Purpose Eosinophilic inflammation is a key component of severe asthma (SA). However, there has been no reliable serum biomarker for the eosinophilic inflammation of SA. We hypothesized that serum eosinophil-derived neurotoxin (EDN) could predict the eosinophilic inflammation of SA in adult asthmatics. Methods Severe asthmatics (n = 235), nonsevere asthmatics (n = 898), and healthy controls (n = 125) were enrolled from Ajou University Hospital, South Korea. The serum levels of EDN and periostin were measured by enzyme-linked immunosorbent assay and compared between severe and nonsevere asthmatics. Their associations with total eosinophil count (TEC) and clinical parameters were evaluated; clinical validation of the K-EDN kit for the measurement of serum EDN was evaluated. Results Severe asthmatics were older and had longer disease duration with significantly lower levels of forced expiratory volume in 1 second and methacholine PC20 than nonsevere asthmatics. Significant differences were found in TEC or sputum eosinophil count (%) between the groups. The serum levels of EDN and periostin were significantly higher in severe asthmatics than in nonsevere asthmatics and in healthy controls (all P < 0.05). Although significant correlations were found between serum EDN levels measured by the 2 kits ( ρ = 0.545, P < 0.0001), higher correlation coefficients between serum EDN levels measured by the K-EDN kit and TEC were higher ( ρ = 0.358, P < 0.0001) than those between serum EDN levels measured by the MBL kit and TEC ( ρ = 0.319, P < 0.0001) or serum periostin level ( ρ = 0.222, P < 0.0001). Multivariate regression analysis demonstrated that serum EDN levels measured by the K-EDN kit predicted the phenotype of SA ( P = 0.003), while 2 other biomarkers did not. Conclusions The serum EDN level may be a useful biomarker for assessing asthma severity in adult asthmatics.

The L p -improving properties of convolution operators with measures supported on space curves have been studied by various authors. If the underlying curve is non-degenerate, the convolution with the (Euclidean) arclength measure is a bounded operator from L 3/2 (R 3 ) into L 2 (R 3 ). Drury suggested that in case the underlying curve has degeneracies the appropriate measure to consider should be the affine arclength measure and he obtained a similar result for homogeneous curves t i-> (/, t 2 , t k ), / > 0 for k > 4. This was further generalized by Pan to curves t i->-(/, t k ,«'), / > 0 for 1 < Jt < /, it + / > 5. In this article, we will extend Pan's result to (smooth) compact curves of finite type whose tangents never vanish. In addition, we give an example of a flat curve with the same mapping properties.2000 Mathematics subject classification: primary 42B15; secondary 42B10.

Background Obesity associated with various complications has increased worldwide. Body weight gain alters lipid metabolites (especially sphingolipids) contributing to obesity‐induced inflammation. However, the significance of the metabolites in the development of obese asthma is not yet clear. Methods The serum levels of sphingolipids were measured using liquid chromatography‐tandem mass spectrometry in obese controls (n = 7) and patients with asthma: the obese group (BMI > 25 kg/m2, n = 13) vs the nonobese (n = 28) group. To examine the relationship between metabolic changes in sphingolipids and macrophage polarization, public microarray data were analyzed. In addition, the alteration in sphingolipid metabolism was investigated in wild‐type BALB/c mice fed a high‐fat diet. Results The obese asthma had higher levels of serum C18:0 and C20:0 ceramides than the nonobese asthma group (P = .028 and P = .040, respectively). The value of the serum C18:0 ceramide (184.3 ng/mL) for discriminating the obese asthma from the nonobese asthma group showed 53.9% sensitivity and 85.7% specificity (AUC = 0.721, P = .024). The microarray data showed significantly increased ceramide synthesis and metabolic shift to ceramide accumulation during M1 macrophage polarization in humans. Increased airway hyperresponsiveness, M1 macrophage polarization, and C18:0 ceramide levels were noted in obese mice, but not in nonobese mice. Increased expression of ceramide synthase (CerS) 1 and CerS6 (not CerS2) was noted in lung tissues of obese mice. Conclusion Alteration in sphingolipid metabolism favoring ceramide accumulation (especially long‐chain ceramides) may contribute to developing obese asthma.

Asthma is a common chronic disease with several variant phenotypes and endotypes. NSAID-exacerbated respiratory disease (NERD) is one such endotype characterized by asthma, chronic rhinosinusitis (CRS) with nasal polyps, and hypersensitivity to aspirin/cyclooxygenase-1 inhibitors. NERD is more associated with severe asthma than other asthma phenotypes. Regarding diagnosis, aspirin challenge tests via the oral or bronchial route are a standard diagnostic method; reliable in vitro diagnostic tests are not available. Recent studies have reported various biomarkers of phenotype, diagnosis, and prognosis. In this review, we summarized the known potential biomarkers of NERD that are distinct from those of aspirin-tolerant asthma. We also provided an overview of the different NERD subgroups.

The L 2 -boundedness of the Marcinkiewicz integrals in product domains with component-wise homogeneous kernels which belong to a certain Orlicz space and satisfy the cancellation property is studied.