Ladder Siamese Network: a Method and Insights for Multi-level Self-Supervised Learning

Siamese-network-based self-supervised learning (SSL) suffers from slow convergence and instability in training. To alleviate this, we propose a framework to exploit intermediate self-supervisions in each stage of deep nets, called the Ladder Siamese Network. Our self-supervised losses encourage the intermediate layers to be consistent with different data augmentations to single samples, which facilitates training progress and enhances the discriminative ability of the intermediate layers themselves. While some existing work has already utilized multi-level self supervisions in SSL, ours is different in that 1) we reveal its usefulness with non-contrastive Siamese frameworks in both theoretical and empirical viewpoints, and 2) ours improves image-level classification, instance-level detection, and pixel-level segmentation simultaneously. Experiments show that the proposed framework can improve BYOL baselines by 1.0% points in ImageNet linear classification, 1.2% points in COCO detection, and 3.1% points in PASCAL VOC segmentation. In comparison with the state-of-the-art methods, our Ladder-based model achieves competitive and balanced performances in all tested benchmarks without causing large degradation in one

Pulmonary Manifestations of Plasma Cell Type Idiopathic Multicentric Castleman Disease: A Clinicopathological Study in Comparison with IgG4-Related Disease

Plasma cell type idiopathic multicentric Castleman disease (PC-iMCD) occasionally manifests as parenchymal lung disease. This study aimed to elucidate the detailed clinicopathological features of lung lesions in PC-iMCD and compare the findings with those in immunoglobulin (Ig) G4-related disease (IgG4-RD), the most difficult differential diagnosis of PC-iMCD. We analyzed the clinicopathological findings and immunohistochemical expression patterns of interleukin-6 (IL-6) and Igs in lung specimens from 16 patients with PC-iMCD and 7 patients with IgG4-RD. Histologically, pulmonary PC-iMCD could not be differentiated from IgG4-RD based on lesion distribution patterns, the number of lymphoid follicles and obliterative vasculitis, or fibrosis types. The eosinophil count was higher in the IgG4-RD group than in the PC-iMCD group (p = 0.004). The IgG4/IgG-positive cell ratio was significantly higher in the IgG4-RD group (p < 0.001). The IgA-positive cell count and IL-6 expression intensity were higher in the PC-iMCD group than in the IgG4-RD group (p < 0.001). Based on these findings, we proposed a new diagnostic approach to differentiate lung lesions of PC-iMCD and IgG4-RD. Our approach can be utilized to stratify patients with suspected lung-dominant PC-iMCD to identify candidates for strong immunosuppressive treatment, including IL-6 blockade, at an early stage

Cortical Factor Feedback Model for Cellular Locomotion and Cytofission

Eukaryotic cells can move spontaneously without being guided by external cues. For such spontaneous movements, a variety of different modes have been observed, including the amoeboid-like locomotion with protrusion of multiple pseudopods, the keratocyte-like locomotion with a widely spread lamellipodium, cell division with two daughter cells crawling in opposite directions, and fragmentations of a cell to multiple pieces. Mutagenesis studies have revealed that cells exhibit these modes depending on which genes are deficient, suggesting that seemingly different modes are the manifestation of a common mechanism to regulate cell motion. In this paper, we propose a hypothesis that the positive feedback mechanism working through the inhomogeneous distribution of regulatory proteins underlies this variety of cell locomotion and cytofission. In this hypothesis, a set of regulatory proteins, which we call cortical factors, suppress actin polymerization. These suppressing factors are diluted at the extending front and accumulated at the retracting rear of cell, which establishes a cellular polarity and enhances the cell motility, leading to the further accumulation of cortical factors at the rear. Stochastic simulation of cell movement shows that the positive feedback mechanism of cortical factors stabilizes or destabilizes modes of movement and determines the cell migration pattern. The model predicts that the pattern is selected by changing the rate of formation of the actin-filament network or the threshold to initiate the network formation

Twisted Superspace on a Lattice

We propose a new formulation which realizes exact twisted supersymmetry for all the supercharges on a lattice by twisted superspace formalism. We show explicit examples of N=2 twisted supersymmetry invariant BF and Wess-Zumino models in two dimensions. We introduce mild lattice noncommutativity to preserve Leibniz rule on the lattice. The formulation is based on the twisted superspace formalism for N=D=2 supersymmetry which was proposed recently. From the consistency condition of the noncommutativity of superspace, we find an unexpected three-dimensional lattice structure which may reduce into two dimensional lattice where the superspace describes semilocally scattered fermions and bosons within a double size square lattice.Comment: 49 pages, 17 figures; v2: Fig.2 is replace

Feasibility of in vivo measurement of carotid wall shear rate using spiral Fourier velocity encoded MRI

Arterial wall shear stress is widely believed to influence the formation and growth of atherosclerotic plaque; however, there is currently no gold standard for its in vivo measurement. The use of phase contrast MRI has proved to be challenging due to partial-volume effects and inadequate signal-to-noise ratio at the high spatial resolutions that are required. This work evaluates the use of spiral Fourier velocity encoded MRI as a rapid method for assessing wall shear rate in the carotid arteries. Wall shear rate is calculated from velocity histograms in voxels spanning the blood/vessel wall interface, using a method developed by Frayne and Rutt (Magn Reson Med 1995;34:378–387). This study (i) demonstrates the accuracy of the velocity histograms measured by spiral Fourier velocity encoding in a pulsatile carotid flow phantom compared with high-resolution two-dimensional Fourier transform phase contrast, (ii) demonstrates the accuracy of Fourier velocity encoding–based shear rate measurements in a numerical phantom designed using a computational fluid dynamics simulation of carotid flow, and (iii) demonstrates in vivo measurement of regional wall shear rate and oscillatory shear index in the carotid arteries of healthy volunteers at 3 T. Magn Reson Med 63:1537–1547, 2010. © 2010 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/75777/1/22325_ftp.pd

Structure of 136Sn and the Z = 50 magicity

The first 2+ excited state in the neutron-rich tin isotope 136Sn has been identified at 682(13) keV by measuring γ -rays in coincidence with the one proton removal channel from 137Sb. This value is higher than those known for heavier even-even N = 86 isotones, indicating the Z = 50 shell closure. It compares well to the first 2+ excited state of the lighter tin isotope 134Sn, which may suggest that the seniority scheme also holds for 136Sn. Our result confirms the trend of lower 2+ excitation energies of even-even tin isotopes beyond N = 82 compared to the known values in between the two doubly magic nuclei 100Sn and 132Sn. © The Author(s) 2014.published_or_final_versio

Conformational changes in quadruplex oligonucleotide structures probed by Raman spectroscopy

Quadruplex structures are higher order structures formed by guanine-rich oligonucleotides. In the present study, temperature-induced conformational changes in the quadruplex structures of aptamers and other guanine-rich oligonucleotides are probed by Raman spectroscopy. In particular, dramatic changes in the fingerprint region are observed in the spectra of thrombin binding aptamer at higher temperatures. These changes are accompanied by a decrease in the intensity of the 1480 cm−1 peak (attributed to C8 = N7-H2), which is diagnostic of the quadruplex structure. We also show that these changes can be reversed (to a certain extent) by addition of K+ ions

Arrangements of human telomere DNA quadruplex in physiologically relevant K+ solutions

The arrangement of the human telomeric quadruplex in physiologically relevant conditions has not yet been unambiguously determined. Our spectroscopic results suggest that the core quadruplex sequence G3(TTAG3)3 forms an antiparallel quadruplex of the same basket type in solution containing either K+ or Na+ ions. Analogous sequences extended by flanking nucleotides form a mixture of the antiparallel and hybrid (3 + 1) quadruplexes in K+-containing solutions. We, however, show that long telomeric DNA behaves in the same way as the basic G3(TTAG3)3 motif. Both G3(TTAG3)3 and long telomeric DNA are also able to adopt the (3 + 1) quadruplex structure: Molecular crowding conditions, simulated here by ethanol, induced a slow transition of the K+-stabilized quadruplex into the hybrid quadruplex structure and then into a parallel quadruplex arrangement at increased temperatures. Most importantly, we demonstrate that the same transitions can be induced even in aqueous, K+-containing solution by increasing the DNA concentration. This is why distinct quadruplex structures were detected for AG3(TTAG3)3 by X-ray, nuclear magnetic resonance and circular dichrosim spectroscopy: Depending on DNA concentration, the human telomeric DNA can adopt the antiparallel quadruplex, the (3 + 1) structure, or the parallel quadruplex in physiologically relevant concentrations of K+ ions

Identification of ChIP-seq mapped targets of HP1β due to bombesin/GRP receptor activation

Epithelial cells lining the adult colon do not normally express gastrin-releasing peptide (GRP) or its receptor (GRPR). In contrast, GRP/GRPR can be aberrantly expressed in human colorectal cancer (CRC) including Caco-2 cells. We have previously shown that GRPR activation results in the up-regulation of HP1β, an epigenetic modifier of gene transcription. The aim of this study was to identify the genes whose expression is altered by HP1β subsequent to GRPR activation. We determined HP1β binding positions throughout the genome using chromatin immunoprecipitation followed by massively parallel DNA sequencing (ChIP-seq). After exposure to GRP, we identified 9,625 genomic positions occupied by HP1β. We performed gene microarray analysis on Caco-2 cells in the absence and presence of a GRPR specific antagonist as well as siRNA to HP1β. The expression of 97 genes was altered subsequent to GRPR antagonism, while the expression of 473 genes was altered by HP1β siRNA exposure. When these data were evaluated in concert with our ChIP-seq findings, 9 genes showed evidence of possible altered expression as a function of GRPR signaling via HP1β. Of these, genomic PCR of immunoprecipitated chromatin demonstrated that GRPR signaling affected the expression of IL1RAPL2, FAM13A, GBE1, PLK3, and SLCO1B3. These findings provide the first evidence by which GRPR aberrantly expressed in CRC might affect tumor progression