Energy/Water Efficiency at Glenwood Elementary

This project focuses on reducing the energy and water footprint of Glenwood Elementary School in Chapel Hill, North Carolina. I inventoried energy and water consumption, modeled costs and benefits of several efficiency upgrades, and implemented those that were possible within a $1000 grant I received from the Kathryn Hoenig Gift. Glenwood is currently responsible for annual emissions of approximately 398 metric tons of CO2 equivalent and 871 kilo gallons of water consumption. Last year, this energy and water consumption carried a price tag of$80,940, of which most ($75,709) was attributable to electricity and natural gas. The energy and water upgrades I chose to implement are low-cost with rapid payback periods. They are very cost-effective, though the magnitude of their impact is small compared to Glenwood’s energy and water consumption as a whole. These measures will save the Chapel Hill-Carrboro City Schools approximately$750, more than 6800 kWh of electricity, and 44,700 gallons of water annually. Because the upgrades were purchased with grant money, this is essentially an annual $750 donation toward helping the school district meet its educational goals. Implementing such initiatives will also avoid 7,089 pounds of carbon dioxide equivalent (CO2e) emissions annually. Efficient energy and water use provide financial and environmental benefits, a sometimes elusive partnership. Approximately$850 of the $1000 grant covered the costs of these upgrades. The remaining funds purchased additional lighting timers for the district to use elsewhere and three Kill-A-Watt energy meters for the Glenwood science teacher (a sustainability advocate) to use in teaching her students about energy efficiency

Comment réussir la tarification incitative au Québec : un outil pour les municipalités

L’objectif de cet essai est de démystifier la tarification incitative et de présenter un outil pratique pour l’implantation réussie d’un système de tarification incitative de la collecte municipale des matières résiduelles au Québec. Cinq sous-objectifs mènent à cette réponse : les raisons du non-emploi de la tarification incitative au Québec, l’analyse des cas à succès en Amérique du Nord et en Europe, l’identification des préalables nécessaires à l’implantation, les étapes opérationnelles de la mise en œuvre et la communication adéquate du processus. L’importance du sujet de cet essai découle des coûts de la gestion des matières résiduelles. Ils voient une augmentation constante due aux redevances à l’élimination et aux nouvelles méthodes de valorisation pour les matières organiques. Une mise à jour de la tarification municipale est donc indispensable. La tarification incitative est un outil efficace pour la réduction des matières résiduelles produites et enfouies ainsi que pour améliorer le taux de récupération résidentiel. De nombreux cas réussis existent en Amérique du Nord. Néanmoins, seulement deux municipalités québécoises utilisent ce système à présent. Des résultats trouvés indiquent qu’une tarification incitative fonctionnelle dépend de l’adaptation du système aux particularités de chaque municipalité. Ceci s’applique au choix du contenant de collecte, des modalités de la facturation et à l’élaboration de la grille tarifaire. En préparation du projet, il est important d’offrir le plus de services complémentaires que possibles afin d’inciter un taux de récupération maximal. Ces services comportent des outils pour le compostage maison, un écocentre pour apport de matières additionnelles ainsi que des collectes spéciales pour les matières organiques, les encombrants et les résidus de construction. Neuf étapes d’une implantation réussie ont été identifiées. La base de chaque projet de tarification incitative est une étude économique et logistique préalable qui permet l’élaboration du scénario choisi. Un projet pilote lancé dans un échantillon de la population aide ensuite à peaufiner la méthode. La préparation de l’appel d’offres et le vote du projet s'en suivent. La mise en œuvre présente un contact avec les citoyens lors de la distribution et mise à jour des contenants de collecte. Par la suite, la municipalité à l’option de commencer par un test à blanc avant d’introduire la tarification complète lors du lancement. Enfin, un suivi par bilans annuels publiés s’impose. Une communication adéquate avant, pendant et après l’implantation est indispensable. La réussite du projet est fortement améliorée par l’allocation d’un chargé de projet responsable dès le début et la portée du projet par les élus

“Nepomuceno Legacy”: The Construction of an Elite Heritage

M.A. University of Hawaii at Manoa 2016.Includes bibliographical references.This thesis examines the manner in which the Nepomuceno family promoted themselves in two books published in the early 21st century. The Nepomucenos are an elite family in the province of Pampanga in the Philippines. They are regionally important in politics and business. Their ancestors founded Holy Angel University, a private Catholic institution. The Nepomucenos used Holy Angel’s press to have two books published which promote the family’s descent from locally prominent elites in the 18th to 20th centuries, including but not limited to a Spanish priest named Guillermo Masnou. The Philippines is dominated, both politically and economically, by nationally powerful oligarchic families. The Nepomucenos are not one of these as their power is limited within their home province. It is clear from their portrayal of themselves in their books that the Nepomucenos would like readers to believe that the family is just as significant as the oligarchs

The effects of crop type, landscape composition and agroecological practices on biodiversity and ecosystem services in tropical smallholder farms

In the tropics, smallholder farming characterizes some of the world's most biodiverse landscapes. Agroecology as a pathway to sustainable agriculture has been proposed and implemented in sub-Saharan Africa, but the effects of agricultural practices in smallholder agriculture on biodiversity and ecosystem services are understudied. Similarly, the contribution of different landscape elements, such as shrubland or grassland cover, on biodiversity and ecosystem services to fields remains unknown.We selected 24 villages situated in landscapes with varying shrubland and grassland cover in Malawi. In each village, we assessed biodiversity of eight taxa and ecosystem services in relation to crop type, shrubland and grassland cover and the number of agroecological pest and soil management practices on smallholder's fields of different crop types (bean monoculture, maize-bean intercrop and maize monoculture).Increasing shrubland cover altered carabid and soil bacteria communities. Carabid abundance increased in maize but decreased in intercrop and bean fields with increasing shrubland cover. Carabid abundance and richness and wasp abundance increased with soil management practices. Carabid, spider and parasitoid abundances were higher in bean monocultures, but this was modulated by surrounding shrubland cover. Natural enemy abundances in beans were especially high in landscapes with little shrubland, possibly leading to lower bean damage in monocultures compared to intercropped fields, whereas maize monocultures had higher damage. In maize, grassland cover and pest management practices were positively related to damage. Carabid abundance was higher fields with high bean damage, and increased carabid richness in fields with high maize damage. Parasitoid abundance was negatively associated with bean damage.Synthesis and application. Our results suggest that maintaining biodiversity and ecosystem services on smallholder farms is not achievable with a 'one size fits all' approach but should instead be adapted to the landscape context and the priorities of smallholders. Shrubland is important to maintain carabid and soil bacterial diversity, but legume cultivation beneficial to natural enemies could complement pest management in landscapes with a low shrubland cover. An increased number of agroecological soil management practices can lead to improved pest control while the effectiveness of agroecological pest management practices needs to be re-evaluated

Loss of inter-cellular cooperation by complete epithelial-mesenchymal transition supports favorable outcomes in basal breast cancer patients.

According to the sequential metastasis model, aggressive mesenchymal (M) metastasis-initiating cells (MICs) are generated by an epithelial-mesenchymal transition (EMT) which eventually is reversed by a mesenchymal-epithelial transition (MET) and outgrowth of life-threatening epithelial (E) macrometastases. Paradoxically, in breast cancer M signatures are linked with more favorable outcomes than E signatures, and M cells are often dispensable for metastasis in mouse models. Here we present evidence at the cellular and patient level for the cooperation metastasis model, according to which E cells are MICs, while M cells merely support E cell persistence through cooperation. We tracked the fates of co-cultured E and M clones and of fluorescent CDH1-promoter-driven cell lines reporting the E state derived from basal breast cancer HMLER cells. Cells were placed in suspension state and allowed to reattach and select an EMT cell fate. Flow cytometry, single cell and bulk gene expression analyses revealed that only pre-existing E cells generated E cells, mixed E/M populations, or stem-like hybrid E/M cells after suspension and that complete EMT manifest in M clones and CDH1-negative reporter cells resulted in loss of cell plasticity, suggesting full transdifferentiation. Mechanistically, E-M coculture experiments supported the persistence of pre-existing E cells where M cells inhibited EMT of E cells in a mutual cooperation via direct cell-cell contact. Consistently, M signatures were associated with more favorable patient outcomes compared to E signatures in breast cancer, specifically in basal breast cancer patients. These findings suggest a potential benefit of complete EMT for basal breast cancer patients

Epithelial transglutaminase 2 is needed for T cell interleukin-17 production and subsequent pulmonary inflammation and fibrosis in bleomycin-treated mice

Inhibition of transglutaminase 2 reduces bleomycin-induced epithelial cell release of interleukin 6 in vitro and pulmonary inflammation and fibrosis in vivo

Extracellular loops 2 and 3 of the calcitonin receptor selectively modify agonist binding and efficacy.

Class B peptide hormone GPCRs are targets for the treatment of major chronic disease. Peptide ligands of these receptors display biased agonism and this may provide future therapeutic advantage. Recent active structures of the calcitonin (CT) and glucagon-like peptide-1 (GLP-1) receptors reveal distinct engagement of peptides with extracellular loops (ECLs) 2 and 3, and mutagenesis of the GLP-1R has implicated these loops in dynamics of receptor activation. In the current study, we have mutated ECLs 2 and 3 of the human CT receptor (CTR), to interrogate receptor expression, peptide affinity and efficacy. Integration of these data with insights from the CTR and GLP-1R active structures, revealed marked diversity in mechanisms of peptide engagement and receptor activation between the CTR and GLP-1R. While the CTR ECL2 played a key role in conformational propagation linked to Gs/cAMP signalling this was mechanistically distinct from that of GLP-1R ECL2. Moreover, ECL3 was a hotspot for distinct ligand- and pathway- specific effects, and this has implications for the future design of biased agonists of class B GPCRs

γδ T cells protect against lung fibrosis via IL-22

Inflammation-induced pulmonary fibrosis (PF) leads to irreversible loss of lung function and is a predictor of mortality in numerous lung diseases. Why some subjects with lung inflammation but not others develop PF is unclear. In a mouse model of hypersensitivity pneumonitis that progresses to lung fibrosis upon repeated exposure to the ubiquitous microorganism Bacillus subtilis, γδ T cells expand in the lung and inhibit collagen deposition. We show that a subset of these γδ cells represents the predominant source of the Th17 cytokine IL-22 in this model. Preventing expression of IL-22, either by mutating the aryl hydrocarbon receptor (AhR) or inhibiting AhR signaling, accelerated lung fibrosis. Direct blockade of IL-22 also enhanced collagen deposition in the lung, whereas administration of recombinant IL-22 inhibited lung fibrosis. Moreover, the presence of protective γδ T cells and IL-22 diminished recruitment of CD4+ T cells to lung. These data reveal a protective pathway that involves the inhibition of αβ T cells by regulatory IL-22–secreting γδ T cells

A Protective Role by Interleukin-17F in Colon Tumorigenesis

Interleukin-17F (IL-17F), produced by Th17 cells and other immune cells, is a member of IL-17 cytokine family with highest homology to IL-17A. IL-17F has been shown to have multiple functions in inflammatory responses. While IL-17A plays important roles in cancer development, the function of IL-17F in tumorigenesis has not yet been elucidated. In the current study, we found that IL-17F is expressed in normal human colonic epithelial cells, but this expression is greatly decreased in colon cancer tissues. To examine the roles of IL-17F in colon cancer, we have used IL-17F over-expressing colon cancer cell lines and IL-17F-deficient mice. Our data showed decreased tumor growth of IL-17F-transfected HCT116 cells comparing to mock transfectants when transplanted in nude mice. Conversely, there were increased colonic tumor numbers and tumor areas in Il-17f−/− mice than those from wild-type controls after colon cancer induction. These results indicate that IL-17F plays an inhibitory role in colon tumorigenesis in vivo. In IL-17F over-expressing tumors, there was no significant change in leukocyte infiltration; instead, we found decreased VEGF levels and CD31+ cells. While the VEGF levels were increased in the colon tissues of Il-17f−/− mice with colon cancer. Together, our findings demonstrate a protective role for IL-17F in colon cancer development, possibly via inhibiting tumor angiogenesis

IL-17A/F-Signaling Does Not Contribute to the Initial Phase of Mucosal Inflammation Triggered by S. Typhimurium

Salmonella enterica subspecies 1 serovar Typhimurium (S. Typhimurium) causes diarrhea and acute inflammation of the intestinal mucosa. The pro-inflammatory cytokines IL-17A and IL-17F are strongly induced in the infected mucosa but their contribution in driving the tissue inflammation is not understood. We have used the streptomycin mouse model to analyze the role of IL-17A and IL-17F and their cognate receptor IL-17RA in S. Typhimurium enterocolitis. Neutralization of IL-17A and IL-17F did not affect mucosal inflammation triggered by infection or spread of S. Typhimurium to systemic sites by 48 h p.i. Similarly, Il17ra−/− mice did not display any reduction in infection or inflammation by 12 h p.i. The same results were obtained using S. Typhimurium variants infecting via the TTSS1 type III secretion system, the TTSS1 effector SipA or the TTSS1 effector SopE. Moreover, the expression pattern of 45 genes encoding chemokines/cytokines (including CXCL1, CXCL2, IL-17A, IL-17F, IL-1α, IL-1β, IFNγ, CXCL-10, CXCL-9, IL-6, CCL3, CCL4) and antibacterial molecules was not affected by Il17ra deficiency by 12 h p.i. Thus, in spite of the strong increase in Il17a/Il17f mRNA in the infected mucosa, IL-17RA signaling seems to be dispensable for eliciting the acute disease. Future work will have to address whether this is attributable to redundancy in the cytokine signaling network