3,046 research outputs found

    Bubble transport by electro-magnetophoretic forces at anode bottom of aluminium cells

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    Electrically conducting and nonconducting particles and bubbles experience additional forcing in a liquid which carries electric current. These so called electro-magnetophoretic forces are well known in metallurgical applications, like metal purification in vacuum-arc remelting, electro-slag processes, impurity removal or concentration change in special castings. However, the effect of electro-magnetophoretic forces has never been considered for aluminium cells where the gas bubbles evolving in the liquid electrolyte are surrounded by an electric current and significant magnetic fields. We present models to estimate the effect of electric current flow in the vicinity of the bubbles and the additional pressure distribution resulting from the magnetic forces in the surrounding liquid electrolyte. According to the estimates, this force becomes important for bubbles exceeding 2 mm in size, and could be sufficient to overcome the typical drag force associated with electrolyte flow thereby opposing motion of the bubble along the base of the anode when it is inclined at a slight angle. The effect could explain certain features of the anode effect onset. Mathematical models and numerical results are presented and a further implementation in the general MHD code for the aluminium cell design is discussed

    MTA1 of the MTA (metastasis-associated) gene family and its encoded proteins: molecular and regulatory functions and role in human cancer progression

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    Deep insight on MTA1 of the MTA (metastasis-associated) gene family and its encoded proteins: molecular and regulatory functions and role in human cancer progression

    MTA1 (metastasis-associated gene 1)

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    Review on MTA1 (metastasis-associated gene 1), with data on DNA, on the protein encoded, and where the gene is implicated

    Role of Interleukin 17 in arthritis chronicity through survival of synoviocytes via regulation of synoviolin expression

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    Background: The use of TNF inhibitors has been a major progress in the treatment of chronic inflammation. However, not all patients respond. In addition, response will be often lost when treatment is stopped. These clinical aspects indicate that other cytokines might be involved and we focus here on the role of IL-17. In addition, the chronic nature of joint inflammation may contribute to reduced response and enhanced chronicity. Therefore we studied the capacity of IL-17 to regulate synoviolin, an E3 ubiquitin ligase implicated in synovial hyperplasia in human rheumatoid arthritis (RA) FLS and in chronic reactivated streptococcal cell wall (SCW)-induced arthritis.<p></p> Methodology/Principal Findings: Chronic reactivated SCW-induced arthritis was examined in IL-17R deficient and wild-type mice. Synoviolin expression was analysed by real-time RT-PCR, Western Blot or immunostaining in RA FLS and tissue, and p53 assessed by Western Blot. Apoptosis was detected by annexin V/propidium iodide staining, SS DNA apoptosis ELISA kit or TUNEL staining and proliferation by PCNA staining. IL-17 receptor A (IL-17RA), IL-17 receptor C (IL-17-RC) or synoviolin inhibition were achieved by small interfering RNA (siRNA) or neutralizing antibodies. IL-17 induced sustained synoviolin expression in RA FLS. Sodium nitroprusside (SNP)-induced RA FLS apoptosis was associated with reduced synoviolin expression and was rescued by IL-17 treatment with a corresponding increase in synoviolin expression. IL-17RC or IL-17RA RNA interference increased SNP-induced apoptosis, and decreased IL-17-induced synoviolin. IL-17 rescued RA FLS from apoptosis induced by synoviolin knockdown. IL-17 and TNF had additive effects on synoviolin expression and protection against apoptosis induced by synoviolin knowndown. In IL-17R deficient mice, a decrease in arthritis severity was characterized by increased synovial apoptosis, reduced proliferation and a marked reduction in synoviolin expression. A distinct absence of synoviolin expressing germinal centres in IL-17R deficient mice contrasted with synoviolin positive B cells and Th17 cells in synovial germinal centre-like structures.<p></p> Conclusion/Significance: IL-17 induction of synoviolin may contribute at least in part to RA chronicity by prolonging the survival of RA FLS and immune cells in germinal centre reactions. These results extend the role of IL-17 to synovial hyperplasia.<p></p&gt

    Hydrodynamic response of rotationally supported flows in the Small Shearing Box model

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    The hydrodynamic response of the inviscid small shearing box model of a midplane section of a rotationally supported astrophysical disk is examined. An energy functional E{\cal E} is formulated for the general nonlinear problem. It is found that the fate of disturbances is related to the conservation of this quantity which, in turn, depends on the boundary conditions utilized: E{\cal E} is conserved for channel boundary conditions while it is not conserved in general for shearing box conditions. Linearized disturbances subject to channel boundary conditions have normal-modes described by Bessel Functions and are qualitatively governed by a quantity Σ\Sigma which is a measure of the ratio between the azimuthal and vertical wavelengths. Inertial oscillations ensue if Σ>1\Sigma >1 - otherwise disturbances must in general be treated as an initial value problem. We reflect upon these results and offer a speculation.Comment: 6 pages, resubmitted to Astronomy and Astrophysics, shortened with references adde

    Transition in pipe flow: the saddle structure on the boundary of turbulence

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    The laminar-turbulent boundary S is the set separating initial conditions which relaminarise uneventfully from those which become turbulent. Phase space trajectories on this hypersurface in cylindrical pipe flow look to be chaotic and show recurring evidence of coherent structures. A general numerical technique is developed for recognising approaches to these structures and then for identifying the exact coherent solutions themselves. Numerical evidence is presented which suggests that trajectories on S are organised around only a few travelling waves and their heteroclinic connections. If the flow is suitably constrained to a subspace with a discrete rotational symmetry, it is possible to find locally-attracting travelling waves embedded within S. Four new types of travelling waves were found using this approach.Comment: 24 pages, 14 figures. Accepted, Jou. Fluid Mec

    p53 expression in squamous dysplasia associated with carcinoma of the oesophagus: evidence for field carcinogenesis

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    Squamous epithelial dysplasia is often observed multifocally in the cancerous oesophagus and is presumably considered to be a pre-cancerous lesion. A mutation of the p53 tumour suppressor gene is commonly identified in oesophageal cancer and dysplasia. p53 mutations can be anticipated immunohistochemically. In order to confirm the biological and clinical significance of p53 expressions in oesophageal field carcinogenesis, immunostaining for p53 in cancerous and multifocal precancerous lesions from resected human oesophagus was systematically investigated, while paying special attention to the contiguity of these lesions. Lesions expressing p53 were detected in 46.5% (20 of 43 lesions) of the invasive carcinoma, and in 51.0% (46 of 90 lesions) of the carcinoma in situ, and in 51.4% (92 of 179 lesions) of the dysplasia. Next, the p53 expression in dysplasia was compared with that in carcinoma for the same case. 37 of 39 (94.8%) dysplasias contiguous to p53-positive carcinomas also expressed p53 (P < 0.0001). On the other hand, the isolated dysplasias without contiguity to p53-positive carcinomas, only expressed p53 protein in 44.0% (11 of 25 lesions). No significant correlations were found between the p53 staining and either the clinicopathological features or prognosis. Discordant p53 alterations, such as those seen in cancerous and isolated precancerous lesions, may thus demonstrate further evidence for a multicentric or field carcinogenesis of the human oesophagus. © 2000 Cancer Research Campaig

    Angiogenically active vascular endothelial growth factor is over-expressed in malignant human and rat prostate carcinoma cells

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    Vascular endothelial growth factor (VEGF) is one of the most potent factors for stimulating angiogenesis, an essential process required for expansion of primary tumour and dissemination of malignant cells. To investigate the possible role of VEGF in facilitating metastasis of prostate cancer via stimulating angiogenesis, we have used Northern and slot blotting, reverse transcription polymerase chain reaction, nucleotide sequence analysis and enzyme-linked immunosorbent assay to compare the VEGF expression in series of human and rat cell lines with either benign or malignant characteristics. We have also employed the chick chorioallantoic membrane (CAM) assay to measure the angiogenic activity of the VEGF derived from both benign and malignant cells. The level of VEGF mRNA expressed in the seven malignant human and rat cell lines is 3.5- to 10-fold higher than that expressed in the benign cell lines. The three metastatic variants, generated by transfection of a benign cell line with DNA extracted from prostate carcinoma cells, expressed 2.5 to 5 times more VEGF mRNA than their parental benign cells. While VEGF 121 and 165 were predominantly expressed by both the benign and malignant cells, the transcript representing VEGF 189 isoform was only detected in the malignant cells. At protein level, three human malignant cell lines produced more VEGF (2.7–7.9 ng ml−1) than the benign cell line (1.3 ng ml−1). CAM assay detected a VEGF-dependent angiogenic activity in the medium from malignant cells, but only a relatively weak VEGF-independent activity in the medium from benign cells. These results demonstrated that malignant cells did over-express VEGF and only the VEGF derived from malignant cells was angiogenically active. Thus, we suggest that the VEGF produced by malignant cells might play an important role in facilitating metastasis of prostatic cancer. © 2000 Cancer Research Campaig
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