Estimating energy consumption from cross-country relationships

World Ban

The hidden world trade in energy

The energy embodied in internationally traded commodities is estimated for the year 1967 by employing United States input-output energy coefficients expressed in physical units. In this year and under the assumption of USA technology and industrial structure, this "hidden" world trade in energy probably exceeded 40 per cent of the directly observed world trade in energy. As a ratio to aggregate energy consumption, the importance of embodied energy flows is smaller, but net embodied energy imports are positively correlated with per capita GDP, and their inclusion in aggregate energy consumption would increase measured income (per capita GDP) elasticities. A country's imports of embodied energy are approximately proportional to the imports of all commodities. Exports of embodied energy, on the other hand, especially those associated with more energy-intensive materials (which are largely products of what is commonly called heavy industry and which account for most of the country net imports of embodied energy) have a much higher elasticity than do imports with respect to per capita GDP. These energy-intensive exports are also significantly affected by a country's relative production of primary energy, total agricultural crops, and other natural resources.World Ban

An objective index of walkability for research and planning in the Sydney Metropolitan Region of New South Wales, Australia: an ecological study

Background: Walkability describes the capacity of the built environment to support walking for various purposes. This paper describes the construction and validation of two objective walkability indexes for Sydney, Australia. Methods: Walkability indexes using residential density, intersection density, land use mix, with and without retail floor area ratio were calculated for 5,858 Sydney Census Collection Districts in a geographical information system. Associations between variables were evaluated using Spearman’s rho (ρ). Internal consistency and factor structure of indexes were estimated with Cronbach’s alpha and principal components analysis; convergent and predictive validity were measured using weighted kappa (κw) and by comparison with reported walking to work at the 2006 Australian Census using logistic regression. Spatial variation in walkability was assessed using choropleth maps and Moran’s I. Results: A three-attribute abridged Sydney Walkability Index comprising residential density, intersection density and land use mix was constructed for all Sydney as retail floor area was only available for 5.3% of Census Collection Districts. A four-attribute full index including retail floor area ratio was calculated for 263 Census Collection Districts in the Sydney Central Business District. Abridged and full walkability index scores for these 263 areas were strongly correlated (ρ=0.93) and there was good agreement between walkability quartiles (κw=0.73). Internal consistency ranged from 0.60 to 0.71, and all index variables loaded highly on a single factor. The percentage of employed persons who walked to work increased with increasing walkability: 3.0% in low income-low walkability areas versus 7.9% in low income-high walkability areas; and 2.1% in high income-low walkability areas versus 11% in high income-high walkability areas. The adjusted odds of walking to work were 1.05 (0.96–1.15), 1.58 (1.45–1.71) and 3.02 (2.76–3.30) times higher in medium, high and very high compared to low walkability areas. Associations were similar for full and abridged indexes. Conclusions: The abridged Sydney Walkability Index has predictive validity for utilitarian walking, will inform urban planning in Sydney, and will be used as an objective measure of neighbourhood walkability in a large population cohort. Abridged walkability indexes may be useful in settings where retail floor area data are unavailable

A semi-automated non-radiactive system for measuring recovery of RNA synthesis and unscheduled DNA synthesis using ethynyluracil derivatives

Nucleotide excision repair (NER) removes the major UV-photolesions from cellular DNA. In humans, compromised NER activity is the cause of several photosensitive diseases, one of which is the skin-cancer predisposition disorder, xeroderma pigmentosum (XP). Two assays commonly used in measurement of NER activity are ‘unscheduled DNA synthesis (UDS)’, and ‘recovery of RNA synthesis (RRS)’, the latter being a specific measure of the transcription-coupled repair sub-pathway of NER. Both assays are key techniques for research in NER as well as in diagnoses of NER-related disorders. Until very recently, reliable methods for these assays involved measurements of incorporation of radio-labeled nucleosides. We have established non-radioactive procedures for determining UDS and RRS levels by incorporation of recently developed alkyne-conjugated nucleoside analogues, 5-ethynyl-2′-deoxyuridine (EdU) and 5-ethynyuridine (EU). EdU and EU are respectively used as alternatives for 3H-thymidine in UDS and for 3H-uridine in RRS. Based on these alkyne-nucleosides and an integrated image analyser, we have developed a semi-automated assay system for NER-activity. We demonstrate the utility of this system for NER-activity assessments of lymphoblastoid samples as well as primary fibroblasts. Potential use of the system for large-scale siRNA-screening for novel NER defects as well as for routine XP diagnosis are also considered

DNA repair, DNA replication and human disorders: A personal journey

I was born in 1946 and grew up in the industrial north-west of England close to the city of Manchester. My parents were German- Jewish refugees, who left Germany fairly early, in 1933. My father helped to establish and was one of the directors of a tannery, which made leather for shoes and handbags. This was part of a group of tanneries established first in Strasbourg by my great-grandfather Ferdinand Oppenheimer. I would describe my childhood and adolescent years as comfortable by general post-war standards. I went to a state primary school and obtained a scholarship to Manchester Grammar School (MGS), a fairly prestigious secondary school. As a child I was always interested in chemistry but had little interest in or knowledge of biology. The educational system in the UK at that time was such that one had to specialise very early and as a consequence I have had no formal biology education since the age of 12, something I have managed to hide reasonably successfully for the rest of my life! In my final two years at MGS I studied just physics, chemistry and mathematics and obtained a scholarship to Pembroke College, Cambridge (England) to study Natural Sciences, with the intention of becoming a chemist. In the second year at Cambridge, one of the options was a course on biochemistry. Having no real idea what this was, I read a book about it in the summer of 1965, and was truly astonished and excited to discover that the basis of life was just a bunch of rather complicated organic chemistry reactions. So I took the biochemistry course in my second year. By the end of that year, I was fed up with chemistry and for my final year I chose to do biochemistry rather than chemistry, a decision I have not regretted. The biochemistry lectures must have been pretty up-to-date, as we were told briefly about the discovery of DNA repair by Dick Setlow [1], a topic that seemed rather esoteric at the time

Mutations in UVSSA cause UV-sensitive syndrome and impair RNA polymerase IIo processing in transcription-coupled nucleotide-excision repair

UV-sensitive syndrome (UVSS) is a genodermatosis characterized by cutaneous photosensitivity without skin carcinoma1, 2, 3, 4. Despite mild clinical features, cells from individuals with UVSS, like Cockayne syndrome cells, are very UV sensitive and are deficient in transcription-coupled nucleotide-excision repair (TC-NER)2, 4, 5, which removes DNA damage in actively transcribed genes6. Three of the seven known UVSS cases carry mutations in the Cockayne syndrome genes ERCC8 or ERCC6 (also known as CSA and CSB, respectively)7, 8. The remaining four individuals with UVSS, one of whom is described for the first time here, formed a separate UVSS-A complementation group1, 9, 10; however, the responsible gene was unknown. Using exome sequencing11, we determine that mutations in the UVSSA gene (formerly known as KIAA1530) cause UVSS-A. The UVSSA protein interacts with TC-NER machinery and stabilizes the ERCC6 complex; it also facilitates ubiquitination of RNA polymerase IIo stalled at DNA damage sites. Our findings provide mechanistic insights into the processing of stalled RNA polymerase and explain the different clinical features across these TC-NER–deficient disorders