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The Endoscopy Computer Vision Challenge (EndoCV) is a crowd-sourcing initiative to address eminent problems in developing reliable computer aided detection and diagnosis endoscopy systems and suggest a pathway for clinical translation of technologies. Whilst endoscopy is a widely used diagnostic and treatment tool for hollow-organs, there are several core challenges often faced by endoscopists, mainly: 1) presence of multi-class artefacts that hinder their visual interpretation, and 2) difficulty in identifying subtle precancerous precursors and cancer abnormalities. Artefacts often affect the robustness of deep learning methods applied to the gastrointestinal tract organs as they can be confused with tissue of interest. EndoCV2020 challenges are designed to address research questions in these remits. In this paper, we present a summary of methods developed by the top 17 teams and provide an objective comparison of state-of-the-art methods and methods designed by the participants for two sub-challenges: i) artefact detection and segmentation (EAD2020), and ii) disease detection and segmentation (EDD2020). Multi-center, multi-organ, multi-class, and multi-modal clinical endoscopy datasets were compiled for both EAD2020 and EDD2020 sub-challenges. The out-of-sample generalization ability of detection algorithms was also evaluated. Whilst most teams focused on accuracy improvements, only a few methods hold credibility for clinical usability. The best performing teams provided solutions to tackle class imbalance, and variabilities in size, origin, modality and occurrences by exploring data augmentation, data fusion, and optimal class thresholding techniques., 32 pages

Analysis of colonoscopy images plays a significant role in early detection of colorectal cancer. Automated tissue segmentation can be useful for two of the most relevant clinical target applications&mdash, lesion detection and classification, thereby providing important means to make both processes more accurate and robust. To automate video colonoscopy analysis, computer vision and machine learning methods have been utilized and shown to enhance polyp detectability and segmentation objectivity. This paper describes a polyp segmentation algorithm, developed based on fully convolutional network models, that was originally developed for the Endoscopic Vision Gastrointestinal Image Analysis (GIANA) polyp segmentation challenges. The key contribution of the paper is an extended evaluation of the proposed architecture, by comparing it against established image segmentation benchmarks utilizing several metrics with cross-validation on the GIANA training dataset. Different experiments are described, including examination of various network configurations, values of design parameters, data augmentation approaches, and polyp characteristics. The reported results demonstrate the significance of the data augmentation, and careful selection of the method&rsquo, s design parameters. The proposed method delivers state-of-the-art results with near real-time performance. The described solution was instrumental in securing the top spot for the polyp segmentation sub-challenge at the 2017 GIANA challenge and second place for the standard image resolution segmentation task at the 2018 GIANA challenge.

Analyses of polyp images play an important role in an early detection of colorectal cancer. An automated polyp segmentation is seen as one of the methods that could improve the accuracy of the colonoscopic examination. The paper describes evaluation study of a segmentation method developed for the Endoscopic Vision Gastrointestinal Image ANAlysis – (GIANA) polyp segmentation sub-challenges. The proposed polyp segmentation algorithm is based on a fully convolutional network (FCN) model. The paper describes cross-validation results on the training GIANA dataset. Various tests have been evaluated, including network configuration, effects of data augmentation, and performance of the method as a function of polyp characteristics. The proposed method delivers state-of-the-art results. It secured the first place for the image segmentation tasks at the 2017 GIANA challenge and the second place for the SD images at the 2018 GIANA challenge.

The elementary Ca2+ release events, Ca2+ sparks, has been found for a quarter of century. However, the molecular regulation of the spark generator, the ryanodine receptor (RyR) on the sarcoplasmic reticulum, remains obscure. Although each subunit of the RyR homotetramer has a site for FK506-binding protein (FKBP), the role of FKBPs in modifying RyR Ca2+ sparks has been debated for long. One of the reasons behind the controversy is that most previous studies detect spontaneous sparks, where the mixture with out-of-focus events and local wavelets prevents an accurate characterization of Ca2+ sparks. In the present study, we detected Ca2+ sparks triggered by single L-type Ca2+ channels (LCCs) under loose-seal patch clamp conditions in FK506-treated or FKBP12.6 knockout cardiomyocytes. We found that FKBP dissociation both by FK506 and by rapamycin decreased the Ca2+ spark amplitude in ventricular cardiomyocytes. This change was neither due to decreased releasable Ca2+ in the sarcoplasmic reticulum, nor explained by changed RyR sensitivity. Actually FK506 increased the LCC-RyR coupling probability and curtailed the latency for an LCC to trigger a RyR Ca2+ spark. FKBP12.6 knockout had similar effects as FK506/rapamycin treatment, indicating that the decreased spark amplitude was attributable to the dissociation of FKBP12.6 rather than FKBP12. We also explained how decreased amplitude of spontaneous sparks after FKBP dissociation sometimes appears to be increased or unchanged due to inappropriate data processing. Our results provided firm evidence that without the inter-RyR coordination by functional FKBP12.6, the RyR recruitment during a Ca2+ spark would be compromised despite the sensitization of individual RyRs.

Aims β-adrenergic receptors (βARs) play pivotal roles in regulating cardiac excitation–contraction (E-C) coupling. Global signalling of β1ARs up-regulates both the influx of Ca2+ through sarcolemmal L-type Ca2+ channels (LCCs) and the release of Ca2+ from the sarcoplasmic reticulum (SR) through the ryanodine receptors (RyRs). However, we recently found that β2AR stimulation meditates ‘offside compartmentalization’, confining β1AR signalling into subsarcolemmal nanodomains without reaching SR proteins. In the present study, we aim to investigate the new question, whether and how compartmentalized β1AR signalling regulates cardiac E-C coupling. Methods and results By combining confocal Ca2+ imaging and patch-clamp techniques, we investigated the effects of compartmentalized βAR signalling on E-C coupling at both cellular and molecular levels. We found that simultaneous activation of β2 and β1ARs, in contrast to global signalling of β1ARs, modulated neither the amplitude and spatiotemporal properties of Ca2+ sparks nor the kinetics of the RyR response to LCC Ca2+ sparklets. Nevertheless, by up-regulating LCC current, compartmentalized β1AR signalling synchronized RyR Ca2+ release and increased the functional reserve (stability margin) of E-C coupling. In circumstances of briefer excitation durations or lower RyR responsivity, compartmentalized βAR signalling, by increasing the intensity of Ca2+ triggers, helped stabilize the performance of E-C coupling and enhanced the Ca2+ transient amplitude in failing heart cells. Conclusion Given that compartmentalized βAR signalling can be induced by stress-associated levels of catecholamines, our results revealed an important, yet unappreciated, heart regulation mechanism that is autoadaptive to varied stress conditions.

Through analyzing the working principle of the technology of maximum power point tracking in the photovoltaic system, the maximum power tracking circuit is designed. In the hybrid energy storage devices of the super capacitor and battery, the super capacitor is a secondary storage device. Through photovoltaic controller is connected with the photovoltaic cells, photovoltaic cells can achieve the status of the maximum power point tracking. Through the bi-directional DC-DC converting circuit connecting with the battery, the battery can effectively decrease the times of the charging and discharging and works stably. It improves the working efficiency and life of the system.

This paper presents a principle that compensation balance is flexible used in a certain context of the power grid load growth, in order to keep the system voltage stability and system to maximize the economic operation. Some questions are analyzed and demonstrated which.

Based on the comparison of battery energy storage system, super capacitor energy storage system, superconducting storage system, flywheel energy storage system, hybrid energy storage system composed by battery and super capacitor is proposed. By Analysis the performance of the system, it can be know that the system has characteristics of high specific power and high specific energy, and the battery and super capacitor device can be flexibly configured, which make energy storage system performance greatly improved. This template explains and demonstrates how to prepare your camera-ready paper for Trans Tech Publications. The best is to read these instructions and follow the outline of this text.

Colorectal adenocarcinoma originating in intestinal glandular structures is the most common form of colon cancer. In clinical practice, the morphology of intestinal glands, including architectural appearance and glandular formation, is used by pathologists to inform prognosis and plan the treatment of individual patients. However, achieving good inter-observer as well as intra-observer reproducibility of cancer grading is still a major challenge in modern pathology. An automated approach which quantifies the morphology of glands is a solution to the problem. This paper provides an overview to the Gland Segmentation in Colon Histology Images Challenge Contest (GlaS) held at MICCAI’2015. Details of the challenge, including organization, dataset and evaluation criteria, are presented, along with the method descriptions and evaluation results from the top performing methods.

In dividing embryos, a localized elevation in intracellular Ca2+ ([Ca2+]i) at the cleavage furrow has been shown to be essential for cytokinesis. However, the underlying mechanisms for generating and maintaining these [Ca2+]i gradients throughout cytokinesis are not fully understood. In the present study, we analyzed the role of inositol 1,4,5-trisphosphate receptors (IP3Rs) and endoplasmic reticulum (ER) distribution in determining the intracellular Ca2+ gradients in early zebrafish blastomeres. Application of the injected Ca2+ indicator, Indo-1, showed that during the first cell division a standing Ca2+ gradient was formed ∼35 min after fertilization, with the [Ca2+]i spatially decaying from 500–600 nmol/L at the cleavage furrow to 100–200 nmol/L around the nucleus. While the IP3R immunohistochemical fluorescence was relatively concentrated in the peri-furrow region, ER labeling was relatively enriched in both peri-furrow and peri-nuclear regions. Numeric simulation suggested that a divergence in the spatial distribution of IP3R and the locations of Ca2+ uptake within the ER was essential for the formation of a standing Ca2+ gradient, and the Ca2+ gradient could only be well-established under an optimal stoichiometry of Ca2+ uptake and release. Indeed, while inhibition of IP3R Ca2+ release blocked the generation of the Ca2+ gradient at a lower [Ca2+]i level, both Ca2+ release stimulation by inositol 1,4,5-trisphosphate (IP3) injection and ER Ca2+ pump inhibition by cyclopiazonic acid also eliminated the Ca2+ gradients at higher [Ca2+]i levels. Our results suggest a dynamic relationship between ER-mediated Ca2+ release and uptake that underlies the maintenance of the perifurrow Ca2+ gradient and is essential for cytokinesis of zebrafish embryos.

As the most prototypical G protein-coupled receptor, β-adrenergic receptor (βAR) regulates the pace and strength of heart beating by enhancing and synchronizing L-type channel (LCC) Ca 2+ influx, which in turn elicits greater sarcoplasmic reticulum (SR) Ca 2+ release flux via ryanodine receptors (RyRs). However, whether and how βAR-protein kinase A (PKA) signaling directly modulates RyR function remains elusive and highly controversial. By using unique single-channel Ca 2+ imaging technology, we measured the response of a single RyR Ca 2+ release unit, in the form of a Ca 2+ spark, to its native trigger, the Ca 2+ sparklet from a single LCC. We found that acute application of the selective βAR agonist isoproterenol (1 μM, ≤20 min) increased triggered spark amplitude in an LCC unitary current-independent manner. The increased ratio of Ca 2+ release flux underlying a Ca 2+ spark to SR Ca 2+ content indicated that βAR stimulation helps to recruit additional RyRs in synchrony. Quantification of sparklet-spark kinetics showed that βAR stimulation synchronized the stochastic latency and increased the fidelity (i.e., chance of hit) of LCC-RyR intermolecular signaling. The RyR modulation was independent of the increased SR Ca 2+ content. The PKA antagonists Rp-8-CPT-cAMP (100 μM) and H89 (10 μM) both eliminated these effects, indicating that βAR acutely modulates RyR activation via the PKA pathway. These results demonstrate unequivocally that RyR activation by a single LCC is accelerated and synchronized during βAR stimulation. This molecular mechanism of sympathetic regulation will permit more fundamental studies of altered βAR effects in cardiovascular diseases.

Mesenchymal stem cells (MSCs) are multipotential stem cells residing in the bone marrow. Several studies have shown that mechanical stimulation modulates MSC differentiation through mobilization of second messengers, but the mechanism of mechanotransduction remains poorly understood. In this study, using fluorescence and laser confocal microcopy as well as patch-clamp techniques, we identified the transient receptor potential melastatin type 7 (TRPM7) channel as the key channel involved in mechanotransduction in bone marrow MSCs. TRPM7 knockdown completely abolished the pressure-induced cytosolic Ca2+ increase and pressure-induced osteogenesis. TRPM7 directly sensed membrane tension, independent of the cytoplasm and the integrity of cytoskeleton. Ca2+ influx through TRPM7 further triggered Ca2+ release from the inositol trisphosphate receptor type 2 on the endoplasmic reticulum and promoted NFATc1 nuclear localization and osteogenesis. These results identified a central role of TRPM7 in MSC mechanical stimulation-induced osteogenesis. Stem Cells 2015;33:615–621

Rationale: During the transition from compensated hypertrophy to heart failure, the signaling between L-type Ca 2+ channels in the cell membrane/T-tubules and ryanodine receptors in the sarcoplasmic reticulum becomes defective, partially because of the decreased expression of a T-tubule–sarcoplasmic reticulum anchoring protein, junctophilin-2. MicroRNA (miR)-24, a junctophilin-2 suppressing miR, is upregulated in hypertrophied and failing cardiomyocytes. Objective: To test whether miR-24 suppression can protect the structural and functional integrity of L-type Ca 2+ channel–ryanodine receptor signaling in hypertrophied cardiomyocytes. Methods and Results: In vivo silencing of miR-24 by a specific antagomir in an aorta-constricted mouse model effectively prevented the degradation of heart contraction, but not ventricular hypertrophy. Electrophysiology and confocal imaging studies showed that antagomir treatment prevented the decreases in L-type Ca 2+ channel–ryanodine receptor signaling fidelity/efficiency and whole-cell Ca 2+ transients. Further studies showed that antagomir treatment stabilized junctophilin-2 expression and protected the ultrastructure of T-tubule–sarcoplasmic reticulum junctions from disruption. Conclusions: MiR-24 suppression prevented the transition from compensated hypertrophy to decompensated hypertrophy, providing a potential strategy for early treatment against heart failure.

Rationale: Failing cardiomyocytes exhibit decreased efficiency of excitation-contraction (E-C) coupling. The downregulation of junctophilin-2 (JP2), a protein anchoring the sarcoplasmic reticulum to T-tubules, has been identified as a major mechanism underlying the defective E-C coupling. However, the regulatory mechanism of JP2 remains unknown. Objective: To determine whether microRNAs regulate JP2 expression. Methods and Results: Bioinformatic analysis predicted 2 potential binding sites of miR-24 in the 3′-untranslated regions of JP2 mRNA. Luciferase assays confirmed that miR-24 suppressed JP2 expression by binding to either of these sites. In the aortic stenosis model, miR-24 was upregulated in failing cardiomyocytes. Adenovirus-directed overexpression of miR-24 in cardiomyocytes decreased JP2 expression and reduced Ca 2+ transient amplitude and E-C coupling gain. Conclusions: MiR-24–mediated suppression of JP2 expression provides a novel molecular mechanism for E-C coupling regulation in heart cells and suggests a new target against heart failure.

To design a platform for microarray data analysis and processing in the browser/server mode running in Linux operating system.Based on the Apache HTTP server, the platform, programmed with Perl language, integrated R language and Bioconductor packages for processing and analysis of the input data of oligonucleotide arrays and two-color spotted arrays. Users were allowed to submit data and parameter configurations to the platform via the web page, and the results of analysis were also returned via the web page.With an easy operation and high performance, the platform fulfilled the functions of processing, quality assessment, biological annotation and statistical analysis of the data from oligonucleotide arrays and two-color spotted arrays. Using the platform, we analyzed the gene expression profiles in Mtb-stimulated macrophages of three clinical phenotypes, namely latent TB (LTB), pulmonary (PTB) and meningeal (TBM), and obtained valuable clues for identifying tuberculosis susceptibility genes. We also analyzed the effect of INH treatment on Mycobacterium tuberculosis gene expression in various dormancy models, such as hypoxia and KatG mutant, and found that a set of genes responded to INH treatment during exponential growth but not in dormancy, and that the overall number of differentially regulated genes was reduced in the cells in low metabolic state.The platform we have constructed integrates comprehensive resources, and with a user-friendly interface, allows direct result visualization to facilitate microarray data analysis.

To design a versatile genome comparison and visualization platform based on browser/server mode supported by a local server.The server of the platform was Apache HTTP server. Perl was used to integrate such genome alignment package and algorithms as MUMmer, LAGAN, and Mauve for different comparison purposes, and the users could submit data and parameters to the platform via the web page. The results of analysis were also returned via the web page.The platform could handle multiple data input formats, compare complete and draft genome sequence, alignment pair-wise or multi genome of more divergent species, identify regions of high similarity, locate local nucleotide mutations and large-scale recombination, and display the results by visualization interface. Analysis of the homology of 10 new strains of influenza A virus indicated that PB1 gene might evolve from human H3N2 viruses, PB2 and PA genes from avian H3N2 viruses, and HA and NS genes from swine H1N1 viruses. Alignment of Mycobacterium tuberculosis (H37Rv, CDC1551) and Mycobacterium bovis (AF2122/97) genomes revealed that sequence insertion/deletion and duplication were the major source of genomic differences.The platform integrate comprehensive resources with a user-friendly interface and intuitive result visualization to facilitate conventional study of comparative genomics.

To establish a method by high-performance liquid chromatography (HPLC) for determining the concentration of magnetic mitomycin C-polybutylcyanoacrylate nanoparticles in mouse plasma.Chromatography was performed on a LiChroCART C18 (250 mm x 4 mm, 5 microm) column with the mobile phase consisting of acetonitrile-NaAC (15:85), the flow rate of 1.0 ml/min, and the detection wavelength of 365 nm. Sample extraction was carried out with ethylacetate.The linear range of mouse plasma mitomycin C concentration was 0.04-1.00 microg/ml, and the linear equation of Y=16 388X-17.17 (r=0.999 8) was derived.This method is very easy to operate and suits the need of perclinical pharmacokinetic studies of mitomycin-magnetic nanoparticles and yields accurate and precise results.