Carbon Footprint of Inbound Tourism to Iceland: A Consumption-Based Life-Cycle Assessment including Direct and Indirect Emissions

The greenhouse gas (GHG) emissions caused by tourism have been studied from several perspectives, but few studies exist that include all direct and indirect emissions, particularly those from aviation. In this study, an input/output-based hybrid life-cycle assessment (LCA) method is developed to assess the consumption-based carbon footprint of the average tourist including direct and indirect emissions. The total inbound tourism-related GHG emissions are also calculated within a certain region. As a demonstration of the method, the full carbon footprint of an average tourist is assessed as well as the total GHG emissions induced by tourism to Iceland over the period of 2010–2015, with the presented approach applicable in other contexts as well. Iceland provides an interesting case due to three features: (1) the tourism sector in Iceland is the fastest-growing industry in the country with an annual growth rate of over 20% over the past five years; (2) almost all tourists arrive by air; and (3) the country has an almost emissions-free energy industry and an import-dominated economy, which emphasise the role of the indirect emissions. According to the assessment, the carbon footprint for the average tourist is 1.35 tons of CO2-eq, but ranges from 1.1 to 3.2 tons of CO2-eq depending on the distance travelled by air. Furthermore, this footprint is increasing due to the rise in average flight distances travelled to reach the country. The total GHG emissions caused by tourism in Iceland have tripled from approximately 600,000 tons of CO2-eq in 2010 to 1,800,000 tons in 2015. Aviation accounts for 50%–82% of this impact (depending on the flight distance) underlining the importance of air travel, especially as tourism-related aviation is forecasted to grow significantly in the near future. From a method perspective, the carbon footprinting application presented in the study would seem to provide an efficient way to study both the direct and indirect emissions and to provide new insights and information to enable the development of appropriate GHG mitigation policies in the tourism sector.Academy of Finland (Grant 286747)Peer Reviewe

The Unintentional Gerrymandering of America: How Population Shifts in Congressional Districts Contribute to the Wasting of Votes, as Measured by the Efficiency Gap

Thanks to the foresight of our Founding Fathers we are required by law to redraw legislative boundaries every ten years, after the decennial census. These boundaries create districts at both the state and federal legislative level, and there are many guidelines which govern how districts can be drawn in order to provide for fair competition and accurate representation. Population distribution is key to how electoral districts are drawn at all levels. In recent decades, increasing concentrated populations of Democrats in urban areas and decreasing population in rural, more Republican areas has made it harder to draw competitive districts at the congressional level. There is evidence to support that this geographic polarization is being driven by citizens themselves, making choices of where to live based upon their lifestyle and ideology. This concept of self-sorting has been termed “unintentional gerrymandering” (Chen and Rodden 2013). This trend of “self-sorting” has been caused by many factors, all of them stemming from a larger movement of generational change. Intentional gerrymandering, that which is done by powerful incumbent legislators, is a known problem in political science. Unintentional gerrymandering, the way that geographic population shifts are affecting legislative and congressional districts in the same way, is a much less developed and affirmed concept. My research question addresses two areas that are missing from the current discussion of political geography and redistricting. The first asks how geographic population distribution (rural vs. urban) affects the amount of wasted votes in an election cycle, specifically looking at Congressional elections. The second is to test whether the efficiency gap is an effective formula to measure how wasted vii votes are affected by population shifts within congressional districts between redistricting cycles. To do this I examine a sample of urban and rural congressional districts to compare the number of wasted votes from the 2012 election cycle (which took place after 2010 redistricting was in effect) to the 2018 election cycle (which is the last available election data before 2020 redistricting will begin). I find that the number of wasted votes in rural districts in 2012 is significant and decreases slightly when looking at the 2018 election results. The effect was smaller and not statistically significant in urban districts when using the 2012 data, but the results in 2018 were much more significant. Supportive of the concept of unintentional gerrymandering, the population shifts from 2012 to 2018 resulted in more wasted votes in the districts which I measured

The pathway to diagnosis of type 1 diabetes in children: a questionnaire study.

OBJECTIVE: To explore the pathway to diagnosis of type 1 diabetes (T1D) in children. DESIGN: Questionnaire completed by parents. PARTICIPANTS: Parents of children aged 1 month to 16 years diagnosed with T1D within the previous 3 months. SETTING: Children and parents from 11 hospitals within the East of England. RESULTS: 88/164 (54%) invited families returned the questionnaire. Children had mean±SD age of 9.41±4.5 years. 35 (39.8%) presented with diabetic ketoacidosis at diagnosis. The most common symptoms were polydipsia (97.7%), polyuria (83.9%), tiredness (75.9%), nocturia (73.6%) and weight loss (64.4%) and all children presented with at least one of those symptoms. The time from symptom onset to diagnosis ranged from 2 to 315 days (median 25 days). Most of this was the appraisal interval from symptom onset until perceiving the need to seek medical advice. Access to healthcare was good but one in five children presenting to primary care were not diagnosed at first encounter, most commonly due to waiting for fasting blood tests or alternative diagnoses. Children diagnosed at first consultation had a shorter duration of symptoms (p=0.022) and children whose parents suspected the diagnosis were 1.3 times more likely (relative risk (RR) 1.3, 95% CI 1.02 to 1.67) to be diagnosed at first consultation. CONCLUSIONS: Children present with the known symptoms of T1D but there is considerable scope to improve the diagnostic pathway. Future interventions targeted at parents need to address the tendency of parents to find alternative explanations for symptoms and the perceived barriers to access, in addition to symptom awareness.The study was funded by the Royal College of General Practitioners Scientific Foundation Board (SFB-2011-15). JUS was supported by a National Institute of Health Research (NIHR) Academic Clinical Fellowship and subsequently Clinical Lectureship, and FMW by an NIHR Clinician Scientist award. SJS was supported by the Medical Research Council www.mrc.ac.uk [Unit Programme number MC_UU_12015/1]. The views expressed in this publication are those of the author(s) and not necessarily those of the NHS, the NIHR or the Department of Health.This is the final version of the article. It was first published by BMJ Group at http://bmjopen.bmj.com/content/5/3/e006470.ful

Cadherin-26 (CDH26) regulates airway epithelial cell cytoskeletal structure and polarity.

Polarization of the airway epithelial cells (AECs) in the airway lumen is critical to the proper function of the mucociliary escalator and maintenance of lung health, but the cellular requirements for polarization of AECs are poorly understood. Using human AECs and cell lines, we demonstrate that cadherin-26 (CDH26) is abundantly expressed in differentiated AECs, localizes to the cell apices near ciliary membranes, and has functional cadherin domains with homotypic binding. We find a unique and non-redundant role for CDH26, previously uncharacterized in AECs, in regulation of cell-cell contact and cell integrity through maintaining cytoskeletal structures. Overexpression of CDH26 in cells with a fibroblastoid phenotype increases contact inhibition and promotes monolayer formation and cortical actin structures. CDH26 expression is also important for localization of planar cell polarity proteins. Knockdown of CDH26 in AECs results in loss of cortical actin and disruption of CRB3 and other proteins associated with apical polarity. Together, our findings uncover previously unrecognized functions for CDH26 in the maintenance of actin cytoskeleton and apicobasal polarity of AECs

Poloxomer 188 Has a Deleterious Effect on Dystrophic Skeletal Muscle Function

Duchenne muscular dystrophy (DMD) is an X-linked, fatal muscle wasting disease for which there is currently no cure and limited palliative treatments. Poloxomer 188 (P188) is a tri-block copolymer that has been proposed as a potential treatment for cardiomyopathy in DMD patients. Despite the reported beneficial effects of P188 on dystrophic cardiac muscle function, the effects of P188 on dystrophic skeletal muscle function are relatively unknown. Mdx mice were injected intraperitoneally with 460 mg/kg or 30 mg/kg P188 dissolved in saline, or saline alone (control). The effect of single-dose and 2-week daily treatment was assessed using a muscle function test on the Tibialis Anterior (TA) muscle in situ in anaesthetised mice. The test comprises a warm up, measurement of the force-frequency relationship and a series of eccentric contractions with a 10% stretch that have previously been shown to cause a drop in maximum force in mdx mice. After 2 weeks of P188 treatment at either 30 or 460 mg/kg/day the drop in maximum force produced following eccentric contractions was significantly greater than that seen in saline treated control mice (P = 0.0001). Two week P188 treatment at either dose did not significantly change the force-frequency relationship or maximum isometric specific force produced by the TA muscle. In conclusion P188 treatment increases susceptibility to contraction-induced injury following eccentric contractions in dystrophic skeletal muscle and hence its suitability as a potential therapeutic for DMD should be reconsidered

The Effects of a Pre-workout Supplement on Collegiate Track Athletes\u27 Sub-max Bench Press

The use of prework out supplements in athletes has been increasing as athletes try to get more of an edge on their competition. Our research looked at the effect of taking Muscle Pharms preworkout supplement Assault in collegiate track athletes. We did this by having them preform a sub-max bench press. We found that there was no significant difference between the placebo and Assault

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

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 Alterations of the MYC Oncogene and Its Proximal Network across the Cancer Genome Atlas

Although theMYConcogene has been implicated incancer, a systematic assessment of alterations ofMYC, related transcription factors, and co-regulatoryproteins, forming the proximal MYC network (PMN),across human cancers is lacking. Using computa-tional approaches, we define genomic and proteo-mic features associated with MYC and the PMNacross the 33 cancers of The Cancer Genome Atlas.Pan-cancer, 28% of all samples had at least one ofthe MYC paralogs amplified. In contrast, the MYCantagonists MGA and MNT were the most frequentlymutated or deleted members, proposing a roleas tumor suppressors.MYCalterations were mutu-ally exclusive withPIK3CA,PTEN,APC,orBRAFalterations, suggesting that MYC is a distinct onco-genic driver. Expression analysis revealed MYC-associated pathways in tumor subtypes, such asimmune response and growth factor signaling; chro-matin, translation, and DNA replication/repair wereconserved pan-cancer. This analysis reveals insightsinto MYC biology and is a reference for biomarkersand therapeutics for cancers with alterations ofMYC or the PMN

Spatial Organization and Molecular Correlation of Tumor-Infiltrating Lymphocytes Using Deep Learning on Pathology Images

Beyond sample curation and basic pathologic characterization, the digitized H&E-stained images of TCGA samples remain underutilized. To highlight this resource, we present mappings of tumorinfiltrating lymphocytes (TILs) based on H&E images from 13 TCGA tumor types. These TIL maps are derived through computational staining using a convolutional neural network trained to classify patches of images. Affinity propagation revealed local spatial structure in TIL patterns and correlation with overall survival. TIL map structural patterns were grouped using standard histopathological parameters. These patterns are enriched in particular T cell subpopulations derived from molecular measures. TIL densities and spatial structure were differentially enriched among tumor types, immune subtypes, and tumor molecular subtypes, implying that spatial infiltrate state could reflect particular tumor cell aberration states. Obtaining spatial lymphocytic patterns linked to the rich genomic characterization of TCGA samples demonstrates one use for the TCGA image archives with insights into the tumor-immune microenvironment