Bistable Helmholtz dark spatial optical solitons in materials with self-defocusing saturable nonlinearity

We present, to the best of our knowledge, the first exact dark spatial solitons of a nonlinear Helmholtz equation with a self-defocusing saturable refractive-index model. These solutions capture oblique (arbitrary-angle) propagation in both the forward and backward directions, and they can also exhibit a bistability characteristic. A detailed derivation is presented, obtained by combining coordinate transformations and direct-integration methods, and the corresponding solutions of paraxial theory are recovered asymptotically as a subset. Simulations examine the robustness of the new Helmholtz solitons, with stationary states emerging from a range of perturbed input beams

Lifelong exposure to BPA significantly increased the allergic airway inflammation.

<p>Nursing mice were exposed to 5 µg/ml BPA via drinking water and offspring during their lifetime. The asthma phenotype was induced by sensitization to OVA followed by an intrapulmonary allergen challenge as described in Materials and Methods. BPA exposure increased total cell number in BAL fluid (a), lung inflammation (b), lung resistance (c), and OVA-specific IgE serum levels (e). Cytokine production was not affected (e+f). Data are expressed as mean ± SEM, n≥6 animals per group. *P<0.05.</p

BPA levels measured in serum.

a<p>BPA drinking water concentration.</p>b<p>BPA levels were measured before weaning from pups of non-exposed and mother mice exposed during pregnancy and breastfeeding.</p><p>**P<0.01, ***P<0.001 compared to non-exposed control.</p><p>Mother mice were exposed during pregnancy and breastfeeding and adult mice for 5 weeks to BPA via drinking water. BPA serum levels of adult mice or pups were measured at the end of the exposure period as described in Methods.</p

Perinatal BPA exposure showed no effect on the asthma phenotype in the offspring.

<p>Mice were exposed to 5 µg/ml BPA via drinking water during pregnancy and breastfeeding. In the offspring an asthma phenotype was induced by sensitization to OVA followed by an intrapulmonary allergen challenge as described in Materials and Methods. BPA exposure did neither affect total cell number in BAL fluid (a), lung inflammation (b), lung resistance (c), OVA-specific IgE serum levels (d) nor cytokine production in splenocytes (e) or lymph node cells (f). Data are expressed as mean ± SEM, n≥22 animals per group. *P<0.05.</p

Glucocorticoid receptor antagonist RU486 abolished the decreased immune response induced by BPA.

<p>Adult mice were exposed to 5 µg/ml BPA via drinking water. RU486 was given intraperitoneally 3 times/week during OVA-immunisation. Treatment with RU486 reversed the BPA-induced effect on total cell number in BAL fluid (a), lung inflammation (b), lung resistance (c) and OVA-specific IgE serum levels (d). Data are expressed as mean ± SEM, n≥5 animals per group. *P<0.05 OVA and ^#P<0.05 OVA+BPA+RU486 <i>vs.</i> OVA+BPA.</p

Exposure of adult mice to BPA during sensitization reduced the allergic immune response.

<p>Adult mice were exposed to 5 µg/ml BPA via drinking water during OVA-immunization. BPA exposure reduced total cell number in BAL fluid (a), lung inflammation (b), lung resistance (c), OVA-specific IgE serum levels (e) and Th2 cytokine production from lymph node cells (f), while cytokine production from spleen was not affected (e). Data are expressed as mean ± SEM, n≥18 animals per group. *P<0.05.</p

Prenatal BPA exposure did not affect the asthma phenotype in the offspring.

<p>Mice were exposed to 5 µg/ml BPA via drinking water during pregnancy. In the offspring an asthma phenotype was induced by sensitization to ovalbumin (OVA) followed by an intrapulmonary allergen challenge as described in Materials and Methods. BPA exposure did neither affect total cell number in BAL fluid (a), lung inflammation (b), lung resistance (c), OVA-specific IgE serum levels (d) nor cytokine production in splenocytes (e) or lymph node cells (f). Data are expressed as mean ± SEM, n≥11 animals per group.</p

Additional file 7: of Tobacco smoking differently influences cell types of the innate and adaptive immune system—indications from CpG site methylation

Sample sizes of the prospective birth cohort study LINA. (DOCX 16 kb

Additional file 4: of Tobacco smoking differently influences cell types of the innate and adaptive immune system—indications from CpG site methylation

Spearman correlation between amount of GPR15+ T cells and methylation at cg05575921 in granulocytes in non-smokers and smokers. Both biomarkers did not correlate significantly with each other. (PDF 101 kb

Additional file 2: of Tobacco smoking differently influences cell types of the innate and adaptive immune system—indications from CpG site methylation

Estimation of the prominent cell type of whole blood accounting for major smoking-associated methylation change (∆meth) at single CpG site based on reports of methylation changes in whole blood and peripheral blood mononuclear cells (PBMC). (DOCX 20 kb