Spinoza

"Spinoza", second edition. Encyclopedia entry for the Springer Encyclopedia of EM Phil and the Sciences, ed. D. Jalobeanu and C. T. Wolfe

Entanglement of dark electron-nuclear spin defects in diamond

A promising approach for multi-qubit quantum registers is to use optically addressable spins to control multiple dark electron-spin defects in the environment. While recent experiments have observed signatures of coherent interactions with such dark spins, it is an open challenge to realize the individual control required for quantum information processing. Here we demonstrate the initialisation, control and entanglement of individual dark spins associated to multiple P1 centers, which are part of a spin bath surrounding a nitrogen-vacancy center in diamond. We realize projective measurements to prepare the multiple degrees of freedom of P1 centers - their Jahn-Teller axis, nuclear spin and charge state - and exploit these to selectively access multiple P1s in the bath. We develop control and single-shot readout of the nuclear and electron spin, and use this to demonstrate an entangled state of two P1 centers. These results provide a proof-of-principle towards using dark electron-nuclear spin defects as qubits for quantum sensing, computation and networks

Robust Smith Predictor Design for Time-Delay Systems with H∞ Performance

A new method for robust fixed-order H∞ controller design for uncertain time-delay systems is presented. It is shown that the H∞ robust performance condition can be represented by a set of convex constraints with respect to the parameters of a linearly parameterized primary controller in the Smith predictor structure. Therefore, the parameters of the primary controller can be obtained by convex optimization. The proposed method can be applied to stable SISO and MIMO models with uncertain dead-time and with multimodel and frequency-dependent uncertainty. It is also shown that how the design method can be extended to unstable SISO models. The design of robust gain-scheduled dead-time compensators is also investigated. The performance of the method is illustrated for both SISO and MIMO systems by simulation examples

Intragenic deletions and a deep intronic mutation affecting pre-mRNA splicing in the dihydropyrimidine dehydrogenase gene as novel mechanisms causing 5-fluorouracil toxicity

Dihydropyrimidine dehydrogenase (DPD) is the initial enzyme acting in the catabolism of the widely used antineoplastic agent 5-fluorouracil (5FU). DPD deficiency is known to cause a potentially lethal toxicity following administration of 5FU. Here, we report novel genetic mechanisms underlying DPD deficiency in patients presenting with grade III/IV 5FU-associated toxicity. In one patient a genomic DPYD deletion of exons 21–23 was observed. In five patients a deep intronic mutation c.1129–5923C>G was identified creating a cryptic splice donor site. As a consequence, a 44 bp fragment corresponding to nucleotides c.1129–5967 to c.1129–5924 of intron 10 was inserted in the mature DPD mRNA. The deleterious c.1129–5923C>G mutation proved to be in cis with three intronic polymorphisms (c.483 + 18G>A, c.959–51T>G, c.680 + 139G>A) and the synonymous mutation c.1236G>A of a previously identified haplotype. Retrospective analysis of 203 cancer patients showed that the c.1129–5923C>G mutation was significantly enriched in patients with severe 5FU-associated toxicity (9.1%) compared to patients without toxicity (2.2%). In addition, a high prevalence was observed for the c.1129–5923C>G mutation in the normal Dutch (2.6%) and German (3.3%) population. Our study demonstrates that a genomic deletion affecting DPYD and a deep intronic mutation affecting pre-mRNA splicing can cause severe 5FU-associated toxicity. We conclude that screening for DPD deficiency should include a search for genomic rearrangements and aberrant splicing

Profound variation in dihydropyrimidine dehydrogenase activity in human blood cells: major implications for the detection of partly deficient patients

Dihydropyrimidine dehydrogenase (DPD) is responsible for the breakdown of the widely used antineoplastic agent 5-fluorouracil (5FU), thereby limiting the efficacy of the therapy. To identify patients suffering from a complete or partial DPD deficiency, the activity of DPD is usually determined in peripheral blood mononuclear cells (PBM cells). In this study, we demonstrated that the highest activity of DPD was found in monocytes followed by that of lymphocytes, granulocytes and platelets, whereas no significant activity of DPD could be detected in erythrocytes. The activity of DPD in PBM cells proved to be intermediate compared with the DPD activity observed in monocytes and lymphocytes. The mean percentage of monocytes in the PBM cells obtained from cancer patients proved to be significantly higher than that observed in PBM cells obtained from healthy volunteers. Moreover, a profound positive correlation was observed between the DPD activity of PBM cells and the percentage of monocytes, thus introducing a large inter- and intrapatient variability in the activity of DPD and hindering the detection of patients with a partial DPD deficiency. © 1999 Cancer Research Campaig

Rank-one LMIs and Lyapunov's inequality

We describe a new proof of the well-known Lyapunov's matrix inequality about the location of the eigenvalues of a matrix in some region of the complex plane. The proof makes use of standard facts from quadratic and semi-definite programming. Links are established between the Lyapunov matrix, rank-one LMI and the Lagrange multiplier arising in duality theory