How to Drink from a Firehose: Systemic Supports for Polytechnic Chairs

This Organizational Improvement Plan (OIP) is centred on the Problem of Practice of the inadequate institutional supports for academic Chairs at Prairie Polytechnic (a pseudonym), a large public higher education institution in Western Canada. Chairs are pivotal for higher education institutions because they impact student, departmental, and institutional outcomes; however, the leadership development needs of Chairs are overlooked, and the limited training available for Chairs is primarily ad hoc, episodic, short-term, and self-guided. The objective of this OIP is to determine how Prairie Polytechnic can provide more effective systemic supports for Chairs. Postmodernism is used to explore the relationships between knowledge and positional power, and Critical Theory highlights the inequities Chairs face. Four potential solutions are explored and compared: increased release time from teaching, increased role clarity, Chair learning communities, and a Chair life cycle strategy. The Chair life cycle strategy is selected as the most feasible, efficacious, and ethical solution, and a change plan is detailed for how the strategy will be implemented at Prairie Polytechnic. The change plan is mapped to the stages of change from the ADKAR change model (awareness; desire; knowledge; ability; reinforcement) and guided by Adaptive Leadership behaviours. A communication plan identifies how collaborators will be engaged in the change process, and a monitoring and evaluation plan identifies how the change plan will be assessed. Successful implementation of the change plan will provide the systemic infrastructure needed to support academic leadership development at Prairie Polytechnic

Plasmodium falciparum Malaria Elicits Inflammatory Responses that Dysregulate Placental Amino Acid Transport

Placental malaria (PM) can lead to poor neonatal outcomes, including low birthweight due to fetal growth restriction (FGR), especially when associated with local inflammation (intervillositis or IV). The pathogenesis of PM-associated FGR is largely unknown, but in idiopathic FGR, impaired transplacental amino acid transport, especially through the system A group of amino acid transporters, has been implicated. We hypothesized that PM-associated FGR could result from impairment of transplacental amino acid transport triggered by IV. In a cohort of Malawian women and their infants, the expression and activity of system A (measured by Na+-dependent 14C-MeAIB uptake) were reduced in PM, especially when associated with IV, compared to uninfected placentas. In an in vitro model of PM with IV, placental cells exposed to monocyte/infected erythrocytes conditioned medium showed decreased system A activity. Amino acid concentrations analyzed by reversed phase ultra performance liquid chromatography in paired maternal and cord plasmas revealed specific alterations of amino acid transport by PM, especially with IV. Overall, our data suggest that the fetoplacental unit responds to PM by altering its placental amino acid transport to maintain adequate fetal growth. However, IV more profoundly compromises placental amino acid transport function, leading to FGR. Our study offers the first pathogenetic explanation for FGR in PM