Epithelial 15LO1 expression increases with increasing asthma severity. IL-13 induction of 15-HETE-PE enhances MUC5AC expression in human airway epithelial cells. High levels of 15LO1 activity could contribute to the increases of MUC5AC observed in asthma.

These results contrast with many previous results to confirm that Th2 stimuli enhance iNOS expression and activity. While arginase 1 protein decreases in response to IL-13, neither arginase appears to substantially impact nitrite levels in this system.

Rationale: Excessive deposition of extracellular matrix occurs in proximal airways of individuals with asthma, but fibrosis in distal lung has not been observed. Whether differing fibrotic capacities of fibroblasts from these two regions contribute to this variability is unknown. Objectives: We compared morphologic and functional characteristics of fibroblasts isolated from proximal airways and distal lung parenchyma to determine phenotypic differences. Methods: Concurrent proximal airway and distal lung biopsies were obtained by bronchoscopy from subjects with asthma to isolate airway and distal lung fibroblasts, respectively. The following characteristics were compared: morphology, proliferation, ␣-smooth muscle actin expression, and synthesis of procollagen type I and eotaxin-1. Results: Airway fibroblasts (AFs) are morphologically distinct from distal lung fibroblasts (DLFs): they are larger (2.3-fold greater surface area vs. matched DLFs; p ϭ 0.02), stellate in appearance, and with more cytoplasmic projections compared with the spindleshaped DLFs. AFs synthesized more procollagen type I than did DLFs at baseline (twofold higher; p ϭ 0.003) and after transforming growth factor-␤ stimulation (1.4-fold higher; p ϭ 0.02). Similarly, AFs produced more eotaxin-1 than did DLFs at baseline (2.5-fold higher; p ϭ 0.004) and after interleukin-13 stimulation (13-fold higher; p ϭ 0.0001). In contrast, DLFs proliferate more than AFs with serum stimulation (about sixfold greater; p ϭ 0.03). Unstimulated DLFs also expressed more ␣-smooth muscle actin than did corresponding AFs (p ϭ 0.006). Conclusions: These studies suggest that at least two phenotypes of fibroblast exist in the lung. These phenotypic differences may partially explain the variable responses to injury and repair between proximal airways and distal lung/parenchyma in asthma and other respiratory diseases.

Color descriptors are among the most important features used in image analysis and retrieval. Due to its compact representation and low complexity, direct histogram comparison is a commonly used technique for measuring the color similarity. However, it has many serious drawbacks, including a high degree of dependency on color codebook design, sensitivity to quantization boundaries, and inefficiency in representing images with few dominant colors. In this paper, we present a new algorithm for color matching that models behavior of the human visual system in capturing color appearance of an image. We first develop a new method for color codebook design in the Lab space. The method is well suited for creating small fixed color codebooks; for image analysis, matching, and retrieval. Then we introduce a statistical technique to extract perceptually relevant colors. We also propose a new color distance measure that is based on the optimal mapping between two sets of color components representing two images. Experiments comparing the new algorithm to some existing techniques show that these novel elements lead to better match to human perception in judging image similarity in terms of color composition.

No abstract

Brain-derived neurotrophic factor (BDNF), a member of the neurotrophin family, exists in several isoforms, which differentially impacts neuronal and immune cell survival and differentiation. The role of BDNF and its isoforms in asthma remains unclear. The objectives of this study were to compare the BDNF protein isoforms and specific splice variant expression in sputum and bronchoscopic samples from healthy control subjects and participants with asthma, and to relate these changes to findings in IL-13-stimulated human airway epithelial cells. Sputum and bronchoscopic samples from healthy control subjects and participants with asthma were evaluated for BDNF protein (ELISA and Western blot) and BDNF mRNA (gel and quantitative real-time PCR) in relation to asthma severity and type 2 inflammatory processes. BDNF mRNA was measured in cultured primary human airway epithelial cells after IL-13 stimulation. Total BDNF protein differed among the groups, and its mature isoform was significantly higher in sputum from subjects with severe asthma compared with healthy control subjects (overall P = 0.008, P = 0.027, respectively). Total BDNF was higher in those with elevated fractional exhaled nitric oxide and sputum eosinophilia. In vitro, IL-13 increased BDNF exon VIb splice variant and the ratio to BDNF common exon IX mRNA (P < 0.001, P = 0.003, respectively). Epithelial brushing exon VIb mRNA and total BDNF protein differed among the groups and were higher in subjects with severe asthma than in healthy control subjects (overall P = 0.01, P = 0.02, respectively). The mature BDNF isoform and the exon VIb splice variant are increased in human asthmatic airways. The in vitro increase in response to IL-13 suggests that type 2 cytokines regulate BDNF levels and activity in asthma.

The protective function of TSA on myocardial ischemia reperfusion injury may be possibly exerted by inhibiting the increase of ROS caused by the reperfusion to attenuate the expression of HMGB1 and inhibit inflammation.

. IL-13 induced increases in nitrite levels are primarily driven by increases in inducible nitric oxide synthase as compared with effects in arginases in human primary bronchial epithelial cells. Clin Exp Allergy 2008; 936-46.