The central nervous system stabilizes unstable dynamics by learning optimal impedance.

To manipulate objects or to use tools we must compensate for any forces arising from interaction with the physical environment. Recent studies indicate that this compensation is achieved by learning an internal model of the dynamics, that is, a neural representation of the relation between motor command and movement. In these studies interaction with the physical environment was stable, but many common tasks are intrinsically unstable. For example, keeping a screwdriver in the slot of a screw is unstable because excessive force parallel to the slot can cause the screwdriver to slip and because misdirected force can cause loss of contact between the screwdriver and the screw. Stability may be dependent on the control of mechanical impedance in the human arm because mechanical impedance can generate forces which resist destabilizing motion. Here we examined arm movements in an unstable dynamic environment created by a robotic interface. Our results show that humans learn to stabilize unstable dynamics using the skillful and energy-efficient strategy of selective control of impedance geometry.     

论竞技健美操技术创新的概念与分类

该研究以竞技健美操技术创新为研究对象,采用文献资料法、案例分析法,对查阅的文献和案例进行综合的归纳分析,在研究竞技健美操技术创新发展现状基础上,结合其他项目技术创新的特点,对竞技健美操技术创新的概念进行了阐述;对竞技健美操技术创新进行了系统的分类.     

Evolutionary genetics: CCR5 mutation and plague protection

A recent and prevalent mutation in the chemokine receptor CCR5 in humans of northern European ancestry has been proposed to provide protection against bubonic plague. Here we infect both normal and CCR5-deficient mice with the bacterium Yersinia pestis, the cause of the plague epidemics that wiped out one-third of Europeans in the Middle Ages, and find no difference in either bacterial growth or survival time between the two groups. Unless the pathogenesis of Yersinia infection differs markedly between mice and humans, our results indicate that CCR5 deficiency in people is unlikely to protect against plague.     

Nucleolar organizer regions inBiomphalaria andBulinus snails

Cellular and Molecular Life Sciences - A method is described for the demonstration of nucleolar organizer regions (NORs) in freshwater snails and is applied to the study of one tetraploid and...     

Bv8 regulates myeloid-cell-dependent tumour angiogenesis

Bone-marrow-derived cells facilitate tumour angiogenesis, but the molecular mechanisms of this facilitation are incompletely understood. We have previously shown that the related EG-VEGF and Bv8 proteins, also known as prokineticin 1 (Prok1) and prokineticin 2 (Prok2), promote both tissue-specific angiogenesis and haematopoietic cell mobilization. Unlike EG-VEGF, Bv8 is expressed in the bone marrow. Here we show that implantation of tumour cells in mice resulted in upregulation of Bv8 in CD11b+Gr1+ myeloid cells. We identified granulocyte colony-stimulating factor as a major positive regulator of Bv8 expression. Anti-Bv8 antibodies reduced CD11b+Gr1+ cell mobilization elicited by granulocyte colony-stimulating factor. Adenoviral delivery of Bv8 into tumours was shown to promote angiogenesis. Anti-Bv8 antibodies inhibited growth of several tumours in mice and suppressed angiogenesis. Anti-Bv8 treatment also reduced CD11b+Gr1+ cells, both in peripheral blood and in tumours. The effects of anti-Bv8 antibodies were additive to those of anti-Vegf antibodies or cytotoxic chemotherapy. Thus, Bv8 modulates mobilization of CD11b+Gr1+ cells from the bone marrow during tumour development and also promotes angiogenesis locally.