Preventing Community-Acquired Pressure Injuries in Spinal Cord Injury: Online Healthcare Provider Curriculum.

PURPOSE: The aim of this study was to develop and pilot an educational curriculum for healthcare providers to better understand community-acquired pressure injury (CAPrI) prevention in veterans living with spinal cord injury (SCI). METHODS: The Thomas six-step process model guided curricular development and evaluation. Curriculum development followed six steps: (1) problem identification and general needs assessment from a literature review and qualitative research triangulating provider and veteran perspectives of CAPrI prevention in SCI, (2) target needs assessment using a focus group with 14 experienced practicing interprofessional SCI providers, (3) creation of module goals and objectives with content review from experts ( n = 8), (4) development of curriculum content and educational strategies, (5) implementation of a pilot ( n = 4), and (6) evaluation of satisfaction and curriculum content via survey and focus group. RESULTS: A five-module online curriculum was evaluated positively and is available publicly. Modules include (1) CAPrI Prevention Clinical Guidelines for the Provider, (2) CAPrI Prevention from the Veteran Perspective, (3) Building Collaborative Relationships, (4) Accessing Resources, and (5) Team Approach. Pilot participants stated objectives were met; they were satisfied with the module. The participants did recommend some changes. CLINICAL RELEVANCE: Understanding CAPrI prevention can inform rehabilitation nursing care. CONCLUSIONS: An asynchronous educational curriculum can support nurses in integrating preventive care in community-dwelling veterans living with SCI.

US Department of Veterans Affairs Post-Baccalaureate Registered Nurse Residency: Developing Nurses Equipped with Knowledge and Skills to Care for Nation's Veterans.

Nurse residency programs were developed to improve novice nurse competencies, mitigate burnout, lower recruitment costs and nurse attrition, and the quality of patient care. The Office of Academic Affiliations (OAA), US Department of Veterans Affairs (VA), established a 12-month postbaccalaureate nurse residency (PB-RNR) program at 49 sites to develop competent, confident, practice-ready registered nurses equipped with the knowledge and skills to care for veterans. The OAA evaluation of the PB-RNR program demonstrated improved new nurse graduate competence, confidence, recruitment, and retention rates after completion of training at participating VA medical facilities.

Spiritual Care in Nursing Practice in Veteran Health Care.

Spiritual care is important in nursing practice, and spiritual well-being and spiritual care are associated with better health. Military veterans, a unique patient population, want spiritual care to cope with chronic conditions. It is unclear whether spiritual care is provided in veteran health care in the United States. This study used a qualitative descriptive method, guided by the Spiritual Care in Nursing Practice (SCNiP) theory, to describe spiritual care in nursing practice and facilitators/barriers in veteran health care. Individual interviews were conducted with 39 registered nurses (RNs) at a U.S. veteran health system. Findings were consistent with the SCNiP theory but revealed additional categorical attributes and processes as it applied to veteran health care. Facilitators that promoted spiritual care include nurse professionalism, collegial support, and available spiritual resources. Barriers included lack of time, task-oriented culture, unclear knowledge of accessing resources, and unclear organization policy in providing spiritual care. Findings further refined the theory.

Embryonic Cerebrospinal Fluid Increases Neurogenic Activity in the Brain Ventricular-Subventricular Zone of Adult Mice.

Neurogenesis is a very intensive process during early embryonic brain development, becoming dramatically restricted in the adult brain in terms of extension and intensity. We have previously demonstrated the key role of embryonic cerebrospinal fluid (CSF) in developing brain neurogenic activity. We also showed that cultured adult brain neural stem cells (NSCs) remain competent when responding to the neurogenic influence of embryonic CSF. However, adult CSF loses its neurogenic inductive properties. Here, by means of an organotypic culture of adult mouse brain sections, we show that local administration of embryonic CSF in the subventricular zone (SVZ) niche is able to trigger a neurogenic program in NSCs. This leads to a significant increase in the number of non-differentiated NSCs, and also in the number of new neurons which show normal migration, differentiation and maturation. These new data reveal that embryonic CSF activates adult brain NSCs, supporting the previous idea that it contains key instructive components which could be useful in adult brain neuroregenerative strategies.

Embryonic cerebrospinal fluid in brain development: neural progenitor control.

Due to the effort of several research teams across the world, today we have a solid base of knowledge on the liquid contained in the brain cavities, its composition, and biological roles. Although the cerebrospinal fluid (CSF) is among the most relevant parts of the central nervous system from the physiological point of view, it seems that it is not a permanent and stable entity because its composition and biological properties evolve across life. So, we can talk about different CSFs during the vertebrate life span. In this review, we focus on the CSF in an interesting period, early in vertebrate development before the formation of the choroid plexus. This specific entity is called "embryonic CSF." Based on the structure of the compartment, CSF composition, origin and circulation, and its interaction with neuroepithelial precursor cells (the target cells) we can conclude that embryonic CSF is different from the CSF in later developmental stages and from the adult CSF. This article presents arguments that support the singularity of the embryonic CSF, mainly focusing on its influence on neural precursor behavior during development and in adult life.

Focal adhesion kinase as a mechanotransducer during rapid brain growth of the chick embryo.

Expansion of the hollow fluid-filled embryonic brain occurs by an increase in intraluminal pressure created by accumulation of cerebrospinal fluid (CSF). Experiments have shown a direct correlation between cavity pressure and cell proliferation within the neuroepithelium. These findings lead us to ask how mechanistically this might come about. Are there perhaps molecules on the luminal surface of the embryonic neuroepithelium, such as focal adhesion kinases (FAKs) known to respond to tension in other epithelial cells? Immunodetection using antibodies to total FAK and p-FAK was performed with subsequent confocal analysis of the pattern of their activation under normal intraluminal pressure and induced chronic pressure. Western analysis was also done to look at the amount of FAK expression, as well as its activation under these same conditions. Using immunolocalization, we have shown that FAK is present and activated on both apical and basolateral surfaces and within the cytoplasm of the neuroepithelial cells. This pattern changed profoundly when the neuroepithelium was under pressure. By Western blot, we have shown that FAK was upregulated and activated in the neuroepithelium of the embryos just after the neural tube becomes a closed pressurized system, with phosphorylation detected on the luminal instead of the basal surface, along with an increase in cell proliferation. Chronic hyper-pressure does not induce an increase in phosphorylation of FAK. In conclusion, here we show that neuroepithelial cells respond to intraluminal pressure via FAK phosphorylation on the luminal surface.

Characterization of intestinal and pancreatic dysfunction in VPAC1-null mutant mouse.

OBJECTIVES: These studies examined the effect of homozygous deletion of vasoactive intestinal peptide receptor type 1 (VPAC1) on development and function of intestines and pancreas. METHODS: Genetically engineered VPAC1-null mutant mice were monitored for growth, development, and glucose homeostasis. Expression of VPAC1 was examined during embryonic development using VPAC1 promoter-driven ß-galactosidase transgenic mice. RESULTS: Homozygous deletion of VPAC1 resulted in fetal, neonatal, and postweaning death owing to failure to thrive, intestinal obstruction, and hypoglycemia. Histological findings demonstrated disorganized hyperproliferation of intestinal epithelial cells with mucus deposition and bowel wall thickening. The pancreas demonstrated small dysmorphic islets of Langerhans containing α, ß, and δ cells. Expression of a VPAC1 promoter-driven transgene was observed in E12.5 and E14.5 intestinal epithelial and pancreatic endocrine cells. Vasoactive intestinal peptide receptor type 1-null mutant animals had lower baseline blood glucose levels compared to both heterozygous and wild-type littermates. Vasoactive intestinal peptide receptor type 1-deficient mice responded to oral glucose challenge with normal rise in blood glucose followed by rapid hypoglycemia and failure to restore baseline glucose levels. Insulin challenge resulted in profound hypoglycemia and inadequate glucose homeostasis in VPAC1-null mutant animals. CONCLUSIONS: These observations support a role for VPAC1 during embryonic and neonatal development of intestines and endocrine pancreas.

Expansion of the human embryonic brain during rapid growth: area analysis.

This report focuses on growth of the brain of the early human embryo, Carnegie stages 12-23. Areas of median sections from 50 to 58 embryos were measured to determine the best mathematical model to describe growth of the three primary brain vesicles and to determine the change in the ratio of tissue to cavity areas (T/C). An exponential model best describes growth of the brain and head during this time period. The head expands 248-fold compared with a 171-fold growth of the brain. The whole brain, forebrain, and midbrain all exhibit larger cavities than tissue initially followed by a reversal of such at a critical time (stages 21-24). The presumptive cerebellar tissue which was twice the cavity initially grows to become more than six times the cavity. Boxplots of the T/C ratios for the head and brain plus its components reveal that initially the tissue is less than the cavity (10-20% and 40-60%, respectively) but eventually becomes larger (60-200%).

Why the embryo still matters: CSF and the neuroepithelium as interdependent regulators of embryonic brain growth, morphogenesis and histiogenesis.

The key focus of this review is that both the neuroepithelium and embryonic cerebrospinal fluid (CSF) work in an integrated way to promote embryonic brain growth, morphogenesis and histiogenesis. The CSF generates pressure and also contains many biologically powerful trophic factors; both play key roles in early brain development. Accumulation of fluid via an osmotic gradient creates pressure that promotes rapid expansion of the early brain in a developmental regulated way, since the rates of growth differ between the vesicles and for different species. The neuroepithelium and ventricles both contribute to this growth but by different and coordinated mechanisms. The neuroepithelium grows primarily by cell proliferation and at the same time the ventricle expands via hydrostatic pressure generated by active transport of Na(+) and transport or secretion of proteins and proteoglycans that create an osmotic gradient which contribute to the accumulation of fluid inside the sealed brain cavity. Recent evidence shows that the CSF regulates relevant aspects of neuroepithelial behavior such as cell survival, replication and neurogenesis by means of growth factors and morphogens. Here we try to highlight that early brain development requires the coordinated interplay of the CSF contained in the brain cavity with the surrounding neuroepithelium. The information presented is essential in order to understand the earliest phases of brain development and also how neuronal precursor behavior is regulated.

Internal luminal pressure during early chick embryonic brain growth: descriptive and empirical observations.

If the intraluminal pressure of the brain is decreased for 24 hr, the brain and neuroepithelium volumes are both reduced in half. The current study measured the intraluminal pressure throughout the period of rapid brain growth using a servo-null micropressure monitoring system. From 613 measurements made on 55 embryos, we show that the intraluminal pressure over this time period is appropriately described by a linear model with correlation coefficient of 0.752. To assess whether sustained hyperpressure would increase mitosis, elevated intraluminal pressure was induced in 10 embryos for 1-hr duration via a gravity-fed drip. The mitotic density and index of the mesencephalon were measured for the 10 embryos. Those embryos, in which the colchicine solution was added to the intraluminal cerebrospinal fluid creating a sustained hyperpressure, exhibited at least a 2.5-fold increase in both the mitotic density and index compared with control embryos. Based on the small sample size, we cautiously conclude that sustained hyper-intraluminal pressure does stimulate mitosis.

Overexpression of connexin43 alters the mutant phenotype of midgestational wnt-1 null mice resulting in recovery of the midbrain and cerebellum.

The midbrain-hindbrain (MHB) junction plays a key role in the patterning of the embryonic neural tube and the formation of brain structures such as the cerebellum. The mitogen wnt-1 is critical for cerebellar development, as evidenced by the lack of MHB region and cerebellar formation in the wnt-1 null embryo. We have generated wnt-1 null embryos overexpressing the gap junction gene connexin43 by crossing wnt-1 null heterozygotes into the CMV43 mouse line. We have confirmed that these mice show an increase in gap junctional communication by dye coupling analysis. Two-thirds of wnt-1 null CMV43(+) mouse embryos at E18.5 have a cerebellum. In addition, changes in the wnt-1 null phenotype in mouse embryos overexpressing connexin43 are observed as early as E9.5. At this stage, one-quarter of wnt-1 null CMV43(+) embryos display extra or expanded tissue present at the MHB boundary (a wnt-1 null enlarged phenotype). In situ hybridization studies conducted on these embryos have indicated no changes in the expression of embryonic brain positional markers in this region. We conclude from these studies that overexpression of the connexin43 gap junction restores cerebellar formation by compensating for the loss of wnt-1.

Brain expansion in the chick embryo initiated by experimentally produced occlusion of the spinal neurocoel.

The brain expands in the early chick embryo from pressure generated by accumulation of cerebrospinal fluid (CSF) in a closed neural tube. The sealing of the neural tube occurs as the result of occlusion of the spinal neurocoel rostral to and before closure of the posterior neuropore. We have previously demonstrated the dependence of normal brain expansion upon intraluminal pressure. We had yet to demonstrate, however, that brain expansion actually depends upon natural occlusion of the spinal neurocoel. To demonstrate such dependence, we experimentally occluded the spinal neurocoels of embryos 5 hr younger than stage 11 embryos (in which occlusion of the neurocoel occurs naturally). The stage 10 chick embryos were cultured ex ovo and critically staged, and their spinal neurocoels were occluded using microcautery. All embryos were photographed immediately and at 5, 12, and 24 hr after cautery. Serial sections were made of selected embryos, in which the areas of both the brain and the head were measured. Wilcoxon-Mann-Whitney rank-sum nonparametric tests, Hodges-Lehmann estimators, bootstrapping techniques, and resampling randomization tests were used to determine whether the increases in the brain and head areas for the experimental embryos were significantly different from those of the control embryos during three distinct intervals of expansion: 0-5, 5-12, and 0-12 hr. From 0 to 5 hr, the brains of the precociously occluded embryos expanded significantly more than the brains of the non-occluded controls. From 5 to 12 hr, the brains of the embryos with naturally occluded neurocoels grew significantly larger than the brains of the embryos with precociously occluded neurocoels. At 12 hr, there appeared to be no difference in brain size for these two groups. We conclude that the data support the hypothesis that brain expansion is directly dependent upon occlusion of the spinal neurocoel.