Information Geometry of Wasserstein Statistics on Shapes and Affine Deformations

Information geometry and Wasserstein geometry are two main structures introduced in a manifold of probability distributions, and they capture its different characteristics. We study characteristics of Wasserstein geometry in the framework of Li and Zhao (2023) for the affine deformation statistical model, which is a multi-dimensional generalization of the location-scale model. We compare merits and demerits of estimators based on information geometry and Wasserstein geometry. The shape of a probability distribution and its affine deformation are separated in the Wasserstein geometry, showing its robustness against the waveform perturbation in exchange for the loss in Fisher efficiency. We show that the Wasserstein estimator is the moment estimator in the case of the elliptically symmetric affine deformation model. It coincides with the information-geometrical estimator (maximum-likelihood estimator) when and only when the waveform is Gaussian. The role of the Wasserstein efficiency is elucidated in terms of robustness against waveform change

High glucose-induced apoptosis in human coronary artery endothelial cells involves up-regulation of death receptors

<p>Abstract</p> <p>Background</p> <p>High glucose can induce apoptosis in vascular endothelial cells, which may contribute to the development of vascular complications in diabetes. We evaluated the role of the death receptor pathway of apoptotic signaling in high glucose-induced apoptosis in human coronary artery endothelial cells (HCAECs).</p> <p>Methods</p> <p>HCAECs were treated with media containing 5.6, 11.1, and 16.7 mM of glucose for 24 h in the presence or absence of tumor necrosis factor (TNF)-α. For detection of apoptosis, DNA fragmentation assay was used. HCAEC expression of death receptors were analyzed by the PCR and flow cytometry methods. Also, using immunohistochemical techniques, coronary expression of death receptors was assessed in streptozotocin-nicotinamide-induced type 2 diabetic mice.</p> <p>Results</p> <p>Exposure of HCAECs to high glucose resulted in a significant increase in TNF-R1 and Fas expression, compared with normal glucose. High glucose increased TNF-α production by HCAECs and exogenous TNF-α up-regulated TNF-R1 and Fas expression in HCAECs. High glucose-induced up-regulation of TNF-R1 and Fas expression was undetectable in the presence of TNF-α. Treatment with TNF-R1 neutralizing peptides significantly inhibited high glucose-induced endothelial cell apoptosis. Type 2 diabetic mice displayed appreciable expression of TNF-R1 and Fas in coronary vessels.</p> <p>Conclusions</p> <p>In association with increased TNF-α levels, the death receptors, TNF-R1 and Fas, are up-regulated in HCAECs under high glucose conditions, which could in turn play a role in high glucose-induced endothelial cell apoptosis.</p

Required and received SNRs in coded modulation

Coded modulation techniques aim at reducing the required signal-to-noise ratio (SNR) over the Gaussian channel with an average energy constraint; however, such techniques tend to degrade the received SNR. We studied the balance of required and received SNRs for a realistic system design

A novel interplay between the Fanconi anemia core complex and ATR-ATRIP kinase during DNA cross-link repair.

When DNA replication is stalled at sites of DNA damage, a cascade of responses is activated in the cell to halt cell cycle progression and promote DNA repair. A pathway initiated by the kinase Ataxia teleangiectasia and Rad3 related (ATR) and its partner ATR interacting protein (ATRIP) plays an important role in this response. The Fanconi anemia (FA) pathway is also activated following genomic stress, and defects in this pathway cause a cancer-prone hematologic disorder in humans. Little is known about how these two pathways are coordinated. We report here that following cellular exposure to DNA cross-linking damage, the FA core complex enhances binding and localization of ATRIP within damaged chromatin. In cells lacking the core complex, ATR-mediated phosphorylation of two functional response targets, ATRIP and FANCI, is defective. We also provide evidence that the canonical ATR activation pathway involving RAD17 and TOPBP1 is largely dispensable for the FA pathway activation. Indeed DT40 mutant cells lacking both RAD17 and FANCD2 were synergistically more sensitive to cisplatin compared with either single mutant. Collectively, these data reveal new aspects of the interplay between regulation of ATR-ATRIP kinase and activation of the FA pathway

SXDF-ALMA 2 Arcmin^2 Deep Survey: Resolving and Characterizing the Infrared Extragalactic Background Light Down to 0.5 mJy

We present a multi-wavelength analysis of five submillimeter sources (S_1.1mm = 0.54-2.02 mJy) that were detected during our 1.1-mm-deep continuum survey in the SXDF-UDS-CANDELS field (2 arcmin^2, 1sigma = 0.055 mJy beam^-1) using the Atacama Large Millimeter/submillimeter Array (ALMA). The two brightest sources correspond to a known single-dish (AzTEC) selected bright submillimeter galaxy (SMG), whereas the remaining three are faint SMGs newly uncovered by ALMA. If we exclude the two brightest sources, the contribution of the ALMA-detected faint SMGs to the infrared extragalactic background light is estimated to be ~ 4.1^{+5.4}_{-3.0} Jy deg^{-2}, which corresponds to ~ 16^{+22}_{-12}% of the infrared extragalactic background light. This suggests that their contribution to the infrared extragalactic background light is as large as that of bright SMGs. We identified multi-wavelength counterparts of the five ALMA sources. One of the sources (SXDF-ALMA3) is extremely faint in the optical to near-infrared region despite its infrared luminosity (L_IR ~ 1e12 L_sun or SFR ~ 100 M_sun yr^{-1}). By fitting the spectral energy distributions (SEDs) at the optical-to-near-infrared wavelengths of the remaining four ALMA sources, we obtained the photometric redshifts (z_photo) and stellar masses (M_*): z_photo ~ 1.3-2.5, M_* ~ (3.5-9.5)e10 M_sun. We also derived their star formation rates (SFRs) and specific SFRs (sSFRs) as ~ 30-200 M_sun yr^{-1} and ~ 0.8-2 Gyr^{-1}, respectively. These values imply that they are main-sequence star-forming galaxies.Comment: PASJ accepted, 15 pages, 6 figures, 2 table