Violation of a Bell-like inequality in single-neutron interferometry

Non-local correlations between spatially separated systems have been extensively discussed in the context of the Einstein, Podolsky and Rosen (EPR) paradox and Bell's inequalities. Many proposals and experiments designed to test hidden variable theories and the violation of Bell's inequalities have been reported; usually, these involve correlated photons, although recently an experiment was performed with (9)Be(+) ions. Nevertheless, it is of considerable interest to show that such correlations (arising from quantum mechanical entanglement) are not simply a peculiarity of photons. Here we measure correlations between two degrees of freedom (comprising spatial and spin components) of single neutrons; this removes the need for a source of entangled neutron pairs, which would present a considerable technical challenge. A Bell-like inequality is introduced to clarify the correlations that can arise between observables of otherwise independent degrees of freedom. We demonstrate the violation of this Bell-like inequality: our measured value is 2.051 +/- 0.019, clearly above the value of 2 predicted by classical hidden variable theories.     

Germ-line transmission of a disrupted beta 2-microglobulin gene produced by homologous recombination in embryonic stem cells

Major histocompatibility complex (MHC) class I molecules are integral membrane proteins present on virtually all vertebrate cells and consist of a heterodimer between the highly polymorphic alpha-chain and the beta 2-microglobulin (beta 2-m) protein of relative molecular mass 12,000 (ref. 1). These cell-surface molecules play a pivotal part in the recognition of antigens, the cytotoxic response of T cells, and the induction of self tolerance. It is possible, however, that the function of MHC class I molecules is not restricted to the immune system, but extends to a wide variety of biological reactions including cell-cell interactions. For example, MHC class I molecules seem to be associated with various cell-surface proteins, including the receptors for insulin, epidermal growth factor, luteinizing hormone and the beta-adrenergic receptor. In mice, class I molecules are secreted in the urine and act as highly specific olfactory cues which influence mating preference. The beta 2-m protein has also been identified as the smaller component of the Fc receptor in neonatal intestinal cells, and it has been suggested that the protein induces collagenase in fibroblasts. Cells lacking beta 2-m are deficient in the expression of MHC class I molecules, indicating that the association with beta 2-m is crucial for the transport of MHC class I molecules to the cell surface. The most direct means of unravelling the many biological functions of beta 2-m is to create a mutant mouse with a defective beta 2-m gene. We have now used the technique of homologous recombination to disrupt the beta 2-m gene. We report here that introduction of a targeting vector into embryonic stem cells resulted in beta 2-m gene disruption with high frequency. Chimaeric mice derived from blastocysts injected with mutant embryonic stem cell clones transmit the mutant allele to their offspring.     

Applications of membrane systems in distributed systems

Based on the biological model of cell-to-cell communication proposed by A. Rustom et al. (Science, 2004, 303: 1007-1010), we investigate the possibilities to apply P systems with dynamic channels transporting membrane vesicles for describing processes in distributed systems.     

Mammalian neural crest cells participate in normal embryonic development on microinjection into post-implantation mouse embryos

The production of chimaeric mice by aggregating pre-implantation mouse embryos or by injection of cells into the blastocyst has been of great value in analysing the regulation of early mammalian development and in dissecting the relationships of early cell lineages. While the totipotent cells of the pre-implantation embryo can be grown in vitro and thus are readily accessible to experimental manipulation, this is not possible after the embryo has implanted into the uterus. This problem has severely hampered the analysis of cell migration and of cell lineage relationships in later stages of mammalian development. In contrast, the chicken embryo can be manipulated experimentally throughout embryo-genesis and this has made the bird a favourable system for studying patterns of cell migration in the development of higher vertebrates. In mammals, the introduction of retroviruses and haematopoietic cells has provided two means of probing post-implantation development by direct intervention. I report here that cultured neural crest cells, when microinjected into 9-day-old mouse embryos, can migrate over considerable distances and participate in normal development, and the resulting chimaeric animals show pigmentation derived from the donor cells in hair and iris. The introduction of cells into post-implantation embryos may provide the means of studying patterns of cell migration in mammalian development at a level of sophistication which so far has been restricted to the chicken system.     

Mice cloned from olfactory sensory neurons

Cloning by nuclear transplantation has been successfully carried out in various mammals, including mice. Until now mice have not been cloned from post-mitotic cells such as neurons. Here, we have generated fertile mouse clones derived by transferring the nuclei of post-mitotic, olfactory sensory neurons into oocytes. These results indicate that the genome of a post-mitotic, terminally differentiated neuron can re-enter the cell cycle and be reprogrammed to a state of totipotency after nuclear transfer. Moreover, the pattern of odorant receptor gene expression and the organization of odorant receptor genes in cloned mice was indistinguishable from wild-type animals, indicating that irreversible changes to the DNA of olfactory neurons do not accompany receptor gene choice.     

Meta-analysis identifies 29 additional ulcerative colitis risk loci, increasing the number of confirmed associations to 47

Genome-wide association studies and candidate gene studies in ulcerative colitis have identified 18 susceptibility loci. We conducted a meta-analysis of six ulcerative colitis genome-wide association study datasets, comprising 6,687 cases and 19,718 controls, and followed up the top association signals in 9,628 cases and 12,917 controls. We identified 29 additional risk loci (P < 5 × 10(-8)), increasing the number of ulcerative colitis-associated loci to 47. After annotating associated regions using GRAIL, expression quantitative trait loci data and correlations with non-synonymous SNPs, we identified many candidate genes that provide potentially important insights into disease pathogenesis, including IL1R2, IL8RA-IL8RB, IL7R, IL12B, DAP, PRDM1, JAK2, IRF5, GNA12 and LSP1. The total number of confirmed inflammatory bowel disease risk loci is now 99, including a minimum of 28 shared association signals between Crohn's disease and ulcerative colitis.     

海克·卡莫林·奥纳斯和超导电性的发现

在实验室条件下创造尽可能接近绝对零度的极端条件,这一19－20世纪之交的国际竞争最终导致了电流无阻流动的惊人发现超导电性即电流在材料中的无阻流动,是自然界众多奇观之一。许多人称1987年3月为物理学的中流批技期,数百位科学家聚集在纽约市希尔顿大厅,接收数百份有关高温超导材料的报告。这些高温超导材料的骤变温度是前所未有的。本世纪50年代约翰·巴了（1．n）、里昂·N·库伯（L．N．Cooper）,以及J·罗伯特·斯莱弗（J．R．Sltrieffer）,就为我们提供了有关超导电性的最佳理论基础。然而如果我们撇开理论贡献,而仅就实…     

A degradation-sensitive anionic trypsinogen (PRSS2) variant protects against chronic pancreatitis

Chronic pancreatitis is a common inflammatory disease of the pancreas. Mutations in the genes encoding cationic trypsinogen (PRSS1) and the pancreatic secretory trypsin inhibitor (SPINK1) are associated with chronic pancreatitis. Because increased proteolytic activity owing to mutated PRSS1 enhances the risk for chronic pancreatitis, mutations in the gene encoding anionic trypsinogen (PRSS2) may also predispose to disease. Here we analyzed PRSS2 in individuals with chronic pancreatitis and controls and found, to our surprise, that a variant of codon 191 (G191R) is overrepresented in control subjects: G191R was present in 220/6,459 (3.4%) controls but in only 32/2,466 (1.3%) affected individuals (odds ratio 0.37; P = 1.1 x 10(-8)). Upon activation by enterokinase or trypsin, purified recombinant G191R protein showed a complete loss of trypsin activity owing to the introduction of a new tryptic cleavage site that renders the enzyme hypersensitive to autocatalytic proteolysis. In conclusion, the G191R variant of PRSS2 mitigates intrapancreatic trypsin activity and thereby protects against chronic pancreatitis.     

Genome-wide meta-analyses of nonsyndromic cleft lip with or without cleft palate identify six new risk loci

We have conducted the first meta-analyses for nonsyndromic cleft lip with or without cleft palate (NSCL/P) using data from the two largest genome-wide association studies published to date. We confirmed associations with all previously identified loci and identified six additional susceptibility regions (1p36, 2p21, 3p11.1, 8q21.3, 13q31.1 and 15q22). Analysis of phenotypic variability identified the first specific genetic risk factor for NSCLP (nonsyndromic cleft lip plus palate) (rs8001641; P(NSCLP) = 6.51 × 10(-11); homozygote relative risk = 2.41, 95% confidence interval (CI) 1.84-3.16).