Fuzzier Logic

From eczema to asthma (in mice)

Eczema and asthma often co-occur, indeed, I suffer from both (albeit mildly). What I wasn’t aware of was that eczema often comes first. Though eczema often precedes asthma (asthma has an underlying rate of 4-8% in the general population, but 70% in individuals with a history of chronic severe eczema), the underlying mechanism for this so called ‘atopic march’ isn’t known, though work published today in PLoS Biology elucidates a possible mechanism.

Researchers genetically engineered mice with chronic skin barrier defects (mice lacking Notch signalling in the skin, leading to impairment of epidermal differentiation), who exhibit an eczema like skin condition. They then used these mice to demonstrate the predisposition of such affected individuals to allergic asthma. Occurance of allergic asthma was 7-fold higher in the mutant mouse population, compared to a wild-type population.

The authors then went on to demonstrate that a cytokine called thymic stromal lymphopoietin (TSLP), which is secreted by the damaged skin into the circulation, is required for atopic march in the mutant mice. They show that by knocking out the TSLP receptor in these mice, they can prevent atopic march. They also show that over-production of TSLP in the skin is sufficient to cause allergic asthma, regardless of the cause of that over-production.

This is a paper a little outside my areas of expertise, which is why this is much more of a skim overview than normal. However, there is clearly good work being done here elucidating the molecular mechanisms of a very common disease process. There are also clear implications in this paper on the future management and treatment of eczema and asthma patients. Even though this is unlikely to improve my own experiences of these conditions, I’m very happy this kind of work is being done.

Demehri, S., Morimoto, M., Holtzman, M., & Kopan, R. (2009). Skin-Derived TSLP Triggers Progression from Epidermal-Barrier Defects to Asthma PLoS Biology, 7 (5) DOI: 10.1371/journal.pbio.1000067

Tags: asthma, eczema, Open Access, Research Blogging, science

Open Access Day

14th October 2008 has been designated the first Open Access Day. Many people will blog on the subject more eloquently than I, but here is my ’syncro-blog’

1. Why does Open Access matter to you?

Whatever some über-competitive people I know may think, science is a collaborative enterprise. The inability to freely access the work of another inhibits this collaboration.

How are we to stand on the shoulders of giants, if we cannot read the work of the giants?

2. How did you first become aware of it?

I was not properly aware of the Open Access movement until I started my current job (late 2005). All I knew before is that the subscriptions of my current institution allowed me access to some articles, but not others.

3. Why should scientific and medical research be an open-access resource for the world?

Mainly, and certainly for the UK and the US, the public pays for the scientific and medical research, so they should be able to access the results of that research without having to pay again.

4. What do you do to support Open Access, and what can others do?

Since I am viewed as ‘technical support’ by many of people I work with, I am not included in nearly enough publications, let alone with any kind of control over where they may be published. I can make the case for OA, but at the end of the day it is up to the grant holder where they publish their findings.

As for others, the OA model will only become widely accepted when it is seen as the usual route to publication, rather than something undertaken by an evangelical few. Requirement by funding bodies or institutions for work to be freely available will be a big step (the NIH currently require all works to be freely available within 12 months of initial publication).

I hope that my ramblings serve to add to the general positive noise being created about OA today.

Tags: Open Access, science