Creating Healthy Communities Through Urban Form

ABSTRACT The manner in which we design and build our communities can affect our physical and mental health. When we think about urban planning, we reflect on the form and arrangement of community, of urban, city and town planning. Urban form looks at the integration of land use and explores a complex range of the built and social environment: the environment, infrastructure, people, form and economics. The research recognizes cultural behaviours and activity patterns that affect air quality and environmental conditions; a lack of physical activity, community cohesion, highlights safety issues, and places individuals at risk for health illness. The research evaluates the built form of the neighbourhood community and asks ‘What are the attributes of a healthy community’? The research will verify the extent to which the neighbourhoods selected in the study replicate these attributes and focus on how these neighbourhoods could be improved from a ‘healthy city’ perspective. Key urban form features related to healthy communities focus on the relationship between land use mix, network connectivity and street design, site design, and density. Sustainable planning of communities and efficient land use planning are relevant to healthy communities with the trend towards increasing population density. While the research reinforces the connection between built form and public health planning, it also provides future direction for urban form policy; with improvements towards street connectivity, non-motorized transportation, expansion of regional trail and cycle networks, increasing transit access, encouraging mixed land use and greater land density to shorten travel distances. The research provides a basis for future studies in Canadian growth policy and healthy neighbourhood form, with significance as a Southwestern Ontario study

Soil methane sink capacity response to a long-term wildfire chronosequence in Northern Sweden

Boreal forests occupy nearly one fifth of the terrestrial land surface and are recognised as globally important regulators of carbon (C) cycling and greenhouse gas emissions. Carbon sequestration processes in these forests include assimilation of CO2 into biomass and subsequently into soil organic matter, and soil microbial oxidation of methane (CH4). In this study we explored how ecosystem retrogression, which drives vegetation change, regulates the important process of soil CH4 oxidation in boreal forests. We measured soil CH4 oxidation processes on a group of 30 forested islands in northern Sweden differing greatly in fire history, and collectively representing a retrogressive chronosequence, spanning 5000 years. Across these islands the build-up of soil organic matter was observed to increase with time since fire disturbance, with a significant correlation between greater humus depth and increased net soil CH4 oxidation rates. We suggest that this increase in net CH4 oxidation rates, in the absence of disturbance, results as deeper humus stores accumulate and provide niches for methanotrophs to thrive. By using this gradient we have discovered important regulatory controls on the stability of soil CH4 oxidation processes that could not have not been explored through shorter-term experiments. Our findings indicate that in the absence of human interventions such as fire suppression, and with increased wildfire frequency, the globally important boreal CH4 sink could be diminished

Multiband tight-binding theory of disordered ABC semiconductor quantum dots: Application to the optical properties of alloyed CdZnSe nanocrystals

Zero-dimensional nanocrystals, as obtained by chemical synthesis, offer a broad range of applications, as their spectrum and thus their excitation gap can be tailored by variation of their size. Additionally, nanocrystals of the type ABC can be realized by alloying of two pure compound semiconductor materials AC and BC, which allows for a continuous tuning of their absorption and emission spectrum with the concentration x. We use the single-particle energies and wave functions calculated from a multiband sp^3 empirical tight-binding model in combination with the configuration interaction scheme to calculate the optical properties of CdZnSe nanocrystals with a spherical shape. In contrast to common mean-field approaches like the virtual crystal approximation (VCA), we treat the disorder on a microscopic level by taking into account a finite number of realizations for each size and concentration. We then compare the results for the optical properties with recent experimental data and calculate the optical bowing coefficient for further sizes

Evaluating methane inventories by isotopic analysis in the London region

A thorough understanding of methane sources is necessary to accomplish methane reduction targets. Urban environments, where a large variety of methane sources coexist, are one of the most complex areas to investigate. Methane sources are characterised by specific δ13C-CH4 signatures, so high precision stable isotope analysis of atmospheric methane can be used to give a better understanding of urban sources and their partition in a source mix. Diurnal measurements of methane and carbon dioxide mole fraction, and isotopic values at King’s College London, enabled assessment of the isotopic signal of the source mix in central London. Surveys with a mobile measurement system in the London region were also carried out for detection of methane plumes at near ground level, in order to evaluate the spatial allocation of sources suggested by the inventories. The measured isotopic signal in central London (−45.7 ±0.5‰) was more than 2‰ higher than the isotopic value calculated using emission inventories and updated δ13C-CH4 signatures. Besides, during the mobile surveys, many gas leaks were identified that are not included in the inventories. This suggests that a revision of the source distribution given by the emission inventories is needed

An Integrated TCGA Pan-Cancer Clinical Data Resource to Drive High-Quality Survival Outcome Analytics

For a decade, The Cancer Genome Atlas (TCGA) program collected clinicopathologic annotation data along with multi-platform molecular profiles of more than 11,000 human tumors across 33 different cancer types. TCGA clinical data contain key features representing the democratized nature of the data collection process. To ensure proper use of this large clinical dataset associated with genomic features, we developed a standardized dataset named the TCGA Pan-Cancer Clinical Data Resource (TCGA-CDR), which includes four major clinical outcome endpoints. In addition to detailing major challenges and statistical limitations encountered during the effort of integrating the acquired clinical data, we present a summary that includes endpoint usage recommendations for each cancer type. These TCGA-CDR findings appear to be consistent with cancer genomics studies independent of the TCGA effort and provide opportunities for investigating cancer biology using clinical correlates at an unprecedented scale. Analysis of clinicopathologic annotations for over 11,000 cancer patients in the TCGA program leads to the generation of TCGA Clinical Data Resource, which provides recommendations of clinical outcome endpoint usage for 33 cancer types

Light induced single molecule frequency shift

Alight induced frequency shift of the 0-0 line was measured in two-photon excitation spectra of single diphenyloctatetraene molecules doped in a crystal matrix. The shifts were proportional to the laser power with a slope of about 600 MHz/W when the laser beam of about 300 mW power was focused to a diameter of 2 mu m. Significantly, the observed line broadenings were an order of magnitude smaller than the shifts. The effect is ascribed mainly to a ''fast'' energy exchange between a local vibration and thermal phonons created by the third harmonic C-H band absorption in the matrix, and partially to an ac Stark shift

High expression of RelA/p65 is associated with activation of nuclear factor-κB-dependent signaling in pancreatic cancer and marks a patient population with poor prognosis

Activation of nuclear factor-κB (NF-κB) signaling was observed in pancreatic adenocarcinoma cell lines and tumours. However, information on the expression of RelA/p65, the major transcription activating NF-κB subunit, in these carcinomas and possible correlations thereof with NF-κB activation and patient survival is not available. To provide this missing translational link, we analysed expression of RelA/p65 in 82 pancreatic adenocarcinomas by immunohistochemistry. Moreover, we measured activation of the NF-κB pathway in 11 tumours by quantitative PCR for NF-κB target genes. We observed strong cytoplasmic or nuclear expression of RelA/p65 in 42 and 37 carcinomas, respectively. High cytoplasmic and nuclear expression of RelA/p65 had negative prognostic impact with 2-year survival rates for patients without cytoplasmic or nuclear RelA/p65 positivity of 41 and 40% and rates for patients with strong cytoplasmic or nuclear RelA/p65 expression of 22 and 20%, respectively. High RelA/p65 expression was correlated to increased expression of NF-κB target genes. The observation that high expression of RelA/p65 is correlated to an activation of the NF-κB pathway and indicates poor patient survival identifies a patient subgroup that might particularly benefit from NF-κB-inhibiting agents in the treatment of pancreatic cancer. Based on our findings, this subgroup could be identified by applying simple immunohistochemical techniques

Immunohistochemical analysis of changes in signaling pathway activation downstream of growth factor receptors in pancreatic duct cell carcinogenesis

<p>Abstract</p> <p>Background</p> <p>The pathogenesis of pancreatic ductal adenocarcinoma (PDAC) involves multi-stage development of molecular aberrations affecting signaling pathways that regulate cancer growth and progression. This study was performed to gain a better understanding of the abnormal signaling that occurs in PDAC compared with normal duct epithelia.</p> <p>Methods</p> <p>We performed immunohistochemistry on a tissue microarray of 26 PDAC, 13 normal appearing adjacent pancreatic ductal epithelia, and 12 normal non-PDAC ducts. We compared the levels of 18 signaling proteins including growth factor receptors, tumor suppressors and 13 of their putative downstream phosphorylated (p-) signal transducers in PDAC to those in normal ductal epithelia.</p> <p>Results</p> <p>The overall profiles of signaling protein expression levels, activation states and sub-cellular distribution in PDAC cells were distinguishable from non-neoplastic ductal epithelia. The ERK pathway activation was correlated with high levels of ^S2448p-mTOR (100%, p = 0.05), ^T389p-S6K (100%, p = 0.02 and ^S235/236p-S6 (86%, p = 0.005). Additionally, ^T389p-S6K correlated with ^S727p-STAT3 (86%, p = 0.005). Advanced tumors with lymph node metastasis were characterized by high levels of ^S276p-NFκB (100%, p = 0.05) and ^S9p-GSK3β (100%, p = 0.05). High levels of PKBβ/AKT2, EGFR, as well as nuclear ^T202/Y204p-ERK and ^T180/Y182p-p38 were observed in normal ducts adjacent to PDAC compared with non-cancerous pancreas.</p> <p>Conclusion</p> <p>Multiple signaling proteins are activated in pancreatic duct cell carcinogenesis including those associated with the ERK, PKB/AKT, mTOR and STAT3 pathways. The ERK pathway activation appears also increased in duct epithelia adjacent to carcinoma, suggesting tumor micro-environmental effects.</p

Genomic, Pathway Network, and Immunologic Features Distinguishing Squamous Carcinomas

This integrated, multiplatform PanCancer Atlas study co-mapped and identified distinguishing molecular features of squamous cell carcinomas (SCCs) from five sites associated with smokin

Pan-Cancer Analysis of lncRNA Regulation Supports Their Targeting of Cancer Genes in Each Tumor Context

Long noncoding RNAs (lncRNAs) are commonly dys-regulated in tumors, but only a handful are known toplay pathophysiological roles in cancer. We inferredlncRNAs that dysregulate cancer pathways, onco-genes, and tumor suppressors (cancer genes) bymodeling their effects on the activity of transcriptionfactors, RNA-binding proteins, and microRNAs in5,185 TCGA tumors and 1,019 ENCODE assays.Our predictions included hundreds of candidateonco- and tumor-suppressor lncRNAs (cancerlncRNAs) whose somatic alterations account for thedysregulation of dozens of cancer genes and path-ways in each of 14 tumor contexts. To demonstrateproof of concept, we showed that perturbations tar-geting OIP5-AS1 (an inferred tumor suppressor) andTUG1 and WT1-AS (inferred onco-lncRNAs) dysre-gulated cancer genes and altered proliferation ofbreast and gynecologic cancer cells. Our analysis in-dicates that, although most lncRNAs are dysregu-lated in a tumor-specific manner, some, includingOIP5-AS1, TUG1, NEAT1, MEG3, and TSIX, synergis-tically dysregulate cancer pathways in multiple tumorcontexts