Quantifying Bell nonlocality of a pure two-qudit state via its entanglement

For the maximal violation of all Bell inequalities by an arbitrary pure two-qudit state of any dimension, we derive a new lower bound expressed via the concurrence of this pure state. This new lower bound and the upper bound on the maximal Bell violation, found in [J. Phys. A: Math. Theor. 55, 285301 (2022)] and also expressed via the concurrence, analytically quantify Bell nonlocality of a pure two-qudit state via its entanglement, in particular, prove explicitly that entanglement of a pure two-qudit state is necessary and sufficient for its Bell nonlocality. By re-visiting the pure two-qubit case, we also find and rigorously prove the new results on the correlation properties of an arbitrary pure two-qubit state.Comment: 12 p

Experimental and theoretical studies of helicopter rotor-fuselage interaction

Communication to : 18th ICAS Congress, Beijing (China), September 20-25, 1992SIGLEAvailable at INIST (FR), Document Supply Service, under shelf-number : 22419, issue : a.1992 n.142 / INIST-CNRS - Institut de l'Information Scientifique et TechniqueFRFranc

Experimental and theoretical studies on helicopter rotor fuselage interaction

SIGLECopy held by FIZ Karlsruhe; available from UB/TIB Hannover / FIZ - Fachinformationszzentrum Karlsruhe / TIB - Technische InformationsbibliothekDEGerman

Prdm12 specifies V1 interneurons through cross-repressive interactions with Dbx1 and Nkx6 genes in Xenopus.

International audienceV1 interneurons are inhibitory neurons that play an essential role in vertebrate locomotion. The molecular mechanisms underlying their genesis remain, however, largely undefined. Here, we show that the transcription factor Prdm12 is selectively expressed in p1 progenitors of the hindbrain and spinal cord in the frog embryo, and that a similar restricted expression profile is observed in the nerve cord of other vertebrates as well as of the cephalochordate amphioxus. Using frog, chick and mice, we analyzed the regulation of Prdm12 and found that its expression in the caudal neural tube is dependent on retinoic acid and Pax6, and that it is restricted to p1 progenitors, due to the repressive action of Dbx1 and Nkx6-1/2 expressed in the adjacent p0 and p2 domains. Functional studies in the frog, including genome-wide identification of its targets by RNA-seq and ChIP-Seq, reveal that vertebrate Prdm12 proteins act as a general determinant of V1 cell fate, at least in part, by directly repressing Dbx1 and Nkx6 genes. This probably occurs by recruiting the methyltransferase G9a, an activity that is not displayed by the amphioxus Prdm12 protein. Together, these findings indicate that Prdm12 promotes V1 interneurons through cross-repressive interactions with Dbx1 and Nkx6 genes, and suggest that this function might have only been acquired after the split of the vertebrate and cephalochordate lineages