Boosting for Bounding the Worst-class Error

This paper tackles the problem of the worst-class error rate, instead of the standard error rate averaged over all classes. For example, a three-class classification task with class-wise error rates of 10\%, 10\%, and 40\% has a worst-class error rate of 40\%, whereas the average is 20\% under the class-balanced condition. The worst-class error is important in many applications. For example, in a medical image classification task, it would not be acceptable for the malignant tumor class to have a 40\% error rate, while the benign and healthy classes have 10\% error rates.We propose a boosting algorithm that guarantees an upper bound of the worst-class training error and derive its generalization bound. Experimental results show that the algorithm lowers worst-class test error rates while avoiding overfitting to the training set

Midkine antisense oligodeoxyribonucleotide inhibits renal damage induced by ischemic reperfusion

Midkine antisense oligodeoxyribonucleotide inhibits renal damage induced by ischemic reperfusion.BackgroundMidkine, a heparin-binding growth factor, is involved in the migration of inflammatory cells. The inflammatory cell migration to the tubulointerstitium of the kidney after ischemia/reperfusion (I/R) injury is attenuated in midkine gene–deficient mice, resulting in better preservation of the tubulointerstitium compared with wild-type mice. In the present investigation, we planned to evaluate the usefulness of antisense midkine for the therapy of ischemic renal failure.MethodsMidkine antisense phosphorothioate oligodeoxyribonucleotide (ODN) at a dose of 1 mg/kg in saline was intravenously administered to mice 1 day before or after I/R. The kidneys were removed for examination 1, 2, 3, and 7 days after I/R.ResultsIt was rapidly incorporated into proximal tubular epithelial cells, and inhibited midkine synthesis, leading to reduced migration of inflammatory cells to the injured epithelial layer. Consequently, the midkine antisense ODN-treated animals exhibited less severe renal damage than untreated or midkine sense ODN-treated animals 2 days after I/R as assessed by morphologic criteria and blood urea nitrogen (BUN) and serum creatinine levels. Midkine expression, BUN, and serum creatinine levels were not significantly different between injection of midkine antisense ODN before and after ischemic injury.ConclusionThese results indicate that intravenous injection of midkine antisense ODN is a candidate for a novel therapeutic strategy against acute tubulointerstitial injury induced by I/R injury

Role of CD59 in experimental glomerulonephritis in rats

Role of CD59 in experimental glomerulonephritis in rats. CD59 is a molecule which is present on the host cell membranes and inhibits formation of membrane attack complex. A monoclonal antibody, 6D1, recognizes a rat analogue of human CD59. 6D1 inhibits function of rat CD59 and can enhance complement-mediated hemolysis in vitro. To assess the role of CD59 in complement-mediated glomerular injury, 6D1 was tested in a model of experimental glomerulonephritis induced by a lectin and its antibodies. The left kidney of a rat was perfused either with 200 µg of Lens culinaris hemoagglutinin (LCH) plus 1mg of 6D1 (IgGl fraction) (Group I and III) or with LCH only (Group II) through a cannula placed in the left renal artery. All the perfusate was discarded from a cannula in the renal vein. The holes in the artery and vein were repaired by microsurgery and the blood circulation was re-established. Rats were injected either with 0.125ml of rabbit anti-LCH serum (Group I and II), or with normal rabbit serum (Group III) via tail vein one minute after the recirculation. Fifteen minutes after injection, significant C9 deposition in the glomeruli was observed only in Group I, whereas C3 deposition in Group I and II were comparable. At Day 4, total glomerular cells, proliferating cells, glomerular expression of intercellular adhesion molecule-1 and fibrin deposition in Group I were all significantly increased when compared with Group II. At Day 7, number of total glomerular cells and leukocytes in the glomeruli of Group I were significantly higher than in Group II. The glomeruli in Group III appeared normal throughout experiments. These data indicate that the functional inhibition of a rat analogue of human CD59 worsens complement-mediated glomerular injury in vivo

Deep Attentive Time Warping

Similarity measures for time series are important problems for time series classification. To handle the nonlinear time distortions, Dynamic Time Warping (DTW) has been widely used. However, DTW is not learnable and suffers from a trade-off between robustness against time distortion and discriminative power. In this paper, we propose a neural network model for task-adaptive time warping. Specifically, we use the attention model, called the bipartite attention model, to develop an explicit time warping mechanism with greater distortion invariance. Unlike other learnable models using DTW for warping, our model predicts all local correspondences between two time series and is trained based on metric learning, which enables it to learn the optimal data-dependent warping for the target task. We also propose to induce pre-training of our model by DTW to improve the discriminative power. Extensive experiments demonstrate the superior effectiveness of our model over DTW and its state-of-the-art performance in online signature verification.Comment: Accepted at Pattern Recognitio

Fish mesonephric model of polycystic kidney disease in medaka (Oryzias latipes) pc mutant

Fish mesonephric model of polycystic kidney disease in medaka (Oryzias latipes) pc mutant.BackgroundPolycystic kidney disease (PKD) is a common hereditary disease. A number of murine and zebrafish mutants have been generated and used for the study of PKD as metanephric and pronephric models, respectively. Here, we report a medaka (Oryzias latipes) mutant that develops numerous cysts in the kidney in adulthood fish in an autosomal-recessive manner as a mesonephric model of PKD.MethodsThe phenotypes of the medaka pc mutant were described in terms of morphologic, histologic, and ultrastructural features. The pc see-through stock was produced by crossing a pc mutant and a fish from the see-through stock and used for observing the kidney through the transparent body wall of a live fish.ResultsThe mutant developed bilateral massive enlargement of the kidney in adulthood. They sexually matured normally within 2 months of age and died within 6 months of age. The affected kidney was occupied by numerous, fluid-filled cysts, which were lined by attenuated squamous epithelial cells. Developmentally, cystic formation began in the pronephros in 10-day-old fry and in the mesonephros in 20-day-old fry at the microscopic level. The pc see-through stock was useful in observing disease progression in live fish.ConclusionThe kidney disorder that develops in the medaka pc mutant is a mesonephric counterpart of PKD, particularly an autosomal-dominant PKD, based on its morphologic, histologic, and ultrastructural features, and slow progression

In-situ Observation of Fracture Behavior on Nano Structure in NITE SiC/SiC Composite by HVEM

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CD59 protects rat kidney from complement mediated injury in collaboration with Crry

CD59 protects rat kidney from complement mediated injury in collaboration with Crry.BackgroundAs previously reported, the membrane-bound complement regulator at the C3 level (Crry/p65) is important in maintaining normal integrity of the kidney in rats. However, the role of a complement regulator at the C8/9 level (CD59) is not clear, especially when activation of complement occurs at the C3 level. The aim of this work was to elucidate the in vivo role of CD59 under C3 activating conditions.MethodsTwo monoclonal antibodies, 5I2 and 6D1, were used to suppress the function of Crry and CD59, respectively. In order to activate alternative the pathway of complement, the left kidney was perfused with 5I2 and/or 6D1 and was recirculated.ResultsIn the kidneys perfused with 5I2 alone, deposition of C3 and membrane attack complex (MAC) was observed in the peritubular capillaries, vasa recta, and tubular basement membranes. Cast formation, tubular dilation and degeneration, and cellular infiltration were observed at days 1 and 4, and they recovered by day 7. Further suppression of CD59 by 6D1 significantly enhanced the deposition of MAC and worsened the already exacerbated tubulointerstitial injury. These effects of 6D1 were dose dependent. Perfusion with 6D1 alone did not induce histologic damage or MAC deposition in the tubulointerstitium.ConclusionsIn rats, CD59 maintains normal integrity of the kidney in collaboration with Crry in rats against complement-mediated damage in vivo

Magnetic Flux Signal Simulation with 16-channel Sensor Array to Specify Accurate IGBT Current Distribution

Current crowding of IGBT and power diodes in a chip or among chips is a barrier to the realization of highlyreliable power modules and power electronics systems. Current crowding occurs because of stray inductance imbalance, difference of chip characteristics and temperature imbalance among chips. Although current crowding among IGBT or power diode chips has been analyzed by numerical simulation, no sensor with sufficiently high special resolution and fast measurement time has yet been developed. Therefore, we developed a 16-channel sensor array and demonstrated IGBT current distribution imaging. By using the developed simulation method for the sensor array, the accuracy of the magnetic flux signals was confirmed. In future work, we will apply the simulation method to specify the IGBT current distribution corresponding to the structure of bonding wire and other wiring.CIPS 2016 International Conference on Integrated Power Electronics Systems, Mar 8-10, 2016, Nuremberg, German

Differential expression of syndecan isoforms during mouse incisor amelogenesis

Syndecans are transmembranous heparan sulfate proteoglycans (HSPGs) with covalently attached glycosaminoglycan side-chains located on the cell surface. The mammalian syndecan family is composed of four types of syndecans (syndecan-1 to -4). Syndecans interact with the intracellular cytoskeleton through the cytoplasmic domains of their core proteins and membrane proteins, extracellular enzymes, growth factors, and matrix components, through their heparan-sulfate chains, to regulate developmental processes. Here, as a first step to assess the possible roles of syndecan proteins in amelogenesis, we examined the expression patterns of all syndecan isoforms in continuously growing mouse incisors, in which we can overview major differentiation stages of amelogenesis at a glance. Understanding the expression domain of each syndecan isoform during specific developmental stages seems useful for investigating their physiological roles in amelogenesis. Immunohistochemical analysis of syndecan core proteins in the lower incisors from postnatal day 1 mice revealed spatially and temporally specific expression patterns, with syndecan-1 expressed in undifferentiated epithelial and mesenchymal cells, and syndecan-2, -3, and -4 in more differentiated cells. These findings suggest that each syndecan isoform functions distinctly during the amelogenesis of the incisors of mice