Determination of Abnormality of IGBT Images Using VGG16

A power device is a semiconductor device for power control used for power conversion such as converting direct current to alternating current and alternating current to direct current. It is widely used such as refrigerators, air conditioners which is implemented electronic components that are closely related to our daily lives. Therefore, high reliability and safety are required, and power cycle tests are conducted for the purpose of evaluating them. In the conventional test, there is a problem that it is difficult to perform analysis because sparks are generated during the test and the device is severely damaged after the test. To solve this problem, a new technology has been developed that adds ultrasonic that enable internal observation during the test. However, there are remains a problem that the method for analyzing the ultrasonic image obtained in the new technology has not been established. Also, few abnormal images are obtained in the test. In this paper, we propose a method for detection of abnormal devices based on CNN. Especially, we implement a Cycle-GAN to extend the abnormal data and classify the known image based on improved VGG16. As an experimental result, classification accuracy of Precision = 97.06%, Recall = 93.58%, F - measure = 95.17% were obtained.21th International Conference on Control, Automation and Systems, ICCAS 2021, October 12-15, 2021, Jeju, Korea and onlin

U-survival for prognostic prediction of disease progression and mortality of patients with COVID-19

The rapid increase of patients with coronavirus disease 2019 (COVID-19) has introduced major challenges to healthcare services worldwide. Therefore, fast and accurate clinical assessment of COVID-19 progression and mortality is vital for the management of COVID-19 patients. We developed an automated image-based survival prediction model, called U-survival, which combines deep learning of chest CT images with the established survival analysis methodology of an elastic-net Cox survival model. In an evaluation of 383 COVID-19 positive patients from two hospitals, the prognostic bootstrap prediction performance of U-survival was significantly higher (P < 0.0001) than those of existing laboratory and image-based reference predictors both for COVID-19 progression (maximum concordance index: 91.6% [95% confidence interval 91.5, 91.7]) and for mortality (88.7% [88.6, 88.9]), and the separation between the Kaplan–Meier survival curves of patients stratified into low- and high-risk groups was largest for U-survival (P < 3 × 10–14). The results indicate that U-survival can be used to provide automated and objective prognostic predictions for the management of COVID-19 patients

Weakly unsupervised conditional generative adversarial network for image-based prognostic prediction for COVID-19 patients based on chest CT

Because of the rapid spread and wide range of the clinical manifestations of the coronavirus disease 2019 (COVID-19), fast and accurate estimation of the disease progression and mortality is vital for the management of the patients. Currently available image-based prognostic predictors for patients with COVID-19 are largely limited to semi-automated schemes with manually designed features and supervised learning, and the survival analysis is largely limited to logistic regression. We developed a weakly unsupervised conditional generative adversarial network, called pix2surv, which can be trained to estimate the time-to-event information for survival analysis directly from the chest computed tomography (CT) images of a patient. We show that the performance of pix2surv based on CT images significantly outperforms those of existing laboratory tests and image-based visual and quantitative predictors in estimating the disease progression and mortality of COVID-19 patients. Thus, pix2surv is a promising approach for performing image-based prognostic predictions

Effects of verapamil and propranolol on early afterdepolarizations and ventricular arrhythmias induced by epinephrine in congenital long QT syndrome

Objectives.This study used monophasic action potentials to investigate the effects of verapamil and propranolol on epinephrineinduced repolarization abnormalities in congenital long QT syndrome.Background.Early afterdepolarizations have been suggested to play a significant role in QT prolongation and ventricular arrhythmias in congenital long QT syndrome. Calcium channel blocking as well as beta-adrenergic blocking agents are reported to be effective in the management of this syndrome.Methods.Monophasic action potentials from 2 to 4 sites were recorded simultaneously in eight patients with the long QT syndrome (22 sites) and in eight control patients (23 sites) and were obtained during constant atrial pacing 1) before epinephrine infusion; 2) during epinephrine infusion (0.1 μg/kg body weight min); 3) after verapamil injection (0.1 mg/kg) during epinephrine infusion; and 4) after both propranolol (0.1 mg/kg) and verapamil injections.Results.Early afterdepolarizations were recorded in two of the eight patients (2 of 22 sites) during the control state. During epinephrine infusion, early afterdepolarizations were recorded in six patients (six sites), and ventricular premature complexes were induced in three and torsade de pointes in one. Epinephrine prolonged 90% monophasic action potential duration from 348 ± 48 (mean ± SD) to 381 ± 49 ms (22 sites, p < 0.0005) and increased the dispersion of action potential duration (difference between the longest and shortest action potential duration) from 36 ± 20 to 64 ± 34 ms (p < 0.005). Verapamil eliminated (two sites) or reduced (four sites) early afterdepolarizations and abolished ventricular premature complexes in two of the three patients as well as suppressing torsade de pointes. Verapamil shortened the action potential duration to 355 ± 28 ms (p < 0.01 vs. epinephrine) and decreased the dispersion to 44 ± 19 ms (p < 0.05 vs. epinephrine). Propranolol further eliminated (two sites) or reduced (two sites) early afterdepolarizations, abolished ventricular premature complexes in the remaining one patient and further shortened the action potential duration to 337 ± 32 ms (p = 0.09 vs. verapamil). In the control patients, none of the early afterdepolarizations, ventricular arrhythmias or marked prolongations of action potential duration were induced by epinephrine, and neither verapamil nor propranolol changed repolarization variables.Conclusions.These results indicate that both verapamil and propranolol can improve repolarization abnormalities induced by epinephrine in congenital long QT syndrome

Copper Transport Protein Antioxidant-1 Promotes Inflammatory Neovascularization via Chaperone and Transcription Factor Function

Supplementary information accompanies this paper at http://www.nature.com/srepCopper (Cu), an essential micronutrient, plays a fundamental role in inflammation and angiogenesis; however, its precise mechanism remains undefined. Here we uncover a novel role of Cu transport protein Antioxidant-1 (Atox1), which is originally appreciated as a Cu chaperone and recently discovered as a Cu-dependent transcription factor, in inflammatory neovascularization. Atox1 expression is upregulated in patients and mice with critical limb ischemia. Atox1-deficient mice show impaired limb perfusion recovery with reduced arteriogenesis, angiogenesis, and recruitment of inflammatory cells. In vivo intravital microscopy, bone marrow reconstitution, and Atox1 gene transfer in Atox1(-/-) mice show that Atox1 in endothelial cells (ECs) is essential for neovascularization and recruitment of inflammatory cells which release VEGF and TNFα. Mechanistically, Atox1-depleted ECs demonstrate that Cu chaperone function of Atox1 mediated through Cu transporter ATP7A is required for VEGF-induced angiogenesis via activation of Cu enzyme lysyl oxidase. Moreover, Atox1 functions as a Cu-dependent transcription factor for NADPH oxidase organizer p47phox, thereby increasing ROS-NFκB-VCAM-1/ICAM-1 expression and monocyte adhesion in ECs inflamed with TNFα in an ATP7A-independent manner. These findings demonstrate a novel linkage between Atox1 and NADPH oxidase involved in inflammatory neovascularization and suggest Atox1 as a potential therapeutic target for treatment of ischemic disease.SS is a British Heart Foundation (BHF) PhD student; GDA is BHF Chair in cardiac surgery and NIHR Senior Investigator; CE is a BHF Senior Research Fellow. Sources of Funding: This research was supported by NIH R01 HL070187 (T.F.), Department of Veterans Affairs Merit Review grant 1I01BX001232 (T.F.), R01HL116976 (T.F., M.U.-F.), NIH R01 HL077524 and HL077524-S1, R21HL112293 (to M.U.-F.), Ruth L. Kirschstein-National Service Research Award (Kirschstein-NRSA) T32 Training Grant (to G-F.C.), AHA Post-doctoral Fellowship 09POST2250151 (to N.U.), and 11POST5740006 (to V.S.).Peer-reviewedPublisher Versio

The whole blood transcriptional regulation landscape in 465 COVID-19 infected samples from Japan COVID-19 Task Force

「コロナ制圧タスクフォース」COVID-19患者由来の血液細胞における遺伝子発現の網羅的解析 --重症度に応じた遺伝子発現の変化には、ヒトゲノム配列の個人差が影響する--. 京都大学プレスリリース. 2022-08-23.Coronavirus disease 2019 (COVID-19) is a recently-emerged infectious disease that has caused millions of deaths, where comprehensive understanding of disease mechanisms is still unestablished. In particular, studies of gene expression dynamics and regulation landscape in COVID-19 infected individuals are limited. Here, we report on a thorough analysis of whole blood RNA-seq data from 465 genotyped samples from the Japan COVID-19 Task Force, including 359 severe and 106 non-severe COVID-19 cases. We discover 1169 putative causal expression quantitative trait loci (eQTLs) including 34 possible colocalizations with biobank fine-mapping results of hematopoietic traits in a Japanese population, 1549 putative causal splice QTLs (sQTLs; e.g. two independent sQTLs at TOR1AIP1), as well as biologically interpretable trans-eQTL examples (e.g., REST and STING1), all fine-mapped at single variant resolution. We perform differential gene expression analysis to elucidate 198 genes with increased expression in severe COVID-19 cases and enriched for innate immune-related functions. Finally, we evaluate the limited but non-zero effect of COVID-19 phenotype on eQTL discovery, and highlight the presence of COVID-19 severity-interaction eQTLs (ieQTLs; e.g., CLEC4C and MYBL2). Our study provides a comprehensive catalog of whole blood regulatory variants in Japanese, as well as a reference for transcriptional landscapes in response to COVID-19 infection

DOCK2 is involved in the host genetics and biology of severe COVID-19

「コロナ制圧タスクフォース」COVID-19疾患感受性遺伝子DOCK2の重症化機序を解明 --アジア最大のバイオレポジトリーでCOVID-19の治療標的を発見--. 京都大学プレスリリース. 2022-08-10.Identifying the host genetic factors underlying severe COVID-19 is an emerging challenge. Here we conducted a genome-wide association study (GWAS) involving 2, 393 cases of COVID-19 in a cohort of Japanese individuals collected during the initial waves of the pandemic, with 3, 289 unaffected controls. We identified a variant on chromosome 5 at 5q35 (rs60200309-A), close to the dedicator of cytokinesis 2 gene (DOCK2), which was associated with severe COVID-19 in patients less than 65 years of age. This risk allele was prevalent in East Asian individuals but rare in Europeans, highlighting the value of genome-wide association studies in non-European populations. RNA-sequencing analysis of 473 bulk peripheral blood samples identified decreased expression of DOCK2 associated with the risk allele in these younger patients. DOCK2 expression was suppressed in patients with severe cases of COVID-19. Single-cell RNA-sequencing analysis (n = 61 individuals) identified cell-type-specific downregulation of DOCK2 and a COVID-19-specific decreasing effect of the risk allele on DOCK2 expression in non-classical monocytes. Immunohistochemistry of lung specimens from patients with severe COVID-19 pneumonia showed suppressed DOCK2 expression. Moreover, inhibition of DOCK2 function with CPYPP increased the severity of pneumonia in a Syrian hamster model of SARS-CoV-2 infection, characterized by weight loss, lung oedema, enhanced viral loads, impaired macrophage recruitment and dysregulated type I interferon responses. We conclude that DOCK2 has an important role in the host immune response to SARS-CoV-2 infection and the development of severe COVID-19, and could be further explored as a potential biomarker and/or therapeutic target