Electrospinning using natural proteins or synthetic polymers is a promising technique for the fabrication of fibrous scaffolds for various tissue engineering applications. However, one limitation of scaffolds electrospun from natural proteins is the need to cross-link with glutaraldehyde for stability, which has been postulated to lead to many complications in vivo including graft failure. In this study, we determined the characteristics of hybrid scaffolds composed of natural proteins including collagen and elastin, as well as gelatin, and the synthetic polymer poly(ε-caprolactone) (PCL), so to avoid chemical cross-linking. Fiber size increased proportionally with increasing protein and polymer concentrations, whereas pore size decreased. Electrospun gelatin/PCL scaffolds showed a higher tensile strength when compared to collagen/elastin/PCL constructs. To determine the effects of pore size on cell attachment and migration, both hybrid scaffolds were seeded with adipose-derived stem cells. Scanning electron microscopy and nuclei staining of cell-seeded scaffolds demonstrated complete cell attachment to the surfaces of both hybrid scaffolds, although cell migration into the scaffold was predominantly seen in the gelatin/PCL hybrid. The combination of natural proteins and synthetic polymers to create electrospun fibrous structures resulted in scaffolds with favorable mechanical and biological properties.

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Nocturnal asthma is a frequent problem, but the mechanism is unclear. We investigated the possibility that airways inflammation occurred during the night. Bronchoalveolar lavage fluid was analyzed in asthmatic patients with (n = 7) and without nocturnal asthma (n = 7) at 1600 and 0400 h. The nocturnal asthma group had an increase in the total leukocyte count (24.0 +/- 7.0 to 41.1 +/- 9.9 x 10(4) cells/ml, p less than 0.05), neutrophils (1.1 +/- 0.6 to 3.7 +/- 1.5 x 10(4) cells/ml, p less than 0.05), and eosinophils (0.5 +/- 0.1 to 1.7 +/- 0.7 x 10(4) cells/ml, p less than 0.05) from 1600 to 0400 h. Cellular components for the non-nocturnal asthma group did not change. Between groups, the 1600-h cells were similar. At 0400 h the nocturnal asthma group had significantly higher total leukocyte, neutrophil, eosinophil, lymphocyte, and epithelial cell counts. For all subjects, the overnight fall in peak expiratory flow rates was correlated to the change in neutrophils (r = 0.54, p less than 0.05) and eosinophils (r = 0.77, p less than 0.05). We conclude that the nocturnal worsening of asthma has an associated cellular inflammatory response that is not seen in patients without overnight decrements in lung function. This inflammatory response together with epithelial damage may be important factors in the etiology of nocturnal asthma.

Prostanoids have been implicated in the pathogenesis of asthma because of their potential role in the modulation of airway tone. In the present study, the bronchoconstrictors prostaglandin D2 (PGD2) and thromboxane (TX), and those prostanoids able to protect against bronchoconstriction, prostaglandin E2 (PGE2), and the stable metabolite of prostacyclin, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), were measured in bronchoalveolar lavage fluid (BALF) before and 5 min after endobronchial allergen challenge in four subject groups: nonatopic nonasthmatics (n = 6), nonatopic asthmatics (n = 3), atopic nonasthmatics (n = 9), and atopic asthmatics (n = 8). There were no significant differences in prechallenge prostanoid levels between the four groups, with the potentially bronchoprotective mediators present in highest concentration. Allergen challenge in atopic asthmatics resulted in significant increases (p less than 0.05) in PGD2 (97.4 +/- 19.4 to 1,053.2 +/- 338.6 pg/ml, mean +/- SEM) and TX (45.5 +/- 7.5 to 150.7 +/- 37.8 pg/ml) over prechallenge levels and control groups. Similarly, histamine increased in the atopic asthmatics after challenge (0.36 +/- 0.22 to 6.84 +/- 1.86 ng/ml; p less than 0.05). Atopic nonasthmatics had slight increases in PGD2 (96.9 +/- 25.4 to 219.7 +/- 47.5 pg/ml; p greater than 0.1) after challenge, whereas PGD2 and TX did not change in nonatopic subjects. A significant positive correlation was found between histamine, PGD2, and TX levels after challenge among all groups (p less than 0.001). There were no significant changes among the four groups after allergen challenge in 6-keto-PGF1 alpha or PGE2.(ABSTRACT TRUNCATED AT 250 WORDS)

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