To evaluate software that is depends on an expired system date, you may want to use this batch that wraps around calling a program.
1: |
|
To evaluate software that is depends on an expired system date, you may want to use this batch that wraps around calling a program.
1: |
|
I have written earlier about the hygiene hypothesis and my doubts that more or less “hygiene” influences the development of allergy (blog | paper). As we are further swamped with regular statements like Continue reading Believe me, it ‘s not hygiene
I am starting here a thread of immigrant studies – seems that there are now ~100 available in the medical literature. This could be the nice question for a meta-analysis: Does the move to a high prevalence country lead to more allergy, e.g. do your peers matter? Continue reading Allergy immigrant studies
-moblog- In my view, epidemiology is not very flexible to adjust to new methods and new techniques. Following some discussion that I had today with STW about eQTLs (quantitative traits derived by RNA microarrays or metabolome profiles) and JMA about system biology, it is likely that we are facing huge changes. Phenotypes may no more called intermediary and we may soon forget old controversies of disease definition. We will instead use new system-terms like NonImm076Trig31Ste0098 or TLR9-096321-Auto5337. Yea, yea.
I will present this poster next Monday in San Francisco at the Annual Conference of the American Thoracic Society. Continue reading Lactase variants in Europe – any connection to allergy?
The J Int Med has a symposium series about the “origins of the developmental origins theory” scienceblog:doi:10.1111/j.1365-2796.2007.01809.x or the so called “Barker hypothesis” Continue reading Why we didn´t find the asthma gene
Ostepopontin (OPN) is a remarkable substance. The many aliases already point towards a multitude of biological functions: SPP1=secreted phosphoprotein 1, BSPI 1=bone sialoprotein-1, CIT, ETA-1, GC110940, nephropontin, osteoprotegerin, uropontin, bone sialoprotein I, early T-lymphocyte activation among others. Continue reading Osteopontin bridging air pollution and immunology of allergic inflammation
There already some rumors – an earlier Lancet perspective named asthma a symptom “like fever” (scienceblog:doi:10.1016/S0140-6736(06)69271-4:). A new editorial now compares it to “diarrhea” Continue reading Asthma no more a disease but a symptom
Two decades ago, 10% calcium gluconate had been recommended for the treatment of anaphylaxis (couldn’t find any explanation for that but renember one of my teachers saying it will stabilize the membranes). There is now an update in scienceblog:doi:10.1038/ni1441: Continue reading Ca2+ and IgE
Here comes the reference to a first molecular system biology paper on asthma – something on my to-do list for 3 years. The authors constructed a biological interaction network using a database of curated molecular interactions. Continue reading Hubs and superhubs in asthma: low activity
Allergy (or at least an associated trait) may have its roots somewhere in Africa – where helminth infections are frequent. A new Nature Immunol Review has an overview but I am quite disappointed. From the abstract Continue reading Wormy world
During my visit last week in Berlin, I found a remarkable letter, that corrects some misbeliefs about the allergy prevalence at that time. Here is my transcript – use Babelfish to translate it. Continue reading Allergy research in Germany 1935
A funny question answered in Allergy.
After adjustment for age, sex, parental predisposition and social status, the risk of hay fever was more than double in subjects who lived together with a partner having the same disease (odds ratio 2.4 […]). If subjects lived together with an affected partner, the risk of developing the disease increased with the time the partners lived together (1-11 years, OR 1; 12-23 years, OR 1.8; 24-35 years, OR 7.4; 36-54 years, OR 13.7).
Whatever that means – improved recall, shared doctor, non random mating, shared food, transmissible agent in descending order – it has been noticed already 40 years ago by Montgomery Smith and Lloyd Knowler in the Am Rev Resp Dis 1965; 92:16:
A 3rd paper in nature genetics details the filaggrin gene structure: exon 3 has 10 repeats (as well as three variants FLG8+, FLG10+, FLF8+10+) and 15 SNPs – one of the few success stories in allergy research. In the discussion section, they ask the rhetoric question:
This study raises questions of interest to the complex trait field. Would SNP tagging of these multiple, relatively rare alleles, with frequencies no greater than 0.013, have readily identified this particularly strong susceptibility gene?
Nay, nay.