846 research outputs found
Principal Components of Short-term Variability in Venus' UV Albedo
We explore the dominant modes of variability in the observed albedo at the
cloud tops of Venus using the Akatsuki UVI 283-nm and 365-nm observations,
which are sensitive to SO2 and unknown UV absorber distributions respectively,
over the period Dec 2016 to May 2018. The observations consist of images of the
dayside of Venus, most often observed at intervals of 2 hours, but interspersed
with longer gaps. The orbit of the spacecraft does not allow for continuous
observation of the full dayside, and the unobserved regions cause significant
gaps in the datasets. Each dataset is subdivided into three subsets for three
observing periods, the unobserved data are interpolated and each subset is then
subjected to a principal component analysis (PCA) to find six oscillating
patterns in the albedo. Principal components in all three periods show similar
morphologies at 283-nm but are much more variable at 365-nm. Some spatial
patterns and the time scales of these modes correspond to well known physical
processes in the atmosphere of Venus such as the ~4 day Kelvin wave, 5 day
Rossby waves and the overturning circulation, while others defy a simple
explanation. We also a find a hemispheric mode that is not well understood and
discuss its implications.Comment: 9 pages, 6 figures, accepted in A&
Coherent transfer of light polarization to electron spins in a semiconductor
We demonstrate that the superposition of light polarization states is
coherently transferred to electron spins in a semiconductor quantum well. By
using time-resolved Kerr rotation we observe the initial phase of Larmor
precession of electron spins whose coherence is transferred from light. To
break the electron-hole spin entanglement, we utilized the big discrepancy
between the transverse g-factors of electrons and light holes. The result
encourages us to make a quantum media converter between flying photon qubits
and stationary electron spin qubits in semiconductors.Comment: 4 pages. Submitted to Physical Review Letter
Induction of Autophagy by Amino Acid Starvation in Fish Cells
Autophagy is well established as a starvation-induced process in yeast and mammalian cells and tissues. To elucidate the cellular mechanisms induced by starvation in fish, we characterized the induction of autophagy in cultured zebrafish cells under starvation conditions. As an autophagic marker protein, the microtubule-associated protein 1-light chain 3B protein (MAP1-LC3B) was cloned from the fish cells, and its expression and localization were characterized. In zebrafish embryonic (ZE) cells, posttranslational modifications produced two distinct forms of MAP1-LC3B, i.e., a cytosolic form and a membrane-bound form (types I and II, respectively). Immunofluorescence microscopy revealed fluorescently labeled autophagosomes in cells stably transfected with a green fluorescent protein (GFP)–MAP1-LC3B fusion protein and showed that this protein accumulated in punctate dots in a time-dependent manner in response to amino acid starvation. Starvation also induced the degradation of long-lived proteins. Treatment with 3-methyladenine and wortmannin, two class-III inhibitors of phosphoinositide 3-kinase (PI3K), repressed autophagy under starvation conditions, indicating that the PI3K class-III pathway regulates starvation-induced autophagy in fish
Tissue Intrinsic Fluorescence Spectra-Based Digital Pathology of Liver Fibrosis by Marker-Controlled Segmentation
Tissue intrinsic emission fluorescence provides useful diagnostic information for various diseases. Because of its unique feature of spectral profiles depending on tissue types, spectroscopic imaging is a promising tool for accurate evaluation of endogenous fluorophores. However, due to difficulties in discriminating those sources, quantitative analysis remains challenging. In this study, we quantitatively investigated spectral-spatial features of multi-photon excitation fluorescence in normal and diseased livers. For morphometrics of multi-photon excitation spectra, we examined a marker-controlled segmentation approach and its application to liver fibrosis assessment by employing a mouse model of carbon tetrachloride (CCl4)-induced liver fibrosis. We formulated a procedure of internal marker selection where markers were chosen to reflect typical biochemical species in the liver, followed by image segmentation and local morphological feature extraction. Image segmentation enabled us to apply mathematical morphology analysis, and the local feature was applied to the automated classification test based on a machine learning framework, both demonstrating highly accurate classifications. Through the analyses, we showed that spectral imaging of native fluorescence from liver tissues have the capability of differentiating not only between normal and diseased, but also between progressive disease states. The proposed approach provides the basics of spectroscopy-based digital histopathology of chronic liver diseases, and can be applied to a range of diseases associated with autofluorescence alterations
SVMによる頑健なピアノ演奏の音高推定
平成21年度研究報告会、統計数理研究所(広尾)、H22.3.18-19ポスター発
The N domain of Smad7 is essential for specific inhibition of transforming growth factor-β signaling
Inhibitory Smads (I-Smads) repress signaling by cytokines of the transforming growth factor-β (TGF-β) superfamily. I-Smads have conserved carboxy-terminal Mad homology 2 (MH2) domains, whereas the amino acid sequences of their amino-terminal regions (N domains) are highly divergent from those of other Smads. Of the two different I-Smads in mammals, Smad7 inhibited signaling by both TGF-β and bone morphogenetic proteins (BMPs), whereas Smad6 was less effective in inhibiting TGF-β signaling. Analyses using deletion mutants and chimeras of Smad6 and Smad7 revealed that the MH2 domains were responsible for the inhibition of both TGF-β and BMP signaling by I-Smads, but the isolated MH2 domains of Smad6 and Smad7 were less potent than the full-length Smad7 in inhibiting TGF-β signaling. The N domains of I-Smads determined the subcellular localization of these molecules. Chimeras containing the N domain of Smad7 interacted with the TGF-β type I receptor (TβR-I) more efficiently, and were more potent in repressing TGF-β signaling, than those containing the N domain of Smad6. The isolated N domain of Smad7 physically interacted with the MH2 domain of Smad7, and enhanced the inhibitory activity of the latter through facilitating interaction with TGF-β receptors. The N domain of Smad7 thus plays an important role in the specific inhibition of TGF-β signaling
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