A quantum scattering interferometer

The collision of two ultracold atoms results in a quantum mechanical superposition of the two possible outcomes: each atom continues without scattering, and each atom scatters as an outgoing spherical wave with an s-wave phase shift. The magnitude of the s-wave phase shift depends very sensitively on the interaction between the atoms. Quantum scattering and the underlying phase shifts are vitally important in many areas of contemporary atomic physics, including Bose-Einstein condensates, degenerate Fermi gases, frequency shifts in atomic clocks and magnetically tuned Feshbach resonances. Precise experimental measurements of quantum scattering phase shifts have not been possible because the number of scattered atoms depends on the s-wave phase shifts as well as the atomic density, which cannot be measured precisely. Here we demonstrate a scattering experiment in which the quantum scattering phase shifts of individual atoms are detected using a novel atom interferometer. By performing an atomic clock measurement using only the scattered part of each atom's wavefunction, we precisely measure the difference of the s-wave phase shifts for the two clock states in a density-independent manner. Our method will enable direct and precise measurements of ultracold atom-atom interactions, and may be used to place stringent limits on the time variations of fundamental constants.     

中美科技产出比较

该文以科技文献为分析基础,从数量与质量方面比较了中美之间科技发展的差距。数量比较选择了
SCI、INSPEC、Ei Compendex三大数据库,而质量比较则是应用了SCI中的引文分析。根据作者以前对中国
科技产出的评估,该文选择了30个技术研究领域,全面考察了中国在物质科学、环境、工程和生命科学重点
发展方向上论文数量情况。
SCI数据显示在几乎所有的技术领域内,虽然中国在论文数量方面增幅很大,但美国仍然处于领先地位
(2002－2007)。到2007年,INSPEC数据表明,在大多数技术领域内,中国的科技论文数量赶上或超过了美国;
但在生物医学和部分环境科学领域,美国仍然保持着较大的领先优势。Ei Compendex的数据分析结果表明,对
于大多数技术领域,到2007年中国的科技论文产量更大;而与日益增长的科研经费恰恰相反,美国发表论文的
数量似乎在2005年就已经到达了顶峰。如果不考虑生物医学领域,中国显然已经成为美国的强劲竞争对手。
为了对质量进行比较,该文对论文和引文数量进行了归一化处理,但仅限于纳米技术领域(1998－2003
年)。结果表明,虽然在过去的10年里美国在质量方面明显地领先中国(以及其他主要纳米技术研究国家),但
依然不能改表中国的论文质量持续提升的事实。中国目前已经达到可以与法国、意大利、日本和澳大利亚的
论文质量相提并论的地步。     

h指数研究在2007－2008年的新进展

该文对近期（2007－2008年）h指数及其衍生指数的发展进行了简单的回顾。     

Mutations in TRPV4 cause an inherited arthropathy of hands and feet

Familial digital arthropathy-brachydactyly (FDAB) is a dominantly inherited condition that is characterized by aggressive osteoarthropathy of the fingers and toes and consequent shortening of the middle and distal phalanges. Here we show in three unrelated families that FDAB is caused by mutations encoding p.Gly270Val, p.Arg271Pro and p.Phe273Leu substitutions in the intracellular ankyrin-repeat domain of the cation channel TRPV4. Functional testing of mutant TRPV4 in HEK-293 cells showed that the mutant proteins have poor cell-surface localization. Calcium influx in response to the synthetic TRPV4 agonists GSK1016790A and 4αPDD was significantly reduced, and mutant channels did not respond to hypotonic stress. Others have shown that gain-of-function TRPV4 mutations cause skeletal dysplasias and peripheral neuropathies. Our data indicate that TRPV4 mutations that reduce channel activity cause a third phenotype, inherited osteoarthropathy, and show the importance of TRPV4 activity in articular cartilage homeostasis. Our data raise the possibility that TRPV4 may also have a role in age- or injury-related osteoarthritis.     

Variants in KCNQ1 are associated with susceptibility to type 2 diabetes mellitus

We carried out a multistage genome-wide association study of type 2 diabetes mellitus in Japanese individuals, with a total of 1,612 cases and 1,424 controls and 100,000 SNPs. The most significant association was obtained with SNPs in KCNQ1, and dense mapping within the gene revealed that rs2237892 in intron 15 showed the lowest Pvalue (6.7 x 10(-13), odds ratio (OR) = 1.49). The association of KCNQ1 with type 2 diabetes was replicated in populations of Korean, Chinese and European ancestry as well as in two independent Japanese populations, and meta-analysis with a total of 19,930 individuals (9,569 cases and 10,361 controls) yielded a P value of 1.7 x 10(-42) (OR = 1.40; 95% CI = 1.34-1.47) for rs2237892. Among control subjects, the risk allele of this polymorphism was associated with impairment of insulin secretion according to the homeostasis model assessment of beta-cell function or the corrected insulin response. Our data thus implicate KCNQ1 as a diabetes susceptibility gene in groups of different ancestries.     

LKB1 signaling in mesenchymal cells required for suppression of gastrointestinal polyposis

Germline mutations in STK11 (also known as LKB1) are found in individuals with Peutz-Jeghers syndrome (PJS) manifesting with gastrointestinal polyps that contain a prominent stromal component. Epithelia in polyps of Stk11(+/-) mice can retain a functional copy of Stk11 (refs. 2,3), and loss of heterozygosity is not an obligate feature of human polyps, raising the possibility of non-epithelial origins in tumorigenesis. Here we show that either monoallelic or biallelic loss of murine Stk11 limited to Tagln-expressing mesenchymal cells results in premature postnatal death as a result of gastrointestinal polyps indistinguishable from those in PJS. Stk11-deficient mesenchymal cells produced less TGFbeta, and defective TGFbeta signaling to epithelial cells coincided with epithelial proliferation. We also noted TGFbeta signaling defects in polyps of individuals with PJS, suggesting that the identified stromal-derived mechanism of tumor suppression is also relevant in PJS.