Achieving Energy Justice in Low Income Communities: Creating a Community-Driven Program for Residential Energy Savings

The cost of residential energy the U.S. is unequally distributed, with low income households paying higher rates and spending 16.8% of their income on utility bills compared to 3.5% of all U.S. Residents.[1] Researchers have found that bringing the housing stock up to the efficiency of the median household would reduce excess energy cost by as much as 68%.[2] However, access to opportunities to reduce residential energy consumption and costs such as tax incentives and utility rebate programs tends to be biased toward wealthier, white homeowners. Additionally, low income residents are most likely to be renters, and residence owners have little incentive to improve the energy effectiveness of their properties. Beyond its economic benefits, energy efficiency is essential to reducing local environmental pollution from high-emissions energy sources and to reducing carbon emissions that contribute to global climate change, the direct and indirect harms of which are more likely to impact low income and non-white populations.[3] Our research explores methods of achieving energy justice in low income communities through a pilot study in the Twin Towers neighborhood of Dayton Ohio. By providing free wifi and smart thermostats, our pilot narrows the digital divide and provides immediate opportunities for residents to exercise more control over their energy use and learn more about how to further reduce their utility bills. Building on existing community resources and organizational capacity, we are developing a peer-to-peer education program with the goal of contributing to the long term eco-economic transformation of the Twin Towers neighborhood and developing a model for the replication of the program in other communities. We propose that engaging the community in the grassroots creation of a neighborhood energy savings initiative is a more effective approach - one that emphasizes energy justice rather than simply energy efficiency - than previous top-down efforts. [1] Drehobl, A., & Ross, L. (2016). “Lifting the High Energy Burden in America’s Largest Cities: How Energy Efficiency Can Improve Low Income and Underserved Communities.” American Council for an Energy Efficient Economy, Washington, DC. [2] Lin, J. (2018). “Energy Affordability and Access in Focus: Metrics and Tools of Relative Energy Vulnerability.” Behavior, Energy & Climate Change Conference. Behavior, Energy & Climate Change Conference, Washington, DC [3] Mohai, P., Pellow, D., & Roberts, J. T. (2009). Environmental Justice. Annual Review of Environment and Resources, 34(1), 405–430

Plasmonic resonators for enhanced diamond NV- center single photon sources

We propose a novel source of non-classical light consisting of plasmonic aperture with single-crystal diamond containing a single Nitrogen-Vacancy (NV) color center. Theoretical calculations of optimal structures show that these devices can simultaneously enhance optical pumping by a factor of 7, spontaneous emission rates by Fp ~ 50 (Purcell factor), and offer collection efficiencies up to 40%. These excitation and collection enhancements occur over a broad range of wavelengths (~30nm), and are independently tunable with device geometry, across the excitation (~530nm) and emission (~600-800nm) spectrum of the NV center. Implementing this system with top-down techniques in bulk diamond crystals will provide a scalable architecture for a myriad of diamond NV center applications.Comment: 9 pages, 7 figure

Reporting rates of opioid-related adverse events since 1965 in Canada : a descriptive retrospective study

Background : Patients with chronic or acute/postoperative pain frequently use opioids. However, opioids may cause considerable adverse reactions (ARs), such as respiratory depression, which could be lethal. Unfortunately, only 5% of drug-related ARs (including those to opioids) are reported to health authorities. Therefore, little is known regarding the occurrence of opioid-related ARs at the population level. Objective : The aim of this study was to investigate how the rates of reported opioid-related ARs have changed in Canada since 1965. Methods : Our retrospective study examined trends of reported opioid-related ARs occurring in hospitalized and outpatients. Data on opioid-related ARs and mortality between 1965 and 2019 were obtained from the Canada Vigilance and Statistics Canada databases. Descriptive and Joinpoint regression analyses were performed. Results : Oxycodone and normethadone were the most and least involved opioid agents, respectively, among the 18,407 reported ARs. The highest rate of reported opioid ARs (3.8 per 100,000 person-years) was recorded in 2012, whereas the lowest was recorded in 1965 (0.1 per 100,000 person-years). Between 1965 and 2019, annual rates climbed by 4.2% (95% confidence interval [CI] 3.1–5.2), and many fluctuations were observed: 1965–1974: +22.3% (95% CI 12.0–33.6); 1974–2000: − 4.1% (95% CI − 5.3 to − 2.9); 2000–2008: +30.3% (95% CI 22.6–38.4); 2008–2014: +4.1% (95% CI − 1.5 to 10.1); 2014–2017: −26.0% (95% CI − 44.7 to − 0.9); and, finally, 2017–2019: +35.4% (95% CI 3.8–76.7). Conclusion : Reported opioid-related ARs have increased since 1965, although fluctuations were observed in recent decades. The absolute number of opioid-related ARs might be seriously underestimated. Future studies should look into how to close this gap

PPAR? Downregulation by TGF in Fibroblast and Impaired Expression and Function in Systemic Sclerosis: A Novel Mechanism for Progressive Fibrogenesis

The nuclear orphan receptor peroxisome proliferator-activated receptor-gamma (PPAR-γ) is expressed in multiple cell types in addition to adipocytes. Upon its activation by natural ligands such as fatty acids and eicosanoids, or by synthetic agonists such as rosiglitazone, PPAR-γ regulates adipogenesis, glucose uptake and inflammatory responses. Recent studies establish a novel role for PPAR-γ signaling as an endogenous mechanism for regulating transforming growth factor-ß (TGF-ß)- dependent fibrogenesis. Here, we sought to characterize PPAR-γ function in the prototypic fibrosing disorder systemic sclerosis (SSc), and delineate the factors governing PPAR-γ expression. We report that PPAR-γ levels were markedly diminished in skin and lung biopsies from patients with SSc, and in fibroblasts explanted from the lesional skin. In normal fibroblasts, treatment with TGF-ß resulted in a time- and dose-dependent down-regulation of PPAR-γ expression. Inhibition occurred at the transcriptional level and was mediated via canonical Smad signal transduction. Genome-wide expression profiling of SSc skin biopsies revealed a marked attenuation of PPAR-γ levels and transcriptional activity in a subset of patients with diffuse cutaneous SSc, which was correlated with the presence of a ''TGF-ß responsive gene signature'' in these biopsies. Together, these results demonstrate that the expression and function of PPAR-γ are impaired in SSc, and reveal the existence of a reciprocal inhibitory cross-talk between TGF-ß activation and PPAR-γ signaling in the context of fibrogenesis. In light of the potent anti-fibrotic effects attributed to PPAR-γ, these observations lead us to propose that excessive TGF-ß activity in SSc accounts for impaired PPAR-γ function, which in turn contributes to unchecked fibroblast activation and progressive fibrosis. © 2010 Wei et al

Introduction: approaching space in intellectual history

This article serves as an introduction to the special issue on Conceptions of Space in Intellectual History. It opens with a brief inquiry into the place of ‘space’, both as a topic and as an analytical lens, in the field of intellectual history. The remainder of the introduction suggests a pathway through the special issue. Under three broad headings – ‘territory,’ ‘oceans and empire’, and ‘geopolitics’ – the volume’s articles are presented, brought into dialogue, and situated within a wider trajectory of recent research on conceptions of ‘space’ in intellectual history.Arts and Humanities Research Council; Cambridge Commonwealth, European & International Trust; Levy-Plumb Fund for the Humanities at Christ's College, Cambridge

Skewed Distribution of Circulating Activated Natural Killer T (NKT) Cells in Patients with Common Variable Immunodeficiency Disorders (CVID)

Common variable immunodeficiency disorder (CVID) is the commonest cause of primary antibody failure in adults and children, and characterized clinically by recurrent bacterial infections and autoimmune manifestations. Several innate immune defects have been described in CVID, but no study has yet investigated the frequency, phenotype or function of the key regulatory cell population, natural killer T (NKT) cells. We measured the frequencies and subsets of NKT cells in patients with CVID and compared these to healthy controls. Our results show a skewing of NKT cell subsets, with CD4+ NKT cells at higher frequencies, and CD8+ NKT cells at lower frequencies. However, these cells were highly activated and expression CD161. The NKT cells had a higher expression of CCR5 and concomitantly expression of CCR5+CD69+CXCR6 suggesting a compensation of the remaining population of NKT cells for rapid effector action

Gamma-Secretase Represents a Therapeutic Target for the Treatment of Invasive Glioma Mediated by the p75 Neurotrophin Receptor

The multifunctional signaling protein p75 neurotrophin receptor (p75NTR) is a central regulator and major contributor to the highly invasive nature of malignant gliomas. Here, we show that neurotrophin-dependent regulated intramembrane proteolysis (RIP) of p75NTR is required for p75NTR-mediated glioma invasion, and identify a previously unnamed process for targeted glioma therapy. Expression of cleavage-resistant chimeras of p75NTR or treatment of animals bearing p75NTR-positive intracranial tumors with clinically applicable γ-secretase inhibitors resulted in dramatically decreased glioma invasion and prolonged survival. Importantly, proteolytic processing of p75NTR was observed in p75NTR-positive patient tumor specimens and brain tumor initiating cells. This work highlights the importance of p75NTR as a therapeutic target, suggesting that γ-secretase inhibitors may have direct clinical application for the treatment of malignant glioma

VAMP7 modulates ciliary biogenesis in kidney cells

Epithelial cells elaborate specialized domains that have distinct protein and lipid compositions, including the apical and basolateral surfaces and primary cilia. Maintaining the identity of these domains is required for proper cell function, and requires the efficient and selective SNARE-mediated fusion of vesicles containing newly synthesized and recycling proteins with the proper target membrane. Multiple pathways exist to deliver newly synthesized proteins to the apical surface of kidney cells, and the post-Golgi SNAREs, or VAMPs, involved in these distinct pathways have not been identified. VAMP7 has been implicated in apical protein delivery in other cell types, and we hypothesized that this SNARE would have differential effects on the trafficking of apical proteins known to take distinct routes to the apical surface in kidney cells. VAMP7 expressed in polarized Madin Darby canine kidney cells colocalized primarily with LAMP2-positive compartments, and siRNA-mediated knockdown modulated lysosome size, consistent with the known function of VAMP7 in lysosomal delivery. Surprisingly, VAMP7 knockdown had no effect on apical delivery of numerous cargoes tested, but did decrease the length and frequency of primary cilia. Additionally, VAMP7 knockdown disrupted cystogenesis in cells grown in a three-dimensional basement membrane matrix. The effects of VAMP7 depletion on ciliogenesis and cystogenesis are not directly linked to the disruption of lysosomal function, as cilia lengths and cyst morphology were unaffected in an MDCK lysosomal storage disorder model. Together, our data suggest that VAMP7 plays an essential role in ciliogenesis and lumen formation. To our knowledge, this is the first study implicating an R-SNARE in ciliogenesis and cystogenesis. © 2014 Szalinski et al

Targeting A20 Decreases Glioma Stem Cell Survival and Tumor Growth

The A20 protein is a known inhibitor of apoptosis that here is shown to be a novel cancer stem cell-promoting factor associated with poor glioma patient survival