162 research outputs found

    Pseudo Trained YOLO R_CNN Model for Weapon Detection with a Real-Time Kaggle Dataset

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    The Recurrent Convolutional Neural Networks (RCNN) based deep learning models has been classified image patterns and deep features through layer architecture. In this world every country doesn’t encouraging violence, so that indirectly nations prohibiting usages of weapons to common people. This study proposes a novel YoLo Faster R-CNN based weapon detection algorithm for unusual weapon object detection. The proposed YoLo V3 R-CNN computer vision application can rapidly find weapons carried by people and highlighted through bounding-box-intimation. The work plan of this research is divided into two stages, at 1st stage pre-processing has been called to Faster R-CNN segmentation. The 2nd stage has been training the dataset as well as extracting 8-features (image_id, detection score, pixels-intensity, resolution, Aspect-ratio, PSNR, CC, SSIM) into .csv file. The labeling can be performed to RCNN-YoLo method such that getting real-time objects detection (Unusual things). The Confusion matrix has been generating performance measures in terms of accuracy 97.12%, SSIM 0.99, sensitivity 97.23%, and throughput 94.23% had been attained which are outperformance methodology

    Pseudo Trained YOLO R_CNN Model for Weapon Detection with a Real-Time Kaggle Dataset

    Get PDF
    The Recurrent Convolutional Neural Networks (RCNN) based deep learning models has been classified image patterns and deep features through layer architecture. In this world every country doesn’t encouraging violence, so that indirectly nations prohibiting usages of weapons to common people. This study proposes a novel YoLo Faster R-CNN based weapon detection algorithm for unusual weapon object detection. The proposed YoLo V3 R-CNN computer vision application can rapidly find weapons carried by people and highlighted through bounding-box-intimation. The work plan of this research is divided into two stages, at 1st stage pre-processing has been called to Faster R-CNN segmentation. The 2nd stage has been training the dataset as well as extracting 8-features (image_id, detection score, pixels-intensity, resolution, Aspect-ratio, PSNR, CC, SSIM) into .csv file. The labeling can be performed to RCNN-YoLo method such that getting real-time objects detection (Unusual things). The Confusion matrix has been generating performance measures in terms of accuracy 97.12%, SSIM 0.99, sensitivity 97.23%, and throughput 94.23% had been attained which are outperformance methodology

    Investigation of Fatigue Crack Initiation and Growth in Cast MAR-M247 Subjected to Low Cycle Fatigue at Room Temperature

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    MC carbide particles (with Hafnium and/or Tantalum as constituent metallic element, M) were observed to crack extensively in a cast polycrystalline nickel-base superalloy, MAR-M247, when subjected to low-cycle fatigue loading at room temperature. High resolution secondary electron images taken on the surface of a double edge notch test specimen revealed that approximately half the carbide particles cracked in the highly-strained notch section of the specimen. These images further illustrated that the average surface area of cracked particles was approximately three times that of the uncracked particles. Additional analysis illustrated that the cracks within a large number of particles aligned nearly perpendicular to the loading direction. However, high aspect ratio particles (with aspect ratio >3) were prone to incubate cracks aligned along its major axis, independent of the loading direction. Additionally, forward-scattered imaging often showed a high density of slip bands interaction with most of the particles which cracked. The life limiting crack growth in MAR-M247 was observed to be crystallographic in nature, as the crack grew along slip bands as measured by high-resolution electron backscatter diffraction, even after spanning many grains. Statistically representative microstructure models of MAR-M247 were generated and used in the crystal plasticity finite element simulations. As expected, there was a significant variation in the computed stress state among constituent carbide particles. The stress state of the carbide particles was found to be heavily influenced by the stress in surrounding grains and the orientation of the major axis of the particles with respect to applied load direction. For particles that intersect the free-surface, stress was found to be highly concentrated at the free surface and a positive correlation between the magnitude of free-surface area and the maximum principal stress was found. Additionally, high stress concentrations were observed in regions where carbide particles intersect grain boundaries

    Angiotensin II stimulates superoxide production by nitric oxide synthase in thick ascending limbs

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    Angiotensin II (Ang II) causes nitric oxide synthase (NOS) to become a source of superoxide (O2 (-)) via a protein kinase C (PKC)-dependent process in endothelial cells. Ang II stimulates both NO and O2 (-) production in thick ascending limbs. We hypothesized that Ang II causes O2 (-) production by NOS in thick ascending limbs via a PKC-dependent mechanism. NO production was measured in isolated rat thick ascending limbs using DAF-FM, whereas O2 (-) was measured in thick ascending limb suspensions using the lucigenin assay. Consistent stimulation of NO was observed with 1 nmol/L Ang II (P \u3c 0.001; n = 9). This concentration of Ang II-stimulated O2 (-) production by 50% (1.77 ± 0.26 vs. 2.62 ± 0.36 relative lights units (RLU)/s/μg protein; P \u3c 0.04; n = 5). In the presence of the NOS inhibitor L-NAME, Ang II-stimulated O2 (-) decreased from 2.02 ± 0.29 to 1.10 ± 0.11 RLU/s/μg protein (P \u3c 0.01; n = 8). L-arginine alone did not change Ang II-stimulated O2 (-) (2.34 ± 0.22 vs. 2.29 ± 0.29 RLU/s/μg protein; n = 5). In the presence of Ang II plus the PKC α/β1 inhibitor Gö 6976, L-NAME had no effect on O2 (-) production (0.78 ± 0.23 vs. 0.62 ± 0.11 RLU/s/μg protein; n = 7). In the presence of Ang II plus apocynin, a NADPH oxidase inhibitor, L-NAME did not change O2 (-) (0.59 ± 0.04 vs. 0.61 ± ×0.08 RLU/s/μg protein; n = 5). We conclude that: (1) Ang II causes NOS to produce O2 (-) in thick ascending limbs via a PKC- and NADPH oxidase-dependent process; and (2) the effect of Ang II is not due to limited substrate

    GaAs on Si epitaxy by aspect ratio trapping: analysis and reduction of defects propagating along the trench direction

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    The Aspect Ratio Trapping technique has been extensively evaluated for improving the quality of III-V heteroepitaxial films grown on Si, due to the potential for terminating defects at the sidewalls of SiO2 patterned trenches that enclose the growth region. However, defects propagating along the trench direction cannot be effectively confined with this technique. We studied the effect of the trench bottom geometry on the density of defects of GaAs fins, grown by metal-organic chemical vapor deposition on 300 mm Si (001) wafers inside narrow (<90 nm wide) trenches. Plan view and cross sectional Scanning Electron Microscopy and Transmission Electron Microscopy, together with High Resolution X-Ray Diffraction, were used to evaluate the crystal quality of GaAs. The prevalent defects that reach the top surface of GaAs fins are {111} twin planes propagating along the trench direction. The lowest density of twin planes, 8 108 cm 2, was achieved on “V” shaped bottom trenches, where GaAs nucleation occurs only on {111} Si planes, minimizing the interfacial energy and preventing the formation of antiphase boundaries

    The autoimmune disease-associated SNP rs917997 of IL18RAP controls IFNγ production by PBMC

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    AbstractType 1 Diabetes (T1D) is an autoimmune disorder characterized by aberrant T cell responses. Innate immune activation defects may facilitate a T helper 1 (Th1) phenotype. The cytokine IL-18 synergizes with IL-12 to induce IFNγ production and Th1 differentiation. The IL-18R subunit (IL18RAP) SNP rs917997 has been linked to decreased IL18RAP gene expression. Prior reports link rs917997 allele A with protection from T1D, and conversely with susceptibility to Celiac disease. However, few studies have investigated the IL-18 pathway in T1D. In this study, we analyzed responsiveness to IL-18 in T1D, and the effect of rs917997 genotype on IL18RAP gene expression post-activation. Upon IL-12 and IL-18 treatment, peripheral blood mononuclear cells from subjects carrying susceptibility alleles at rs917997 produced higher levels of IFNγ than those with protective genotypes. Additionally, the SNP modified IL18RAP surface protein expression by NK cells and gene expression in activated T cells. Taken together, these data suggest that the disease-associated rs917997 allele G permits hyperresponsiveness to IL-18, providing a novel target for therapeutic intervention in T1D

    Characterization of Titanium Alloys Produced by Electron Beam Directed Energy Deposition

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    Functionally graded materials offer the potential to improve structural efficiency by allowing the material composition and/or microstructural features to spatially vary within a component. Additive manufacturing techniques enable the fabrication of such graded materials and structures. While examining several titanium alloys, this paper focuses on Ti-8Al-1Er as it has a unique microstructure that is only feasible when produced by rapid solidification methods like electron beam directed energy deposition, an additive manufacturing process. The results show that, when mixed, Ti-8Al-1Er and commercially-pure titanium uniformly mix at various ratios and the resultant static tensile properties of the mixed alloys behave according to rule-of-mixtures. At discontinuous interfaces between Ti-8Al-1Er and commercially-pure titanium, the crack growth behavior progresses smoothly across the discontinuity as the crack transitions from one crack growth regime into another. Studies on monolithic samples shows the mechanisms of damage in the Ti-8Al-1Er; specifically, that strain localization occurs near grain boundaries of high mis-orientation on the microscale and that twinning and dislocation density is concentrated near erbia-strengthening particles (Er2O3) on the nanoscale

    Interplay between IL-10, IFN-γ, IL-17A and PD-1 Expressing EBNA1-Specific CD4+ and CD8+ T Cell Responses in the Etiologic Pathway to Endemic Burkitt Lymphoma

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    Children diagnosed with endemic Burkitt lymphoma (eBL) are deficient in interferon-γ (IFN-γ) responses to Epstein–Barr Nuclear Antigen1 (EBNA1), the viral protein that defines the latency I pattern in this B cell tumor. However, the contributions of immune-regulatory cytokines and phenotypes of the EBNA1-specific T cells have not been characterized for eBL. Using a bespoke flow cytometry assay we measured intracellular IFN-γ, IL-10, IL-17A expression and phenotyped CD4+ and CD8+ T cell effector memory subsets specific to EBNA1 for eBL patients compared to two groups of healthy children with divergent malaria exposures. In response to EBNA1 and a malaria antigen (PfSEA-1A), the three study groups exhibited strikingly different cytokine expression and T cell memory profiles. EBNA1-specific IFN-γ-producing CD4+ T cell response rates were lowest in eBL (40%) compared to children with high malaria (84%) and low malaria (66%) exposures (p < 0.0001 and p = 0.0004, respectively). However, eBL patients did not differ in CD8+ T cell response rates or the magnitude of IFN-γ expression. In contrast, eBL children were more likely to have EBNA1-specific CD4+ T cells expressing IL-10, and less likely to have polyfunctional IFN-γ+IL-10+ CD4+ T cells (p = 0.02). They were also more likely to have IFN-γ+IL-17A+, IFN-γ+ and IL-17A+ CD8+ T cell subsets compared to healthy children. Cytokine-producing T cell subsets were predominantly CD45RA+CCR7+ TNAIVE-LIKE cells, yet PD-1, a marker of persistent activation/exhaustion, was more highly expressed by the central memory (TCM) and effector memory (TEM) T cell subsets. In summary, our study suggests that IL-10 mediated immune regulation and depletion of IFN-γ+ EBNA1-specific CD4+ T cells are complementary mechanisms that contribute to impaired T cell cytotoxicity in eBL pathogenesis

    Essential versus accessory aspects of cell death: recommendations of the NCCD 2015

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    Cells exposed to extreme physicochemical or mechanical stimuli die in an uncontrollable manner, as a result of their immediate structural breakdown. Such an unavoidable variant of cellular demise is generally referred to as ‘accidental cell death’ (ACD). In most settings, however, cell death is initiated by a genetically encoded apparatus, correlating with the fact that its course can be altered by pharmacologic or genetic interventions. ‘Regulated cell death’ (RCD) can occur as part of physiologic programs or can be activated once adaptive responses to perturbations of the extracellular or intracellular microenvironment fail. The biochemical phenomena that accompany RCD may be harnessed to classify it into a few subtypes, which often (but not always) exhibit stereotyped morphologic features. Nonetheless, efficiently inhibiting the processes that are commonly thought to cause RCD, such as the activation of executioner caspases in the course of apoptosis, does not exert true cytoprotective effects in the mammalian system, but simply alters the kinetics of cellular demise as it shifts its morphologic and biochemical correlates. Conversely, bona fide cytoprotection can be achieved by inhibiting the transduction of lethal signals in the early phases of the process, when adaptive responses are still operational. Thus, the mechanisms that truly execute RCD may be less understood, less inhibitable and perhaps more homogeneous than previously thought. Here, the Nomenclature Committee on Cell Death formulates a set of recommendations to help scientists and researchers to discriminate between essential and accessory aspects of cell death

    Expression of Bcl-2 and Bax in Mouse Renal Tubules during Kidney Development

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    Bcl-2 and Bax play an important role in apoptosis regulation, as well as in cell adhesion and migration during kidney morphogenesis, which is structurally and functionally related to mitochondria. In order to elucidate the role of Bcl-2 and Bax during kidney development, it is essential to establish the exact location of their expression in the kidney. The present study localized their expression during kidney development. Kidneys from embryonic (E) 16-, 17-, 18-day-old mouse fetuses, and postnatal (P) 1-, 3-, 5-, 7-, 14-, 21-day-old pups were embedded in Epon. Semi-thin serial sections from two E17 kidneys underwent computer assisted 3D tubule tracing. The tracing was combined with a newly developed immunohistochemical technique, which enables immunohistochemistry on glutaraldehyde fixated plastic embedded sections. Thereby, the microstructure could be described in detail, and the immunochemistry can be performed using exactly the same sections. The study showed that Bcl-2 and Bax were strongly expressed in mature proximal convoluted tubules at all time points, less strongly expressed in proximal straight tubules, and only weakly in immature proximal tubules and distal tubules. No expression was detected in ureteric bud and other earlier developing structures, such as comma bodies, S shaped bodies, glomeruli, etc. Tubules expressing Bcl-2 only were occasionally observed. The present study showed that, during kidney development, Bcl-2 and Bax are expressed differently in the proximal and distal tubules, although these two tubule segments are almost equally equipped with mitochondria. The functional significance of the different expression of Bcl-2 and Bax in proximal and distal tubules is unknown. However, the findings of the present study suggest that the mitochondrial function differs between mature proximal tubules and in the rest of the tubules. The function of Bcl-2 and Bax during tubulogenesis still needs to be investigated
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