Unbounded violation of tripartite Bell inequalities

We prove that there are tripartite quantum states (constructed from random unitaries) that can lead to arbitrarily large violations of Bell inequalities for dichotomic observables. As a consequence these states can withstand an arbitrary amount of white noise before they admit a description within a local hidden variable model. This is in sharp contrast with the bipartite case, where all violations are bounded by Grothendieck's constant. We will discuss the possibility of determining the Hilbert space dimension from the obtained violation and comment on implications for communication complexity theory. Moreover, we show that the violation obtained from generalized GHZ states is always bounded so that, in contrast to many other contexts, GHZ states do in this case not lead to extremal quantum correlations. The results are based on tools from the theories of operator spaces and tensor norms which we exploit to prove the existence of bounded but not completely bounded trilinear forms from commutative C*-algebras.Comment: Substantial changes in the presentation to make the paper more accessible for a non-specialized reade

Large violation of Bell inequalities with low entanglement

In this paper we obtain violations of general bipartite Bell inequalities of order $\frac{\sqrt{n}}{\log n}$ with $n$ inputs, $n$ outputs and $n$-dimensional Hilbert spaces. Moreover, we construct explicitly, up to a random choice of signs, all the elements involved in such violations: the coefficients of the Bell inequalities, POVMs measurements and quantum states. Analyzing this construction we find that, even though entanglement is necessary to obtain violation of Bell inequalities, the Entropy of entanglement of the underlying state is essentially irrelevant in obtaining large violation. We also indicate why the maximally entangled state is a rather poor candidate in producing large violations with arbitrary coefficients. However, we also show that for Bell inequalities with positive coefficients (in particular, games) the maximally entangled state achieves the largest violation up to a logarithmic factor.Comment: Reference [16] added. Some typos correcte

Allotopic expression of mitochondrial-encoded genes in mammals: achieved goal, undemonstrated mechanism or impossible task?

Mitochondrial-DNA diseases have no effective treatments. Allotopic expression—synthesis of a wild-type version of the mutated protein in the nuclear-cytosolic compartment and its importation into mitochondria—has been proposed as a gene-therapy approach. Allotopic expression has been successfully demonstrated in yeast, but in mammalian mitochondria results are contradictory. The evidence available is based on partial phenotype rescue, not on the incorporation of a functional protein into mitochondria. Here, we show that reliance on partial rescue alone can lead to a false conclusion of successful allotopic expression. We recoded mitochondrial mt-Nd6 to the universal genetic code, and added the N-terminal mitochondrial-targeting sequence of cytochrome c oxidase VIII (C8) and the HA epitope (C8Nd6HA). The protein apparently co-localized with mitochondria, but a significant part of it seemed to be located outside mitochondria. Complex I activity and assembly was restored, suggesting successful allotopic expression. However, careful examination of transfected cells showed that the allotopically-expressed protein was not internalized in mitochondria and that the selected clones were in fact revertants for the mt-Nd6 mutation. These findings demonstrate the need for extreme caution in the interpretation of functional rescue experiments and for clear-cut controls to demonstrate true rescue of mitochondrial function by allotopic expression

Unus pro omnibus, omnes pro uno: A novel, evidence-based, unifying theory for the pathogenesis of endometriosis

The theory of retrograde menstruation as aetiopathogenesis of endometriosis formulated by John Sampson in 1927 shows clear shortcomings: this does not explain why retrograde menstruation is a physiological process that affects 90% of women, while endometriosis occurs in only 10% of cases; it also does not explain the endometriotic foci distant from the pelvis, nor explains the cases of endometriosis in male patients. The immunological alterations of the peritoneal fluid explains the effects of disease, such as the inhibition of the physiological processes of cytolysis, but does not explain the cause. There is evidence to support the hypothesis that ectopic müllerian remnants of the endometrium, endocervix and endosalpinx are items from the genital ridge leaked during organogenesis. It is known that tissues derived from coelomatic epithelial and mesenchymal cells have the potential to metaplastically differentiate into epithelium and stroma. In addition, the phenotype of the ectopic endometrial cells is significantly different from those ectopic. There is scientific evidence that, during organogenesis, the genes of the Homeobox and Wingless family play a fundamental role in the differentiation of the ducts of Muller and development of the anatomical structure of the urogenital tract. We present here a hypothesis that deregulation of genes and the Wnt signaling pathway Wnt/β-catenin leads to aberrations and deregulation within the mesoderm, thus, may cause aberrant placement of stem cells. In addition, immune cells, adhesion molecules, extracellular matrix metalloproteinase and pro-inflammatory cytokines activate/alter peritoneal microenvironment, creating the conditions for differentiation, adhesion, proliferation and survival of ectopic endometrial cells