Implementing Strengths-Based Nursing and Healthcare Leadership Values to Promote Equitable, Diverse and Inclusive Workplaces: A Guide for Healthcare Leaders.

Inequities in healthcare persist despite equity, diversity and inclusion (EDI) being embedded in the nursing code of ethics (CNA 2017). Strengths-Based Nursing and Healthcare Leadership (SBNH-L) is "a unique, value-driven, embodied approach that guides leaders and managers to create equitable and safe workplace cultures and environments that honour, develop, mobilize and capitalize on the strengths of individuals and their team" (Gottlieb et al. 2021a: 173) that can be used as a framework to promote EDI in the workplace. Herein, we present concrete suggestions for focusing on EDI through an SBNH-L lens in order to improve healthcare environments for practitioners.

DCC expression by neurons regulates synaptic plasticity in the adult brain.

The transmembrane protein deleted in colorectal cancer (DCC) and its ligand, netrin-1, regulate synaptogenesis during development, but their function in the mature central nervous system is unknown. Given that DCC promotes cell-cell adhesion, is expressed by neurons, and activates proteins that signal at synapses, we hypothesized that DCC expression by neurons regulates synaptic function and plasticity in the adult brain. We report that DCC is enriched in dendritic spines of pyramidal neurons in wild-type mice, and we demonstrate that selective deletion of DCC from neurons in the adult forebrain results in the loss of long-term potentiation (LTP), intact long-term depression, shorter dendritic spines, and impaired spatial and recognition memory. LTP induction requires Src activation of NMDA receptor (NMDAR) function. DCC deletion severely reduced Src activation. We demonstrate that enhancing NMDAR function or activating Src rescues LTP in the absence of DCC. We conclude that DCC activation of Src is required for NMDAR-dependent LTP and certain forms of learning and memory.

Training-induced plasticity in rats with cervical spinal cord injury: effects and side effects.

We investigated the contribution of corticospinal tract (CST) plasticity to training-induced recovery and side effects following spinal cord injury (SCI). Rats were divided into three lesion groups: a unilateral lesion of the dorsal funiculus, the lateral funiculus or a lesion of the entire dorsolateral quadrant (DLQ). Following surgery, rats were distributed into a training group and an untrained group. Trained rats received rehabilitative training in skilled reaching 6 days a week, starting 4 days post-lesion. Following 6 weeks, all rats were tested in reaching (trained task) and crossing a horizontal ladder (untrained task). We found that trained rats with a lesion involving the dorsal column were significantly better in reaching compared to untrained animals. However, when crossing the horizontal ladder, trained rats made significantly more mistakes than untrained animals. Interestingly, rats with a lateral funiculus lesion did not show either effect. A subsequent ablation of the pyramidal tract (pyramidotomy) in rats with a DLQ-lesion significantly reduced but did not eliminate the reaching success. This spared function suggests that other descending systems contributed to the training-induced recovery. In addition, motor-evoked potentials (MEP) from cortical stimulation could still be evoked after pyramidotomy. Further, blocking synaptic transmission passing through the red nucleus using muscimol did not influence the occurrence of MEP's, suggesting that other descending pathways, like the reticulospinal tract, were involved in functional recovery. In summary, this study demonstrates that training-induced CST plasticity may contribute to recovery of motor function, but may also negatively affect untrained tasks as previously reported.

Delayed onset of prolonged hypothermia improves outcome after intracerebral hemorrhage in rats.

Prolonged hypothermia reduces ischemic brain injury, but its efficacy after intracerebral hemorrhagic (ICH) stroke is unresolved. Rats were implanted with core temperature telemetry probes and subsequently subjected to an ICH, which was produced by infusing bacterial collagenase into the striatum. Animals were kept normothermic (NORMO), or were made mildly hypothermic (33-35 degrees C) for over 2 days starting 1 hour (HYP-1), 6 hours (HYP-6), or 12 hours (HYP-12) after collagenase infusion. Others were cooled for 7 hours beginning 1 hour after infusion (BRIEF). Skilled reaching, walking, and spontaneous forelimb use were assessed. Normothermic ICH rats sustained, on average, a 36.9-mm3 loss of tissue at 1 month. Only the HYP-12 group had a significantly smaller lesion (25.5 mm3). Some functional improvements were found with this and other hypothermia treatments. Cerebral edema was observed in NORMO rats, and was not lessened significantly by hypothermia (HYP-12). Blood pressure measurements, as determined by telemetry, in BRIEF rats showed that hypothermia increased blood pressure. This BRIEF treatment also resulted in significantly more bleeding at 12 hours after ICH (79.2 microL) versus NORMO-treated rats (58.4 microL) as determined by a spectrophotometric hemoglobin assay. Accordingly, these findings suggest that early hypothermia may fail to lessen lesion size owing to complications, such as elevated blood pressure, whereas much-delayed hypothermia is beneficial after ICH. Future experiments should assess whether counteracting the side effects of early hypothermia enhances protection.