Roots Project Identity System

These PDF documents contain the identity system and campaign that was designed for PCL\u27s Roots Project- a local not for profit organization that works with young adults with intellectual and development disabilities. The campaign consists of a logo family, a brochure, stationary, and two t shirt designs that perfectly encompass the core concepts of the program: trustworthiness, professionalism, hopefulness, inclusivity, and uniqueness

Cover

Inspiration for the cover was pulled from topics within the journal and includes graphic, photo, and textual elements from several of Makena Harris\u27 previous projects in order to create this collage. The cover features women in STEM/STEAM and research careers who blazed trails and opened doors for many women to come. Her work was rooted in positivity, hopefulness, determination, and strength; all of which are qualities she feels that the two women featured on the cover, Sheila de Bretteville and Neri Oxman, possess. Additionally, color was a major driving force in this piece, with the rosey hue being reclaimed to demonstrate power and strength in femininity

Biochemical characterization of New Delhi metallo-beta-lactamase variants reveals differences in protein stability

Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.Rhodes Trust (UK); a Clarendon Scholarship; a St Hugh's College W. Louey Scholarship; the Biotechnology & Biological Sciences Research Council (BBSRC); a Royal Society Dorothy Hodgkin Research Fellowship; and the Medical Research Council (MRC)/Canadian Grant G1100135

Deficiency of the two-pore-domain potassium channel TREK-1 promotes hyperoxia-induced lung injury

Copyright © 2014 by the Society of Critical Care Medicine and Lippincott Williams & Wilkins. Objectives: We previously reported the expression of the twoporedomain K+ channel TREK-1 in lung epithelial cells and proposed a role for this channel in the regulation of alveolar epithelial cytokine secretion. In this study, we focused on investigating the role of TREK-1 in vivo in the development of hyperoxia-induced lung injury. Design: Laboratory animal experiments. Setting: University research laboratory. Subjects: Wild-type and TREK-1-deficient mice. Interventions: Mice were anesthetized and exposed to 1) room air, no mechanical ventilation, 2) 95% hyperoxia for 24 hours, and 3) 95% hyperoxia for 24 hours followed by mechanical ventilation for 4 hours. Measurements and Main Results: Hyperoxia exposure accentuated lung injury in TREK-1-deficient mice but not controls, resulting in increase in lung injury scores, bronchoalveolar lavage fluid cell numbers, and cellular apoptosis and a decrease in quasi-static lung compliance. Exposure to a combination of hyperoxia and injurious mechanical ventilation resulted in further morphological lung damage and increased lung injury scores and bronchoalveolar lavage fluid cell numbers in control but not TREK-1-deficient mice. At baseline and after hyperoxia exposure, bronchoalveolar lavage cytokine levels were unchanged in TREK-1-deficient mice compared with controls. Exposure to hyperoxia and mechanical ventilation resulted in an increase in bronchoalveolar lavage interleukin-6, monocyte chemotactic protein-1, and tumor necrosis factor-á levels in both mouse types, but the increase in interleukin-6 and monocyte chemotactic protein-1 levels was less prominent in TREK-1-deficient mice than in controls. Lung tissue macrophage inflammatory protein-2, keratinocytederived cytokine, and interleukin-1β gene expression was not altered by hyperoxia in TREK-1-deficient mice compared with controls. Furthermore, we show for the first time TREK-1 expression on alveolar macrophages and unimpaired tumor necrosis factor-á secretion from TREK-1-deficient macrophages. Conclusions: TREK-1 deficiency resulted in increased sensitivity of lungs to hyperoxia, but this effect is less prominent if overwhelming injury is induced by the combination of hyperoxia and injurious mechanical ventilation. TREK-1 may constitute a new potential target for the development of novel treatment strategies against hyperoxiainduced lung injury

Are Kenyan water customers willing to pay a pro-poor sanitation surcharge?

The Kenyan government estimates that 500 billion KES ($5 billion USD) are needed to achieve sanitation coverage targets in urban areas by 2030. To finance these infrastructure improvements, the Ministry of Environment, Water, and Natural Resources is looking at various financing options, including private sector participation, foreign aid, and cross-subsidies. Using a double-bound dichotomous choice method coupled with qualitative interviews, this study investigated willingness to pay for a pro-poor sanitation surcharge among customers of two Kenyan water utilities. 75$1 USD) per month. The primary determinants of willingness to pay were trust in the water utility to manage the pro-poor surcharge, feelings of solidarity towards people living without sanitation, and satisfaction with current water services

Cross-subsidies for improved sanitation in low income settlements: Assessing the willingness to pay of water utility customers in Kenyan cities

Most residents of the developing world do not have access to safely managed sanitation services, and large financial investments are required to address this need. Here we evaluate surcharges on water/sewerage tariffs as an option for supporting these investments in low-income neighborhoods. We investigated willingness-to-pay (WTP) for a pro-poor sanitation surcharge among customers of two urban water utilities in Kenya. Applying qualitative and quantitative methods, we conducted semi-structured in-depth interviews, focus-group discussions, and a double-bounded contingent valuation method for measuring WTP. We varied scenarios quasi-experimentally to study the effects of messaging and surcharge characteristics and evaluated factors associated with WTP. Our study finds that mean WTP was 290 KES (USD 2.9) per month, about 8% of the average water bill; median WTP was 100 KES (USD 1). In a multivariate analysis, WTP was significantly higher among customers that were younger, wealthier, shared toilets, and had higher water bills. WTP was also higher among customers that trusted the utility and distrusted the county government. Of our randomized scenarios, only the bill type was found to significantly influence WTP; WTP was higher if the surcharge was presented as a proportion of the customers’ last water bill vs a flat amount. Our findings suggest that in a sector that struggles to provide universal access to sanitation services, cross-subsidies may offer a means to support financing of safe sanitation for low-income households. These results indicate there are opportunities for cross-subsidies in urban Kenya that may be relevant for a wider understanding of surcharge payments that support basic services for low-income citizens

Preexposure to hyperoxia causes increased lung injury and epithelial apoptosis in mice ventilated with high tidal volumes

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 μl/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 μl/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