Meta-analysis identifies seven susceptibility loci involved in the atopic March

Eczema often precedes the development of asthma in a disease course called the a 'atopic march'. To unravel the genes underlying this characteristic pattern of allergic disease, we conduct a multi-stage genome-wide association study on infantile eczema followed by childhood asthma in 12 populations including 2,428 cases and 17,034 controls. Here we report two novel loci specific for the combined eczema plus asthma phenotype, which are associated with allergic disease for the first time; rs9357733 located in EFHC1 on chromosome 6p12.3 (OR 1.27; P=2.1 × 10 a'8) and rs993226 between TMTC2 and SLC6A15 on chromosome 12q21.3 (OR 1.58; P=5.3 × 10 a'9). Additional susceptibility loci identified

Determination of peak expiratory flow

It is still unknown whether peak expiratory flow (PEF) is determined by 'wave speed' flow limitation in the airways. To investigate the influences of airway mechanical properties on PEF, five healthy adults performed maximal forced expiratory effort (MFEE) manoeuvres, in the standard manner and following breathholds at total lung capacity (TLC) of 2 s and 10 s. Oesophageal pressure (Poes) was measured as an index of respiratory effort. Subjects also performed a MFEE following a 10 s breathhold during which intrathoracic pressure was voluntarily raised by a Valsalva manoeuvre, which would increase transmural pressure and cross-sectional area of the extrathoracic airway. Addition MFEEs were performed with the neck fully flexed and extended, to change longitudinal tracheal tension. In separate studies, PEF was measured with a spirometer and with a pneumotachograph. Breathholds at TLC (2 s and 10 s), and neck flexion reduced PEF by a mean of 9.8% (SD 2.9%), 9.6% (SD 1.6%), and 8.7% (SD 2.8%), respectively, when measured with the spirometer. The same pattern of results was seen when measured with the pneumotachograph. These reductions occurred despite similar respiratory effort. Voluntarily raising intrathoracic pressure during a 10 s breathhold did not reverse a fall in PEF. MFEE manoeuvre with neck extension did not result in an increase in PEF, the group mean % changes being -3.0% (SD 5.0%). We conclude that these results do not allow the hypothesis that 'wave-speed' (V̇ws) is reached at PEF to be rejected. A breathhold at TLC could increase airway wall compliance by allowing stress-relaxation of the airway, thus reducing the 'V̇ws' achievable

Identificação de roedores silvestres como hospedeiros do Angiostrongylus costaricensis no sul do Brasil Identification of wild rodents as hosts of Angiostrongylus costaricensis in the South of Brazil

Um número crescente de casos de angiostrongilíase abdominal tem sido detectado no sul do Brasil. O principal hospedeiro do Angiostrongylus costaricensis na América Central, o rato do algodão (Sigmodon hispidus), não ocorre na América do Sul, exceto no norte do Peru, Colômbia e Venezuela. Foram realizadas capturas na área endêmica do Rio Grande do Sul (RS), visando identificar hospedeiros para obtenção de vermes em laboratório e produção de antígeno. Pela primeira vez no Brasil foi constatada a infecção em roedores: Oryzomys nigripes e Oryzomys ratticeps. O. nigripes é um roedor silvestre de pequeno porte e parece ser o principal hospedeiro definitivo do A. costaricensis na região serrana do RS.<br>Increasing number of human cases of abdominal angiostrongyliasis has been diagnosed in the south of Brazil. The main definitive host of Angiostrongylus costaricensis in Central America is the cotton rat (Sigmodon hispidus) that does not occur in South America, except in the north of Colombia, Peru and Venezuela. Rodents were captured in the endemic area in Rio Grande do Sul (RS) and definitive hosts were identified for the first time in Brazil: Oryzomys nigripes and Oryzomys ratticeps. O. nigripes is a small wild rodent and it appears to be the main definitive host of A. costaricensis in the highlands of RS, Brazil's southermost State

Meta-analysis identifies seven susceptibility loci involved in the atopic march.

Eczema often precedes the development of asthma in a disease course called the &#39;atopic march&#39;. To unravel the genes underlying this characteristic pattern of allergic disease, we conduct a multi-stage genome-wide association study on infantile eczema followed by childhood asthma in 12 populations including 2,428 cases and 17,034 controls. Here we report two novel loci specific for the combined eczema plus asthma phenotype, which are associated with allergic disease for the first time; rs9357733 located in EFHC1 on chromosome 6p12.3 (OR 1.27; P=2.1 &times; 10(-8)) and rs993226 between TMTC2 and SLC6A15 on chromosome 12q21.3 (OR 1.58; P=5.3 &times; 10(-9)). Additional susceptibility loci identified at genome-wide significance are FLG (1q21.3), IL4/KIF3A (5q31.1), AP5B1/OVOL1 (11q13.1), C11orf30/LRRC32 (11q13.5) and IKZF3 (17q21). We show that predominantly eczema loci increase the risk for the atopic march. Our findings suggest that eczema may play an important role in the development of asthma after eczema