School nurses race to the top: the pilot year of how one district's school nurses revised their evaluation process.

During the 2013-2014 school year, the Shaker Heights, Ohio City school district was mandated to change its evaluation process as part of the Race to the Top initiative. Although not required by the federal or state Departments of Education, the Shaker Heights City school district tasked all members of their faculty and staff, including school nurses, to change their evaluation process in an effort to improve students' performances and outcomes. This article chronicles how the Shaker Heights school nurses modified their evaluation process by adhering to the scopes and standards of school nursing as described by the American Nurses Association and National Association of School Nurses. Their revised evaluation tool could usefully serve as a model for school districts nationwide; it improves student outcomes, increases the professionalism of the school nurse specialty, increases administrative understanding of their role, and increases their accountability as independent health providers in the school.

JBI systematic review protocol of text/opinions on how to best collect race-based data in healthcare contexts.

INTRODUCTION: Racialized population groups have worse health outcomes across the world compared with non-racialized populations. Evidence suggests that collecting race-based data should be done to mitigate racism as a barrier to health equity, and to amplify community voices, promote transparency, accountability, and shared governance of data. However, limited evidence exists on the best ways to collect race-based data in healthcare contexts. This systematic review aims to synthesize opinions and texts on the best practices for collecting race-based data in healthcare contexts. METHODS AND ANALYSES: We will use the Joanna Briggs Institute (JBI) method for synthesizing text and opinions. JBI is a global leader in evidence-based healthcare and provides guidelines for systematic reviews. The search strategy will locate both published and unpublished papers in English in CINAHL, Medline, PsycINFO, Scopus and Web of Science from 1 January 2013 to 1 January 2023, as well as unpublished studies and grey literature of relevant government and research websites using Google and ProQuest Dissertations and Theses. The Preferred Reporting Items for Systematic Reviews and Meta-Analyses statement methodology for systematic reviews of text and opinion will be applied, including screening and appraisal of the evidence by two independent reviewers and data extraction using JBI's Narrative, Opinion, Text, Assessment, Review Instrument. This JBI systematic review of opinion and text will address gaps in knowledge about the best ways to collect race-based data in healthcare. Improvements in race-based data collection, may be related to structural policies that address racism in healthcare. Community participation may also be used to increase knowledge about collecting race-based data. ETHICS AND DISSEMINATION: The systematic review does not involve human subjects. Findings will be disseminated through a peer-reviewed publication in JBI evidence synthesis, conferences and media. PROSPERO REGISTRATION NUMBER: CRD42022368270.

alpha3beta1 integrin-controlled Smad7 regulates reepithelialization during wound healing in mice.

Effective reepithelialization after injury is essential for correct wound healing. The upregulation of keratinocyte alpha3beta1 integrin during reepithelialization suggests that this adhesion molecule is involved in wound healing; however, its precise role in this process is unknown. We have shown here that retarded reepithelialization in Itga3(-/-) mouse skin wounds is due predominantly to repressed TGF-beta1-mediated responses. Specifically, expression of the inhibitor of TGF-beta1-signaling Smad7 was elevated in Itga3(-/-) keratinocytes. Indeed, in vivo blockade of Smad7 increased the rate of reepithelialization in Itga3(-/-) and WT wounds to similar levels. Our data therefore indicate that the function of alpha3beta1 integrin as a mediator of keratinocyte migration is not essential for reepithelialization but suggest instead that alpha3beta1 integrin has a major new in vivo role as an inhibitor of Smad7 during wound healing. Moreover, our study may identify a previously undocumented function for Smad7 as a regulator of reepithelialization in vivo and implicates Smad7 as a potential novel target for the treatment of cutaneous wounds.

Fibroblast growth factor 22 is not essential for skin development and repair but plays a role in tumorigenesis.

Fibroblast Growth Factors play critical roles during development, tissue homeostasis and repair by controlling cell proliferation, survival, migration and differentiation. Of the 22 mammalian FGFs, FGF22, a member of the FGF7/10/22 subfamily, has been shown to have a clear role in synaptogenesis, but its roles in other tissues have not been studied. We have investigated the in vivo functions of FGF22 in mice. Fgf22 null animals were viable, fertile and did not display any obvious abnormalities. Despite the known expression profile of FGF22 in the skin, no differences in either skin or pelage were observed, demonstrating that FGF22 is dispensable during embryogenesis and in unchallenged adult skin. Mice lacking FGF22 were able to heal acute wounds just as efficiently as wild type mice. However, classical two-step skin carcinogenesis challenge revealed that FGF22 null mice developed fewer papillomas than wild type controls, suggesting a potential pro-oncogenic role for FGF22 in the skin.

The role of fibroblast growth factor receptor 2b in skin homeostasis and cancer development.

The epithelial isoform of fibroblast growth factor receptor 2 (Fgfr2b) is essential for embryogenesis, and Fgfr2b-null mice die at birth. Using Cre-Lox transgenics to delete Fgfr2b in cells expressing keratin 5, we show that mice lacking epidermal Fgfr2b survive into adulthood but display striking abnormalities in hair and sebaceous gland development. Epidermal hyperthickening develops with age, and 10% of mutant mice develop spontaneous papillomas, demonstrating the role of Fgfr2b in post-natal skin development and in adult skin homeostasis. Mice lacking epithelial Fgfr2b show great sensitivity to chemical carcinogenic insult, displaying several oncogenic ha-ras mutations with dramatic development of papillomas and squamous cell carcinomas. Mutant mice have increased inflammation in the skin, with increased numbers of macrophages and gammadeltaT cells with abnormal morphology. Mutant skin shows several changes in gene expression, including enhanced expression of the pro-inflammatory cytokine interleukin 18 and decreased expression of Serpin a3b, a potential tumor suppressor. Thus we describe a novel role of Fgfr2b and provide the first evidence of a tyrosine kinase receptor playing a tumor suppressive role in the skin.