Energy, carbon and cost performance of building stocks : upgrade analysis, energy labelling and national policy development

The area of policy formulation for the energy and carbon performance of buildings is coming under increasing focus. A major challenge is to account for the large variation within building stocks relative to factors such as location, climate, age, construction, previous upgrades, appliance usage, and type of heating/cooling/lighting system. Existing policy-related tools that rely on simple calculation methods have limited ability to represent the dynamic interconnectedness of technology options and the impact of possible future changes in climate and occupant behaviour. The use of detailed simulation tools to address these limitations in the context of policy development has hitherto been focussed on the modelling of a number of representative designs rather than dealing with the spread inherent in large building stocks. Further, these tools have been research-oriented and largely unsuitable for direct use by policy-makers, practitioners and, ultimately, building owners/occupiers. This paper summarises recent initiatives that have applied advanced modelling and simulation in the context of policy formulation for large building stocks. To exemplify the stages of the process, aspects of the ESRU Domestic Energy Model (EDEM) are described. EDEM is a policy support tool built on detailed simulation models aligned with the outcomes of national surveys and future projections for the housing stock. On the basis of pragmatic inputs, the tool is able to determine energy use, carbon emissions and upgrade/running cost for any national building stock or sub-set. The tool has been used at the behest of the Scottish Building Standards Agency and South Ayrshire Council to determine the impact of housing upgrades, including the deployment of new and renewable energy systems, and to rate the energy/carbon performance of individual dwellings as required by the European Commission's Directive on the Energy Performance of Buildings (EC 2002)

Occupant behaviour in naturally ventilated and hybrid buildings

Adaptive thermal comfort criteria for building occupants are now becoming established. In this paper we illustrate their use in the prediction of occupant behaviour and make a comparison with a non-adaptive temperature threshold approach. A thermal comfort driven adaptive behavioural model for window opening is described and its use within dynamic simulation illustrated for a number of building types. Further development of the adaptive behavioural model is suggested including use of windows, doors, ceiling fans, night cooling, air conditioning and heating, also the setting of opportunities and constraints appropriate to a particular situation. The integration in dynamic simulation of the thermal adaptive behaviours together with non-thermally driven behaviours such as occupancy, lights and blind use is proposed in order to create a more complete model of occupant behaviour. It is further proposed that this behavioural model is implemented in a methodology that includes other uncertainties (e.g. in internal gains) so that a realistic range of occupant behaviours is represented at the design stage to assist in the design of robust, comfortable and low energy buildings

Autophagic cell death exists.

The term autophagic cell death (ACD) initially referred to cell death with greatly enhanced autophagy, but is increasingly used to imply a death-mediating role of autophagy, as shown by a protective effect of autophagy inhibition. In addition, many authors require that autophagic cell death must not involve apoptosis or necrosis. Adopting these new and restrictive criteria, and emphasizing their own failure to protect human osteosarcoma cells by autophagy inhibition, the authors of a recent Editor's Corner article in this journal argued for the extreme rarity or nonexistence of autophagic cell death. We here maintain that, even with the more stringent recent criteria, autophagic cell death exists in several situations, some of which were ignored by the Editor's Corner authors. We reject their additional criterion that the autophagy in ACD must be the agent of ultimate cell dismantlement. And we argue that rapidly dividing mammalian cells such as cancer cells are not the most likely situation for finding pure ACD

Multiple interacting cell death mechanisms in the mediation of excitotoxicity and ischemic brain damage: A challenge for neuroprotection.

There is currently no approved neuroprotective pharmacotherapy for acute conditions such as stroke and cerebral asphyxia. One of the reasons for this may be the multiplicity of cell death mechanisms, because inhibition of a particular mechanism leaves the brain vulnerable to alternative ones. It is therefore essential to understand the different cell death mechanisms and their interactions. We here review the multiple signaling pathways underlying each of the three main morphological types of cell death - apoptosis, autophagic cell death and necrosis - emphasizing their importance in the neuronal death that occurs during cerebral ischemia and hypoxia-ischemia, and we analyze the interactions between the different mechanisms. Finally, we discuss the implications of the multiplicity of cell death mechanisms for the design of neuroprotective strategies

Radioisotopes and coastal research in the Great Barrier Reef

Radioisotopes are efficient tracers of coastal processes on various spatial and temporal scales. The isotopes of radon and radium are particularly useful tools to understand hydrological land-ocean interaction because (a) activities of these isotopes are elevated in groundwater by two to three orders of magnitude in comparison with seawater, and (b) these isotopes have half-lives similar to the time scales of coastal hydrological processes such as river and groundwater discharge to the ocean, as well as coastal ocean mixing (or residence) time. The application of these isotopes to studies of land-ocean interaction in the central Great Barrier Reef region (Townsville to Cooktown) is illustrated in three recent studies: (1) coastal mapping of radon on a regional scale improves the understanding of the spatial variability of river and groundwater fluxes to the Great Barrier Reef lagoon; (2) quantification of tidal water exchange between mangrove forests and creeks demonstrates the significant contributions this process makes to water flux and associated geochemical fluxes along tropical coastlines; (3) estimates of coastal water residence time contribute to the understanding of the fate of land-derived solutes in the Great Barrier Reef Lagoon. Concurrent mapping of 222Rn (half-life 3.8 days) and salinity allows an efficient qualitative assessment of land–ocean interaction on various spatial and temporal scales. From shore-parallel transects along the Central Great Barrier Reef coastline with a surface-towed and continuously recording multi-detector system, numerous locations of elevated radon activities can be identified as terrestrially-derived submarine groundwater discharge, riverine sources, and the recirculation of seawater through crustacean burrows in mangrove forests. Variations in the inverse relationship of 222Rn and salinity in different tropical wet seasons reveal ‘timing’ aspects of large-scale freshwater input during the tropical wet season into the lagoon. Subsequently, 222Rn was used together with radium isotopes to quantify the tidal water exchange between a mangrove forest on Hinchinbrook Island and the ocean. Significant export of these radio-nuclides from the forest into a tidal creek indicates continuous tidally-driven circulation through animal burrows in the forest. The forest floor is efficiently flushed, with water flux of about 30 L m-2 day-1 of forest floor, which is equivalent to about 10% of the total burrow volume in the forest per tidal cycle. This work illustrates the physical process which supports export of organic and inorganic matter from mangrove forests to the coastal zone. Importantly, annual average circulation fluxes through mangrove forest floors are of the same order as annual river discharge in the central GBR. Finally, an improved understanding of the fate of land-derived waters is of great importance to current discussions about water quality management in the Great Barrier Reef. The mixing of coastal waters is an important parameter influencing the health of these ecosystems. Time constants associated with the decay of four naturally-occurring isotopes of radium span large time scales; 224Ra, 223Ra, 228Ra and 226Ra have half-lives of 4 days, 11 days, 6 years and 1620 years respectively. The radium quartet has been used to determine time scales of mixing of near-shore water and deep ocean water. This study demonstrates that central GBR water within 20 km of the coast is flushed with outer lagoon water on a timescale of 18–45 days, with the flushing time increasing northward. This difference likely reflects the different reef matrix density in the two zones, affecting exchange with offshore Coral Sea water

Beclin 1-independent autophagy contributes to apoptosis in cortical neurons.

Neuronal autophagy is enhanced in many neurological conditions, such as cerebral ischemia and traumatic brain injury, but its role in associated neuronal death is controversial, especially under conditions of apoptosis. We therefore investigated the role of autophagy in the apoptosis of primary cortical neurons treated with the widely used and potent pro-apoptotic agent, staurosporine (STS). Even before apoptosis, STS enhanced autophagic flux, as shown by increases in autophagosomal (LC3-II level, LC3 punctate labeling) and lysosomal (cathepsin D, LAMP1, acid phosphatase, β-hexasominidase) markers. Inhibition of autophagy by 3-methyladenine, or by lentivirally-delivered shRNAs against Atg5 and Atg7, strongly reduced the STS-induced activation of caspase-3 and nuclear translocation of AIF, and gave partial protection against neuronal death. Pan-caspase inhibition with Q-VD-OPH likewise protected partially against neuronal death, but failed to affect autophagy. Combined inhibition of both autophagy and caspases gave strong synergistic neuroprotection. The autophagy contributing to apoptosis was Beclin 1-independent, as shown by the fact that Beclin 1 knockdown failed to reduce it but efficiently reduced rapamycin-induced autophagy. Moreover the Beclin 1 knockdown sensitized neurons to STS-induced apoptosis, indicating a cytoprotective role of Beclin 1 in cortical neurons. Caspase-3 activation and pyknosis induced by two other pro-apoptotic stimuli, MK801 and etoposide, were likewise found to be associated with Beclin 1-independent autophagy and reduced by the knockdown of Atg7 but not Beclin 1. In conclusion, Beclin 1-independent autophagy is an important contributor to both the caspase-dependent and -independent components of neuronal apoptosis and may be considered as an important therapeutic target in neural conditions involving apoptosis

Necessary and sufficient condition on global optimality without convexity and second order differentiability

The main goal of this paper is to give a necessary and sufficient condition of global optimality for unconstrained optimization problems, when the objective function is not necessarily convex. We use Gâteaux differentiability of the objective function and its bidual (the latter is known from convex analysis)

Role of phosphoinositide 3-kinase in the autophagic death of serum-deprived PC12 cells.

The death of serum-deprived undifferentiated PC12 cells shows both autophagic and apoptotic features. Since it is still controversial whether the autophagy is instrumental in the cell death or a mere epiphenomenon, we tested the effects of inhibiting the autophagy by a variety of phosphoinositide 3-kinase inhibitors, and provided evidence that the autophagy, or a related trafficking event, is indeed instrumental in the cell death. Furthermore, by comparing the effects of PI3-K inhibition and caspase-inhibition on autophagic and apoptotic cellular events, we showed that in this case the autophagic and apoptotic mechanisms mediate cell death by parallel pathways and do not act in series

Involvement of autophagy in hypoxic-excitotoxic neuronal death.

Neuronal autophagy is increased in numerous excitotoxic conditions including neonatal cerebral hypoxia-ischemia (HI). However, the role of this HI-induced autophagy remains unclear. To clarify this role we established an in vitro model of excitotoxicity combining kainate treatment (Ka, 30 µM) with hypoxia (Hx, 6% oxygen) in primary neuron cultures. KaHx rapidly induced excitotoxic death that was completely prevented by MK801 or EGTA. KaHx also stimulated neuronal autophagic flux as shown by a rise in autophagosome number (increased levels of LC3-II and punctate LC3 labeling) accompanied by increases in lysosomal abundance and activity (increased SQSTM1/p62 degradation, and increased LC3-II levels in the presence of lysosomal inhibitors) and fusion (shown using an RFP-GFP-LC3 reporter). To determine the role of the enhanced autophagy we applied either pharmacological autophagy inhibitors (3-methyladenine or pepstatinA/E64) or lentiviral vectors delivering shRNAs targeting Becn1 or Atg7. Both strategies reduced KaHx-induced neuronal death. A prodeath role of autophagy was also confirmed by the enhanced toxicity of KaHx in cultures overexpressing BECN1 or ATG7. Finally, in vivo inhibition of autophagy by intrastriatal injection of a lentiviral vector expressing a Becn1-targeting shRNA increased the volume of intact striatum in a rat model of severe neonatal cerebral HI. These results clearly show a death-mediating role of autophagy in hypoxic-excitotoxic conditions and suggest that inhibition of autophagy should be considered as a neuroprotective strategy in HI brain injuries

Disorder Effects in Superconducting Multiple Loop Quantum Interferometers

A theoretical study is presented on a number N of resistively shunted Josephson junctions connected in parallel as a disordered 1D array by superconducting wiring in such a manner that there are N-1 individual SQUID loops with arbitrary shape formed.Comment: 4 pages, 2 figure