Direct observation of Anderson localization of matter waves in a controlled disorder

In 1958, Anderson predicted the localization of electronic wavefunctions in disordered crystals and the resulting absence of diffusion. It is now recognized that Anderson localization is ubiquitous in wave physics because it originates from the interference between multiple scattering paths. Experimentally, localization has been reported for light waves, microwaves, sound waves and electron gases. However, there has been no direct observation of exponential spatial localization of matter waves of any type. Here we observe exponential localization of a Bose-Einstein condensate released into a one-dimensional waveguide in the presence of a controlled disorder created by laser speckle. We operate in a regime of pure Anderson localization, that is, with weak disorder-such that localization results from many quantum reflections of low amplitude-and an atomic density low enough to render interactions negligible. We directly image the atomic density profiles as a function of time, and find that weak disorder can stop the expansion and lead to the formation of a stationary, exponentially localized wavefunction-a direct signature of Anderson localization. We extract the localization length by fitting the exponential wings of the profiles, and compare it to theoretical calculations. The power spectrum of the one-dimensional speckle potentials has a high spatial frequency cutoff, causing exponential localization to occur only when the de Broglie wavelengths of the atoms in the expanding condensate are greater than an effective mobility edge corresponding to that cutoff. In the opposite case, we find that the density profiles decay algebraically, as predicted in ref. 13. The method presented here can be extended to localization of atomic quantum gases in higher dimensions, and with controlled interactions.     

Paraneoplastic myasthenic syndrome IgG inhibits 45Ca2+ flux in a human small cell carcinoma line

Certain cancers exert unexplained remote effects on the nervous system. Small cell carcinoma (SCC) of the lung, a tumour capable of spike electrogenesis and which is of possible neural crest origin, is present in approximately 70% of patients with the Lambert-Eaton myasthenic syndrome (LEMS), a disorder characterized by fatigable muscle weakness. Patients with this syndrome have a defect in the (Ca2+-dependent) quantal release of acetylcholine from motor nerve terminals evoked by a nerve impulse or by high K+ (ref.5), and a decreased number of presynaptic active zone particles. The physiological and morphological features of the syndrome can be transferred to mice by the patients' IgG, consistent with an autoantibody interfering with the function of voltage-dependent Ca2+ channels. Here we demonstrate that K+-induced 45Ca2+ flux in a cultured human SCC line is significantly reduced by LEMS IgG, suggesting that in SCC-LEMS an autoantibody to tumour Ca2+-channel determinants is triggered; its cross-reaction with similar determinants at the motor nerve terminal could lead to the remote neurological syndrome.     

从中国大陆产银环蛇毒纯化的第三个K－神经毒素Ⅱ．功能检测

从中国大陆产银环蛇毒纯化得到两个Ｋ－神经毒素：Ⅵ２６及Ⅷ１ｂ峰，其中Ⅵ２ｄ峰的部分氨基酸顺序与Ｋ－银环蛇毒素结构均一。Ⅵ２６及Ⅷ１ｂ峰在浓度分别为１５０ｎｍｏｌ／Ｌ及２００ｎｍｏｌ／Ｌ经３０分钟可完全阻断小鸡睫状神经节的烟碱传递，表明这两个Ｋ－神经毒素均为高效神经元烟碱乙酰胆碱受体拮抗剂。以Ａｆｆｉ－ｇｅｌ４０１亲和层析柱纯化的电鳐烟碱受体在严格的脂－蛋白比例下重构至人工微团上，以￣（８６）Ｒｂ￣＋内流至荷有烟碱乙酰胆碱受体的囊泡来衡量离子通道功能．测定了α－银环蛇毒素及Ｋ－神经毒素对受体离子内流的抑制作用．毒素（μｍｏｌ）与受体（μｍｏｌ）比值为０．５时，α－银环蛇毒素１００％阻断氨甲酰胆碱作用下的受体离子内流。１０倍于此浓度的Ｋ－神经毒素对离子通道活动无影响。     

Proteases of Antarctic krill—a new system for effective enzymatic debridement of necrotic ulcerations

Summary The Antarctic krill (Euphausia superba) possesses an over-dimensioned digestive system, which is of vital importance for the survival of this euphaucean shrimp in the extreme marine environment. The isolated enzymes contain a well-balanced mixture of both endo- and exopeptidases, assuring fast and complete breakdown of proteinaceous material. These unique properties have now been shown to be extremely valuable for the effective removal of necrotic debris, fibrin or blood crusts in vitro. Therefore the krill enzymes should be considered as an important resource in the future management of necrotic wounds.     

TARDBP mutations in individuals with sporadic and familial amyotrophic lateral sclerosis

Recently, TDP-43 was identified as a key component of ubiquitinated aggregates in amyotrophic lateral sclerosis (ALS), an adult-onset neurological disorder that leads to the degeneration of motor neurons. Here we report eight missense mutations in nine individuals--six from individuals with sporadic ALS (SALS) and three from those with familial ALS (FALS)--and a concurring increase of a smaller TDP-43 product. These findings further corroborate that TDP-43 is involved in ALS pathogenesis.     

Robust associations of four new chromosome regions from genome-wide analyses of type 1 diabetes

The Wellcome Trust Case Control Consortium (WTCCC) primary genome-wide association (GWA) scan on seven diseases, including the multifactorial autoimmune disease type 1 diabetes (T1D), shows associations at P < 5 x 10(-7) between T1D and six chromosome regions: 12q24, 12q13, 16p13, 18p11, 12p13 and 4q27. Here, we attempted to validate these and six other top findings in 4,000 individuals with T1D, 5,000 controls and 2,997 family trios independent of the WTCCC study. We confirmed unequivocally the associations of 12q24, 12q13, 16p13 and 18p11 (P(follow-up) 相似文献   

Bee visitors of sweetvetch, Hedysarum boreale boreale (Leguminosae), and their pollen-collecting activities

Normal 0 false false false EN-US X-NONE X-NONE MicrosoftInternetExplorer4 st1\:*{behavior:url(#ieooui) } /* Style Definitions */ table.MsoNormalTable {mso-style-name:"Table Normal"; mso-tstyle-rowband-size:0; mso-tstyle-colband-size:0; mso-style-noshow:yes; mso-style-priority:99; mso-style-qformat:yes; mso-style-parent:""; mso-padding-alt:0in 5.4pt 0in 5.4pt; mso-para-margin:0in; mso-para-margin-bottom:.0001pt; mso-pagination:widow-orphan; font-size:11.0pt; font-family:"Calibri","sans-serif"; mso-ascii-font-family:Calibri; mso-ascii-theme-font:minor-latin; mso-fareast-font-family:"Times New Roman"; mso-fareast-theme-font:minor-fareast; mso-hansi-font-family:Calibri; mso-hansi-theme-font:minor-latin; mso-bidi-font-family:"Times New Roman"; mso-bidi-theme-font:minor-bidi;} The native bee fauna visiting and pollinating a population of sweetvetch in Grand Teton National Park was surveyed. The papilionaceous flowers were exploited by 37 bee species, most of which had long mouthparts. Most species collected pollen as well as nectar. Bees foraged most heavily in early afternoon when pollen was most abundant. However, there was no indication that bee species were competing for limited pollen resources: there was no difference among three time periods in percent sweetvetch pollen carried in the scopal pollen loads of bees nor was there any evidence that some species were displacing the foraging times of others. The advantages of developing a native species as a commercial pollinator of sweetvetch are discussed and several potential candidates are mentioned.     

Partial complementation of a DNA ligase I deficiency by DNA ligase III and its impact on cell survival and telomere stability in mammalian cells

DNA ligase I (LigI) plays a central role in the joining of strand interruptions during replication and repair. In our current study, we provide evidence that DNA ligase III (LigIII) and XRCC1, which form a complex that functions in single-strand break repair, are required for the proliferation of mammalian LigI-depleted cells. We show from our data that in cells with either dysfunctional LigI activity or depleted of this enzyme, both LigIII and XRCC1 are retained on the chromatin and accumulate at replication foci. We also demonstrate that the LigI and LigIII proteins cooperate to inhibit sister chromatid exchanges but that only LigI prevents telomere sister fusions. Taken together, these results suggest that in cells with dysfunctional LigI, LigIII contributes to the ligation of replication intermediates but not to the prevention of telomeric instability.     

From carrot to clinic: an overview of the retinoic acid signaling pathway

Vitamin A is essential for the formation and maintenance of many body tissues. It is also important for embryonic growth and development and can act as a teratogen at critical periods of development. Retinoic acid (RA) is the biologically active form of vitamin A and its signaling is mediated by the RA and retinoid X receptors. In addition to its role as an important molecule during development, RA has also been implicated in clinical applications, both as a potential anti-tumor agent as well as for the treatment of skin diseases. This review presents an overview of how dietary retinoids are converted to RA, hence presenting the major players in RA metabolism and signaling, and highlights examples of treatment applications of retinoids. Moreover, we discuss the origin and diversification of the retinoid pathway, which are important factors for understanding the evolution of ligand-specificity among retinoid receptors.