Perturbation of frame sequences and its applications to shift-invariant spaces

AbstractWe generalize the main result in [O. Christensen, H.O. Kim, R.Y. Kim, J.K. Lim, Perturbation of frame sequences in shift-invariant spaces, J. Geom. Anal. 15 (2005) 181–191] in order to make it comparable with existing results. Then we compare the special cases of the three results in the literature in the setting of the perturbation of the generating sets of finitely generated shift-invariant spaces of L2(Rd)

Rate-dependent inhomogeneous-to-homogeneous transition of plastic flows during nanoindentation of bulk metallic glasses: Fact or artifact?

There has been considerable controversy over the "apparent" rate-dependent transition from inhomogeneous-to-homogeneous flow during nanoindentation of bulk metallic glasses (BMGs) at room temperature: whether it arises from the existence of homogeneous-flow regime in BMG deformation map or is an artifact due to the instrumental blurring at high rates. To provide a clue to address this dispute, the authors performed nanoindentation experiments on a Zr-based BMG with two geometrically self-similar indenters. The results are discussed in terms of the discrete plasticity ratio, which is a useful parameter in analyzing the contribution of inhomogeneous plasticity to the total plastic deformation.open232

Invariances of Frame Sequences under Perturbations

This paper determines the exact relationships that hold among the major Paley–Wiener perturbation theorems for frame sequences. It is shown that major properties of a frame sequence such as excess, deficit, and rank remain invariant under Paley–Wiener perturbations, but need not be preserved by compact perturbations. For localized frames, which are frames with additional structure, it is shown that the frame measure function is also preserved by Paley–Wiener perturbations

Production of Transgenic Cloned Miniature Pigs with Membrane-bound Human Fas Ligand (FasL) by Somatic Cell Nuclear Transfer

Cell-mediated xenograft rejection, including NK cells and CD8+ CTL, is a major obstacle in successful pig-to-human xenotransplantation. Human CD8+ CTL and NK cells display high cytotoxicity for pig cells, mediated at least in part by the Fas/FasL pathway. To prevent cell-mediated xenocytotoxicity, a membrane-bound form of human FasL (mFasL) was generated as an inhibitor for CTL and NK cell cytotoxicity that could not be cleaved by metalloproteinase to produce putative soluble FasL. We produced two healthy transgenic pigs harboring the mFasL gene via somatic cell nuclear transfer (SCNT). In a cytotoxicity assay using transgenic clonal cell lines and transgenic pig ear cells, the rate of CD8+ CTL-mediated cytotoxicity was significantly reduced in transgenic pig's ear cells compared with that in normal minipig fetal fibroblasts. Our data indicate that grafts of transgenic pigs expressing membrane-bound human FasL control the cellular immune response to xenografts, creating a window of opportunity to facilitate xenograft survival

Dirac Bilayer Metasurfaces as an Inverse Gires-Tournois Etalon

Efficient transmissive pure-phase resonances are highly desirable for optical modulation and wavefront engineering. Here, we propose a novel principle to realize a pure-phase resonance in an extremely broad transmission band, as opposed to previous approaches restricted to operating in reflection mode or over a narrow spectral band. We show that a glide-symmetric bilayer metasurface mathematically mimicking a two-dimensional Dirac semimetal induces unidirectional guided-mode excitation and perfect leakage-radiation blazing at the transmission channel. These effects create a peculiar resonant-scattering configuration, similar to the classical reflective Gires-Tournois etalon, but in transmission, providing full 2pi phase modulation with constant transmittance near 100%. Most importantly, this effect persists over an extremely wide band, associated with topological effects. Hence, our proposed approach produces a spectrally and parametrically robust pure-phase resonance effect in transmission, which is highly beneficial for practical applications.Comment: 11 pages, 5 figure

Inhibition of Hypoxic Pulmonary Vasoconstriction of Rats by Carbon Monoxide

Hypoxic pulmonary vasoconstriction (HPV), a unique response of pulmonary circulation, is critical to prevent hypoxemia under local hypoventilation. Hypoxic inhibition of K+ channel is known as an important O2-sensing mechanism in HPV. Carbon monoxide (CO) is suggested as a positive regulator of Ca2+-activated K+ channel (BKCa), a stimulator of guanylate cyclase, and an O2-mimetic agent in heme moiety-dependent O2 sensing mechanisms. Here we compared the effects of CO on the HPV (Po2, 3%) in isolated pulmonary artery (HPVPA) and in blood-perfused/ventilated lungs (HPVlung) of rats. A pretreatment with CO (3%) abolished the HPVPA in a reversible manner. The inhibition of HPVPA was completely reversed by 1H-[1,2,4]oxadiazolo-[4,3-a]quinoxalin-1-one (ODQ), a guanylate cyclase inhibitor. In contrast, the HPVlung was only partly decreased by CO. Moreover, the partial inhibition of HPVlung by CO was affected neither by the pretreatment with ODQ nor by NO synthase inhibitor (L-NAME). The CO-induced inhibitions of HPVPA and HPVlung were commonly unaffected by tetraethylammonium (TEA, 2 mM), a blocker of BKCa. As a whole, CO inhibits HPVPA via activating guanylate cyclase. The inconsistent effects of ODQ on HPVPA and HPVlung suggest that ODQ may lose its sGC inhibitory action when applied to the blood-containing perfusate

The uncalibrated pulse contour cardiac output during off-pump coronary bypass surgery: performance in patients with a low cardiac output status and a reduced left ventricular function

BACKGROUND: We compared the continuous cardiac index measured by the FloTrac/Vigileo™ system (FCI) to that measured by a pulmonary artery catheter (CCI) with emphasis on the accuracy of the FCI in patients with a decreased left ventricular ejection fraction (LVEF) and a low cardiac output status during off-pump coronary bypass surgery (OPCAB). We also assessed the influence of several factors affecting the pulse contour, such as the mean arterial pressure (MAP), the systemic vascular resistance index (SVRI) and the use of norepinephrine. METHODS: Fifty patients who were undergoing OPCAB (30 patients with a LVEF ≥ 40%, 20 patients with a LVEF < 40%) were enrolled. The FCI and CCI were measured and we performed a Bland-Altman analysis. Subgroup analyses were done according to the LVEF (< 40%), the CCI (≤ 2.4 L/min/m), the MAP (60-80 mmHg), the SVRI (1,600-2,600 dyne/s/cm(5)/m(2)) and the use of norepinephrine. RESULTS: The FCI was reliable at all the time points of measurement with an overall bias and limit of agreement of -0.07 and 0.67 L/min/m(2), respectively, resulting in a percentage error of 26.9%. The percentage errors in the patients with a decreased LVEF and in a low cardiac output status were 28.2% and 22.3%, respectively. However, the percentage error in the 91 data pairs outside the normal range of the SVRI was 40.2%. CONCLUSIONS: The cardiac output measured by the FloTrac/Vigileo™ system was reliable even in patients with a decreased LVEF and in a low cardiac output status during OPCAB. Acceptable agreement was also noted during the period of heart displacement and grafting of the obtuse marginalis branch.ope

A genetic screen for modifiers of Drosophila caspase Dcp-1 reveals caspase involvement in autophagy and novel caspase-related genes

BACKGROUND: Caspases are cysteine proteases with essential functions in the apoptotic pathway; their proteolytic activity toward various substrates is associated with the morphological changes of cells. Recent reports have described non-apoptotic functions of caspases, including autophagy. In this report, we searched for novel modifiers of the phenotype of Dcp-1 gain-of-function (GF) animals by screening promoter element- inserted Drosophila melanogaster lines (EP lines). RESULTS: We screened ~15,000 EP lines and identified 72 Dcp-1-interacting genes that were classified into 10 groups based on their functions and pathways: 4 apoptosis signaling genes, 10 autophagy genes, 5 insulin/IGF and TOR signaling pathway genes, 6 MAP kinase and JNK signaling pathway genes, 4 ecdysone signaling genes, 6 ubiquitination genes, 11 various developmental signaling genes, 12 transcription factors, 3 translation factors, and 11 other unclassified genes including 5 functionally undefined genes. Among them, insulin/IGF and TOR signaling pathway, MAP kinase and JNK signaling pathway, and ecdysone signaling are known to be involved in autophagy. Together with the identification of autophagy genes, the results of our screen suggest that autophagy counteracts Dcp-1-induced apoptosis. Consistent with this idea, we show that expression of eGFP-Atg5 rescued the eye phenotype caused by Dcp-1 GF. Paradoxically, we found that over-expression of full-length Dcp-1 induced autophagy, as Atg8b-GFP, an indicator of autophagy, was increased in the eye imaginal discs and in the S2 cell line. Taken together, these data suggest that autophagy suppresses Dcp-1-mediated apoptotic cell death, whereas Dcp-1 positively regulates autophagy, possibly through feedback regulation. CONCLUSIONS: We identified a number of Dcp-1 modifiers that genetically interact with Dcp-1-induced cell death. Our results showing that Dcp-1 and autophagy-related genes influence each other will aid future investigations of the complicated relationships between apoptosis and autophagy