RESUMO
Purpose@#This study aimed to develop an intentional rounding protocol to enhance the clinical competence of nursing students. @*Methods@#An intentional rounding protocol for nursing students’ clinical practice was developed following the ADDIE (Analysis, Design, Development, Implementation, and Evaluation) model. A convenient sampling method was used to select 23 junior year university nursing students during their clinical practice in adult nursing. The program evaluation included a quantitative assessment (communication and relationship efficacy, empathy, and patient safety competency) and focus group interviews. @*Results@#The intentional rounding protocol focused on the 4Ps (pain, position, potty, and possessions) and encompassed aspects such as level of consciousness, pain management, personal care needs, intravenous injection, oxygen administration, nasogastricasoenteric tube care, maintenance of urine collection bags, and the identification of environmental fall risks. Nursing students performed intentional rounding at least twice a day. Following the implementation of this protocol, nursing students demonstrated a significant improvement in communication and interpersonal efficacy. The focus group interviews revealed four main themes: growth of human relationships, acquiring knowledge in and about the clinical field, becoming a nurse, and barriers in reality. @*Conclusion@#The intentional rounding protocol has the potential to enhance nursing students’ communication and interpersonal skills during clinical practice and to provide them with positive experiences in nursing clinical education. Therefore, it is recommended that this protocol be incorporated into nursing clinical practice education.
RESUMO
Hematopoiesis involves a series of lineage differentiation programs initiated in hematopoietic stem cells (HSCs) found in bone marrow (BM). To ensure lifelong hematopoiesis, various molecular mechanisms are needed to maintain the HSC pool. CCCTC-binding factor (CTCF) is a DNA-binding, zinc-finger protein that regulates the expression of its target gene by organizing higher order chromatin structures. Currently, the role of CTCF in controlling HSC homeostasis is unknown. Using a tamoxifen-inducible CTCF conditional knockout mouse system, we aimed to determine whether CTCF regulates the homeostatic maintenance of HSCs. In adult mice, acute systemic CTCF ablation led to severe BM failure and the rapid shrinkage of multiple c-Kit(hi) progenitor populations, including Sca-1⁺ HSCs. Similarly, hematopoietic system-confined CTCF depletion caused an acute loss of HSCs and highly increased mortality. Mixed BM chimeras reconstituted with supporting BM demonstrated that CTCF deficiency-mediated HSC depletion has both cell-extrinsic and cell-intrinsic effects. Although c-Kit(hi) myeloid progenitor cell populations were severely reduced after ablating Ctcf, c-Kit(int) common lymphoid progenitors and their progenies were less affected by the lack of CTCF. Whole-transcriptome microarray and cell cycle analyses indicated that CTCF deficiency results in the enhanced expression of the cell cycle-promoting program, and that CTCF-depleted HSCs express higher levels of reactive oxygen species (ROS). Importantly, in vivo treatment with an antioxidant partially rescued c-Kit(hi) cell populations and their quiescence. Altogether, our results suggest that CTCF is indispensable for maintaining adult HSC pools, likely by regulating ROS-dependent HSC quiescence.