When principles and pedagogy clash: Moving beyond the limits of scholarly practices in an academic-community partnership with sex worker activists.

While U.S. public health education increasingly promotes community-based participatory research (CBPR) as a mode of socially-responsive research, today's intertwined health and social injustice crises demand honest reckoning with the limitations of CBPR as a framework for change. We are a team of students, fellows, and faculty reflecting on the complexities encountered over three years of collaborative work with street-based sex worker activists, in a city characterised by stark wealth disparities reinforced by policies of the university within which we operate. We centre a peer-based needs assessment survey and report on barriers to resources and services for sex workers to highlight hard choices and often unacknowledged challenges to academic partnerships. Our process intends to unsettle the too-sanguine narratives of CBPR, draw from insights arising in the discipline of law, and illuminate practices needed to honour commitments, translate knowledge to power-shifting action, and constructively engage with those most affected in determining the policies that structure their lives.We ask: Can our privileged position within the academy be usefully analysed, confronted, instrumentalised, and even subverted as we shape new practices and interventions in the name of health justice? How might we imagine principles and practices towards a movement public health?

Effects of leukoreduction on N-methylhistamine concentration in stored units of canine whole blood.

OBJECTIVE: To determine the effects of leukoreduction on N-methylhistamine (NMH; a stable histamine metabolite) concentration in units of canine whole blood during storage and incubation at room temperature (approx 22 °C) to simulate temperature conditions during transfusion. ANIMALS: 8 healthy adult Walker Hounds. PROCEDURES: A standard unit of blood (450 mL) was obtained from each dog twice, with at least 28 days between donations. Blood units collected from 4 dogs during the first donation underwent leukoreduction, whereas the blood units collected from the other 4 dogs did not undergo leukoreduction, prior to storage at 4 °C. The alternate treatment was applied to blood units collected during the second donation. A sample from each unit was obtained for determination of plasma NMH concentration the day of donation (before and after leukoreduction when applicable) and before and after incubation at room temperature for 5 hours on days 14 and 28 of storage. RESULTS: Units that underwent leukoreduction had substantially lower leukocyte and platelet counts than nonleukoreduced units. Plasma NMH concentration increased immediately after leukoreduction but did not change significantly during the subsequent 28 days of storage, nor did it differ between units that did and did not undergo leukoreduction. CONCLUSIONS AND CLINICAL RELEVANCE: Leukoreduction and simulated transfusion temperature did not affect the histamine load in units of canine whole blood during the first 28 days of storage. Further research is necessary to determine whether histamine contributes to the development and severity of blood transfusion reactions in dogs.

Cobalt Schiff-base complexes for electrocatalytic hydrogen generation.

Two cobalt(iii) complexes containing inexpensive Schiff-base ligands have been found to be active for proton reduction at low overpotentials. The dinitro and tetranitro derivatized Schiff-base complexes show catalytic activity at -0.96 V and -1.1 V vs. Fc+/Fc, respectively, resulting in overpotentials of 120 mV and 280 mV. Foot-of-the-wave analysis is used to examine the kinetic properties of these complexes, yielding a theoretical TOFmax of up to 4100 s-1. Experimental TOFs of 7 s-1and 3 s-1 are observed. Catalytic Tafel plots are also presented in order to benchmark the relationship between turnover frequency and overpotential.

Hydrogen evolution catalyzed by a cobalt complex containing an asymmetric Schiff-base ligand.

A cobalt(iii) complex containing an asymmetric Schiff-base ligand has been found to be active for proton reduction. Catalysis occurs at -1.2 V vs. Fc(+)/Fc (0.56 V vs. NHE), resulting in an overpotential of 350 mV. Additionally, the complex is active with a turnover frequency of 420 s(-1). An enhancement in activity is observed upon addition of water.

Febrile-range hyperthermia augments neutrophil accumulation and enhances lung injury in experimental gram-negative bacterial pneumonia.

We previously demonstrated that exposure to febrile-range hyperthermia (FRH) accelerates pathogen clearance and increases survival in murine experimental Klebsiella pneumoniae peritonitis. However, FRH accelerates lethal lung injury in a mouse model of pulmonary oxygen toxicity, suggesting that the lung may be particularly susceptible to injurious effects of FRH. In the present study, we tested the hypothesis that, in contrast with the salutary effect of FRH in Gram-negative peritonitis, FRH would be detrimental in multilobar Gram-negative pneumonia. Using a conscious, temperature-clamped mouse model and intratracheal inoculation with K. pneumoniae Caroli strain, we showed that FRH tended to reduce survival despite reducing the 3 day-postinoculation pulmonary pathogen burden by 400-fold. We showed that antibiotic treatment rescued the euthermic mice, but did not reduce lethality in the FRH mice. Using an intratracheal bacterial endotoxin LPS challenge model, we found that the reduced survival in FRH-treated mice was accompanied by increased pulmonary vascular endothelial injury, enhanced pulmonary accumulation of neutrophils, increased levels of IL-1beta, MIP-2/CXCL213, GM-CSF, and KC/CXCL1 in the bronchoalveolar lavage fluid, and bronchiolar epithelial necrosis. These results suggest that FRH enhances innate host defense against infection, in part, by augmenting polymorphonuclear cell delivery to the site of infection. The ultimate effect of FRH is determined by the balance between accelerated pathogen clearance and collateral tissue injury, which is determined, in part, by the site of infection.

Febrile-range hyperthermia augments pulmonary neutrophil recruitment and amplifies pulmonary oxygen toxicity.

Febrile-range hyperthermia (FRH) improves survival in experimental infections by accelerating pathogen clearance, but may also increase collateral tissue injury. We hypothesized that FRH would worsen the outcome of inflammation stimulated by a non-replicating agonist and tested this hypothesis in a murine model of pulmonary oxygen toxicity. Using a conscious, temperature-controlled mouse model, we showed that maintaining a core temperature at FRH (39 degrees C to 40 degrees C) rather than at euthermic levels (36.5 degrees C to 37 degrees C) during hyperoxia exposure accelerated lethal pulmonary vascular endothelial injury, reduced the inspired oxygen threshold for lethality, induced expression of granulocyte-colony stimulating factor, and expanded the circulating neutrophil pool. In these same mice, FRH augmented pulmonary expression of the ELR(+) CXC chemokines, KC and LPS-induced CXC chemokine, enhanced recruitment of neutrophils, and changed the histological pattern of lung injury to a neutrophilic interstitial pneumonitis. Immunoblockade of CXC receptor-2 abrogated neutrophil recruitment, reduced pulmonary vascular injury, and delayed death. These combined data demonstrate that FRH may enlist distinct mediators and effector cells to profoundly shift the host response to a defined injurious stimulus, in part by augmenting delivery of neutrophils to sites of inflammation, such as may occur in infections. In certain conditions, such as in the hyperoxic lung, this process may be deleterious.