2 resultados para Ovine - Stress indicator
em DigitalCommons@The Texas Medical Center
Resumo:
Studies have demonstrated a variable response to ozone among individuals and animal species and strains. For instance, C57BL/6J mice have a greater inflammatory response to ozone exposure than C3H/HeJ mice. In these studies, I utilized these strain differences in an effort to derive a mechanistic explanation to the variable strain sensitivity to ozone exposure. Therefore, alveolar macrophages (AM) from C57BL/6J and C3H/HeJ mice were exposed in vitro to hydrogen peroxide ($\rm H\sb2O\sb2$), heat and acetyl ceramide or in vivo to ozone. Necrosis and DNA fragmentation in macrophages from the two murine strains were determined to assess cytotoxicity following these treatments. In addition, synthesis and expression of the stress proteins, stress protein 72 (SP72) and heme oxygenase (HO-1), were examined following treatments. The in vitro experiments were conducted to eliminate the possibility of in vivo confounders (i.e., differences in breathing rates in the two strains) and thus directly implicate some inherent difference between cells from the two murine strains. $\rm H\sb2O\sb2$ and heat caused greater cytotoxicity in AM from C57BL/6J than C3H/HeJ mice and DNA fragmentation was a particularly sensitive indicator of cell injury. Similarly, AM from C57BL/6J mice were more sensitive to ozone exposure than cells from C3H/HeJ mice. Exposure to either 1 or 0.4 ppm ozone caused greater cytotoxicity in macrophages from C57BL/6J mice compared to macrophages from C3H/HeJ mice. The increased sensitivity of AM to injury was associated with decreased synthesis and expression of stress proteins. AM from C57BL/6J mice synthesized and expressed significantly less stress proteins in response to heat and ozone than AM from C3H/HeJ mice. Heat treatment resulted in greater synthesis and expression of SP72. In addition, macrophages from C57BL/6J mice expressed lower amounts of HO-1 than macrophages from C3H/HeJ mice following 0.4 ppm ozone exposure. Therefore, AM from C57BL/6J mice are more susceptible to oxidative injury than AM from C3H/HeJ mice which might be due to differential expression of stress proteins in these cells. ^
Resumo:
This analysis provides an emergent framework that emphasizes a neglected component of both direct practice with families and organizational development. Human emotions, both beneficial (positive emotional labor) and harmful (negative emotional labor), have received short shrift in leadership development, supervision, direct practice preparation and supports, and workforce stabilization, and professionalization. Significantly, a key indicator of negative emotional labor—secondary traumatic stress (STS)—often has been ignored and neglected, despite the fact that it may be endemic in the workforce. STS typically results from traumatic events in practice, but it also stems from workplace violence. Often undetected and untreated, STS is at least a hidden correlate and perhaps a probable cause of myriad problems such as questionable practice with families, life-work conflicts, undesirable workforce turnover, and a sub-optimal organizational climate. Special interventions are needed. At the same time, new organizational designs are needed to promote and reinforce positive emotional labor. Arguably, positive emotional labor and the positive organizational climates it facilitates are requisites for harmonious relations between jobs and personal lives, desirable workforce retention, and better outcomes for children and families. What’s more, specialized interventions for positive emotional labor constitute a key component in the prevention system for STS. A dual design for positive emotional labor and STS (and other negative emotional labor) prevention/intervention is provided herewith. Early detection and rapid response systems for STS, with social work leadership, receive special attention. Guidelines for new organizational designs for emotional labor in child welfare are offered in conclusion.