Life course building epidemiology: An alternative approach to the collection and analysis of carbon emission data

Developing policy for the reduction of the carbon emissions due to buildings requires models for energy usage that incorporate social, behavioural, and environmental factors in addition to the physical properties and technical specifications of the buildings. Marked parallels exist with some of the more intractable public health issues, such as rising levels of obesity. Recently, health researchers have recognized the importance of taking a broader life-course approach to epidemiology in order to examine the degree that long-term health outcomes are set in early life and the extent that these may be mediated or mitigated by subsequent growth and development, as well as by intervention strategies. Life course epidemiology as applied in building science, where energy usage is treated as analogous to poor health outcomes, provides an alternative approach for the construction of causal models that allow for complex interactions between social and technical factors as well as long term effects. It can provide a useful framework for the successful management and analysis of longitudinal studies and may prove particularly effective in identifying the type, timing, and targeting of intervention strategies to produce optimal outcomes in terms of absolute reductions of carbon emissions and resilience of building performance to external stresses, such as those imposed by climate change. An example based on a study in Milton Keynes (London), which is currently in progress, is used to illustrate the way causal models may help elucidate the complex interactions between factors that influence energy usage

Milton Keynes Park Revisited: changes in internal temperatures

27-30 April 2006 The Carbon Reduction in Buildings project has undertaken a pilot longitudinal survey based on a study of 160 ‘low-energy’ homes in 1989 in Milton Keynes Energy Park. In that study, a sub-sample of 29 dwellings was monitored on an hourly basis for internal temperature for the living room and main bedroom over 2 years. The follow up study has been in progress since 2005 and consists of 15 dwellings from the original detailed survey. Findings include that under an average daily external temperature of 5 ºC, internal temperatures were predicted from regression analysis to be 20.1ºC (95%CI:19.7, 20.5) for the living room in 2005 and 19.5 ºC (95 %CI:19.1, 19.9) for the bedroom. This was not significantly different from the 1990 baseline study, except for main bedroom evening temperatures (6pm-11pm) which were found to have decreased by -1.3°C (95%CI -2.4, 0.08; p-value 0.04). This may be indicative of higher ventilation rates since almost all participants in 2005 reported opening bedroom windows through winter

NK cells and cancer: you can teach innate cells new tricks

Natural killer (NK) cells are the prototype innate lymphoid cells endowed with potent cytolytic function that provide host defence against microbial infection and tumours. Here, we review evidence for the role of NK cells in immune surveillance against cancer and highlight new therapeutic approaches for targeting NK cells in the treatment of cancer

A bispecific antibody against human IgE and human FcgammaRII that inhibits antigen-induced histamine release by human mast cells and basophils

To whom correspondence should be sent. Tam 2 Hal-Pasteur author manuscript pasteur-00271629, version 1 Background: FcγRIIB are low-affinity IgG receptors that we previously demonstrated to negatively regulate IgE-induced mast cell activation when coaggregated with FcεRI. Here, we engineered and characterized a bispecific reagent capable of coaggregating FcγRIIB with FcεRI on human mast cells and basophils. Methods: A bispecific antibody was constructed by chemically crosslinking one Fab ' fragment against human IgE and one Fab ' fragment against human FcγRII. This molecule was used to coaggregate FcεRI with FcγRII on human mast cells and basophils sensitized with human IgE antibodies, and the effect of coaggregation was examined on mediator release upon challenge with specific antigen. Results: When used under these conditions, this bispecific antibody not only failed to trigger the release of histamine by IgE-sensitized cells, but it also prevented specific antigen from triggering histamine release. Comparable inhibitions were observed with mast cells and basophils derived in vitro from cord blood cells and with peripheral blood basophils. Conclusions: The bispecific antibody described here is the prototype of similar molecules that could be used in new therapeutic approaches of allergic diseases based on the coaggregation of activating receptors, such as FcεRI, with inhibitory receptors, such as FcγRIIB, that are constitutively expressed by mast cells and basophils. Key words