Lipid-coated microdroplet array for in vitro protein synthesis

Monitoring complex biological assays such as in vitro protein synthesis over long periods in micrometer-sized cavities of poly(dimethyl siloxane) (PDMS) microfluidic devices requires a strategy that solves the adsorption and absorption problems on PDMS surfaces. In this study, we developed a technique that instantaneously arrays aqueous microdroplets coated with a phospholipid membrane within a single microfluidic device. The simple lipid bilayer coating effectively inhibits the adsorption of proteins and DNA, whereas the encapsulation of the droplet reduces the area in contact with the PDMS surface, resulting in decreased absorption in part. Although the size becomes smaller during the first few hours, a lipid-coated microdroplet array demonstrated a temporal stability of more than 20 h and a size uniformity of CV 3% in the device. Furthermore, we succeeded in expressing a green fluorescent protein by confining an in vitro translation system in the microdroplets, which was confirmed by scanning the fluorescence spectrum of the droplets, demonstrating that the lipid coat secured the synthetic reaction from the adsorption problem.     

桦树沟V矿体无底柱分段崩落法开采技术分析

结合酒钢镜铁山矿桦树沟矿区倾斜矿体赋存条件及开采工艺,就矿体倾角对无底柱分段崩落法矿石残留和放矿条件的影响以及矿山开采技术进行了分析研究,发现采场的退采方向、切割方法以及回采上盘沿脉巷道等矿山现行开采技术存在一定的缺陷,严重影响矿山的正常生产和矿石的正常回收。通过对采场的退采方向、切割槽位置、分段联络巷道的布置等开采技术优化分析,建议矿山采取分段退采方向改为由上盘向下盘退采,切割立槽布置在上分段下盘矿岩交界处,上盘联络巷道布置距上盘矿岩交界3~5m处等技术措施,有助于充分回收残留矿石,提高矿石回采率。     

Locally Secreted Semaphorin 4D Is Engaged in Both Pathogenic Bone Resorption and Retarded Bone Regeneration in a Ligature-Induced Mouse Model of Periodontitis

It is well known that Semaphorin 4D (Sema4D) inhibits IGF-1-mediated osteogenesis by binding with PlexinB1 expressed on osteoblasts. However, its elevated level in the gingival crevice fluid of periodontitis patients and the broader scope of its activities in the context of potential upregulation of osteoclast-mediated periodontal bone-resorption suggest the need for further investigation of this multifaceted molecule. In short, the pathophysiological role of Sema4D in periodontitis requires further study. Accordingly, attachment of the ligature to the maxillary molar of mice for 7 days induced alveolar bone-resorption accompanied by locally elevated, soluble Sema4D (sSema4D), TNF-α and RANKL. Removal of the ligature induced spontaneous bone regeneration during the following 14 days, which was significantly promoted by anti-Sema4D-mAb administration. Anti-Sema4D-mAb was also suppressed in vitro osteoclastogenesis and pit formation by RANKL-stimulated BMMCs. While anti-Sema4D-mAb downmodulated the bone-resorption induced in mouse periodontitis, it neither affected local production of TNF-α and RANKL nor systemic skeletal bone remodeling. RANKL-induced osteoclastogenesis and resorptive activity were also suppressed by blocking of CD72, but not Plexin B2, suggesting that sSema4D released by osteoclasts promotes osteoclastogenesis via ligation to CD72 receptor. Overall, our data indicated that ssSema4D released by osteoclasts may play a dual function by decreasing bone formation, while upregulating bone-resorption.     

Effective highlighting modes of graphical user interfaces in visual information search

Universal Access in the Information Society - This study discusses the preferred highlighting mode for graphical user interface (GUI) design. The study investigated the effects of different...