303 research outputs found

    Detecting and Counting Small Animal Species Using Drone Imagery by Applying Deep Learning

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    This work represents deep learning approach for detecting lizards on the summer grass background. It is the main part of general use case formulation—“how many animals are located now on this substitute habitat. Determine in which parts they prefer to stay”. For this purpose, the U-Net architecture neural network was implemented. Dilated convolution layer was added to usual U-Net. Smoothly blending filter was applied to result probability patches for connecting them in one big probability map without sewed edges. Designed flexible architecture allows to train neural network for pixel-wise semantic segmentation with accuracy value 0.9863 on the tiny dataset

    Expression of the platelet-activating factor receptor enhances benzyl isothiocyanate-induced apoptosis in murine and human melanoma cells

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    Melanoma cells often express platelet‑activating factor receptor (PAF‑R), which has been demonstrated to increase metastatic behavior. However, the effect of PAF‑R on the responsiveness of melanoma to naturally occurring cytotoxic agents remains to be elucidated. The present study aimed to determine the relative cytotoxicity and mechanism of benzyl isothiocyanate (BITC), a component of cruciferous vegetables, in melanoma cells expressing PAF‑R. To evaluate the importance of PAF‑R signaling in melanoma cell growth, PAF‑R‑negative murine B16F10 cells were transduced with a retrovirus containing the cDNA for PAF‑R to generate cells stably expressing PAF‑R (B16‑PAF‑R) or an empty vector (MSCV) to generate PAF‑R‑deficient B16‑MSCV control cells. Activation of PAF‑R, using the PAF‑R agonist, 1‑hexadecyl‑2‑N‑methylcarbamoyl‑3‑glycerophosphocholine, induced an increase in the proliferation of B16‑PAF‑R cells compared with the B16‑MSCV cells. Reverse transcription quantitative polymerase chain reaction revealed the presence of functional PAF‑R in human melanoma SK23MEL cells, but not in SK5MEL cells. The present study investigated the effect of BITC treatments on the survival of murine and human melanoma cells, in the presence or absence of functional PAF‑R. The results revealed that treatment with BITC decreased the survival rate of the PAF‑R‑positive and negative murine and human melanoma cells. However, the expression of PAF‑R substantially augmented BITC‑mediated cytotoxicity in the PAF‑R‑positive cells at lower concentrations compared with the PAF‑R‑negative cells. In order to determine the underlying mechanism, flow cytometric analysis was used, which demonstrated a significant increase in the generation of reactive oxygen species (ROS) in the B16‑PAF‑R cells compared with the B16‑MSCV cells, which enhanced apoptosis by BITC, as measured by increased caspase‑3/7 luminescence. Notably, the BITC‑mediated decreased cell survival rate, increased ROS and increased apoptosis in the B16‑PAF‑R cells were significantly attenuated by the antioxidant, vitamin C, indicating ROS involvement. Additionally, the WEB2086 PAF‑R antagonist, inhibited the BITC‑mediated enhancement of apoptosis in the B16‑PAF‑R cells, indicating a role for PAF‑R‑signaling in the BITC‑mediated effects. These findings indicated that the selectivity of BITC towards PAF‑R in melanoma offers a promising chemopreventive agent for PAF‑R‑positive melanoma treatment

    Analysis of Heat Transfer and Flow Due to Natural Convection in Air Around Heated Triangular Cylinders of Different Sizes Inside a Square Enclosure

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    AbstractHeat transfer and flow due to natural convection in air around heated equilateral triangular cylinders of different sizes inside a square enclosure has been analyzed. The triangular cylinder is at higher temperature and the vertical walls of the enclosure are at lower temperature with insulated horizontal walls. The computational model is developed using Ansys Fluent 13 commercial CFD package. The Rayleigh number is varied from 104 to 106. For a given size of enclosure, cylinders of different size are taken corresponding to aspect ratios of 0.2, 0.3, 0.4 and 0.5. Results are presented in the form of contours of isotherm and stream function

    Cluster expansion Monte Carlo study of phase stability of vanadium nitrides

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    Phase stability of stable and metastable vanadium nitrides is studied using density functional theory (DFT) based total-energy calculations combined with cluster expansion Monte Carlo simulation and supercell methods. We have computed the formation enthalpy of the various stable and metastable vanadium nitride phases considering the available structural models and found that the formation enthalpies of the different phases decrease in the same order as they appear in the experimental aging sequence. DFT calculations are known to show stoichiometric V2N to be polymorphic in Ï”-Fe_2N and ζ-Fe2_N structures within a few meV and VN to be more stable in WC(B_h) phase than in the experimentally observed NaCl(B1) structure. As these nitrides are known to be generally nonstoichiometric due to presence of nitrogen vacancies, we used cluster expansion and supercell methods for examining the effect of nitrogen vacancies on the phase stability. It is found that nitrogen vacancies, represented by ◻, stabilize Ï”-Fe_2N phase of V_2N_(1−x◻x) and NaCl(B1) phase of VN_(1−x◻x) compared to ζ-Fe_2N and WC(B_h) phases respectively, rendering the computed phase stability scenario to be in agreement with experiments. Analysis of supercell calculated electronic density of states (DOS) of VN_(1−x◻x) with varying x, shows that the nitrogen vacancies increase the DOS at Fermi level in WC phase, whereas they decrease the DOS in NaCl phase. And this serves as the mechanism of enhancement of the stability of the NaCl phase. Monte Carlo simulations were used for computing the finite temperature formation enthalpies of these phases as a function of nitrogen-vacancy concentration and found close agreement for NaCl(B1) phase of VN_(1−x◻x) for which measured values are available

    The PPARÎł Agonist Rosiglitazone Suppresses Syngeneic Mouse SCC (Squamous Cell Carcinoma) Tumor Growth through an Immune-Mediated Mechanism

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    Recent evidence suggests that PPARγ agonists may promote anti-tumor immunity. We show that immunogenic PDV cutaneous squamous cell carcinoma (CSCC) tumors are rejected when injected intradermally at a low cell number (1 × 106) into immune competent syngeneic hosts, but not immune deficient mice. At higher cell numbers (5 × 106 PDV cells), progressively growing tumors were established in 14 of 15 vehicle treated mice while treatment of mice with the PPARγ agonist rosiglitazone resulted in increased tumor rejection (5 of 14 tumors), a significant decrease in PDV tumor size, and a significant decrease in tumor cell Ki67 labeling. Rosiglitazone treatment had no effect on tumor rejection, tumor volume or PDV tumor cell proliferation in immune deficient NOD.CB17-PrkdcSCID/J mice. Rosiglitazone treatment also promoted an increase in tumor infiltrating CD3+ T-cells at both early and late time points. In contrast, rosiglitazone treatment had no significant effect on myeloid cells expressing either CD11b or Gr-1 but suppressed a late accumulation of myeloid cells expressing both CD11b and Gr-1, suggesting a potential role for CD11b+Gr-1+ myeloid cells in the late anti-tumor immune response. Overall, our data provides evidence that the PPARγ agonist rosiglitazone promotes immune-mediated anti-neoplastic activity against tumors derived from this immunogenic CSCC cell line

    Identification and characterization of geometrical isomeric photo degradation product of eprosartan using LC-MS and LC-NMR

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    The degradation of eprosartan was evaluated under ICH/WHO prescribed stress conditions. The drug degraded to only one product under photo alkali condition, whereas it was stable to conditions of hydrolysis, oxidation and thermal stress. The drug and its co-eluting product were well separated on RP-HPLC in a gradient mode. Subsequently, LC-MS/TOF and on-line H/D exchange studies were performed on both of them. The two showed same molecular mass, similar fragment ions and even the same number of labile hydrogens indicating the product to be an isomer of the drug. To confirm the same, 1H and COSY LC-NMR studies were carried out by using an enriched sample. Distinguishing behaviour of chemical shifts proved the product to be (Z)-4-((2-butyl-5-(2-carboxy-3-(thiophen-2-yl)prop-1-enyl)-1H-imidazol-1-yl)methyl)benzoic acid. The structure was further supported by differential LC-MS ion intensities of the drug and the product

    Growth of Boundary Layer on Smooth and Rough Surface

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    At the point when genuine liquid streams past a strong body or a strong divider, the liquid particles follow to the limit and condition of no slip happens. This implies that the velocity of liquid near to the limit will be same as that of limit. On the off chance that the limit is stationary, the speed of liquid at the limit will be zero. Further away from the Limit, the speed will be higher and as a consequence of this variety of velocity, the speed inclination will exist. The speed of liquid increments from zero speed on the stationary limit to the free stream speed of the liquid in the heading typical to the limit. This variety of speed from zero to free stream speed in the course typical to the limit takes place in a limited area in the region of strong limit. This thin district of liquid is called Boundary Layer. For the basic understanding of flow characteristics over a flat smooth plate and rough surfaces, the experiment was carried out in the laboratory using Airflow Bench (AF14). Readings of the boundary layer were taken at giving Reynolds number corresponding to laminar through turbulent flows. The height of the boundary layer ranges from 0.5 mm to 1.3mm.then the parameters like displacement thickness were calculated from the velocity profile .The boundary layer growth over the glass plate and rough surface was found out with the help of velocity profiles at different locations. The boundary layer growth gives a brief idea of fluid flow over a flat surface and Rough Surface

    Platelet-Activating Factor-Receptor and Tumor Immunity

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    First described in 1972 by Benveniste and colleagues, platelet-activating factor (PAF) remains one of the potent phospholipid known to date. The role of PAF produced enzymatically in mediating diverse biological and pathophysiological processes including inflammatory and allergic diseases and cancers in response to various stimuli has been extensively studied. However, little is known about the role of non-enzymatically-generated PAF-like lipids produced in response to pro-oxidative stressors, particularly in modulating the host immune responses to tumor immunity, which is the focus of this review

    Benzyl Isothiocyanate Suppresses Pancreatic Tumor Angiogenesis and Invasion by Inhibiting HIF-α/VEGF/Rho-GTPases: Pivotal Role of STAT-3

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    Our previous studies have shown that benzyl isothiocyanate (BITC) suppresses pancreatic tumor growth by inhibiting STAT-3; however, the exact mechanism of tumor growth suppression was not clear. Here we evaluated the effects and mechanism of BITC on pancreatic tumor angiogenesis. Our results reveal that BITC significantly inhibits neovasularization on rat aorta and Chicken-Chorioallantoic membrane. Furthermore, BITC blocks the migration and invasion of BxPC-3 and PanC-1 pancreatic cancer cells in a dose dependant manner. Moreover, secretion of VEGF and MMP-2 in normoxic and hypoxic BxPC-3 and PanC-1 cells was significantly suppressed by BITC. Both VEGF and MMP-2 play a critical role in angiogenesis and metastasis. Our results reveal that BITC significantly suppresses the phosphorylation of VEGFR-2 (Tyr-1175), and expression of HIF-α. Rho-GTPases, which are regulated by VEGF play a crucial role in pancreatic cancer progression. BITC treatment reduced the expression of RhoC whereas up-regulated the expression of tumor suppressor RhoB. STAT-3 over-expression or IL-6 treatment significantly induced HIF-1α and VEGF expression; however, BITC substantially suppressed STAT-3 as well as STAT-3-induced HIF-1α and VEGF expression. Finally, in vivo tumor growth and matrigel-plug assay show reduced tumor growth and substantial reduction of hemoglobin content in the matrigel plugs and tumors of mice treated orally with 12 ”mol BITC, indicating reduced tumor angiogenesis. Immunoblotting of BITC treated tumors show reduced expression of STAT-3 phosphorylation (Tyr-705), HIF-α, VEGFR-2, VEGF, MMP-2, CD31 and RhoC. Taken together, our results suggest that BITC suppresses pancreatic tumor growth by inhibiting tumor angiogenesis through STAT-3-dependant pathway

    Utilisation of Scholarly Communication through DRDO E-journal Consortium during 2012-2017

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    Timely, speedy dissemination of latest information is the benchmark of any information and documentation center, but utilisation of e-journals is an important factor for its significance and cost effectiveness. However, in R&D community especially for defence R&D, where scientists are involved in core technology areas, value of information is more important instead of its utilisation. The aim of the study is to find out the utilisation of e-journals with cost effectiveness under Consortium, which was established in the year 2009 for resource sharing among DRDO labs with least expenses. The data was analysed for the period 2011-2017 to know the current trends of utilisation under Consortium. Feedbacks and suggestions were collected from all DRDO users to evaluate the importance of information and its effectiveness. The study shows that productivity of DRDO scientists in publications were increased in high impact factor journal and majority of scientists preferred e-journals instead of print subscriptions
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