumour growth and metastasis. While different nuclear Ccnd1·Cdk4 targets participating in cell proliferation and tissue development have been identified, little is known about how Ccnd1·Cdk4 controls cell adherence and invasion. Here, we show that the focal adhesion component paxillin is a cytoplasmic substrate of Ccnd1·Cdk4. This complex phosphorylates a fraction of paxillin specifically associated to the cell membrane, and promotes Rac1 activation, thereby triggering membrane ruffling and cell invasion in both normal fibroblasts and tumour cells. Our results demonstrate that localization of Ccnd1·Cdk4 to the cytoplasm does not simply act to restrain cell proliferation, but constitutes a functionally relevant mechanism operating under normal and pathological conditions to control cell adhesion, migration and metastasis through activation of a Ccnd1·Cdk4-paxillin-Rac1 axis.

Characterization of cytoplasmic cyclin D1 as a marker of invasiveness in cancer.

Cyclin D1 (Ccnd1) is a proto-oncogen amplified in many different cancers and nuclear accumulation of Ccnd1 is a characteristic of tumor cells. Ccnd1 activates the transcription of a large set of genes involved in cell cycle progress and proliferation. However, Ccnd1 also targets cytoplasmic proteins involved in the regulation of cell migration and invasion. In this work, we have analyzed by immunohistochemistry the localization of Ccnd1 in endometrial, breast, prostate and colon carcinomas with different types of invasion. The number of cells displaying membranous or cytoplasmic Ccnd1 was significantly higher in peripheral cells than in inner cells in both collective and pushing invasion patterns of endometrial carcinoma, and in collective invasion pattern of colon carcinoma. Also, the cytoplasmic localization of Ccnd1 was higher when tumors infiltrated as single cells, budding or small clusters of cells. To evaluate cytoplasmic function of cyclin D1, we have built a variant (Ccnd1-CAAX) that remains attached to the cell membrane therefore sequestering this cyclin in the cytoplasm. Tumor cells harboring Ccnd1-CAAX showed high levels of invasiveness and metastatic potential compared to those containing the wild type allele of Ccnd1. However, Ccnd1-CAAX expression did not alter proliferative rates of tumor cells. We hypothesize that the role of Ccnd1 in the cytoplasm is mainly associated with the invasive capability of tumor cells. Moreover, we propose that subcellular localization of Ccnd1 is an interesting guideline to measure cancer outcome.