317 research outputs found

    Characterization and evaluation of Paulownia elongota as a raw material for paper production

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    Paulownia elongota, one of the most fast growing species of the world, was evaluated as raw material for pulp and paper production. The chemical, morphological and anatomical aspects of paulownia woodwere determined. The lignin, holocellulose and ∝-cellulose contents in P. elongota wood were comparable to those of some common non-wood and hardwood raw materials. Different chemical pulping procedures were applied to P. elongota wood to evaluate its pulping potential. Paper strength properties and acidic group content bound to the cell wall were determined. The alkali solubility, water solubility and alcohol-benzene extractive content were higher than those from wood and most nonwoods. The fiber length of 0.83 mm was observed, which is close to low end of the hardwoods but fiber diameter was very wide, similar to that of softwoods. The pulpability of paulownia wood was alsostudied. The pulp yield and viscosity were very low and the kappa numbers were high. The strength properties were comparable to those of some wood and non-wood pulps. Although, paulownia pulpsare considered as low quality materials, it can be used for paper production when mixed with long fibrous materials

    Effects of shading and covering material application for delaying harvest on gray mold disease severity

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    To delay the harvest of Sultani Cekirdeksiz grape variety and to reduce pre and post-harvest botrytis bunch rot severity, shading and covering material application were tested in 2009 to 2010 growing periods. In this study, grape vines were shaded with shading materials which had three different shading densities (35, 55, and 75% shading density) from veraison period to harvest. The grape vines were also covered with four different covering materials (transparent polyethylene, mogul, polypropen cross-stich and lifepack) before rainfall, at the end of August until harvest. The gray mold severity was recorded three times (before shading at unriped grape stage, veraison period, shortly after shading and twice at 20 day interval) during growing period. Based on the results of this study, the highest gray mold (Botrytis cinerea) severity was obtained in the control (uncovered and unshaded) treatment and the lowest disease severity was observed in lifepack treatment with or without shading. Since gray mold disease of grape was the main factor affecting harvest date of the crop lifepack, + 35 or 55% shading could be recommended to delay harvest and reduce the gray mold severity of grape in Manisa province-Turkey.Key words: Sultani seedless, table grape, shading, cover material, delaying harvest disease severity, Botrytis cinerea

    Applying Deep Learning in Augmented Reality Tracking

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    An existing deep learning architecture has been adapted to solve the detection problem in camera-based tracking for augmented reality (AR). A known target, in this case a planar object, is rendered under various viewing conditions including varying orientation, scale, illumination and sensor noise. The resulting corpus is used to train a convolutional neural network to match given patches in an incoming image. The results show comparable or better performance compared to state of art methods. Timing performance of the detector needs improvement but when considered in conjunction with the robust pose estimation process promising results are shown. © 2016 IEEE

    Omacetaxine may have a role in chronic myeloid leukaemia eradication through downregulation of Mcl-1 and induction of apoptosis in stem/progenitor cells

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    Chronic myeloid leukaemia (CML) is maintained by a rare population of tyrosine kinase inhibitor (TKI)-insensitive malignant stem cells. Our long-term aim is to find a BcrAbl-independent drug that can be combined with a TKI to improve overall disease response in chronic-phase CML. Omacetaxine mepesuccinate, a first in class cetaxine, has been evaluated by clinical trials in TKI-insensitive/resistant CML. Omacetaxine inhibits synthesis of anti-apoptotic proteins of the Bcl-2 family, including (myeloid cell leukaemia) Mcl-1, leading to cell death. Omacetaxine effectively induced apoptosis in primary CML stem cells (CD34<sup>+</sup>38<sup>lo</sup>) by downregulation of Mcl-1 protein. In contrast to our previous findings with TKIs, omacetaxine did not accumulate undivided cells <i>in vitro</i>. Furthermore, the functionality of surviving stem cells following omacetaxine exposure was significantly reduced in a dose-dependant manner, as determined by colony forming cell and the more stringent long-term culture initiating cell colony assays. This stem cell-directed activity was not limited to CML stem cells as both normal and non-CML CD34<sup>+</sup> cells were sensitive to inhibition. Thus, although omacetaxine is not leukaemia stem cell specific, its ability to induce apoptosis of leukaemic stem cells distinguishes it from TKIs and creates the potential for a curative strategy for persistent disease

    Inverted type-I CdS/CdSe core/crown colloidal quantum ring

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    [No abstract available

    The Effect of N-nitrosodimethylamine (NDMA) on Bax and Mcl-1 Expression in Human Neutrophils

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    In the present study we examined a role of pro-apoptotic Bax and anti-apoptotic Mcl-1 proteins, participating in the regulation of intrinsic apoptosis pathway in human neutrophils (PMNs) exposed to N-nitrosodimethylamine (NDMA), the environmental xenobiotic. For the purpose comparison, the same studies were conducted in autologous peripheral blood mononuclear cells (PBMCs). The production of cytochrome c by PMNs was also determined. A deficit of anti-apoptotic Mcl-1 and overexpression of the pro-apoptotic protein Bax suggest that the apoptosis process in human neutrophils exposed to NDMA is dependent on changes in the expression of these proteins. PMNs were more sensitive to NDMA than PBMCs

    Downregulation of Mcl-1 has anti-inflammatory pro-resolution effects and enhances bacterial clearance from the lung

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    Phagocytes not only coordinate acute inflammation and host defense at mucosal sites, but also contribute to tissue damage. Respiratory infection causes a globally significant disease burden and frequently progresses to acute respiratory distress syndrome, a devastating inflammatory condition characterized by neutrophil recruitment and accumulation of protein-rich edema fluid causing impaired lung function. We hypothesized that targeting the intracellular protein myeloid cell leukemia 1 (Mcl-1) by a cyclin-dependent kinase inhibitor (AT7519) or a flavone (wogonin) would accelerate neutrophil apoptosis and resolution of established inflammation, but without detriment to bacterial clearance. Mcl-1 loss induced human neutrophil apoptosis, but did not induce macrophage apoptosis nor impair phagocytosis of apoptotic neutrophils. Neutrophil-dominant inflammation was modelled in mice by either endotoxin or bacteria (Escherichia coli). Downregulating inflammatory cell Mcl-1 had anti-inflammatory, pro-resolution effects, shortening the resolution interval (R(i)) from 19 to 7 h and improved organ dysfunction with enhanced alveolar–capillary barrier integrity. Conversely, attenuating drug-induced Mcl-1 downregulation inhibited neutrophil apoptosis and delayed resolution of endotoxin-mediated lung inflammation. Importantly, manipulating lung inflammatory cell Mcl-1 also accelerated resolution of bacterial infection (R(i); 50 to 16 h) concurrent with enhanced bacterial clearance. Therefore, manipulating inflammatory cell Mcl-1 accelerates inflammation resolution without detriment to host defense against bacteria, and represents a target for treating infection-associated inflammation

    Resistance to HSP90 inhibition involving loss of MCL1 addiction

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    YesInhibition of the chaperone heat-shock protein 90 (HSP90) induces apoptosis, and it is a promising anti-cancer strategy. The mechanisms underpinning apoptosis activation following HSP90 inhibition and how they are modified during acquired drug resistance are unknown. We show for the first time that, to induce apoptosis, HSP90 inhibition requires the cooperation of multi BH3-only proteins (BID, BIK, PUMA) and the reciprocal suppression of the pro-survival BCL-2 family member MCL1, which occurs via inhibition of STAT5A. A subset of tumour cell lines exhibit dependence on MCL1 expression for survival and this dependence is also associated with tumour response to HSP90 inhibition. In the acquired resistance setting, MCL1 suppression in response to HSP90 inhibitors is maintained; however, a switch in MCL1 dependence occurs. This can be exploited by the BH3 peptidomimetic ABT737, through non-BCL-2-dependent synthetic lethality

    The MCL-1 BH3 helix is an exclusive MCL-1 inhibitor and apoptosis sensitizer

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    available in PMC 2011 February 3.MCL-1 has emerged as a major oncogenic and chemoresistance factor. A screen of stapled peptide helices identified the MCL-1 BH3 domain as selectively inhibiting MCL-1 among the related anti-apoptotic Bcl-2 family members, providing insights into the molecular determinants of binding specificity and a new approach for sensitizing cancer cells to apoptosis.National Institutes of Health (U.S.) (NIH award 5RO1GM084181)National Institutes of Health (U.S.) (NIH grant 5P01CA92625)National Institutes of Health (U.S.) (Ruth L. Kirschstein National Research Service Award 1F31CA144566)Burroughs Wellcome Fund (Career Award
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