Atom laser dynamics in a tight-waveguide

We study the transient dynamics that arise during the formation of an atom laser beam in a tight waveguide. During the time evolution the density profile develops a series of wiggles which are related to the diffraction in time phenomenon. The apodization of matter waves, which relies on the use of smooth aperture functions, allows to suppress such oscillations in a time interval, after which there is a revival of the diffraction in time. The revival time scale is directly related to the inverse of the harmonic trap frequency for the atom reservoir.Comment: 6 pages, 5 figures, to be published in the Proceedings of the 395th WE-Heraeus Seminar on "Time Dependent Phenomena in Quantum Mechanics ", organized by T. Kramer and M. Kleber (Blaubeuren, Germany, September 2007

Bilateral symmetry breaking in a nonlinear Fabry-Perot cavity exhibiting optical tristability

We show the existence of a region in the parameter space that defines the field dynamics in a Fabry-Perot cylindrical cavity, where three output stable stationary states of the light are possible for a given localized incident field. Two of these states do not preserve the bilateral (i.e. left-right) symmetry of the entire system. These broken-symmetry states are the high-transmission nonlinear modes of the system. We also discuss how to excite these states.Comment: 5 pages, 5 figure

Atomic matter wave scanner

We report on the experimental realization of an atom optical device, that allows scanning of an atomic beam. We used a time-modulated evanescent wave field above a glass surface to diffract a continuous beam of metastable Neon atoms at grazing incidence. The diffraction angles and efficiencies were controlled by the frequency and form of modulation, respectively. With an optimized shape, obtained from a numerical simulation, we were able to transfer more than 50% of the atoms into the first order beam, which we were able to move over a range of 8 mrad.Comment: 4 pages, 4 figure

Electromagnetic energy penetration in the self-induced transparency regime of relativistic laser-plasma interactions

Two scenarios for the penetration of relativistically intense laser radiation into an overdense plasma, accessible by self-induced transparency, are presented. For supercritical densities less than 1.5 times the critical one, penetration of laser energy occurs by soliton-like structures moving into the plasma. At higher background densities laser light penetrates over a finite length only, that increases with the incident intensity. In this regime plasma-field structures represent alternating electron layers separated by about half a wavelength by depleted regions.Comment: 9 pages, 4 figures, submitted for publication to PR

Bi-allelic variants in RNF170 are associated with hereditary spastic paraplegia.

Alterations of Ca2+ homeostasis have been implicated in a wide range of neurodegenerative diseases. Ca2+ efflux from the endoplasmic reticulum into the cytoplasm is controlled by binding of inositol 1,4,5-trisphosphate to its receptor. Activated inositol 1,4,5-trisphosphate receptors are then rapidly degraded by the endoplasmic reticulum-associated degradation pathway. Mutations in genes encoding the neuronal isoform of the inositol 1,4,5-trisphosphate receptor (ITPR1) and genes involved in inositol 1,4,5-trisphosphate receptor degradation (ERLIN1, ERLIN2) are known to cause hereditary spastic paraplegia (HSP) and cerebellar ataxia. We provide evidence that mutations in the ubiquitin E3 ligase gene RNF170, which targets inositol 1,4,5-trisphosphate receptors for degradation, are the likely cause of autosomal recessive HSP in four unrelated families and functionally evaluate the consequences of mutations in patient fibroblasts, mutant SH-SY5Y cells and by gene knockdown in zebrafish. Our findings highlight inositol 1,4,5-trisphosphate signaling as a candidate key pathway for hereditary spastic paraplegias and cerebellar ataxias and thus prioritize this pathway for therapeutic interventions

Efficient production and enhanced tumor delivery of engineered extracellular vesicles

Extracellular vesicles (EV), including exosomes and microvesicles, are nano-sized intercellular communication vehicles that participate in a multitude of physiological processes. Due to their biological properties, they are also promising candidates for the systemic delivery of therapeutic compounds, such as cytokines, chemotherapeutic drugs, siRNAs and viral vectors. However, low EV production yield and rapid clearance of administered EV by liver macrophages limit their potential use as therapeutic vehicles. We have used a hollow-fiber bioreactor for the efficient production of bioactive EV bearing the heterodimeric cytokine complex Interleukin-15:Interleukin-15 receptor alpha. Bioreactor culture yielded ∼40-fold more EV per mL conditioned medium, as compared to conventional cell culture. Biophysical analysis and comparative proteomics suggested a more diverse population of EV in the bioreactor preparations, while serum protein contaminants were detectable only in conventional culture EV preparations. We also identified the Scavenger Receptor Class A family (SR-A) as a novel monocyte/macrophage uptake receptor for EV. In vivo blockade of SR-A with dextran sulfate dramatically decreased EV liver clearance in mice, while enhancing tumor accumulation. These findings facilitate development of EV therapeutic methods. © 201

Terminological challenges in the translation of science documentaries: a case-study

This article aims to describe some of the main terminological problems audiovisual translators have to face when dealing with the translation of science documentaries, specifically in the English-Catalan combination. The first section of the article presents some theoretical concepts which underlie this research and which are taken, for the most part, from Cabré's Communicative Theory of Terminology. Then, specific terminological problems audiovisual translators have to solve are described using the data provided by a corpus of four science documentaries lasting approximately 50 minutes each. These challenges include identifying a term, understanding a term, finding the right equivalent, dealing with the absence of an adequate equivalent, solving denominative variations, choosing between in vivo and in vitro terminology, and overcoming mistranscriptions

Substrate cycling between de novo lipogenesis and lipid oxidation: a thermogenic mechanism against skeletal muscle lipotoxicity and glucolipotoxicity

Life is a combustion, but how the major fuel substrates that sustain human life compete and interact with each other for combustion has been at the epicenter of research into the pathogenesis of insulin resistance ever since Randle proposed a 'glucose-fatty acid cycle' in 1963. Since then, several features of a mutual interaction that is characterized by both reciprocality and dependency between glucose and lipid metabolism have been unravelled, namely: 1. the inhibitory effects of elevated concentrations of fatty acids on glucose oxidation (via inactivation of mitochondrial pyruvate dehydrogenase or via desensitization of insulin-mediated glucose transport), 2. the inhibitory effects of elevated concentrations of glucose on fatty acid oxidation (via malonyl-CoA regulation of fatty acid entry into the mitochondria), and more recently 3. the stimulatory effects of elevated concentrations of glucose on de novo lipogenesis, that is, synthesis of lipids from glucose (via SREBP1c regulation of glycolytic and lipogenic enzymes). This paper first revisits the physiological significance of these mutual interactions between glucose and lipids in skeletal muscle pertaining to both blood glucose and intramyocellular lipid homeostasis. It then concentrates upon emerging evidence, from calorimetric studies investigating the direct effect of leptin on thermogenesis in intact skeletal muscle, of yet another feature of the mutual interaction between glucose and lipid oxidation: that of substrate cycling between de novo lipogenesis and lipid oxidation. It is proposed that this energy-dissipating substrate cycling that links glucose and lipid metabolism to thermogenesis could function as a 'fine-tuning' mechanism that regulates intramyocellular lipid homeostasis, and hence contributes to the protection of skeletal muscle against lipotoxicity

Implantation Serine Proteinase 1 Exhibits Mixed Substrate Specificity that Silences Signaling via Proteinase-Activated Receptors

Implantation S1 family serine proteinases (ISPs) are tryptases involved in embryo hatching and uterine implantation in the mouse. The two different ISP proteins (ISP1 and ISP2) have been detected in both pre- and post-implantation embryo tissue. To date, native ISP obtained from uterus and blastocyst tissues has been isolated only as an active hetero-dimer that exhibits trypsin-like substrate specificity. We hypothesised that in isolation, ISP1 might have a unique substrate specificity that could relate to its role when expressed alone in individual tissues. Thus, we isolated recombinant ISP1 expressed in Pichia pastoris and evaluated its substrate specificity. Using several chromogenic substrates and serine proteinase inhibitors, we demonstrate that ISP1 exhibits trypsin-like substrate specificity, having a preference for lysine over arginine at the P1 position. Phage display peptide mimetics revealed an expanded but mixed substrate specificity of ISP1, including chymotryptic and elastase activity. Based upon targets observed using phage display, we hypothesised that ISP1 might signal to cells by cleaving and activating proteinase-activated receptors (PARs) and therefore assessed PARs 1, 2 and 4 as potential ISP1 targets. We observed that ISP1 silenced enzyme-triggered PAR signaling by receptor-disarming. This PAR-disarming action of ISP1 may be important for embryo development and implantation