269 research outputs found

    NMR and GC/MS investigation of the saturate and distillate fractions from the Cerro Negro heavy petroleum crude

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    Six fractions of the Cerro Negro heavy petroleum crude have been evaluated using nuclear magnetic resonance spectroscopy (NMR) and gas chromatography/mass spectrometry (GC/MS). The fractions include four saturated hydrocarbon distillate fractions distilling above 200/sup 0/C (200 to 425/sup 0/C (392 to 797/sup 0/F), 425 to 550/sup 0/C (797 to 1022/sup 0/F), 550 to 700/sup 0/C (1022 to 1292/sup 0/F), and >700/sup 0/C (>1292/sup 0/F)) and two distillate subfractions designated as <200/sup 0/C and >200/sup 0/C. The >700/sup 0/C and 550 to 700/sup 0/C saturated hydrocarbon fractions are not suited for analyses by combined GC/MS because their distillation ranges are higher than the upper limit of material that will elute from the gas chromatographic column. The /sup 1/H and /sup 13/C NMR spectral data for the 550 to 700/sup 0/C and >700/sup 0/C fractions indicate that normal and branched alkanes with an average carbon chainlength of C/sub 10/ are present but must be bonded to a larger molecular moiety based upon mass spectral evidence and boiling point considerations. Normal and branched alkanes were not detected in either 200 to 425/sup 0/C or 425 to 550/sup 0/C samples at concentrations of 0.01% by weight. NMR data for the 200 to 425/sup 0/C fraction give no indication of normal alkanes with C chainlengths >9. Branched alkanes possibly of the isoprenoid-like structure are present. The average molecular structural representation is an alkyl-substituted dicyclic alkane. Average molecular structural representation for the 425 to 550/sup 0/C fraction is also an alkyl-substituted dicyclic alkane. However, at least one of the alkyl substituents has a chainlength >10. Both normal and branched alkanes of C/sub 7-12/ were detected in the <200/sup 0/C subfraction. Alkanes of C/sub 12-31/ were in the >200/sup 0/C sample. /sup 1/H and /sup 13/C spectra for both subfractions indicate similar chemical composition. 12 refs., 6 figs., 8 tabs

    Phenotypic Overlap between MMP-13 and the Plasminogen Activation System during Wound Healing in Mice

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    BACKGROUND: Proteolytic degradation of extracellular matrix is a crucial step in the healing of incisional skin wounds. Thus, healing of skin wounds is delayed by either plasminogen-deficiency or by treatment with the broad-spectrum metalloproteinase (MP) inhibitor Galardin alone, while the two perturbations combined completely prevent wound healing. Both urokinase-type plasminogen activator and several matrix metallo proteinases (MMPs), such as MMP-3, -9 and -13, are expressed in the leading-edge keratinocytes of skin wounds, which may account for this phenotypic overlap between these classes of proteases. METHODOLOGY: To further test that hypothesis we generated Mmp13;Plau and Mmp13;Plg double-deficient mice in a cross between Mmp13- and Plau-deficient mice as well as Mmp13- and Plg-deficient mice. These mice were examined for normal physiology in a large cohort study and in a well-characterized skin wound healing model, in which we made incisional 20 mm-long full-thickness skin wounds. PRINCIPAL FINDINGS: While mice that are deficient in Mmp13 have a mean healing time indistinguishable to wild-type mice, wound healing in both Plau- and Plg-deficient mice is significantly delayed. Histological analysis of healed wounds revealed a significant increase in keratin 10/14 immunoreactive layers of kerationcytes in the skin surface in Mmp13;Plau double-deficient mice. Furthermore, we observe, by immunohistological analysis, an aberrant angiogenic pattern during wound healing induced by Plau-deficiency, which has not previously been described. CONCLUSIONS: We demonstrate a phenotypic overlap, defined as an additional delay in wound healing in the double-deficient mice compared to the individual single-deficient mice, between MMP-13 and the plasminogen activation system in the process of wound healing, but not during gestation and in postnatal development. Thus, a dual targeting of uPA and MMP-13 might be a possible future strategy in designing therapies aimed at tissue repair or other pathological processes, such as cancer invasion, where proteolytic degradation is a hallmark

    Desmoglein 2 is a substrate of kallikrein 7 in pancreatic cancer

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    <p>Abstract</p> <p>Background</p> <p>In a previous report we have demonstrated that the chymotryptic-like serine protease kallikrein 7 (<it>KLK7</it>/hK7) is overexpressed in pancreatic cancer. In normal skin, hK7 is thought to participate in skin desquamation by contributing in the degradation of desmosomal components, such as desmogleins. Thus, the ability of hK7 to degrade desmogleins was assessed and the effect of hK7 expression on desmoglein 2 was examined in cultured pancreatic cancer cells.</p> <p>Methods</p> <p>The expression of Dsg1, Dsg2, and Dsg3 in pancreatic tissues was examined by immunohistochemistry and their expression in two pancreatic cancer cell lines, BxPC-3 and Panc-1, was determined by western blot analysis. The ability of hK7 to degrade Dsg1 and Dsg2 was investigated using <it>in vitro </it>degradation assays. BxPC-3 cells stably transfected to overexpress hK7 were used to examine the effect of hK7 on cell-surface resident Dsg2.</p> <p>Results</p> <p>The levels of immunoreactive Dsg1 and Dsg2 were reduced in pancreatic adenocarcinomas compared with both normal pancreatic and chronic pancreatitis tissues. Among the desmosomal proteins examined, Dsg2 exhibited robust expression on the surface of BxPC-3 cells. When hK7 was overexpressed in this cell line, there was a significant increase in the amount of soluble Dsg2 released into the culture medium compared with vector-transfected control cells.</p> <p>Conclusion</p> <p>A reduction in the amount of the cell adhesion components Dsg1 and Dsg2 in pancreatic tumors suggests that loss of these desmosomal proteins may play a role in pancreatic cancer invasion. Using <it>in vitro </it>degradation assays, both Dsg1 and Dsg2 could be readily proteolyzed by hK7, which is overexpressed in pancreatic adenocarcinomas. The enforced expression of hK7 in BxPC-3 cells that express significant amounts of Dsg2 resulted in a marked increase in the shedding of soluble Dsg2, which is consistent with the notion that aberrant expression of hK7 in pancreatic tumors may result in diminished cell-cell adhesion and facilitate tumor cell invasion.</p

    Linking genes to literature: text mining, information extraction, and retrieval applications for biology

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    Efficient access to information contained in online scientific literature collections is essential for life science research, playing a crucial role from the initial stage of experiment planning to the final interpretation and communication of the results. The biological literature also constitutes the main information source for manual literature curation used by expert-curated databases. Following the increasing popularity of web-based applications for analyzing biological data, new text-mining and information extraction strategies are being implemented. These systems exploit existing regularities in natural language to extract biologically relevant information from electronic texts automatically. The aim of the BioCreative challenge is to promote the development of such tools and to provide insight into their performance. This review presents a general introduction to the main characteristics and applications of currently available text-mining systems for life sciences in terms of the following: the type of biological information demands being addressed; the level of information granularity of both user queries and results; and the features and methods commonly exploited by these applications. The current trend in biomedical text mining points toward an increasing diversification in terms of application types and techniques, together with integration of domain-specific resources such as ontologies. Additional descriptions of some of the systems discussed here are available on the internet
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