Bose-Einstein condensation on a microelectronic chip

Although Bose-Einstein condensates of ultracold atoms have been experimentally realizable for several years, their formation and manipulation still impose considerable technical challenges. An all-optical technique that enables faster production of Bose-Einstein condensates was recently reported. Here we demonstrate that the formation of a condensate can be greatly simplified using a microscopic magnetic trap on a chip. We achieve Bose-Einstein condensation inside the single vapour cell of a magneto-optical trap in as little as 700 ms-more than a factor of ten faster than typical experiments, and a factor of three faster than the all-optical technique. A coherent matter wave is emitted normal to the chip surface when the trapped atoms are released into free fall; alternatively, we couple the condensate into an 'atomic conveyor belt', which is used to transport the condensed cloud non-destructively over a macroscopic distance parallel to the chip surface. The possibility of manipulating laser-like coherent matter waves with such an integrated atom-optical system holds promise for applications in interferometry, holography, microscopy, atom lithography and quantum information processing.     

Initial sequencing and analysis of the human genome

The human genome holds an extraordinary trove of information about human development, physiology, medicine and evolution. Here we report the results of an international collaboration to produce and make freely available a draft sequence of the human genome. We also present an initial analysis of the data, describing some of the insights that can be gleaned from the sequence.     

Integration of cytogenetic landmarks into the draft sequence of the human genome

We have placed 7,600 cytogenetically defined landmarks on the draft sequence of the human genome to help with the characterization of genes altered by gross chromosomal aberrations that cause human disease. The landmarks are large-insert clones mapped to chromosome bands by fluorescence in situ hybridization. Each clone contains a sequence tag that is positioned on the genomic sequence. This genome-wide set of sequence-anchored clones allows structural and functional analyses of the genome. This resource represents the first comprehensive integration of cytogenetic, radiation hybrid, linkage and sequence maps of the human genome; provides an independent validation of the sequence map and framework for contig order and orientation; surveys the genome for large-scale duplications, which are likely to require special attention during sequence assembly; and allows a stringent assessment of sequence differences between the dark and light bands of chromosomes. It also provides insight into large-scale chromatin structure and the evolution of chromosomes and gene families and will accelerate our understanding of the molecular bases of human disease and cancer.     

木乃伊七号(之二)

30. 在随后的5天内,一场生死搏斗在临护室307病房中进行着。在比森的指导下,住院医师们持续不断地观察着,护士詹妮弗和她的伙伴们则寸步不离地守护着他,谁也不许来访。     

使用生物类天然材料包衣种子的效果测试（英文）

用黄瓜种子作试验材料 ,用不同的处理方法包衣种子 ,试验种子的发芽率 ,幼苗生长势及种子抗病能力 ,这三种处理方法是 :对照 (裸种子 )、化学杀菌材料包衣及选择非化学 (生物类 )天然无害材料作为杀菌材料包衣 (用以防止化学杀菌材料的污染提出的新天然包衣材料 ) .实验结果表明 ,使用天然材料和化学材料包衣种子均使种子发芽时间延长和非正常幼苗增多及单株生物量提高 ,并比对照组裸种子杀死了大部分的病菌 ;但化学杀菌包衣种子处理使幼苗的非正常率更明显的增多 ;生物类天然材料包衣相对对照同样也能杀死许多病菌 ,但比化学包衣材料杀菌力弱 ,将进一步研制和改进 .     

半群环成为预布尔环

本文给出半群环ＲＳ（其中：Ｒ为环，Ｓ为半群）为预布尔环的条件为：环Ｒ为指数３的幂零环，且Ｓ为任一可交换半群；或者Ｒ为指数３的预布尔非幂零环，且Ｓ为预布尔半群．     

Neuronal defects and posterior pituitary hypoplasia in mice lacking the receptor tyrosine phosphatase PTPsigma

The LAR-family protein tyrosine phosphatase sigma (PTPsigma, encoded by the gene Ptprs) consists of a cell adhesion-like extracellular domain composed of immunoglobulin and fibronectin type-III repeats, a single transmembrane domain and two intracellular catalytic domains. It was previously shown to be expressed in neuronal and lung epithelial tissues in a developmentally regulated manner. To study the role of PTPsigma in mouse development, we inactivated Ptprs by gene targeting. All Ptprs+/- mice developed normally, whereas 60% of Ptprs-/- mice died within 48 hours after birth. The surviving Ptprs-/- mice demonstrated stunted growth, developmental delays and severe neurological defects including spastic movements, tremor, ataxic gait, abnormal limb flexion and defective proprioception. Histopathology of brain sections revealed reduction and hypocellularity of the posterior pituitary of Ptprs-/- mice, as well as a reduction of approximately 50-75% in the number of choline acetyl transferase-positive cells in the forebrain. Moreover, peripheral nerve electrophysiological analysis revealed slower conduction velocity in Ptprs-/- mice relative to wild-type or heterozygous animals, associated with an increased proportion of slowly conducting, small-diameter myelinated fibres and relative hypomyelination. By approximately three weeks of age, most remaining Ptprs-/- mice died from a wasting syndrome with atrophic intestinal villi. These results suggest that PTPsigma has a role in neuronal and epithelial development in mice.     

The dual role model for p53 in maintaining genomic integrity

The tumour suppressor p53 is a potent mediator of cellular responses against genotoxic insults. In this review we describe the multiple functions of p53 in response to DNA damage, with an emphasis on p53's role in DNA repair. We summarize data demonstrating that p53 actively participates in various processes of DNA repair and DNA recombination via its ability to interact with components of the repair and recombination machinery, and by its various biochemical activities. An important aspect in evaluating p53 functions is provided by the finding that the core domain of p53 harbours two mutually exclusive biochemical activities, sequence-specific DNA binding required for its transactivation function, and 3'-5' exonuclease activity, possibly involved in aspects of DNA repair. Based on the finding that modifications of p53 which lead to activation of its sequence-specific DNA-binding activity result in inactivation of its 3'-5' exonuclease activity, we propose that p53 exerts its functions as a 'guardian of the genome' at various levels: in its noninduced state, p53 should not be regarded as a 'dead' protein but, for example, via its exonuclease activity might be actively involved in prevention and repair of endogenous DNA damage. Upon induction through exogenous DNA damage, p53 will exert its well-documented functions as a superior response element in various types of cellular stress. This dual role model for p53 in maintaining genomic integrity significantly enhances p53's possibilities as a guardian of the genome.     

Bacterial targets and antibiotics: genome-based drug discovery

The requirement for novel classes of antibiotics to combat the emergence of resistant and multi-resistant bacteria has coincided with the completion sequencing of a number of bacterial genomes. The in silico analysis of these genomes coupled with innovative genetic manipulation has already led to the identification of conserved essential (either in vitro or in vivo, depending on the methodology) genes that are potential targets for antibacterial research. New technologies, made possible by access to the genomic sequences, are capable of simultaneously quantifying almost the entire complement of gene products synthesised by bacterial cells. These technologies are opening up the way for the analysis of expression patterns elicited in cells in response to changes in their environment. The integration of these technologies into the drug discovery process is still in its infancy and the potential wealth of information, some of it already available, has yet to be fully realised.     

Heterozygous mutations in the gene encoding noggin affect human joint morphogenesis

The secreted polypeptide noggin (encoded by the Nog gene) binds and inactivates members of the transforming growth factor beta superfamily of signalling proteins (TGFbeta-FMs), such as BMP4 (ref. 1). By diffusing through extracellular matrices more efficiently than TGFbeta-FMs, noggin may have a principal role in creating morphogenic gradients. During mouse embryogenesis, Nog is expressed at multiple sites, including developing bones. Nog-/- mice die at birth from multiple defects that include bony fusion of the appendicular skeleton. We have identified five dominant human NOG mutations in unrelated families segregating proximal symphalangism (SYM1; OMIM 185800) and a de novo mutation in a patient with unaffected parents. We also found a dominant NOG mutation in a family segregating multiple synostoses syndrome (SYNS1; OMIM 186500); both SYM1 and SYNS1 have multiple joint fusion as their principal feature. All seven NOG mutations alter evolutionarily conserved amino acid residues. The findings reported here confirm that NOG is essential for joint formation and suggest that NOG requirements during skeletogenesis differ between species and between specific skeletal elements within species.