How to create Alice string (half-quantum vortex) in a vector Bose-Einstein condensate

We suggest a procedure how to prepare the vortex with N=1/2 winding number -- the counterpart of the Alice string -- in a Bose--Einstein condensate with hyperfine spin F=1. Other possible vortices in Bose-condensates are also discussed.Comment: RevTex file, 3 pages, no figures, extended version submitted to JETP Letter

Spin Dynamics and Spin Transport

Spin-orbit (SO) interaction critically influences electron spin dynamics and spin transport in bulk semiconductors and semiconductor microstructures. This interaction couples electron spin to dc and ac electric fields. Spin coupling to ac electric fields allows efficient spin manipulating by the electric component of electromagnetic field through the electric dipole spin resonance (EDSR) mechanism. Usually, it is much more efficient than the magnetic manipulation due to a larger coupling constant and the easier access to spins at a nanometer scale. The dependence of the EDSR intensity on the magnetic field direction allows measuring the relative strengths of the competing SO coupling mechanisms in quantum wells. Spin coupling to an in-plane electric field is much stronger than to a perpendicular field. Because electron bands in microstructures are spin split by SO interaction, electron spin is not conserved and spin transport in them is controlled by a number of competing parameters, hence, it is rather nontrivial. The relation between spin transport, spin currents, and spin populations is critically discussed. Importance of transients and sharp gradients for generating spin magnetization by electric fields and for ballistic spin transport is clarified.Comment: Invited talk at the 3rd Intern. Conf. on Physics and Applications of Spin-Related Phenomena in Semiconductors, Santa Barbara (CA), July 21 - 23. To be published in the Journal of Superconductivity. 7 pages, 2 figure

A Local Proinflammatory Signalling Loop Facilitates Adverse Age-Associated Arterial Remodeling

Background: The coincidence of vascular smooth muscle cells (VSMC) infiltration and collagen deposition within a diffusely thickened intima is a salient feature of central arterial wall inflammation that accompanies advancing age. However, the molecular mechanisms involved remain undefined. Methodology/Principal Findings: Immunostaining and immunoblotting of rat aortae demonstrate that a triad of proinflammatory molecules, MCP-1, TGF-b1, and MMP-2 increases within the aortic wall with aging. Exposure of VSMC isolated from 8-mo-old rats (young) to MCP-1 effects, via CCR-2 signaling, both an increase in TGF-b1 activity, up to levels of untreated VSMC from 30-mo-old (old) rats, and a concurrent increase in MMP-2 activation. Furthermore, exposure of young VSMC to TGF-b1 increases levels of MCP-1, and MMP-2 activation, to levels of untreated VSMC from old rats. This autocatalytic signaling loop that enhances collagen production and invasiveness of VSMC is effectively suppressed by si-MCP-1, a CCR2 antagonist, or MMP-2 inhibition. Conclusions/Significance: Threshold levels of MCP-1, MMP-2, or TGF-b1 activity trigger a feed-forward signaling mechanism that is implicated in the initiation and progression of adverse age-associated arterial wall remodeling. Intervention that suppressed this signaling loop may potentially retard age-associated adverse arterial remodeling

Drug-induced acute myocardial infarction: identifying 'prime suspects' from electronic healthcare records-based surveillance system.

BACKGROUND: Drug-related adverse events remain an important cause of morbidity and mortality and impose huge burden on healthcare costs. Routinely collected electronic healthcare data give a good snapshot of how drugs are being used in 'real-world' settings. OBJECTIVE: To describe a strategy that identifies potentially drug-induced acute myocardial infarction (AMI) from a large international healthcare data network. METHODS: Post-marketing safety surveillance was conducted in seven population-based healthcare databases in three countries (Denmark, Italy, and the Netherlands) using anonymised demographic, clinical, and prescription/dispensing data representing 21,171,291 individuals with 154,474,063 person-years of follow-up in the period 1996-2010. Primary care physicians' medical records and administrative claims containing reimbursements for filled prescriptions, laboratory tests, and hospitalisations were evaluated using a three-tier triage system of detection, filtering, and substantiation that generated a list of drugs potentially associated with AMI. Outcome of interest was statistically significant increased risk of AMI during drug exposure that has not been previously described in current literature and is biologically plausible. RESULTS: Overall, 163 drugs were identified to be associated with increased risk of AMI during preliminary screening. Of these, 124 drugs were eliminated after adjustment for possible bias and confounding. With subsequent application of criteria for novelty and biological plausibility, association with AMI remained for nine drugs ('prime suspects'): azithromycin; erythromycin; roxithromycin; metoclopramide; cisapride; domperidone; betamethasone; fluconazole; and megestrol acetate. LIMITATIONS: Although global health status, co-morbidities, and time-invariant factors were adjusted for, residual confounding cannot be ruled out. CONCLUSION: A strategy to identify potentially drug-induced AMI from electronic healthcare data has been proposed that takes into account not only statistical association, but also public health relevance, novelty, and biological plausibility. Although this strategy needs to be further evaluated using other healthcare data sources, the list of 'prime suspects' makes a good starting point for further clinical, laboratory, and epidemiologic investigation