Life cycle cost analysis of the UK housing stock

Purpose

The aim of the paper is to estimate life cycle costs (LCC) of the current housing stock in the UK as part of sustainability assessment of the residential construction sector. This is carried out by first estimating the life cycle costs of individual houses considering detached, semi-detached and terraced homes. These results are then extrapolated to the UK housing stock consisting of seven million each of semi-detached and terraced houses and four million of detached houses. A brief discussion of life cycle environmental impacts is also included to help identify improvement opportunities for both costs and impacts.

Methods

The life cycle costing methodology followed in the study is congruent with the life cycle assessment methodology. The system boundary for the study is from ‘cradle to grave’, including all activities from extraction and manufacture of construction materials to construction and use of the house to its demolition. The functional unit is defined as the construction and occupation of a house in the UK over the lifetime of 50 years.

Results and discussion

The total life cycle costs are estimated at £247,000 for the detached house, £192,000 for the semi-detached and £142,000 for the terraced house. The running costs in the use stage contribute 52 % to the total life cycle costs of which half is from energy use. The construction costs contribute 35 % to the total LCC with the walls and the roof being the most expensive items. The remaining 13 % of the costs are incurred at the end of life of the house which are largely (85 %) due to the cost of labour for demolition. Recovery of end-of-life materials has a limited potential to reduce the overall life cycle costs of a house. The life cycle costs of the whole housing stock are estimated at £67 billion per year or £3,360 billion over the 50-year lifetime.

Conclusions

The existing housing stock in the UK is facing a number of challenges that will need to be addressed in the near future. These include improving energy efficiency and reducing the dependency on fossil fuels to reduce energy demand, fuel poverty and environmental impacts. Furthermore, the disparity between the construction costs and house market prices will need to be addressed to ensure that access to housing and house ownership do not become the privilege of a few.     

Extending the Schizosaccharomyces pombe Molecular Genetic Toolbox

Targeted alteration of the genome lies at the heart of the exploitation of S. pombe as a model system. The rate of analysis is often determined by the efficiency with which a target locus can be manipulated. For most loci this is not a problem, however for some loci, such as fin1 ⁺, rates of gene targeting below 5% can limit the scope and scale of manipulations that are feasible within a reasonable time frame. We now describe a simple modification of transformation procedure for directing integration of genomic sequences that leads to a 5-fold increase in the transformation efficiency when antibiotic based dominant selection markers are used. We also show that removal of the pku70 ⁺ and pku80 ⁺ genes, which encode DNA end binding proteins required for the non-homologous end joining DNA repair pathway, increases the efficiency of gene targeting at fin1 ⁺ to around 75–80% (a 16-fold increase). We describe how a natMX6/rpl42 ⁺ cassette can be used for positive and negative selection for integration at a targeted locus. To facilitate the evaluation of the impact of a series of mutations on the function of a gene of interest we have generated three vector series that rely upon different selectable markers to direct the expression of tagged/untagged molecules from distinct genomic integration sites. pINTL and pINTK vectors use ura4 ⁺ selection to direct disruptive integration of leu1 ⁺ and lys1 ⁺ respectively, while pINTH vectors exploit nourseothricin resistance to detect the targeted disruption of a hygromycin B resistance conferring hphMX6 cassette that has been integrated on chromosome III. Finally, we have generated a series of multi-copy expression vectors that use resistance to nourseothricin or kanamycin/G418 to select for propagation in prototrophic hosts. Collectively these protocol modifications and vectors extend the versatility of this key model system.     

A time course study on dose-response relationship between alcohol exposure and its effects on lipid profile and biomarkers of tissue damage

This present research investigated variations in lipid profiles and important biomarkers of tissue damage in response to graded concentrations of alcohol administration in male Wistar rats. Group A (control) received distilled water while group B, C and D received 30%, 40% and 50% (v/v) alcohol respectively. Five rats each from groups A-D were sacrificed after day(s) 1, 7, 14, 21 and 28 of administration. A significant increase was observed at day 28 for serum cholesterol by 79% (group B), 78% (group C) and 47% (group D) together with serum phospholipid 58% (group B), 50% (group C) and 92% (group D). Serum triacylglycerol increased by 71% (group B), 43% (group C) and 16% (group D) at day 21, while concentration of serum albumin decreased at day 28 by 40.9% (group B), 50.2% (group C), 53.3% (group D) respectively when compared with control (group A). Serum aminotransferases and alkaline phosphatase specific activities, as well as creatinine and uric acid concentration increased in a concentration-dependent manner, following alcohol administration. Though most of these effects induced by alcohol were time- and concentration-dependent, 40% alcohol appear to be more stable, giving results consistent with alcohol-induced damages, with minimal mortality. This study therefore further validated dyslipidemia and imbalance in clinical biomarkers as hallmarks of tissue damage induced by excessive alcohol consumption with an insight on the time- and concentration-response relationship between alcohol consumption and its toxicity.     

Global gene expression profiling of endothelium exposed to heme reveals an organ-specific induction of cytoprotective enzymes in sickle cell disease

Background

Sickle cell disease (SCD) is characterized by hemolysis, vaso-occlusion and ischemia reperfusion injury. These events cause endothelial dysfunction and vasculopathies in multiple systems. However, the lack of atherosclerotic lesions has led to the idea that there are adaptive mechanisms that protect the endothelium from major vascular insults in SCD patients. The molecular bases for this phenomenon are poorly defined. This study was designed to identify the global profile of genes induced by heme in the endothelium, and assess expression of the heme-inducible cytoprotective enzymes in major organs impacted by SCD.

Methods and Findings

Total RNA isolated from heme-treated endothelial monolayers was screened with the Affymetrix U133 Plus 2.0 chip, and the microarray data analyzed using multiple bioinformatics software. Hierarchical cluster analysis of significantly differentially expressed genes successfully segregated heme and vehicle-treated endothelium. Validation studies showed that the induction of cytoprotective enzymes by heme was influenced by the origin of endothelial cells, the duration of treatment, as well as the magnitude of induction of individual enzymes. In agreement with these heterogeneities, we found that induction of two major Nrf2-regulated cytoprotective enzymes, heme oxygenase-1 and NAD(P)H:quinone oxidoreductase-1 is organ-specific in two transgenic mouse models of SCD. This data was confirmed in the endothelium of post-mortem lung tissues of SCD patients.

Conclusions

Individual organ systems induce unique profiles of cytoprotective enzymes to neutralize heme in SCD. Understanding this heterogeneity may help to develop effective therapies to manage vasculopathies of individual systems.     

Allocation of environmental burdens in co-product systems: Process and product-related burdens (part 2)

ISO 14041 requires that allocation by physical causality must reflect the quantitative changes in product outputs or functions and will not necessarily be in proportion to simple physical measure such as mass. This paper examines the instances where physical causality can be represented by mass. However, it also goes further than ISO to demonstrate that the type of causality in the system is not necessarily always the same and can change depending on the way the system is operated. Whole system modelling and the marginal allocation approach are used to identify the correct type of causality for different operating states of the system and the corresponding changes in the environmental burdens. This is generally not possible with the other allocation methods, also examined in this paper. Both process- and product-related burdens are considered and the approach is illustrated by a reference to an existing system producing five boron co-products     

An unusual class of PITX2 mutations in Axenfeld-Rieger syndrome

BACKGROUND: Mutations in the PITX2 homeobox gene are known to contribute to Axenfeld-Rieger syndrome (ARS), an autosomal-dominant developmental disorder. Although most mutations are in the homeodomain and result in a loss of function, there is a growing subset in the C-terminal domain that has not yet been characterized. These mutations are of particular interest because the C-terminus has both inhibitory and stimulatory activities. METHODS: In this study we used a combination of in vitro DNA binding and transfection reporter assays to investigate the fundamental issue of whether C-terminal mutations result in gain or loss of function at a cellular level. RESULTS: We report a new frameshift mutation in the PITX2 allele that predicts a truncated protein lacking most of the C-terminal domain (D122FS). This newly reported mutant and another ARS C-terminal mutant (W133Stop) both have greater binding than wild-type to the bicoid element. Of interest, the mutants yielded approximately 5-fold greater activation of the prolactin promoter in CHO cells, even though the truncated proteins were expressed at lower levels than the wild-type protein. The truncated proteins also had greater than wild-type activity in 2 other cell lines, including the LS8 oral epithelial line that expresses the endogenous Pitx2 gene. CONCLUSIONS: The results indicate that the PITX2 C-terminal domain has inhibitory activity and support the notion that ARS may also be caused by gain-of-function mutations.     

Serum lipoproteins promote efficient presentation of the malaria virulence protein PfEMP1 at the erythrocyte surface

The virulence of the malaria parasite Plasmodium falciparum is related to its ability to express a family of adhesive proteins known as P. falciparum erythrocyte membrane protein 1 (PfEMP1) at the infected red blood cell surface. The mechanism for the transport and delivery of these adhesins to the erythrocyte membrane is only poorly understood. In this work, we have used specific immune reagents in a flow cytometric assay to monitor the effects of serum components on the surface presentation of PfEMP1. We show that efficient presentation of the A4 and VAR2CSA variants of PfEMP1 is dependent on the presence of serum in the bathing medium during parasite maturation. Lipid-loaded albumin supports parasite growth but allows much less efficient presentation of PfEMP1 at the red blood cell surface. Analysis of the serum components reveals that lipoproteins, especially those of the low-density lipoprotein fraction, promote PfEMP1 presentation. Cytoadhesion of infected erythrocytes to the host cell receptors CD36 and ICAM-1 is also decreased in infected erythrocytes cultured in the absence of serum. The defect appears to be in the transfer of PfEMP1 from parasite-derived structures known as the Maurer's clefts to the erythrocyte membrane or in surface conformation rather than a down-regulation or switching of particular PfEMP1 variants.     

Allocation of environmental burdens in co-product systems: Product-related burdens (Part 1)

This paper uses an industrial case study of a boron system producing five co-products to examine different allocation methods recommended by ISO 14041 and compare them with the allocation methods most commonly used by LCA practitioners. In particular, allocation by physical causality is discussed. The paper illustrates how the use of whole system modelling can help to identify the correct type of causality for allocation. The case examined here concerns marginal changes of product-related parameters in the system, in this case represented by the output of boron co-products. The analysis shows that in some cases it can he correct to allocate the burdens on the basis of a simple physical quantity, such as mass, as long as the allocation parameter is based on physical causation and is not chosen arbitrarily. In whole system modelling, the correct causality is identified by the model itself, so that the possibility of allocation by an arbitrary parameter is avoided. However, as for system disaggregation and expansion, allocation through mathematical modelling may only be possible if detailed data for the system are available.