2,205 research outputs found
Barbara Ras - Sowell Conference 2017
No full textBarbara Ras, San Antonio, Poet, author of "Bite Every Sorrow" and "The Last Skin
Author Correction: Tumour-selective activity of RAS-GTP inhibition in pancreatic cancer
No full textAuthor Correction to "Tumour-selective activity of RAS-GTP inhibition in pancreatic cancer
T1, an immunoglobulin superfamily member, is expressed in H-ras-dependent epithelial tumours of mammary cells.
No full textT1 is a glycosylated protein in the carcinoembryonic antigen (CEA) family of tumour marker molecules. It was originally identified by virtue of its transient induction after the expression of p21H-ras in NIH3T3 fibroblasts. Here we show that the T1 gene is activated in mammary adenocarcinomas of transgenic mice harbouring an H-ras transgene under the control of the mammary-specific whey acidic protein (WAP) promoter. By contrast, T1 mRNA was not, or only faintly, detectable in mammary carcinomas of transgenic mice bearing a WAP-myc transgene. Thus, T1 overexpression does not appear to be a general tumour-specific phenomenon. A dependence of T1 gene expression on the action of p21H-ras is suggested by the observation of T1 mRNA in nude mouse tumours generated from H-ras-transformed cultured mammary epithelial cells. Interestingly, activation of the T1 gene is also found during the maturation of the mammary gland (3-4 weeks after birth), whereas it is absent during its terminal differentiation in pregnancy and lactation. This expression pattern suggests a role for the secreted T1 glycoprotein in the phase of epithelial proliferation of the mammary gland. It appears that p21H-ras-induced transformation of mammary epithelial cells mimicks the situation occurring in puberty. In both developmental stages the T1 glycoprotein might affect cell interactions of the proliferating epithelial cells with the surrounding stroma. It might thus promote ductal outgrowth in gland maturation as well as invasive growth of p21H-ras-transformed mammary epithelial cells
Performance based selection of RAP-RAS and binder grade in asphalt mixtures
No full textThis archived document is maintained by the Oregon State Library as part of the Oregon Documents Depository Program. It is for informational purposes and may not be suitable for legal purposes.Title from PDF cover (viewed on December 21, 2015)."SPR 755.""Work Order Number 13-07."The intent of this study is to use performance based tests to evaluate mixtures with increased recycled asphalt pavement (RAP) and recycled asphalt shingles (RAS) content (up to 40 percent, or possibly higher) resulting in minimizing the potential cost, and providing environmental and performance benefits.Includes bibliographical references (page 7).Mode of access: Internet from the Oregon Government Publications Collection.Text in English
A Relational Unsupervised Approach to Author Identification
No full textIn the last decades speaking and writing habits have changed.
Many works faced the author identification task by exploiting frequencybased
approaches, numeric techniques or writing style analysis. Following
the last approach we propose a technique for author identification
based on First-Order Logic. Specifically, we translate the complex data
represented by natural language text to complex (relational) patterns
that represent the writing style of an author. Then, we model an author
as the result of clustering the relational descriptions associated to the
sentences. The underlying idea is that such a model can express the typical
way in which an author composes the sentences in his writings. So,
if we can map such writing habits from the unknown-author model to
the known-author model, we can conclude that the author is the same.
Preliminary results are promising and the approach seems viable in real
contexts since it does not need a training phase and performs well also
with short texts
Transcription factor 8 activates R-Ras to regulate angiogenesis
No full textWe have recently reported that transcription factor 8 (TCF8) negatively regulates pathological angiogenesis by regulating endothelial invasiveness by acting as a transcriptional attenuator of matrix metalloproteinase 1. TCF8 also modulates cell–matrix and cell–cell adhesion; however molecular mechanism of this TCF8 function remains obscure. Here, we provide evidence that TCF8 activates R-Ras, another class of angiogenic regulator, to suppress angiogenesis by a mechanism other than a transcriptional attenuator. Tube formation by human umbilical vein endothelial cells (HUVECs) facilitated by TCF8 suppression was significantly inhibited by the expression of onstitutive active mutant of R-Ras. When we examined the mRNA expression levels of R-Ras regulators, no significant changes were observed to explain the R-Ras activation by TCF8. Interestingly, we found that TCF8 bound to CalDAG-GEFIII, an R-Ras activator, in the cytosol, indicating that TCF8 emanates signaling for R-Ras activation from cytosol to regulate angiogenesis negatively
Modelonderzoek "Dikke Kop", golfonderzoek haven "Ras Lanuf"
No full textHet is bekend dat de toepassing van een dikke kop aan een golfbreker met verticale wanden invloed heeft op de golfhoogteverdeling achter de golfbreker. Dit onderzoek is verricht om een methode te vinden om deze invloed te bepalen en tevens te verklaren. Nadat dit vooronderzoek is afgerond is er begonnen met een zo economisch mogelijk ontwerp van de haven van Ras Lanuf.Hydraulic EngineeringCivil Engineering and Geoscience
Visualization of Ras-PI3K interaction in the endosome using BiFC
No full textRecent studies indicate the importance of spatiotemporal regulation in the diversity and specificity of intracellular signaling. Here, we show that Ras-PI3K signaling plays an important role in the local regulation of phosphatidylinositol metabolism in the endosome through live-cell imaging by using a bimolecular fluorescence complementation technique, in which molecular interaction is indicated by fluorescence emission. Using several possible combinations of Ras and the Ras-binding domain, we identified an optimal set of probe molecules that yielded the most significant increase in fluorescence intensity between the active and inactive forms of Ras. This combination revealed that, among the Ras effectors tested, phosphatidylinositol 3-kinase (PI3K) was specifically implicated in signaling in the endosome. We also found that full length PI3K was recruited to the endosome in EGF- and Ras-dependent manners, which appears to be essential for the activation of PI3K in this compartment. Taken together, these findings demonstrate that the spatiotemporal regulation of Ras-PI3K signaling may dictate the activation of PI3K and subsequent downstream signaling in the endosome
Twist1 promotes tumor initiation <i>in vivo</i>.
No full text<p>Transgene expression was driven by WAP-Cre. While WAP-Cre;<i>Twist1</i> (TWIST1; n = 25) and WAP-Cre;K-<i>RasG12D</i> (RAS; n = 19) mice remained healthy, WAP-Cre;<i>K-RasG12D</i>;<i>Twist1</i> females (RAS+TWIST1; n = 21) developed metaplastic mammary carcinomas. (A) Kaplan-Meier survival curves of transgenic mice. Survival corresponds to the end point of the experiment, the tumor burden requiring euthanasia of the animal. Open circles indicate mice censored from the dataset. (B) HPS staining of mammary glands from either wild-type (wt), <i>Twist1</i> or <i>K-rasG12D</i> transgenic mice. (C) Expression analysis of ectopic TWIST1 in mammary glands of nulliparous WAP-Cre;<i>Twist1</i> mice as assessed by IHC shows that the WAP promoter is active in a few epithelial cells. (D) Characterization of the WAP-Cre;<i>K-RasG12D</i>;<i>Twist1</i> mice-derived mammary carcinomas (RAS+TWIST1). RAS and TWIST coexpression leads to the development of metaplastic carcinomas characterized by a predominant E-cadherin<sup>−</sup>, vimentin<sup>+</sup> fusiform contingent (tumors A, C, E, F) or the presence of two epithelial-like (E-cadherin<sup>+</sup>) and fusiform (vimentin<sup>+</sup>) cell contingents (tumors B and D). For tumors B and D, both epithelial (upper panel) and fusiform (lower panel) cell contingents express the tagged-TWIST1 transgenic protein, demonstrating that fusiform cells originate from the epithelial ones. Normal epithelial cells are arrowed.</p
Neuroblastoma RAS viral oncogene homolog (N-RAS) deficiency aggravates liver injury and fibrosis
No full textProgressive hepatic damage and fibrosis are major features of chronic liver diseases of different etiology, yet the underlying molecular mechanisms remain to be fully defined. N-RAS, a member of the RAS family of small guanine nucleotide-binding proteins also encompassing the highly homologous H-RAS and K-RAS isoforms, was previously reported to modulate cell death and renal fibrosis; however, its role in liver damage and fibrogenesis remains unknown. Here, we approached this question by using N-RAS deficient (N-RAS-/-) mice and two experimental models of liver injury and fibrosis, namely carbon tetrachloride (CCl4) intoxication and bile duct ligation (BDL). In wild-type (N-RAS+/+) mice both hepatotoxic procedures augmented N-RAS expression in the liver. Compared to N-RAS+/+ counterparts, N-RAS-/- mice subjected to either CCl4 or BDL showed exacerbated liver injury and fibrosis, which was associated with enhanced hepatic stellate cell (HSC) activation and leukocyte infiltration in the damaged liver. At the molecular level, after CCl4 or BDL, N-RAS-/- livers exhibited augmented expression of necroptotic death markers along with JNK1/2 hyperactivation. In line with this, N-RAS ablation in a human hepatocytic cell line resulted in enhanced activation of JNK and necroptosis mediators in response to cell death stimuli. Of note, loss of hepatic N-RAS expression was characteristic of chronic liver disease patients with fibrosis. Collectively, our study unveils a novel role for N-RAS as a negative controller of the progression of liver injury and fibrogenesis, by critically downregulating signaling pathways leading to hepatocyte necroptosis. Furthermore, it suggests that N-RAS may be of potential clinical value as prognostic biomarker of progressive fibrotic liver damage, or as a novel therapeutic target for the treatment of chronic liver disease
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