3,496 research outputs found

    Multiple forms of glucose-6-phosphate dehydrogenase of Neurospora crassa

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    Multiple forms of glucose-6-phosphate dehydrogenase of Neurospora crassa

    Concentration of chromatographic effluent for gel electrophoresis

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    Concentration of chromatographic effluent for gel electrophoresi

    A Bayesian Climate Change Detection and Attribution Assessment

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    Development of physical and mathematical models for the Porous Ceramic Tube Plant Nutrification System (PCTPNS)

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    A physical model of the Porous Ceramic Tube Plant Nutrification System (PCTPNS) was developed through microscopic observations of the tube surface under various operational conditions. In addition, a mathematical model of this system was developed which incorporated the effects of the applied suction pressure, surface tension, and gravitational forces as well as the porosity and physical dimensions of the tubes. The flow of liquid through the PCTPNS was thus characterized for non-biological situations. One of the key factors in the verification of these models is the accurate and rapid measurement of the 'wetness' or holding capacity of the ceramic tubes. This study evaluated a thermistor based moisture sensor device and recommendations for future research on alternative sensing devices are proposed. In addition, extensions of the physical and mathematical models to include the effects of plant physiology and growth are also discussed for future research

    The application of ultrasonic NDT techniques in tribology

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    The use of ultrasonic reflection is emerging as a technique for studying tribological contacts. Ultrasonic waves can be transmitted non-destructively through machine components and their behaviour at an interface describes the characteristics of that contact. This paper is a review of the current state of understanding of the mechanisms of ultrasonic reflection at interfaces, and how this has been used to investigate the processes of dry rough surface contact and lubricated contact. The review extends to cover how ultrasound has been used to study the tribological function of certain engineering machine elements

    Further observations on mechanisms of bone destruction by squamous carcinomas of the head and neck: the role of host stroma.

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    Mechanisms of bone invasion by squamous carcinomas of the head and neck have been investigated using fresh tumours and established tumour cell lines in an in vitro bone resorption assay with 45Ca-labelled mouse calvaria. Fresh tumours regularly resorb bone in vitro. Activity is consistently reduced by indomethacin. The tumours release E2 prostaglandins (PGE2) in amounts sufficient to account for approximately 50% of the bone resorption observed. Small amounts of non-prostaglandin (indomethacin-resistant) osteolytic factors are also produced. Control non-neoplastic tissues show a variable capacity to resorb bone in vitro; PGE2 levels in these tissues may be related to their content of inflammatory cells. Tumour cell lines also resorb bone in vitro but, for most lines, activity is not significantly blocked by indomethacin and PGE2 levels are generally insufficient to account for the osteolysis observed. Non-prostaglandin bone resorbing factors thus predominate. It is concluded that most squamous cancers of the head and neck are osteolytic in vitro and release a mixture of prostaglandin and non-prostaglandin factors which stimulate osteoclastic bone resorption. These factors are derived from both neoplastic and stromal elements, and are "tumour-associated" rather than "tumour-specific". In vitro bone resorption and prostaglandin release does not correlate with pathological features of the tumour or with post-operative survival

    Regulation and targeting of antiapoptotic XIAP in acute myeloid leukemia

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    : XIAP is a member of the inhibitors-of-apoptosis family of proteins, which inhibit caspases and block cell death, with prognostic importance in AML. Here we demonstrate that cytokines regulate the expression of XIAP in leukemic cell lines and primary AML blasts. Inhibition of phosphatidylinositol-3 kinase (PI3K) with LY294002 and of the mitogen-activated protein kinase (MAPK) cascade by PD98059 resulted in decreased XIAP levels (34+/-8.7 and 23+/-5.7%, respectively). We then generated OCI-AML3 cells with constitutively phosphorylated Akt (p473-Akt) by retroviral gene transfer. Neither these nor Akt inhibitor-treated OCI-AML3 cells showed changes in XIAP levels, suggesting that XIAP expression is regulated by PI3K downstream effectors other than Akt. The induction of XIAP expression by cytokines through PI3K/MAPK pathways is consistent with its role in cell survival. Exposure of leukemic cells to chemotherapeutic agents decreased XIAP protein levels by caspase-dependent XIAP cleavage. Targeting XIAP by XIAP antisense oligonucleotide resulted in downregulation of XIAP, activation of caspases and cell death, and sensitized HL-60 cells to Ara-C. Our results suggest that XIAP is regulated by cytokines through PI3K, and to a lesser degree through MAPK pathways. Selective downregulation of XIAP expression might be of therapeutic benefit to leukemic patients

    Expression of the neuroprotective slow Wallerian degeneration (WldS) gene in non-neuronal tissues

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    <p>Abstract</p> <p>Background</p> <p>The slow Wallerian Degeneration (<it>Wld</it><sup><it>S</it></sup>) gene specifically protects axonal and synaptic compartments of neurons from a wide variety of degeneration-inducing stimuli, including; traumatic injury, Parkinson's disease, demyelinating neuropathies, some forms of motor neuron disease and global cerebral ischemia. The <it>Wld</it><sup><it>S </it></sup>gene encodes a novel Ube4b-Nmnat1 chimeric protein (Wld<sup>S </sup>protein) that is responsible for conferring the neuroprotective phenotype. How the chimeric Wld<sup>S </sup>protein confers neuroprotection remains controversial, but several studies have shown that expression in neurons <it>in vivo </it>and <it>in vitro </it>modifies key cellular pathways, including; NAD biosynthesis, ubiquitination, the mitochondrial proteome, cell cycle status and cell stress. Whether similar changes are induced in non-neuronal tissue and organs at a basal level <it>in vivo </it>remains to be determined. This may be of particular importance for the development and application of neuroprotective therapeutic strategies based around <it>Wld</it><sup><it>S</it></sup>-mediated pathways designed for use in human patients.</p> <p>Results</p> <p>We have undertaken a detailed analysis of non-neuronal <it>Wld</it><sup><it>S </it></sup>expression in <it>Wld</it><sup><it>S </it></sup>mice, alongside gravimetric and histological analyses, to examine the influence of <it>Wld</it><sup><it>S </it></sup>expression in non-neuronal tissues. We show that expression of <it>Wld</it><sup><it>S </it></sup>RNA and protein are not restricted to neuronal tissue, but that the relative RNA and protein expression levels rarely correlate in these non-neuronal tissues. We show that <it>Wld</it><sup><it>S </it></sup>mice have normal body weight and growth characteristics as well as gravimetrically and histologically normal organs, regardless of Wld<sup>S </sup>protein levels. Finally, we demonstrate that previously reported <it>Wld</it><sup><it>S</it></sup>-induced changes in cell cycle and cell stress status are neuronal-specific, not recapitulated in non-neuronal tissues at a basal level.</p> <p>Conclusions</p> <p>We conclude that expression of Wld<sup>S </sup>protein has no adverse effects on non-neuronal tissue at a basal level <it>in vivo</it>, supporting the possibility of its safe use in future therapeutic strategies targeting axonal and/or synaptic compartments in patients with neurodegenerative disease. Future experiments determining whether Wld<sup>S </sup>protein can modify responses to injury in non-neuronal tissue are now required.</p

    Measuring kinetic coefficients by molecular dynamics simulation of zone melting

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    Molecular dynamics simulations are performed to measure the kinetic coefficient at the solid-liquid interface in pure gold. Results are obtained for the (111), (100) and (110) orientations. Both Au(100) and Au(110) are in reasonable agreement with the law proposed for collision-limited growth. For Au(111), stacking fault domains form, as first reported by Burke, Broughton and Gilmer [J. Chem. Phys. {\bf 89}, 1030 (1988)]. The consequence on the kinetics of this interface is dramatic: the measured kinetic coefficient is three times smaller than that predicted by collision-limited growth. Finally, crystallization and melting are found to be always asymmetrical but here again the effect is much more pronounced for the (111) orientation.Comment: 8 pages, 9 figures (for fig. 8 : [email protected]). Accepted for publication in Phys. Rev.
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