832 research outputs found
Wide-Area Mapping of 155 Micron Continuum Emission from the Orion Molecular Cloud Complex
We present the results of a wide-area mapping of the far-infrared continuum
emission toward the Orion complex by using a Japanese balloon-borne telescope.
The 155-um continuum emission was detected over a region of 1.5 deg^2 around
the KL nebula with 3' resolution similar to that of the IRAS 100-um map.
Assuming a single-temperature model of the thermal equilibrium dust, maps of
the temperature and the optical depth were derived from the 155 um intensity
and the IRAS 100 um intensity. The derived dust temperature is 5 - 15 K lower
and the derived dust optical thickness were derived from the 155-um intensity
and the IRAS 100-um intensity. The derived dust temperature is 5 - 15 K lower
and the derived dust optical depth is 5 - 300 times larger than those derived
from the IRAS 60 and 100-um intensities due to the significant contribution of
the statistically heated very small grains to the IRAS 60-um intensity. The
optical-thickness distribution shows a filamentary dust ridge that has a 1.5
degrees extent in the north - south direction and well resembles the
Integral-Shaped Filament (ISF) molecular gas distribution. The gas-to-dust
ratio derived from the CO molecular gas distribution along the ISF is in the
range 30 - 200, which may be interpreted as being an effect of CO depletion due
to the photodissociation and/or the freezing on dust grains.Comment: 23 pages, 7 figures, 1 table, to appear in PASJ, Vol. 56, No.
Low-frequency noise assessment of work function engineering cap layers in high-k gate stacks
Engineering the effective work function of scaled-down devices is commonly achieved by the implementation of capping layers in the gate stack. Typical cap layers are Al2O3 for pMOSFETs and La-oxide or Mg for nMOSFETs. Besides introducing a dipole layer at the SiO2/high-κ interface, the in-diffusion of the metal ions may lead to either passivation or generation of traps in the SiO2/high-κ layer. This paper uses low frequency noise studies to determine the impact of capping layers on the quality of the SiO2/HfO2 gate stacks. The influence on the trap profiles of different types of cap layers, different locations of the cap layer (below or on top of the HfO2 dielectric) and the impact of different thermal budgets, typically used for the fabrication of Dynamic Random Access Memory (DRAM) logic devices, are investigated. The differences between several metal oxides are outlined and discussed
[Phe4]somatostatin: a potent, selective inhibitor of growth hormone release.
[Phe4]Somatostatin was twice as active as somatostatin (SS) in suppressing rat growth hormone release in vitro but had only weak activity toward inhibition of insulin and glucagon release in vivo. The ability of this analogue to inhibit growth hormone release more actively than SS was confirmed in vivo by two separately designed bioassays. Further structure/activity studies of position 4 were carried out with [Glu4]SS, [Thr4]SS, and des-Lys4-SS, all of which had negligible inhibiting activity in the pituitary and pancreas. In this context the strikingly selective activity of [Phe4]SS suggests a fundamental difference in the SS receptors of pituitary and pancreas and the normal side-chain basicity of position 4 appears to be more important for action in pancreas than in pituitary. [Phe4]SS has properties that may be useful in the development of agents for the treatment of acromegaly or other disorders associated with increased growth hormone levels
Beyond Hypergraph Dualization
International audienceThis problem concerns hypergraph dualization and generalization to poset dualization. A hypergraph H = (V, E) consists of a finite collection E of sets over a finite set V , i.e. E ⊆ P(V) (the powerset of V). The elements of E are called hyperedges, or simply edges. A hypergraph is said simple if none of its edges is contained within another. A transversal (or hitting set) of H is a set T ⊆ V that intersects every edge of E. A transversal is minimal if it does not contain any other transversal as a subset. The set of all minimal transversal of H is denoted by T r(H). The hypergraph (V, T r(H)) is called the transversal hypergraph of H. Given a simple hypergraph H, the hypergraph dualization problem (Trans-Enum for short) concerns the enumeration without repetitions of T r(H). The Trans-Enum problem can also be formulated as a dualization problem in posets. Let (P, ≤) be a poset (i.e. ≤ is a reflexive, antisymmetric, and transitive relation on the set P). For A ⊆ P , ↓ A (resp. ↑ A) is the downward (resp. upward) closure of A under the relation ≤ (i.e. ↓ A is an ideal and ↑ A a filter of (P, ≤)). Two antichains (B + , B −) of P are said to be dual if ↓ B + ∪ ↑ B − = P and ↓ B + ∩ ↑ B − = ∅. Given an implicit description of a poset P and an antichain B + (resp. B −) of P , the poset dualization problem (Dual-Enum for short) enumerates the set B − (resp. B +), denoted by Dual(B +) = B − (resp. Dual(B −) = B +). Notice that the function dual is self-dual or idempotent, i.e. Dual(Dual(B)) = B
Herbivore-induced terpenoid emission in Medicago truncatula: concerted action of jasmonate, ethylene and calcium signaling
Plant volatiles emitted by Medicago truncatula in response to feeding larvae of Spodoptera exigua are composed of a complex blend of terpenoids. The cDNAs of three terpene synthases (TPSs), which contribute to the blend of terpenoids, were cloned from M. truncatula. Their functional characterization proved MtTPS1 to be a β-caryophyllene synthase and MtTPS5 to be a multi-product sesquiterpene synthase. MtTPS3 encodes a bifunctional enzyme producing (E)-nerolidol and geranyllinalool (precursors of C11 and C16 homoterpenes) from different prenyl diphosphates serving as substrates. The addition of jasmonic acid (JA) induced expression of the TPS genes, but terpenoid emission was higher from plants treated with JA and the ethylene precursor 1-amino-cyclopropyl-1-carboxylic acid. Compared to infested wild-type M. truncatula plants, lower amounts of various sesquiterpenes and a C11–homoterpene were released from an ethylene-insensitive mutant skl. This difference coincided with lower transcript levels of MtTPS5 and of 1-deoxy-d-xylulose-5-phosphate synthase (MtDXS2) in the damaged skl leaves. Moreover, ethephon, an ethylene-releasing compound, modified the extent and mode of the herbivore-stimulated Ca2+ variations in the cytoplasm that is necessary for both JA and terpene biosynthesis. Thus, ethylene contributes to the herbivory-induced terpenoid biosynthesis at least twice: by modulating both early signaling events such as cytoplasmic Ca2+-influx and the downstream JA-dependent biosynthesis of terpenoids
The effect of dexamethasone on defective nephrin transport caused by ER stress: A potential mechanism for the therapeutic action of glucocorticoids in the acquired glomerular diseases
The mechanism by which glucocorticoids govern antiproteinuric effect in nephrotic syndrome remains unknown. Present study examined the protective role of dexamethasone (DEX) in the intracellular trafficking of nephrin under endoplasmic reticulum (ER) stress. Human embryonic kidney-293 cell line expressing a full-length human nephrin was cultured in mediums containing 5.5 or 25 mM glucose with or without DEX. The result revealed that glucose starvation evoked a rapid ER stress leading to formation of underglycosylated nephrin that was remained in the ER as a complex with calreticulin/calnexin. DEX rescued this interfered trafficking through binding to its receptor and stimulating the mitochondrial transcripts and adenosine 5′ triphosphate (ATP) production, leading to synthesis of fully glycosylated nephrin. These results suggest that ER-stress in podocytes may cause alteration of nephrin N-glycosylation, which may be an underlying factor in the pathomechanism of the proteinuria in nephrotic syndrome. DEX may restore this imbalance by stimulating expression of mitochondrial genes, resulted in the production of ATP that is essential factor for proper folding machinery aided by the ER chaperones
ANKRD1, the gene encoding cardiac ankyrin repeat protein, is a novel dilated cardiomyopathy gene.
OBJECTIVES: We evaluated ankyrin repeat domain 1 (ANKRD1), the gene encoding cardiac ankyrin repeat protein (CARP), as a novel candidate gene for dilated cardiomyopathy (DCM) through mutation analysis of a cohort of familial or idiopathic DCM patients, based on the hypothesis that inherited dysfunction of mechanical stretch-based signaling is present in a subset of DCM patients.
BACKGROUND: CARP, a transcription coinhibitor, is a member of the titin-N2A mechanosensory complex and translocates to the nucleus in response to stretch. It is up-regulated in cardiac failure and hypertrophy and represses expression of sarcomeric proteins. Its overexpression results in contractile dysfunction.
METHODS: In all, 208 DCM patients were screened for mutations/variants in the coding region of ANKRD1 using polymerase chain reaction, denaturing high-performance liquid chromatography, and direct deoxyribonucleic acid sequencing. In vitro functional analyses of the mutation were performed using yeast 2-hybrid assays and investigating the effect on stretch-mediated gene expression in myoblastoid cell lines using quantitative real-time reverse transcription-polymerase chain reaction.
RESULTS: Three missense heterozygous ANKRD1 mutations (P105S, V107L, and M184I) were identified in 4 DCM patients. The M184I mutation results in loss of CARP binding with Talin 1 and FHL2, and the P105S mutation in loss of Talin 1 binding. Intracellular localization of mutant CARP proteins is not altered. The mutations result in differential stretch-induced gene expression compared with wild-type CARP.
CONCLUSIONS: ANKRD1 is a novel DCM gene, with mutations present in 1.9% of DCM patients. The ANKRD1 mutations may cause DCM as a result of disruption of the normal cardiac stretch-based signaling
Performance Evaluation of Radiologists with Artificial Neural Network for Differential Diagnosis of Intra-Axial Cerebral Tumors on MR Images
Uterine selection of human embryos at implantation
Human embryos frequently harbor large-scale complex chromosomal errors that impede normal development. Affected embryos may fail to implant although many first breach the endometrial epithelium and embed in the decidualizing stroma before being rejected via mechanisms that are poorly understood. Here we show that developmentally impaired human embryos elicit an endoplasmic stress response in human decidual cells. A stress response was also evident upon in vivo exposure of mouse uteri to culture medium conditioned by low-quality human embryos. By contrast, signals emanating from developmentally competent embryos activated a focused gene network enriched in metabolic enzymes and implantation factors. We further show that trypsin, a serine protease released by pre-implantation embryos, elicits Ca2+ signaling in endometrial epithelial cells. Competent human embryos triggered short-lived oscillatory Ca2+ fluxes whereas low-quality embryos caused a heightened and prolonged Ca2+ response. Thus, distinct positive and negative mechanisms contribute to active selection of human embryos at implantation
Genetics of Mechanosensation in the Heart
Mechanosensation (the ultimate conversion of a mechanical stimulus into a biochemical signal) as well as mechanotransduction (transmission of mechanically induced signals) belong to the most fundamental processes in biology. These effects, because of their dynamic nature, are particularly important for the cardiovascular system. Therefore, it is not surprising that defects in cardiac mechanosensation, are associated with various types of cardiomyopathy and heart failure. However, our current knowledge regarding the genetic basis of impaired mechanosensation in the cardiovascular system is beginning to shed light on this subject and is at the centre of this brief review
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