An assessment of the potential returns of energy certificates for the UK household sector

Purpose – This article seeks to investigate the interconnections between the expectations of the impact of energy certificates issued within the UK domestic building sector through the Energy Performance of Buildings Directive (EPBD) and the actual number and financial implications of the energy saving measures (ESMs) achieved. Design/methodology/approach – The methodology uses two previously published surveys and compares these with a third independent survey by the authors focusing upon the discrepancies between planned action and implemented action, introducing the term human factor element (hfe). Findings – The article concludes that annual carbon savings arising from implementation of the Energy Performance Certificate (EPC) may be as low as 73.4?ktC over the five year term of the Kyoto Protocol even though 44 per cent of energy saving measure costs of £200 million are recouped within the same time period and savings will continue for up to 40 years. Achieving annual savings of only 14.7?ktC by 2010, such a figure represents a mere 0.3 per cent of the annual domestic 4.8?MtC savings announced by the government in its 2006 Climate Change Programme. Practical implications – Since the principal determinant in the uptake of ESMs is initial cost, it is considered that the EPBD is likely to remain an under-performing instrument in the promotion of energy sufficiency until such time as other complementary provisions are introduced. Originality/value – Sheds light upon the likely financial impact upon energy efficiency in domestic buildings by energy certificates

A magneto-optic trap using a reversible, solid-state alkali-metal source

We demonstrate a novel way to form and deplete a vapor-cell magneto-optic trap (MOT) using a reversible, solid-state alkali-metal source (AMS) via an applied polarized voltage. Using ~100 mW of electrical power, a trapped-atom number of 5x10^6 has been achieved starting from near zero and the timescales of the MOT formation and depletion of ~1 s. This fast, reversible, and low power alkali-atom source is desirable in both tabletop and portable cold-atom systems. The core technology of this device should translate readily to other alkali and alkaline-earth elements that could find a wide range of uses in cold-atom systems and instruments.Comment: 7 page

Dynamic characterization of an alkali-ion battery as a source for laser-cooled atoms

We investigate a solid-state, reversible, alkali-ion battery (AIB) capable of regulating the density of alkali atoms in a vacuum system used for the production of laser-cooled atoms. The cold-atom sample can be used with in-vacuum chronoamperometry as a diagnostic for the voltage-controlled electrochemical reaction that sources or sinks alkali atoms into the vapor. In a combined reaction-diffusion-limited regime, we show that the number of laser-cooled atoms in a magneto-optical trap can be increased both by initially loading the AIB from the vapor for longer, and by using higher voltages across the AIB when atoms are subsequently sourced back into the vapor. The time constants associated with the change in atom number in response to a change in AIB voltage are in the range of 0.5 s - 40 s. The AIB alkali reservoir is demonstrated to survive oxidization during atmospheric exposure, simplifying reservoir loading prior to vacuum implementation as a replacement for traditional resistively-heated dispensers. The AIB capabilities may provide an improved atom number stability in next-generation atomic clocks and sensors, while also facilitating fast loading and increased interrogation times.Comment: 7 pages, 5 figure

Staphylococcus aureus Activates the NLRP3 Inflammasome in Human and Rat Conjunctival Goblet Cells

The conjunctiva is a moist mucosal membrane that is constantly exposed to an array of potential pathogens and triggers of inflammation. The NACHT, leucine rich repeat (LRR), and pyrin domain-containing protein 3 (NLRP3) is a Nod-like receptor that can sense pathogens or other triggers, and is highly expressed in wet mucosal membranes. NLRP3 is a member of the multi-protein complex termed the NLRP3 inflammasome that activates the caspase 1 pathway, inducing the secretion of biologically active IL-1β, a major initiator and promoter of inflammation. The purpose of this study was to: (1) determine whether NLRP3 is expressed in the conjunctiva and (2) determine whether goblet cells specifically contribute to innate mediated inflammation via secretion of IL-1β. We report that the receptors known to be involved in the priming and activation of the NLRP3 inflammasome, the purinergic receptors P2X4 and P2X7 and the bacterial Toll-like receptor 2 are present and functional in conjunctival goblet cells. Toxin-containing Staphylococcus aureus (S. aureus), which activates the NLRP3 inflammasome, increased the expression of the inflammasome proteins NLRP3, ASC and pro- and mature caspase 1 in conjunctival goblet cells. The biologically active form of IL-1β was detected in goblet cell culture supernatants in response to S. aureus, which was reduced when the cells were treated with the caspase 1 inhibitor Z-YVAD. We conclude that the NLRP3 inflammasome components are present in conjunctival goblet cells. The NRLP3 inflammasome appears to be activated in conjunctival goblet cells by toxin-containing S. aureus via the caspase 1 pathway to secrete mature IL1-β. Thus goblet cells contribute to the innate immune response in the conjunctiva by activation of the NLRP3 inflammasome

A novel role for CRIM1 in the corneal response to UV and pterygium development

Pterygium is a pathological proliferative condition of the ocular surface, characterised by formation of a highly vascularised, fibrous tissue arising from the limbus that invades the central cornea leading to visual disturbance and, if untreated, blindness. Whilst chronic ultraviolet (UV) light exposure plays a major role in its pathogenesis, higher susceptibility to pterygium is observed in some families, suggesting a genetic component. In this study, a Northern Irish family affected by pterygium but reporting little direct exposure to UV was identified carrying a missense variant in CRIM1 NM_016441.2: c.1235 A > C (H412P) through whole-exome sequencing and subsequent analysis. CRIM1 is expressed in the developing eye, adult cornea and conjunctiva, having a role in cell differentiation and migration but also in angiogenesis, all processes involved in pterygium formation. We demonstrate elevated CRIM1 expression in pterygium tissue from additional individual Northern Irish patients compared to unaffected conjunctival controls. UV irradiation of HCE-S cells resulted in an increase in ERK phosphorylation and CRIM1 expression, the latter further elevated by the addition of the MEK1/2 inhibitor, U0126. Conversely, siRNA knockdown of CRIM1 led to decreased UV-induced ERK phosphorylation and increased BCL2 expression. Transient expression of the mutant H412P CRIM1 in corneal epithelial HCE-S cells showed that, unlike wild-type CRIM1, it was unable to reduce the cell proliferation, increased ERK phosphorylation and apoptosis induced through a decrease of BCL2 expression levels. We propose here a series of intracellular events where CRIM1 regulation of the ERK pathway prevents UV-induced cell proliferation and may play an important role in the in the pathogenesis of pterygium

Selectivity and Mechanism of Hydrogen Atom Transfer by an Isolable Imidoiron(III) Complex

This article discusses a mechanistic study of hydrogen atom transfer by an isolable iron (III) imido complex, LᴹᵉFeNAd (Lᴹᵉ = bulky β-diketiminate ligand, 2,4-bis(2,6-diisopropylphenylimido)pentyl; Ad = 1-adamantyl)

Cigarette Smoke Extract (CSE) Delays NOD2 Expression and Affects NOD2/RIPK2 Interactions in Intestinal Epithelial Cells

Genetic and environmental factors influence susceptibility to Crohn's disease (CD): NOD2 is the strongest individual genetic determinant and smoking the best-characterised environmental factor. Carriage of NOD2 mutations predispose to small-intestinal, stricturing CD, a phenotype also associated with smoking. We hypothesised that cigarette smoke extract (CSE) altered NOD2 expression and function in intestinal epithelial cells.Intestinal epithelial cell-lines (SW480, HT29, HCT116) were stimulated with CSE and nicotine (to mimic smoking) ±TNFα (to mimic inflammation). NOD2 expression was measured by qRT-PCR and western blotting; NOD2-RIPK2 interactions by co-immunoprecipitation (CoIP); nuclear NFκB-p65 by ELISA; NFκB activity by luciferase reporter assays and chemokines (CCL20, IL8) in culture supernatants by ELISA. In SW480 and HT29 cells the TNFα-induced NOD2 expression at 4 hours was reduced by CSE (p = 0.0226), a response that was dose-dependent (p = 0.003) and time-dependent (p = 0.0004). Similar effects of CSE on NOD2 expression were seen in cultured ileal biopsies from healthy individuals. In SW480 cells CSE reduced TNFα-induced NFκB-p65 translocation at 15 minutes post-stimulation, upstream of NOD2. Levels of the NOD2-RIPK2 complex were no different at 8 hours post-stimulation with combinations of CSE, nicotine and TNFα, but at 18 hours it was increased in cells stimulated with TNFα+CSE but decreased with TNFα alone (p = 0.0330); CSE reduced TNFα-induced NFκB activity (p = 0.0014) at the same time-point. At 24 hours, basal CCL20 and IL8 (p<0.001 for both) and TNFα-induced CCL20 (p = 0.0330) production were decreased by CSE. CSE also reduced NOD2 expression, CCL20 and IL8 production seen with MDP-stimulation of SW480 cells pre-treated with combinations of TNFα and CSE.CSE delayed TNFα-induced NOD2 mRNA expression and was associated with abnormal NOD2/RIPK2 interaction, reduced NFκB activity and decreased chemokine production. These effects may be involved in the pathogenesis of small-intestinal CD and may have wider implications for the effects of smoking in NOD2-mediated responses