gebhart/patrepeval huggingface dataset:
Fullerenes Broaden Scientists' View of Molecular Structure (1993)

RETURN TO ISSUEPREVNewsNEXTFullerenes Broaden Scientists' View of Molecular StructureFullerene structure of atoms bonded in a cage also occurs in nanotubes, graphite 'onions,' and metallocarbohedrenesRUDY M. BAUMView Author Information C&EN West Coast BureauCite this: Chem. Eng. News 1993, 71, 1, 29–34Publication Date (Print):January 4, 1993Publication History Published online12 November 2010Published inissue 4 January 1993https://pubs.acs.org/doi/10.1021/cen-v071n001.p029https://doi.org/10.1021/cen-v071n001.p029newsACS PublicationsCopyright © 1993 AMERICAN CHEMICAL SOCIETYArticle Views11Altmetric-Citations1LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access options SUBJECTS:Carbon nanomaterials,Nanospheres Get e-Alerts
Cardiolipin Binding a Light Chain from Lupus-Prone Mice, (1998)

Autoantibodies in systemic lupus erythematosus react with multiple epitopes on highly conserved molecules such as nucleic acids, cytoskeletal proteins, phospholipids, and phospholipid-binding proteins. Analysis of the heavy- and light-chain variable sequences (VH and VL) has shown that a restricted set of V genes gives rise to these autoantibodies. Several monoclonal antibodies were developed from a strain of mouse prone to lupus (F1 male NZW x BXSB). Two of these antibodies, A1.72 and A1.84, reacted directly with cardiolipin and their VH and VL sequences were analyzed. Surprisingly, these two antibodies had identical light-chain variable sequences despite having substantially different heavy-chain variable sequences. This VL sequence, VL 72/84 was 97% identical with the germ-line sequences with only four single nucleotide substitutions. When this VL sequence was shuffled with the VH sequence of other monoclonal antibodies and expressed as single chain variable fragment (scFv) in Escherichia coli, it imparted cardiolipin-binding activity to the hybrids. Furthermore, the VL 72/84 sequence, when expressed alone without any VH sequence, also bound to cardiolipin. The antibodies and their recombinant fragments were immunoaffinity-purified on cardiolipin liposomes. The dissociation constant of the light chain for cardiolipin was similar to the intact molecule (21 +/- 0.01 vs 20 +/- 0.03 nM). These studies demonstrate that the VL sequence alone, in the absence of any other immunoglobulin domains, can mediate cardiolipin binding, raising the possibility that antigen specificity of certain antibodies may exclusively reside in their light-chain sequences.
Tumor necrosis factor alpha (rhTNF) fails to stimulate angiogenesis in the rabbit cornea (1996)

Background The objective of this study was to thoroughly examine the in vivo angiogenesis activity of human recombinant tumor necrosis factor alpha (rhTNF). Methods rhTNF (0.5 ng to 1.0 μg) was incorporated into the slow release polymers Hydron or HYPAN® and implanted into the rabbit cornea. Release of biologically active rhTNF from the polymers was determined with the L929 cytotoxicity assay. Results All concentrations tested failed to elicit capillary formation beyond that observed for controls. Less than 2% of the rhTNF was released from the Hydron over 7 days. HYPAN® released five times the amount of rhTNF in vitro, but even at doses of 500 ng (104.3 ng suggested release) no angiogenesis was stimulated. Conclusion Under the circumstances tested, rhTNF is not angiogenic in vivo. © 1996 Wiley-Liss, Inc.
Viral Control of Phytoplankton Populations—a Review1 (2004)

Phytoplankton population dynamics are the result of imbalances between reproduction and losses. Losses include grazing, sinking, and natural mortality. As the importance of microbes in aquatic ecology has been recognized, so has the potential significance of viruses as mortality agents for phytoplankton. The field of algal virus ecology is steadily changing and advancing as new viruses are isolated and new methods are developed for quantifying the impact of viruses on phytoplankton dynamics and diversity. With this development, evidence is accumulating that viruses can control phytoplankton dynamics through reduction of host populations, or by preventing algal host populations from reaching high levels. The identification of highly specific host ranges of viruses is changing our understanding of population dynamics. Viral-mediated mortality may not only affect algal species succession, but may also affect intraspecies succession. Through cellular lysis, viruses indirectly affect the fluxes of energy, nutrients, and organic matter, especially during algal bloom events when biomass is high. Although the importance of viruses is presently recognized, it is apparent that many aspects of viral-mediated mortality of phytoplankton are still poorly understood. It is imperative that future research addresses the mechanisms that regulate virus infectivity, host resistance, genotype richness, abundance, and the fate of viruses over time and space.
Word normalization for online handwritten word recognition (2002)

We introduce a new approach to normalizing words written with an electronic stylus that applies to all styles of handwriting (upper case, lower case, printed, cursive, or mixed). A geometrical model of the word spatial structure is fitted to the pen trajectory using the expectation-maximisation algorithm. The fitting process maximizes the likelihood of the trajectory given the model and a set a priors on its parameters. The method was evaluated and integrated to a recognition system that combines neural networks and hidden Markov models.
A Protective Role for Inflammasome Activation Following Injury (2011)

The inflammasome is activated in response to pathogen or endogenous danger signals and acts as an initiator and mediator of inflammatory reactions. In this study, we wished to identify whether the inflammasome is activated in vivo by injury. And if so, we wanted to characterize the kinetics, the immune cell distribution, and the functional impact of inflammasome activation on the injury response. Because caspase-1 activation is the final product of the inflammasome pathway, we used cleaved caspase-1 p10 and p20 as a measure for inflammasome activation in cells. We first developed a procedure to stain for caspase-1 p10 and p20 by flow cytometry (FACS) in lipopolysaccharide + adenosine triphosphate-stimulated spleen cells. This method for measuring caspase-1 activation was validated using FLICA (fluorochrome inhibitor of caspase), a fluorescently tagged specific binding reagent for activated caspase-1. Once validated by in vitro studies, we measured caspase-1 activation by FACS in immune cell subsets prepared from the lymph nodes and spleens of sham- or burn-injured mice at different time points. Lastly, the functional significance of inflammasome activation following burn injury was tested in mice treated with the specific caspase-1 inhibitor, AC-YVAD-CMK. The results of in vitro studies indicated that adenosine triphosphate and lipopolysaccharide stimulation induced significant caspase-1 activation in dendritic cells, macrophages, and natural killer (NK) cells. This approach also revealed caspase-1 activation in CD4 and CD8 T cells as well as B cells. We then measured caspase-1 activation in cells prepared from the lymph nodes and spleens of sham- or burn-injured mice. Significant caspase-1 activation was detected in macrophages and dendritic cells by 4 h after injury and peaked by day 1 after injury. FLICA staining confirmed that caspase-1 activation occurred in these cells at 1 day after injury. We also found significant injury-induced caspase-1 activation in NK cells, CD4 T cells, and B cells, but CD8 T cells did not demonstrate caspase-1 activation. Surprisingly, we found that blocking caspase-1 activation with AC-YVAD-CMK in vivo caused significantly higher mortality in burn-injured mice (P < 0.01). Taken together, these findings document that injury induces inflammasome activation in many immune cell subsets, but primarily in macrophages, and that inflammasome activation plays a protective role in the host response to severe injury.
Inhibition of Human Endogenous Retrovirus-K10 Protease in Cell-free and Cell-based Assays (2001)

A full-length and C-terminally truncated version of human endogenous retrovirus (HERV)-K10 protease were expressed in Escherichia coli and purified to homogeneity. Both versions of the protease efficiently processed HERV-K10 Gag polyprotein substrate. HERV-K10 Gag was also cleaved by human immunodeficiency virus, type 1 (HIV-1) protease, although at different sites. To identify compounds that could inhibit protein processing dependent on the HERV-K10 protease, a series of cyclic ureas that had previously been shown to inhibit HIV-1 protease was tested. Several symmetric bisamides acted as very potent inhibitors of both the truncated and full-length form of HERV-K10 protease, in subnanomolar or nanomolar range, respectively. One of the cyclic ureas, SD146, can inhibit the processing of in vitro translated HERV-K10 Gag polyprotein substrate by HERV-K10 protease. In addition, in virus-like particles isolated from the teratocarcinoma cell line NCCIT, there is significant accumulation of Gag and Gag-Pol precursors upon treatment with SD146, suggesting the compound efficiently blocks HERV-K Gag processing in cells. This is the first report of an inhibitor able to block cell-associated processing of Gag polypeptides of an endogenous retrovirus.
Sodium butyrate suppresses apoptosis in human Burkitt lymphomas and murine plasmacytomas bearing c‐myc translocations (1998)

We report that sodium butyrate, a natural product of fiber degradation by colonic bacteria, markedly suppresses c-Myc-mediated apoptosis induced in murine plasmacytomas and human Burkitt lymphomas by growth factor deprivation, but not in cell lines devoid of c-myc translocations. Attenuation of cell death is associated with downregulation of the rearranged c-myc and activation of pRb via its dephosphorylation. We suggest that in vivo sodium butyrate may play an important role in plasmacytomagenesis by supporting the survival of cells with c-myc translocations, which otherwise would be eliminated by the lack of growth factors.
Polymer−Cisplatin Conjugate Nanoparticles for Acid-Responsive Drug Delivery (2009)

We report the synthesis of novel acid-responsive therapeutic nanoparticles (NPs) with sub-100 nm size consisting of polymer--cisplatin conjugates. The uniqueness of these drug delivery polymeric NPs lies in the covalent conjugation of each cisplatin drug to the hydrophobic segment of two biocompatible diblock copolymer chains through a hydrazone bond, resulting in highly differential drug release profile at different environmental acidity. We demonstrate that the synthesized polymer--cisplatin conjugates can readily precipitate to form sub-100 nm NPs in aqueous solution due to their very low critical micelle concentration (CMC). The resulting NPs show well-controlled cisplatin loading yield, excellent acid-responsive drug release kinetics, and enhanced in vitro cytotoxicity against ovarian cancer cells as compared to free cisplatin. As an environmentally sensitive drug delivery vehicle, these NPs can potentially minimize the drug loss during NP circulation in the blood, where the pH value is neutral, and trigger rapid intracellular drug release after the NPs are endocytosed by the target cells. This characteristic drug release profile holds the promise to suppress cancer cell chemoresistance by rapidly releasing a high dose of chemotherapy drugs inside the tumor cells, thereby improving the therapeutic efficacy of the drug payload.
Analysis of the Roles of ICAM-1 in Neutrophil Transmigration Using a Reconstituted Mammalian Cell Expression Model: Implication of ICAM-1 Cytoplasmic Domain and Rho-Dependent Signaling Pathway (2001)

Interaction between ICAM-1 (CD54) and fibrinogen (fg) has been shown to enhance leukocyte adhesion, but its specific role in the process of migration across endothelial cell junctions remains unclear. To overcome the problem of multiple adhesion receptors found on endothelial cells, we have engineered stable Chinese hamster ovary cell lines expressing ICAM-1 (Chinese hamster ovary ICAM-1). The transfection of ICAM-1 alone in these cells is sufficient to recapitulate the entire process of neutrophil adhesion and transmigration. This phenomenon was mediated by fg-ICAM-1 interactions, as depletion of fg, as well as the use of an Ab that specifically inhibits ICAM-1-fg interaction (2D5), completely abolished the effect of ICAM-1 expression on PMN transmigration. In addition, this ICAM-1-mediated transmigration is clearly dependent on the occurrence of fg-ICAM-1 interactions on the monolayer, and not on neutrophils, as the preincubation of the PMN with the mAb was ineffective. Furthermore, PMN transmigration, but not adhesion, is totally abolished when the ICAM-1 cytoplasmic domain is deleted, indicating that signaling inside the cell is required to mediate the fg-ICAM-1 effect on transmigration. Using a specific inhibitor of the small GTP-binding protein Rho, we have obtained evidence that this signaling cascade is involved. Thus, our results clearly show that ICAM-1 plays a key role in the migration of leukocytes across cell junctions, and indicate that this phenomenon is not a direct consequence of the enhanced adhesion mediated by the expression of ICAM-1.
Histatin and lactoferrin-derived anti-microbial peptides; in vitro and in vivo studies on the treatment and prevention of osteomyelitis (2007)

Door de toegenomen resistentie van ziekenhuis bacterien is er een behoefte aan nieuwe antibiotica voor de behandeling osteomyelitis. AMPs zijn natuurlijk antibiotica, onder andere werkzaam tegen methicylline resistente Staphylococcus aureus (MRSA). Het proefschrift beschrijft een in vitro en in vivo onderzoek naar een nieuwe behandeling van osteomyelitis met antimicrobiële peptiden (AMP), hLF1-11 en Dhvar-5. Voor de lokale behandeling van osteomyelitis is een dragersysteem noodzakelijk, daarom werd de afgifte van Dhvar-5 uit PMMA botcement onderzocht. Deze afgifte bleek veel hoger te zijn dan voor andere antibiotica. Daarnaast verviervoudigde de afgifte van gentamicine door toevoeging van Dhvar-5. De invloed van Dhvar-5 op het PMMA botcement werd onderzocht door onder andere elektronen microscopie. In vivo onderzoek van Dhvar-5 antibiotica kralen in een MRSA osteomyelitis model toonde aan dat Dhvar-5 de infectie kan remmen, maar niet verhinderen. Daarentegen bleek hLF1-11 geïncorporeerd in een calcium fosfaat botcement zeer goed MRSA osteomyelitis te kunnen behandelen in vivo. hLF1-11 is daarmee een veel belovend kandidaat antibioticum voor de behandeling van osteomyelitis veroorzaakt door resistente bacteriën.
Integration of intra- and extravasation in one cell-based microfluidic chip for the study of cancer metastasis (2011)

Most studies of cancer metastasis focus on cancer cell invasion utilizing adhesion assays that are performed independently, and are thus limited in their ability to mimic complex cancer metastasis on a chip. Here we report the development of an integrated cell-based microfluidic chip for intra- and extravasation that combines two assays on one chip for the study of the complex cascade of cancer metastasis. This device consists of two parts; one is an intravasation chamber for the three-dimensional (3-D) culture of cancer cells using a Matrigel matrix, and the other is an extravasation chamber for the detection of metastasized cancer cells by adhesion molecules expressed by epithelial cells. In this novel system, the intravasation and extravasation processes of cancer metastasis can be studied simultaneously using four screw valves. Metastatic LOVO and non-metastatic SW480 cells were used in this study, and the invasion of LOVOs was found to be higher compared to SW480. In contrast, invasion of cells treated with metalloproteinase (MMP) inhibitors decreased within the intravasation chamber. Degraded cancer cells from the intravasation chamber were detected within the extravasation chamber under physiological conditions of shear stress, and differences in binding efficiency were also detected when CA19-9 antibody, an inhibitor of cancer cell adhesion, was used to treat degraded cancer cells. Our results support the potential usefulness of this new 3D cell-based microfluidic system as a drug screening tool to select targets for the development of new drugs and to verify their effectiveness.
Projection defocus analysis for scene capture and image display (2006)

In order to produce bright images, projectors have large apertures and hence narrow depths of field. In this paper, we present methods for robust scene capture and enhanced image display based on projection defocus analysis. We model a projector's defocus using a linear system. This model is used to develop a novel temporal defocus analysis method to recover depth at each camera pixel by estimating the parameters of its projection defocus kemel in frequency domain. Compared to most depth recovery methods, our approach is more accurate near depth discontinuities. Furthermore, by using a coaxial projector-camera system, we ensure that depth is computed at all camera pixels, without any missing parts. We show that the recovered scene geometry can be used for refocus synthesis and for depth-based image composition. Using the same projector defocus model and estimation technique, we also propose a defocus compensation method that filters a projection image in a spatially-varying, depth-dependent manner to minimize its defocus blur after it is projected onto the scene. This method effectively increases the depth of field of a projector without modifying its optics. Finally, we present an algorithm that exploits projector defocus to reduce the strong pixelation artifacts produced by digital projectors, while preserving the quality of the projected image. We have experimentally verified each of our methods using real scenes.
Using Prediction Markets and Twitter to Predict a Swine Flu Pandemic (2009)

We explore the hypothesis that social media such as Twitter encodes the belief of a large number of people about some concrete statement about the world. Here, these beliefs are aggregated using a Prediction Market specifically concerning the possibility of a Swine Flu Pandemic in 2009. Using a regression framework, we are able to show that simple features extracted from Tweets can reduce the error associated with modelling these beliefs. Our approach is also shown to outperform some baseline methods based purely on time-series information from the Market. 1
Pseudomonas fluorescens subsp. cellulosa : an alternative model for bacterial cellulase (1992)

Pseudomonas fluorescens subsp. cellulosa, a Gram-negative soil bacterium, can utilize crystalline cellulose or xylan as main sources of carbon and energy. Synthesis of endoglucanases and xylanases is induced by Avicel, filter paper, carboxymethylcellulose or xylan and is repressed by cellobiose, glucose or xylose. These enzymes are secreted into the culture supernatant fluid and do not form aggregates or associate with the cell surface. Cells of Ps. fluorescens subsp. cellulosa do not adhere to cellulose. In cultures containing Avicel or filter paper, a significant proportion of the secreted cellulase and xylanase activities becomes tightly bound to the insoluble cellulose. Western blotting has revealed that endoglucanase B, xylanase A and a cellodextrinase encoded by genes previously isolated from Ps. fluorescens subsp. cellulosa and expressed in Escherichia coli, are synthesized by the pseudomonad under a variety of conditions. These enzymes appear to be post-translationally modified, probably through glycosylation. Overall, it appears that the cellulase/hemicellulase system of Ps. fluorescens subsp. cellulosa differs from the model established for celluloytic anaerobes such as Clostridium thermocellum.
Mutagenesis and Functional Characterization of the glnB , glnA , and nifA Genes from the Photosynthetic Bacterium Rhodospirillum rubrum (2000)

Nitrogen fixation is tightly regulated in Rhodospirillum rubrum at two different levels: transcriptional regulation of nif expression and posttranslational regulation of dinitrogenase reductase by reversible ADP-ribosylation catalyzed by the DRAT-DRAG (dinitrogenase reductase ADP-ribosyltransferase-dinitrogenase reductase-activating glycohydrolase) system. We report here the characterization of glnB, glnA, and nifA mutants and studies of their relationship to the regulation of nitrogen fixation. Two mutants which affect glnB (structural gene for P(II)) were constructed. While P(II)-Y51F showed a lower nitrogenase activity than that of wild type, a P(II) deletion mutant showed very little nif expression. This effect of P(II) on nif expression is apparently the result of a requirement of P(II) for NifA activation, whose activity is regulated by NH(4)(+) in R. rubrum. The modification of glutamine synthetase (GS) in these glnB mutants appears to be similar to that seen in wild type, suggesting that a paralog of P(II) might exist in R. rubrum and regulate the modification of GS. P(II) also appears to be involved in the regulation of DRAT activity, since an altered response to NH(4)(+) was found in a mutant expressing P(II)-Y51F. The adenylylation of GS plays no significant role in nif expression or the ADP-ribosylation of dinitrogenase reductase, since a mutant expressing GS-Y398F showed normal nitrogenase activity and normal modification of dinitrogenase reductase in response to NH(4)(+) and darkness treatments.
Software architecture recovery and modelling (2002)

This paper covers current trends and issues in software architecture recovery. It consists of a summary of the presentations and discussions of the Software Architecture Recovery and Modelling discussion forum held during WCRE 2001, the Working Conference on Reverse Engineering, Stuttgart, Germany, October 2, 2001.
Inhibition of G-protein betagamma-subunit functions by phosducin-like protein. (1996)

Phosducin is a cytosolic protein predominantly expressed in the retina and the pineal gland that can interact with the betagamma subunits of guanine nucleotide binding proteins (G proteins) and thereby may regulate transmembrane signaling. A cDNA encoding a phosducin-like protein (PhLP) has recently been isolated from rat brain [Miles, M. F., Barhite, S., Sganga, M. & Elliott, M. (1993) Proc. Natl. Acad. Sci. USA 90, 10831-10835. Here we report the expression of PhLP in Escherichia coli and its purification. Recombinant purified PUP inhibited multiple effects of G-protein betagamma subunits. First, it inhibited the betagamma-subunit-dependent ADP-ribosylation of purified alpha(o) by pertussis toxin. Second, it inhibited the GTPase activity of purified G(o). The IC50 value of PhLP in the latter assay was 89 nM, whereas phosducin caused half-maximal inhibition at 17 nM. And finally, PhLP antagonized the enhancement of rhodopsin phosphorylation by purified betagamma subunits. The N terminus of PhLP shows no similarity to the much longer N terminus of phosducin, the region shown to be critical for phosducin-betagamma-subunit interactions. Therefore, PhLP appears to bind to G-protein betagamma subunits by an as yet unknown mode of interaction and may represent an endogenous regulator of G-protein function.