The Microwave Thermal Thruster Concept

The microwave thermal thruster heats propellant via a heat-exchanger then expands it through a rocket nozzle to produce thrust. The heat-exchanger is simply a microwave-absorbent structure through which propellant flows in small channels. Nuclear thermal thrusters are based on an analogous principle, using neutrons rather than microwaves, and have experimentally demonstrated specific impulses exceeding 850 seconds. A microwave equivalent will likely have a similar specific impulse, since both nuclear and microwave thermal thrusters are ultimately constrained by material thermal limits, rather than the energy-density limits of chemical propellants. We present the microwave thermal thruster concept by characterizing a novel variation for beamed-energy launch. In reducing the thruster concept to practice, the enabling physical process is microwave absorption by refractory materials, and we examine semiconductor and susceptor-based approaches to achieving this absorption within the heat-exchanger structure

Fidelity of Quantum Interferometers

For a generic interferometer, the conditional probability density distribution, $p(\phi|m)$, for the phase $\phi$ given measurement outcome $m$, will generally have multiple peaks. Therefore, the phase sensitivity of an interferometer cannot be adequately characterized by the standard deviation, such as $\Delta\phi\sim 1/\sqrt{N}$ (the standard limit), or $\Delta\phi\sim 1/N$ (the Heisenberg limit). We propose an alternative measure of phase sensitivity--the fidelity of an interferometer--defined as the Shannon mutual information between the phase shift $\phi$\ and the measurement outcomes $m$. As an example application of interferometer fidelity, we consider a generic optical Mach-Zehnder interferometer, used as a sensor of a classical field. We find the surprising result that an entangled {\it N00N} state input leads to a lower fidelity than a Fock state input, for the same photon number.Comment: 4 pages, 3 figure

Suppression of flavor violation in an A4 warped extra dimensional model

In an attempt to simultaneously explain the observed masses and mixing patterns of both quarks and leptons, we recently proposed a model (JHEP08(2010)115) based on the non abelian discrete flavor group A4, implemented in a custodial RS setup with a bulk Higgs. We showed that the standard model flavor structure can be realized within the zero mode approximation (ZMA), with nearly tribimaximal (TBM) neutrino mixing and a realistic CKM matrix with rather mild assumptions. An important advantage of this framework with respect to flavor anarchic models is the vanishing of the dangerous tree level KK gluon contribution to \epsilon_K and the suppression of the new physics one loop contributions to the neutron EDM, \epsilon'/\epsilon, b->s\gamma and Higgs mediated flavor changing neutral current (FCNC) processes. These results are obtained beyond the ZMA, in order to account for the the full flavor structure and mixing of the zero modes and first Kaluza-Klein (KK) modes of all generations. The resulting constraints on the KK mass scale are shown to be significantly relaxed compared to the flavor anarchic case, showing explicitly the role of non abelian discrete flavor symmetries in relaxing flavor violation bounds within the RS setup. As a byproduct of our analysis we also obtain the same contributions for the custodial anarchic case with two SU(2)_R doublets for each fermion generation.Comment: 8 pages, 4 figures; contribution prepared for DISCRETE'10 - Symposium on Prospects in the Physics of Discrete Symmetrie

Heterovalent and A-atom effects in A(B'B'')O3 perovskite alloys

Using first-principles supercell calculations, we have investigated energetic, structural and dielectric properties of three different A(B'B'')O_3 perovskite alloys: Ba(Zn_{1/3}Nb_{2/3})O_3 (BZN), Pb(Zn_{1/3}Nb_{2/3})O_3 (PZN), and Pb(Zr_{1/3}Ti_{2/3})O_3 (PZT). In the homovalent alloy PZT, the energetics are found to be mainly driven by atomic relaxations. In the heterovalent alloys BZN and PZN, however, electrostatic interactions among B' and B'' atoms are found to be very important. These electrostatic interactions are responsible for the stabilization of the observed compositional long-range order in BZN. On the other hand, cell relaxations and the formation of short Pb--O bonds could lead to a destabilization of the same ordered structure in PZN. Finally, comparing the dielectric properties of homovalent and heterovalent alloys, the most dramatic difference arises in connection with the effective charges of the B' atom. We find that the effective charge of Zr in PZT is anomalous, while in BZN and PZN the effective charge of Zn is close to its nominal ionic value.Comment: 7 pages, two-column style with 2 postscript figures embedded. Uses REVTEX and epsf macros. Also available at http://www.physics.rutgers.edu/~dhv/preprints/index.html#lb_he

Saccharomyces cerevisiae chitin biosynthesis activation by N-acetylchitooses depends on size and structure of chito-oligosaccharides

<p>Abstract</p> <p>Background</p> <p>To explore chitin synthesis initiation, the effect of addition of exogenous oligosaccharides on <it>in vitro </it>chitin synthesis was studied. Oligosaccharides of various natures and lengths were added to a chitin synthase assay performed on a <it>Saccharomyces cerevisiae </it>membrane fraction.</p> <p>Findings</p> <p><it>N</it>-acetylchito-tetra, -penta and -octaoses resulted in 11 to 25% [¹⁴C]-GlcNAc incorporation into [¹⁴C]-chitin, corresponding to an increase in the initial velocity. The activation appeared specific to <it>N</it>-acetylchitooses as it was not observed with oligosaccharides in other series, such as beta-(1,4), beta-(1,3) or alpha-(1,6) glucooligosaccharides.</p> <p>Conclusions</p> <p>The effect induced by the <it>N</it>-acetylchitooses was a saturable phenomenon and did not interfere with free GlcNAc and trypsin which are two known activators of yeast chitin synthase activity <it>in vitro</it>. The magnitude of the activation was dependent on both oligosaccharide concentration and oligosaccharide size.</p

Hyperthermia Induces the ER Stress Pathway

The ER chaperone GRP78/BiP is a homolog of the Hsp70 family of heat shock proteins, yet GRP78/BiP is not induced by heat shock but instead by ER stress. However, previous studies had not considered more physiologically relevant temperature elevation associated with febrile hyperthermia. In this report we examine the response of GRP78/BiP and other components of the ER stress pathway in cells exposed to 40°C.AD293 cells were exposed to 43°C heat shock to confirm inhibition of the ER stress response genes. Five mammalian cell types, including AD293 cells, were then exposed to 40°C hyperthermia for various time periods and induction of the ER stress pathway was assessed.The inhibition of the ER stress pathway by heat shock (43°C) was confirmed. In contrast cells subjected to more mild temperature elevation (40°C) showed either a partial or full ER stress pathway induction as determined by downstream targets of the three arms of the ER stress pathway as well as a heat shock response. Cells deficient for Perk or Gcn2 exhibit great sensitivity to ER stress induction by hyperthermia.The ER stress pathway is induced partially or fully as a consequence of hyperthermia in parallel with induction of Hsp70. These findings suggest that the ER and cytoplasm of cells contain parallel pathways to coordinately regulate adaptation to febrile hyperthermia associated with disease or infection

ROR2 blockade as a therapy for osteoarthritis

Osteoarthritis is characterized by the loss of the articular cartilage, bone remodeling, pain, and disability. No pharmacological intervention can currently halt progression of osteoarthritis. Here, we show that blocking receptor tyrosine kinase–like orphan receptor 2 (ROR2) improves cartilage integrity and pain in osteoarthritis models by inhibiting yes-associated protein (YAP) signaling. ROR2 was up-regulated in the cartilage in response to inflammatory cytokines and mechanical stress. The main ligand for ROR2, WNT5A, and the targets YAP and connective tissue growth factor were up-regulated in osteoarthritis in humans. In vitro, ROR2 overexpression inhibited chondrocytic differentiation. Conversely, ROR2 blockade triggered chondrogenic differentiation of C3H10T1/2 cells and suppressed the expression of the cartilage-degrading enzymes a disintegrin and metalloproteinase with thrombospondin motifs (ADAMTS)–4 and ADAMTS-5. The chondrogenic effect of ROR2 blockade in the cartilage was independent of WNT signaling and was mediated by down-regulation of YAP signaling. ROR2 signaling induced G protein and Rho-dependent nuclear accumulation of YAP, and YAP inhibition was required but not sufficient for ROR2 blockade–induced chondrogenesis. ROR2 silencing protected mice from instability-induced osteoarthritis with improved structural outcomes, sustained pain relief, and without apparent side effects or organ toxicity. Last, ROR2 silencing in human articular chondrocytes transplanted in nude mice led to the formation of cartilage organoids with more and better differentiated extracellular matrix, suggesting that the anabolic effect of ROR2 blockade is conserved in humans. Thus, ROR2 blockade is efficacious and well tolerated in preclinical animal models of osteoarthritis

The SR Protein B52/SRp55 Is Required for DNA Topoisomerase I Recruitment to Chromatin, mRNA Release and Transcription Shutdown

DNA- and RNA-processing pathways are integrated and interconnected in the eukaryotic nucleus to allow efficient gene expression and to maintain genomic stability. The recruitment of DNA Topoisomerase I (Topo I), an enzyme controlling DNA supercoiling and acting as a specific kinase for the SR-protein family of splicing factors, to highly transcribed loci represents a mechanism by which transcription and processing can be coordinated and genomic instability avoided. Here we show that Drosophila Topo I associates with and phosphorylates the SR protein B52. Surprisingly, expression of a high-affinity binding site for B52 in transgenic flies restricted localization, not only of B52, but also of Topo I to this single transcription site, whereas B52 RNAi knockdown induced mis-localization of Topo I in the nucleolus. Impaired delivery of Topo I to a heat shock gene caused retention of the mRNA at its site of transcription and delayed gene deactivation after heat shock. Our data show that B52 delivers Topo I to RNA polymerase II-active chromatin loci and provide the first evidence that DNA topology and mRNA release can be coordinated to control gene expression