Purpose
Universities can do more to deliver against the sustainable development goals (SDGs), working with faculty, staff and students, as well as their wider stakeholder community and alumni body. They play a critical role in helping shape new ways for the world, educating global citizens and delivering knowledge and innovation into society. Universities can be engines of societal transformation. Using a multiple case study approach, this study aims to explore different ways of strategizing sustainability toward delivering the SDGs are explored in a university setting with an example from the UK, Bulgaria (Europe) and USA.
Design/methodology/approach
The first case is a public UK university that adopted enterprise and sustainability as its academic mission to secure differentiation in a disrupted and increasingly marketized global higher education sector; this became a source of inspiration for change in regional businesses and the local community. The second case is a business sector-led sustainability-driven transformation working with a private university in Bulgaria to catalyze economic regeneration and social innovation. Finally, a case from the office for sustainability in a major US research university is given to show how its engagement program connected faculty and students in sustainability projects within the institution and with external partners.
Findings
Each case is in effect a “living lab,” positioning sustainability as an intentional and aspirational strategy with sustainable development and the SDG framework a means to that end. Leadership at all levels, and by students, was key to success in acting with a shared purpose. Partnerships within and with universities can help accelerate delivery of the SDGs, enabling higher education to make a fuller contribution to sustaining the economic, environmental, cultural and intellectual well-being of our global communities.
Originality/value
The role of universities as the engine of transformational sustainability toward delivering the SDGs has been explored by way of three case studies that highlight different means toward that end. The collegiate nature of the higher education sector, with its shared governance models and different constituencies and performance drivers, means that sustainability at a strategic level must be led with leaders at all levels acting with purpose. The “living lab” model can become a part of transformative institutional change that draws on both top-down and bottom-up strategies in pursuit of sustainable development.
The kill rates for keratinocytes were 18-200-fold slower than those previously determined for cutaneous microbial species, suggesting that in vivo, APDT sufficient to reduce microbes by seven log cycles would have little cytotoxic effect on keratinocytes. This approach may offer a safe alternative to conventional antimicrobial treatment.
1 We have examined the generation of intracellular reactive oxygen species (ROS) and release of histamine by rat peritoneal mast cells (RPMC) in response to stimulation with antigen (ovalbumin), compound 48/80, nerve growth factor (NGF) and substance P (SP). 2 We have also examined the eects of the non-speci®c nitric oxide synthase inhibitor, L-NAME (100 mM) upon the release of histamine and generation of intracellular ROS in response to the named secretagogues. 3 Ovalbumin (100 ± 1000 mg ml 71 ), compound 48/80 (0.1 ± 100 mg ml 71 ), NGF (0.1 ± 100 mg ml 71 ), and SP (5 ± 50 mM), caused a concentration-dependent release of histamine from RPMC. 4 Ovalbumin (1 ng ml 71 ± 0.1 mg ml
71), compound 48/80 (1 ± 100 mg ml 71 ), NGF (1 pg ml 71 ± 1 mg ml 71 ), and SP (0.005 ± 50 mM) caused a concentration-dependent generation of intracellular ROS by RPMC. 5 Pre-incubation of RPMC with L-NAME (100 mM) caused a signi®cant enhancement of both histamine release and intracellular ROS from RPMC in response to ovalbumin, compound 48/80, NGF and SP. 6 Our data demonstrate that NGF, SP and ovalbumin are capable of causing intracellular ROS generation by RPMC at lower concentrations than those causing signi®cant histamine release and we speculate that this may contribute to the activation of cytokine production. 7 The data also show that NO modulates histamine release, and ROS generation in response to the secretagogues used. This may have signi®cance in pathologies where NO synthesis is decreased, leading to an increased activation of mast cells.
Mast cells are located in close proximity to neurons in the peripheral and central nervous systems, suggesting a functional role in normal and aberrant neurodegenerative states. They also possess many of the features of neurons, in terms of monoaminergic systems, responsiveness to neurotrophins and neuropeptides and the ability to synthesise and release bioactive neurotrophic factors. Mast cells are able to secrete an array of potent mediators which may orchestrate neuroinflammation and affect the integrity of the blood-brain barrier. The 'cross-talk' between mast cells, lymphocytes, neurons and glia constitutes a neuroimmune axis which is implicated in a range of neurodegenerative diseases with an inflammatory and/or autoimmune component, such as multiple sclerosis and Alzheimer's disease. Mast cells appear to make an important contribution to developing, mature and degenerating nervous systems and this should now be recognised when assessing the neurotoxic potential of xenobiotics.
Three-dimensional culture systems are an ideal in vitro model being capable of sustaining cell functionalities in a manner that resembles the in vivo conditions. In the present study, we developed an ultrasound trap-based technique to rapidly produce HepG2 hepatocarcinoma cell aggregates within 30 min. Enhanced junctional F-actin was observed at the points of cell-cell contact throughout the aggregates. HepG2 aggregates prepared by the ultrasound trap can be maintained in culture on a P-HEMA-coated surface for up to 3 weeks. The cells in these aggregates proliferated during the initial 3 days and cell number was consistent during the following maintenance period. Albumin secretion from these HepG2 aggregates recovered after 3 days of aggregate formation and remained relatively stable for the following 12 days. Cytochrome P450-1A1 activity was significantly enhanced after 6 days with maximal enzyme activity observed between 9 and 18 days. In addition, comparison experiments demonstrated that HepG2 aggregates generated by the ultrasound trap had comparable functional characterizations with HepG2 spheroids formed by a traditional gyrotatory-mediated method. Our results suggest that HepG2 aggregate cultures prepared through the ultrasound trap-based technique may provide a novel approach to produce in vitro models for hepatocyte functional studies.
APDT sufficient to reduce microbes by seven log cycles showed no detectable genotoxic effects on keratinocytes. APDT applied in vivo may represent a useful low-risk alternative to conventional antimicrobial treatment in dermatology.
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