On Series of Multiqubit Bell's Inequalities

We overview series of multiqubit Bell's inequalities which apply to correlation functions. We present conditions that quantum states must satisfy to violate such inequalities.Comment: 10 page

Detection of N-particle entanglement with generalized Bell inequalities

We show that the generalized Bell-type inequality, explicitly involving rotational symmetry of physical laws, is very efficient in distinguishing between true N-particle quantum correlations and correlations involving less particles. This applies to various types of generalized partial separabilities. We also give a rigorous proof that the new Bell inequalities are maximally violated by the GHZ states, and find a very handy description of the N-qubit correlation function.Comment: 5 pages, minor typos corrected, journal versio

Rotational invariance as an additional constraint on local realism

Rotational invariance of physical laws is a generally accepted principle. We show that it leads to an additional external constraint on local realistic models of physical phenomena involving measurements of multiparticle spin 1/2 correlations. This new constraint rules out such models even in some situations in which standard Bell inequalities allow for explicit construction of such models. The whole analysis is performed without any additional assumptions on the form of local realistic models.Comment: 4 page

Nonclassicality of pure two-qutrit entangled states

We report an exhaustive numerical analysis of violations of local realism by two qutrits in all possible pure entangled states. In Bell type experiments we allow any pairs of local unitary U(3) transformations to define the measurement bases. Surprisingly, Schmidt rank-2 states, resembling pairs of maximally entangled qubits, lead to the most noise-robust violations of local realism. The phenomenon seems to be even more pronounced for four and five dimensional systems, for which we tested a few interesting examples.Comment: 6 pages, journal versio

Magnetic groundstate and Fermi surface of bcc Eu

Using spin-spiral technique within the full potential linearized augmented-plane-waves (LAPW) electronic structure method we investigate the magnon spectrum and N\'eel temperature of bcc Eu. Ground state corresponding to an incommensurate spin-spiral is obtained in agreement with experiment and previous calculations. We demonstrate that the magnetic coupling is primarily through the intra-atomic $f-s$ and $f-d$ exchange and Ruderman-Kittel-Kasuya-Yosida mechanism. We show that the existence of this spin-spiral is closely connected to a nesting feature of the Fermi surface which was not noticed before.Comment: 6 pages 8 figure

Bell inequality with an arbitrary number of settings and its applications

Based on a geometrical argument introduced by Zukowski, a new multisetting Bell inequality is derived, for the scenario in which many parties make measurements on two-level systems. This generalizes and unifies some previous results. Moreover, a necessary and sufficient condition for the violation of this inequality is presented. It turns out that the class of non-separable states which do not admit local realistic description is extended when compared to the two-setting inequalities. However, supporting the conjecture of Peres, quantum states with positive partial transposes with respect to all subsystems do not violate the inequality. Additionally, we follow a general link between Bell inequalities and communication complexity problems, and present a quantum protocol linked with the inequality, which outperforms the best classical protocol.Comment: 8 pages, To appear in Phys. Rev.

Do all pure entangled states violate Bell's inequalities for correlation functions?

Any pure entangled state of two particles violates a Bell inequality for two-particle correlation functions (Gisin's theorem). We show that there exist pure entangled N>2 qubit states that do not violate any Bell inequality for N particle correlation functions for experiments involving two dichotomic observables per local measuring station. We also find that Mermin-Ardehali-Belinskii-Klyshko inequalities may not always be optimal for refutation of local realistic description.Comment: 4 pages, journal versio

Protein structure and phenotypic analysis of pathogenic and population missense variants in STXBP1

Background: Syntaxin-binding protein 1, encoded by STXBP1, is highly expressed in the brain and involved in fusing synaptic vesicles with the plasma membrane. Studies have shown that pathogenic loss-of-function variants in this gene result in various types of epilepsies, mostly beginning early in life. We were interested to model pathogenic missense variants on the protein structure to investigate the mechanism of pathogenicity and genotype–phenotype correlations. Methods: We report 11 patients with pathogenic de novo mutations in STXBP1 identified in the first 4293 trios of the Deciphering Developmental Disorder (DDD) study, including six missense variants. We analyzed the structural locations of the pathogenic missense variants from this study and the literature, as well as population missense variants extracted from Exome Aggregation Consortium (ExAC). Results: Pathogenic variants are significantly more likely to occur at highly conserved locations than population variants, and be buried inside the protein domain. Pathogenic mutations are also more likely to destabilize the domain structure compared with population variants, increasing the proportion of (partially) unfolded domains that are prone to aggregation or degradation. We were unable to detect any genotype–phenotype correlation, but unlike previously reported cases, most of the DDD patients with STXBP1 pathogenic variants did not present with very early-onset or severe epilepsy and encephalopathy, though all have developmental delay with intellectual disability and most display behavioral problems and suffered seizures in later childhood. Conclusion: Variants across STXBP1 that cause loss of function can result in severe intellectual disability with or without seizures, consistent with a haploinsufficiency mechanism. Pathogenic missense mutations act through destabilization of the protein domain, making it prone to aggregation or degradation. The presence or absence of early seizures may reflect ascertainment bias in the literature as well as the broad recruitment strategy of the DDD study

Crystal structure of monomeric human β-2- microglobulin reveals clues to its amyloidogenic properties

Dissociation of human β-2-microglobulin (β(2)m) from the heavy chain of the class I HLA complex is a critical first step in the formation of amyloid fibrils from this protein. As a consequence of renal failure, the concentration of circulating monomeric β(2)m increases, ultimately leading to deposition of the protein into amyloid fibrils and development of the disorder, dialysis-related amyloidosis. Here we present the crystal structure of a monomeric form of human β(2)m determined at 1.8-Å resolution that reveals remarkable structural changes relative to the HLA-bound protein. These involve the restructuring of a β bulge that separates two short β strands to form a new six-residue β strand at one edge of this β sandwich protein. These structural changes remove key features proposed to have evolved to protect β sheet proteins from aggregation [Richardson, J.&Richardson, D. (2002) Proc. Natl. Acad. Sci. USA 99, 2754–2759] and replaces them with an aggregationcompetent surface. In combination with solution studies using (1)H NMR, we show that the crystal structure presented here represents a rare species in solution that could provide important clues about the mechanism of amyloid formation from the normally highly soluble native protein