Quantum chaos with spin-chains in pulsed magnetic fields

Recently it was found that the dynamics in a Heisenberg spin-chain subjected to a sequence of periodic pulses from an external, parabolic, magnetic field can have a close correspondence with the quantum kicked rotor (QKR). The QKR is a key paradigm of quantum chaos; it has as its classical limit the well-known Standard Map. It was found that a single spin excitation could be converted into a pair of non-dispersive, counter-propagating spin coherent states equivalent to the accelerator modes of the Standard Map. Here we consider how other types of quantum chaotic systems such as a double-kicked quantum rotor or a quantum rotor with a double-well potential might be realized with spin chains; we discuss the possibilities regarding manipulation of the one-magnon spin waves.Comment: 10 pages, 4 figures. Submitted to PTP special issue for QMC200

Classical diffusion in double-delta-kicked particles

We investigate the classical chaotic diffusion of atoms subjected to {\em pairs} of closely spaced pulses (`kicks) from standing waves of light (the $2\delta$-KP). Recent experimental studies with cold atoms implied an underlying classical diffusion of type very different from the well-known paradigm of Hamiltonian chaos, the Standard Map. The kicks in each pair are separated by a small time interval $\epsilon \ll 1$, which together with the kick strength $K$, characterizes the transport. Phase space for the $2\delta$-KP is partitioned into momentum `cells' partially separated by momentum-trapping regions where diffusion is slow. We present here an analytical derivation of the classical diffusion for a $2\delta$-KP including all important correlations which were used to analyze the experimental data. We find a new asymptotic ($t \to \infty$) regime of `hindered' diffusion: while for the Standard Map the diffusion rate, for $K \gg 1$, $D \sim K^2/2[1- J_2(K)..]$ oscillates about the uncorrelated, rate $D_0 =K^2/2$, we find analytically, that the $2\delta$-KP can equal, but never diffuses faster than, a random walk rate. We argue this is due to the destruction of the important classical `accelerator modes' of the Standard Map. We analyze the experimental regime $0.1\lesssim K\epsilon \lesssim 1$, where quantum localisation lengths $L \sim \hbar^{-0.75}$ are affected by fractal cell boundaries. We find an approximate asymptotic diffusion rate $D\propto K^3\epsilon$, in correspondence to a $D\propto K^3$ regime in the Standard Map associated with 'golden-ratio' cantori.Comment: 14 pages, 10 figures, error in equation in appendix correcte

Beyond deficiency:Potential benefits of increased intakesof vitamin K for bone and vascular health

Vitamin K is wellknown for its role in the synthesisof a number of blood coagulationfactors.During recent years vitaminK-dependent proteins werediscovered to be of vital importancefor bone and vascular health.Recommendations for dietary vitaminK intake have been made onthe basis of the hepatic requirementsfor the synthesis of bloodcoagulation factors.Accumulatingevidence suggests that the requirementsfor other functions thanblood coagulation may be higher.This paper is the result of a closedworkshop (Paris,November 2002)in which a number of Europeanvitamin K experts reviewed theavailable data and formulated theirstandpoint with respect to recommendeddietary vitamin K intakeand the use of vitamin K-containingsupplements

Gymnemic acids inhibit hyphal growth and virulence in Candida albicans

Candida albicans is an opportunistic and polymorphic fungal pathogen that causes mucosal, disseminated and invasive infections in humans. Transition from the yeast form to the hyphal form is one of the key virulence factors in C. albicans contributing to macrophage evasion, tissue invasion and biofilm formation. Nontoxic small molecules that inhibit C. albicans yeast-to-hypha conversion and hyphal growth could represent a valuable source for understanding pathogenic fungal morphogenesis, identifying drug targets and serving as templates for the development of novel antifungal agents. Here, we have identified the triterpenoid saponin family of gymnemic acids (GAs) as inhibitor of C. albicans morphogenesis. GAs were isolated and purified from Gymnema sylvestre leaves, the Ayurvedic traditional medicinal plant used to treat diabetes. Purified GAs had no effect on the growth and viability of C. albicans yeast cells but inhibited its yeast-to-hypha conversion under several hypha-inducing conditions, including the presence of serum. Moreover, GAs promoted the conversion of C. albicans hyphae into yeast cells under hypha inducing conditions. They also inhibited conidial germination and hyphal growth of Aspergillus sp. Finally, GAs inhibited the formation of invasive hyphae from C. albicans-infected Caenorhabditis elegans worms and rescued them from killing by C. albicans. Hence, GAs could be useful for various antifungal applications due to their traditional use in herbal medicine

STAT5 Is an Ambivalent Regulator of Neutrophil Homeostasis

BACKGROUND: Although STAT5 promotes survival of hematopoietic progenitors, STAT5-/- mice develop mild neutrophilia. METHODOLOGY/PRINCIPAL FINDINGS: Here, we show that in STAT5-/- mice, liver endothelial cells (LECs) autonomously secrete high amounts of G-CSF, allowing myeloid progenitors to overcompensate for their intrinsic survival defect. However, when injected with pro-inflammatory cytokines, mutant mice cannot further increase neutrophil production, display a severe deficiency in peripheral neutrophil survival, and are therefore unable to maintain neutrophil homeostasis. In wild-type mice, inflammatory stimulation induces rapid STAT5 degradation in LECs, G-CSF production by LECs and other cell types, and then sustained mobilization and expansion of long-lived neutrophils. CONCLUSION: We conclude that STAT5 is an ambivalent factor. In cells of the granulocytic lineage, it exerts an antiapoptotic function that is required for maintenance of neutrophil homeostasis, especially during the inflammatory response. In LECs, STAT5 negatively regulates granulopoiesis by directly or indirectly repressing G-CSF expression. Removal of this STAT5-imposed brake contributes to induction of emergency granulopoiesis.Journal ArticleResearch Support, Non-U.S. Gov'tinfo:eu-repo/semantics/publishe