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This article introduces a project, School Leadership for Quality Global Learning, which focuses on the relationship between leadership at different levels within educational institutions and quality global learning. The article outlines briefly the changing societal context within which education is operating currently before exploring key ideas, issues and strategies by reporting on a workshop involving some 25 student primary teachers. The workshop was designed to challenge the student teachers' thinking about leadership in an increasingly globalised society, how the education system should respond and the implications for learners and education leaders. It also raised questions about the purposes of schools and the roles of learning and of educational leadership. Following introductory activities that allowed the participants to share their initial perceptions about globalisation and raise their overall awareness, the student teachers used a "World Cafe activity" to investigate in greater depth the educational implications of two aspects of globalisation: the potential for individuals to be overwhelmed by the scale and complexity of the challenges faced by society and the nature of difference and commonality that have always been features of society. In the final phase of the workshop, the participants synthesised their thinking by considering the implications of their discussions for learners and for educational leaders. The workshop revealed that the student teachers welcomed engagement with issues relating to globalisation, but that they had previously given little thought as to how these issues may impact on learners. Furthermore, it would appear that few had considered previously their roles in school beyond that of "teachers" and certainly not as "leaders". The workshop left some of the student teachers frustrated, for example in wanting to explore further the implications of their debates for the taught primary school curriculum and how they could to teach it. In effect, the students generated a substantial agenda for further exploration. School Leadership for Quality Global Learning seeks to identify ways for such agendas to be more central to education so that it meets more effectively the needs of learners, teachers and leaders. (Contains 3 tables.)

Both high tidal volume mechanical ventilation (HV) and hyperoxia (HO) have been implicated in ventilator-induced lung injury. However, patients with acute lung injury are often exposed to HO before the application of mechanical ventilation. The potential priming of the lungs for subsequent injury by exposure to HO has not been extensively studied. We provide evidence that HO (90%) for 12 h followed by HV (25 [micro]l/g) combined with HO for 2 or 4 h (HO-12h+HVHO-2h or -4h) induced severe lung injury in mice. Analysis of lung homogenates showed that lung injury was associated with cleavage of executioner caspases, caspases-3 and -7, and their downstream substrate poly(ADP-ribose) polymerase-1 (PARP-1). No significant lung injury or caspase cleavage was seen with either HO for 16 h or HV for up to 4 h. Ventilation for 4 h with HO (HVHO) did not cause significant lung injury without preexposure to HO. Twelve-hour HO followed by lower tidal volume (6 [micro]l/g) mechanical ventilation failed to produce significant injury or caspase cleavage. We also evaluated the initiator caspases, caspases-8 and -9, to determine whether the death receptor or mitochondrial-mediated pathways were involved. Caspase-9 cleavage was observed in HO-12h+HVHO-2h and -4h as well as HO for 16 h. Caspase-8 activation was observed only in HO-12h+HVHO-4h, indicating the involvement of both pathways. Immunohistochemistry and in vitro stretch studies showed caspase cleavage in alveolar epithelial cells. In conclusion, preexposure to HO followed by HV produced severe lung injury associated with alveolar epithelial cell apoptosis. mechanical ventilation; mouse doi: 10.1152/ajplung.00072.2010.

Patients with acute respiratory distress syndrome undergoing mechanical ventilation may be exposed to both high levels of stretch and high levels of oxygen. We hypothesized that the combination of high stretch and hyperoxia promotes loss of epithelial adhesion and impairs epithelial repair mechanisms necessary for restoration of barrier function. We utilized a model of high tidal volume mechanical ventilation (25 ml/kg) with hyperoxia (50% 02) in rats to investigate alveolar type II (AT2) cell adhesion and focal adhesion signaling. AT2 cells isolated from rats exposed to hyperoxia and high tidal volume mechanical ventilation (MVHO) exhibited significantly decreased cell adhesion and reduction in phosphotyrosyl levels of local adhesion kinase (FAK) and paxillin compared with control rats, rats exposed to hyperoxia without ventilation (HO), or rats ventilated with normoxia (MV). MV alone increased phosphorylation of [p130.sup.Cas] RhoA activation was increased by MV, HO, and the combination of MV and HO. Treatment of MVHO cells with keratinocyte growth factor (KGF) for 1 h upon isolation reduced RhoA activity and restored attachment to control levels. Attachment and migration of control AT2 cells was significantly decreased by constitutively active RhoA or a kinase inactive form of FAK (FRNK), whereas expression of dominant negative RhoA in cells from MVHO-treated rats restored cell adhesion. Mechanical ventilation with hyperoxia promotes changes in focal adhesion proteins and RhoA in AT2 cells that may be deleterious for cell adhesion and migration. keratinocyte growth factor; RhoA; focal adhesion kinase

Overdistention of lung tissue during mechanical ventilation may be one of the factors that initiates ventilator-induced lung injury (VILI). We hypothesized that cyclic mechanical stretch (CMS) of the lung epithelium is involved in the early events of VILI through the production of reactive oxygen species (ROS). Cultures of an immortalized human airway epithelial cell line (16HBE), a human alveolar type II cell line (A549), and primary cultures of rat alveolar type II cells were cyclically stretched, and the production of superoxide ([O.sub.2]) was measured by dihydroethidium fluorescence. CMS stimulated increased production of [O.sup.-.sub.2] after 2 h in each type of cell. 16HBE cells exhibited no significant stimulation of ROS before 2 h of CMS (20% strain, 30 cycles/min), and ROS production returned to control levels after 24 h. Oxidation of glutathione (GSH), a cellular antioxidant, increased with CMS as measured by a decrease in the ratio of the reduced GSH level to the oxidized GSH level. Strain levels of 10% did not increase [O.sup.-.sub.2] production in 16HBE cells, whereas 15, 20, and 30% significantly increased generation of [O.sup.-.sub.2]. Rotenone, a mitochondrial complex I inhibitor, partially abrogated the stretch-induced generation of [O.sup.-.sub.2] after 2 h CMS in 16HBE cells. NADPH oxidase activity was increased after 2 h of CMS, contributing to the production of [O.sup.-.sub.2]. Increased ROS production in lung epithelial cells in response to elevated stretch may contribute to the onset of VILI. mechanotransduction; ventilator-induced lung injury