Public School Elementary Teachers’ Perspectives on Levels of Workplace Stress and Needed Supports

The problem addressed through this study was that public elementary school teachers in the United States have reported increasing levels of workplace stress. Teachers’ stress levels need to be studied and addressed because they affect students as well. The purpose of this basic qualitative study was to explore elementary public school K-3 teachers’ perspectives on their levels of workplace stress and institutional supports needed to reduce workplace stress. Coping-competence-context theory was the conceptual framework. Research questions explored elementary public school teachers’ perspectives on their levels of workplace stress, and their perspectives on the institutional supports needed to reduce workplace stress. Participants were selected purposefully in a sample of 13 K-3 U.S. public school teachers with 3 or more years of classroom experience. Data analysis procedures included interview transcription and the process of coding and categorizing data into emerging themes. Key results included teachers’ perspectives on stress and needed supports along three themes: time, balance, and institutional support. The reported average level of weekly stress was 6.4 on a scale of 1 to 10. Future studies may widen the geographic area and the representation of the sample. Implications for positive social change include aiding district leaders in developing institutional supports to assist elementary teachers and generating additional research on the influence stress has on their work. This study may lead to positive social change and fill a gap in practice by providing public school districts with the data to address K-3 elementary public school teachers’ perspectives on the institutional supports needed to reduce workplace stress

Complement system activation contributes to the ependymal damage induced by microbial neuraminidase

Background In the rat brain, a single intracerebroventricular injection of neuraminidase from Clostridium perfringens induces ependymal detachment and death. This injury occurs before the infiltration of inflammatory blood cells; some reports implicate the complement system as a cause of these injuries. Here, we set out to test the role of complement. Methods The assembly of the complement membrane attack complex on the ependymal epithelium of rats injected with neuraminidase was analyzed by immunohistochemistry. Complement activation, triggered by neuraminidase, and the participation of different activation pathways were analyzed by Western blot. In vitro studies used primary cultures of ependymal cells and explants of the septal ventricular wall. In these models, ependymal cells were exposed to neuraminidase in the presence or absence of complement, and their viability was assessed by observing beating of cilia or by trypan blue staining. The role of complement in ependymal damage induced by neuraminidase was analyzed in vivo in two rat models of complement blockade: systemic inhibition of C5 by using a function blocking antibody and testing in C6-deficient rats. Results The complement membrane attack complex immunolocalized on the ependymal surface in rats injected intracerebroventricularly with neuraminidase. C3 activation fragments were found in serum and cerebrospinal fluid of rats treated with neuraminidase, suggesting that neuraminidase itself activates complement. In ventricular wall explants and isolated ependymal cells, treatment with neuraminidase alone induced ependymal cell death; however, the addition of complement caused increased cell death and disorganization of the ependymal epithelium. In rats treated with anti-C5 and in C6-deficient rats, intracerebroventricular injection of neuraminidase provoked reduced ependymal alterations compared to non-treated or control rats. Immunohistochemistry confirmed the absence of membrane attack complex on the ependymal surfaces of neuraminidase-exposed rats treated with anti-C5 or deficient in C6. Conclusions These results demonstrate that the complement system contributes to ependymal damage and death caused by neuraminidase. However, neuraminidase alone can induce moderate ependymal damage without the aid of complement