Resistance of mice suppressed for IgM production to Babesia microti infection.

The immunological mechanisms responsible for overcoming infections with Babesia, an intra-erythrocytic protozoan, are not fully understood. Although high titres of specific anti-babesial antibodies have been observed in several species of animals, and protection has been obtained by transfer of large volumes of recovery serum, the role of antibody in the immune response to an infection is uncertain. The present study investigates the nature of B-cell participation during Babesia microti infections by observing the course of the disease in mice in which IgM production has been suppressed from birth and which contain no B cells. The results show that, in contrast to control mice, which develop and subsequently clear circulating parasitaemias, suppressed mice show an unexpected resistance to infection as reflected by a virtual absence of parasites in the peripheral circulation.     

管状曲面的奇点

研究管状曲面和它的平行曲面的奇点问题.所谓管状曲面,是沿着E3里一条曲线的双参数空间运动产生的.选定曲线的Frenet向量T作为旋转轴,用不同的方法得到了运动管状曲面的特征.然后,给出管状曲面奇点的一些定理和结果.     

The mechanism of sodium and substrate release from the binding pocket of vSGLT

Membrane co-transport proteins that use a five-helix inverted repeat motif have recently emerged as one of the largest structural classes of secondary active transporters. However, despite many structural advances there is no clear evidence of how ion and substrate transport are coupled. Here we report a comprehensive study of the sodium/galactose transporter from Vibrio parahaemolyticus (vSGLT), consisting of molecular dynamics simulations, biochemical characterization and a new crystal structure of the inward-open conformation at a resolution of 2.7??. Our data show that sodium exit causes a reorientation of transmembrane helix 1 that opens an inner gate required for substrate exit, and also triggers minor rigid-body movements in two sets of transmembrane helical bundles. This cascade of events, initiated by sodium release, ensures proper timing of ion and substrate release. Once set in motion, these molecular changes weaken substrate binding to the transporter and allow galactose readily to enter the intracellular space. Additionally, we identify an allosteric pathway between the sodium-binding sites, the unwound portion of transmembrane helix 1 and the substrate-binding site that is essential in the coupling of co-transport.     

Poröse blutgefässe beiScutigera coleoptrata L. (Chilopoda,Notostigmophora)

Summary A hitherto unknown structure of the wall of blood vessels inScutigera coleoptrata is described. It is lacking in a continuous adventitia and a dense endocard, and between its muscle fibres there are irregular clefts filled with stroma.