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Cai, Feng

Publications and source records attributed to Cai, Feng.

NSTX-U Machine Core Vacuum Seals Upgrade Design

The vacuum in the National Spherical Torus Experiment Upgrade (NSTX-U) is in the range of 2.66x10⁻⁶ Pa (2x 10⁻⁸ torr). To enhance vacuum seals and lower gas permeation in the NSTX-U and therefore ensuring operation safety and quality, the machine core vacuum seal design has been upgraded using double elastomeric seals and pumped interspaces (guard channels). In NSTX-U machine core, there are six major vacuum seals, including upper and lower vacuum vessel main flanges, upper and lower bellows flanges, and two in the ceramic isolation ring assembly that are mounted to the upper vacuum vessel main flange. The elastomeric seals are commercially available and customized fluorocarbon (Viton) O-rings. To ensure appropriate O-ring compression ratios for the vacuum seal, the O-ring grooves are customized with appropriate tolerances considering specific situations for each seal. In this upgrade, the vacuum in each interspace is designed to reach 13.33 Pa (0.1 torr), thus the overall pressure difference crossing each double O-ring seal is expected to be reduced by at least three orders of magnitude, and accordingly the overall rates of leakage and permeation will be lowered by three orders of magnitude. The corresponding pump-down times for each seal, at room temperature, are estimated at about 60 s. Additionally, the vacuum pumped interspaces will be able to function as a real-time leak monitor.

70 PLASMA PHYSICS AND FUSION TECHNOLOGY↗

Galectin-1 secreted by bone marrow-derived mesenchymal stem cells mediates anti-inflammatory responses in acute airway disease

The hallmarks of allergic airway disease (AAD) include infiltration of inflammatory cells into the bronchoalveolar space. Bone marrow derived mesenchymal stem cells (BMSCs) show anti-inflammatory properties in AAD. In addition, galectin-1 (Gal-1) is a lectin significantly upregulated upon inflammation and is also known to mediate potential anti-inflammatory responses. We hypothesized that BMSCs regulated inflammatory responses by secretion of Gal-1 during AAD pathogenesis. BMSCs were isolated from murine femurs and tibiae and adoptively transferred into an ovalbumin-induced AAD mouse model. Knockdown of Gal-1 in BMSCs was performed using shRNA. Flow cytometry, ELISAs, and immunohistology were performed to analyze inflammatory responses in mice, and a Transwell system was used to establish an in vitro co-culture system of lung epithelial cells (MLE-12) and BMSCs. Administration of BMSCs significantly upregulated Gal-1 expression upon inflammation and decreased infiltration of inflammatory cells and secretion of proinflammatory cytokines in vivo. In addition, we showed that this function was mediated by reduced activation of the MAPK p38 signaling pathway. Similar observations were found using an in vitro lipopolysaccharide-induced model when MLE-12 cells were co-cultured with BMSCs. Gal-1 secretion by BMSCs alleviated inflammatory responses observed in AAD and hence provides a promising therapeutic alternative to AAD patients insensitive to conventional drug treatments.

60 APPLIED LIFE SCIENCES↗