A turbulent wake as a tracer of 30,000 years of Mira's mass loss history

Mira is one of the first variable stars ever discovered and it is the prototype (and also the nearest example) of a class of low-to-intermediate-mass stars in the late stages of stellar evolution. These stars are relatively common and they return a large fraction of their original mass to the interstellar medium (ISM) (ref. 2) through a processed, dusty, molecular wind. Thus stars in Mira's stage of evolution have a direct impact on subsequent star and planet formation in their host galaxy. Previously, the only direct observation of the interaction between Mira-type stellar winds and the ISM was in the infrared. Here we report the discovery of an ultraviolet-emitting bow shock and turbulent wake extending over 2 degrees on the sky, arising from Mira's large space velocity and the interaction between its wind and the ISM. The wake is visible only in the far ultraviolet and is consistent with an unusual emission mechanism whereby molecular hydrogen is excited by turbulent mixing of cool molecular gas and shock-heated gas. This wind wake is a tracer of the past 30,000 years of Mira's mass-loss history and provides an excellent laboratory for studying turbulent stellar wind-ISM interactions.     

An ancient nova shell around the dwarf nova Z Camelopardalis

Cataclysmic variables (classical novae and dwarf novae) are binary star systems in which a red dwarf transfers hydrogen-rich matter, by way of an accretion disk, to its white dwarf companion. In dwarf novae, an instability is believed to episodically dump much of the accretion disk onto the white dwarf. The liberation of gravitational potential energy then brightens these systems by up to 100-fold every few weeks or months. Thermonuclear-powered eruptions thousands of times more luminous occur in classical novae, accompanied by significant mass ejection and formation of clearly visible shells from the ejected material. Theory predicts that the white dwarfs in all dwarf novae must eventually accrete enough mass to undergo classical nova eruptions. Here we report a shell, an order of magnitude more extended than those detected around many classical novae, surrounding the prototypical dwarf nova Z Camelopardalis. The derived shell mass matches that of classical novae, and is inconsistent with the mass expected from a dwarf nova wind or a planetary nebula. The shell observationally links the prototypical dwarf nova Z Camelopardalis with an ancient nova eruption and the classical nova process.     

核物理学基础——从核结构到宇宙学

本书是法国埃库勒理工学院一套著名的教科书中的一本．是作者为高年级大学生讲授原子核物理相关的一些专题课发展而成的教材。作者们认为大多数核现象都可以从基于泡利原理与库仑势垒的一些简单的论证理解。因此本书并不打算对于核理论现代发展深人讨论，而是把重点放在核物理学各方面的实际应用。本书充分利用了从网上可以得到的大量核物理的实验数据资源。     

A chimaeric 11 beta-hydroxylase/aldosterone synthase gene causes glucocorticoid-remediable aldosteronism and human hypertension.

Glucocorticoid-remediable aldosteronism (GRA), an autosomal dominant disorder, is characterized by hypertension with variable hyperaldosteronism and by high levels of the abnormal adrenal steroids 18-oxocortisol and 18-hydroxycortisol, which are all under control of adrenocorticotropic hormone and suppressible by glucocorticoids. These abnormalities could result from ectopic expression of aldosterone synthase, which is normally expressed only in adrenal glomerulosa, in the adrenal fasciculata. Genes encoding aldosterone synthase and steroid 11 beta-hydroxylase (expressed in both adrenal fasciculata and glomerulosa), which are 95% identical and lie on chromosome 8q (refs 7, 10), are therefore candidate genes for GRA. Here we demonstrate complete linkage of GRA in a large kindred to a gene duplication arising from unequal crossing over, fusing the 5' regulatory region of 11 beta-hydroxylase to the coding sequences of aldosterone synthase (maximum lod score 5.23 for complete linkage, odds ratio of 170,000:1). This mutation can account for all the physiological abnormalities of GRA. Our result represents the demonstration of a mutation causing hypertension in otherwise phenotypically normal animals or humans.     

Mechanism of glutamate receptor desensitization

Ligand-gated ion channels transduce chemical signals into electrical impulses by opening a transmembrane pore in response to binding one or more neurotransmitter molecules. After activation, many ligand-gated ion channels enter a desensitized state in which the neurotransmitter remains bound but the ion channel is closed. Although receptor desensitization is crucial to the functioning of many ligand-gated ion channels in vivo, the molecular basis of this important process has until now defied analysis. Using the GluR2 AMPA-sensitive glutamate receptor, we show here that the ligand-binding cores form dimers and that stabilization of the intradimer interface by either mutations or allosteric modulators reduces desensitization. Perturbations that destabilize the interface enhance desensitization. Receptor activation involves conformational changes within each subunit that result in an increase in the separation of portions of the receptor that are linked to the ion channel. Our analysis defines the dimer interface in the resting and activated state, indicates how ligand binding is coupled to gating, and suggests modes of dimer dimer interaction in the assembled tetramer. Desensitization occurs through rearrangement of the dimer interface, which disengages the agonist-induced conformational change in the ligand-binding core from the ion channel gate.