gebhart/patrepeval huggingface dataset:
Networks of ultra-fine Ag nanocrystals in a Teflon AF®matrix by vapour phase e-beam-assisted deposition (2007)

We have fabricated nanocomposite thin films comprising silver (Ag) nanoparticles dispersed in a Teflon AF polymer matrix using electron-beam-assisted physical vapour deposition.Four different Ag nanoparticle volume fillings (20%, 35%, 70% and 75%) were achieved by varying the relative metal-polymer evaporation rates with the formation of highly crystalline Ag nanoparticles regardless of the filling ratio.The present fabrication technique allowed full control over dispersion uniformity of nanoparticles in the polymer network.At 20% and 35% metal volume fillings, the nanocomposite film morphology consists of a uniformly dispersed assembly of equiaxed isolated Ag nanoparticles.At higher metal volume fractions the nanocomposite structures displayed two different and unique Ag nanoparticle arrangements within the polymer matrix.In particular, at 70% metal filling, the formation of irregularly shaped clusters of individually assembled nanocrystals was observed.At a slightly higher volume filling (75%), larger irregularly shaped Ag nanocrystals that appeared to be the result of coalescence and grain growth were observed.Finally, a composite theory developed by Tandon and Weng was used to estimate various elastic properties of the nanocomposite films.At high metal filling, the reinforcing effect of the Ag nanoparticles was reflected as approximately a sixfold increase in the elastic modulus compared to the virgin polymer film.Possible applications of such ultra-fine metal nanoparticles networks are discussed.
Type I IFN Protects Against Murine Lupus (2004)

Both the type I (IFN-alpha beta) and type II (IFN-gamma) IFNs have been heavily implicated in the pathogenesis of systemic lupus erythematosus. To test the relative roles of these systems, congenic lupus-prone MRL/CD95(lpr/lpr) (MRL/lpr) mice lacking the type I IFN receptor (IFN-RI), type II IFN receptor (IFN-RII), or both, were derived. As expected, deficiency for IFN-RII protected MRL/lpr mice from the development of significant autoimmune-associated lymphadenopathy, autoantibodies, and renal disease. However, deficiency for the IFN-RI surprisingly worsened lymphoproliferation, autoantibody production, and end organ disease; animals doubly deficient for IFN-RI and IFN-RII developed an autoimmune phenotype intermediate between wild-type and IFN-RII-deficient animals, all correlating with an ability of type I IFN to suppress MRL B cell activation. Thus, type I IFNs protect against both the humoral and end organ autoimmune syndrome of MRL/lpr mice, independent of IFN-gamma. These findings warrant caution in the use of type I IFN antagonists in the treatment of autoimmune diseases and suggest further investigation into the interplay between the types I and II IFNs during the ontogeny of pathogenic autoantibodies.
CD28/B7 SYSTEM OF T CELL COSTIMULATION (1996)

T cells play a central role in the initiation and regulation of the immune response to antigen. Both the engagement of the TCR with MHC/Ag and a second signal are needed for the complete activation of the T cell. The CD28/B7 receptor/ligand system is one of the dominant costimulatory pathways. Interruption of this signaling pathway with CD28 antagonists not only results in the suppression of the immune response, but in some cases induces antigen-specific tolerance. However, the CD28/B7 system is increasingly complex due to the identification of multiple receptors and ligands with positive and negative signaling activities. This review summarizes the state of CD28/B7 immunobiology both in vitro and in vivo; summarizes the many experiments that have led to our current understanding of the participants in this complex receptor/ligand system; and illustrates the current models for CD28/B7-mediated T cell and B cell regulation. It is our hope and expectation that this review will provoke additional research that will unravel this important, yet complex, signaling pathway.
The induction of 72-kD gelatinase in T cells upon adhesion to endothelial cells is VCAM-1 dependent. (1994)

T cell extravasation from the bloodstream into the perivascular tissue during inflammation involves transmigration through the endothelial cell layer and basement membrane into the interstitial matrix. The specific mechanisms by which T cells transmigrate, however, are poorly understood. Matrix degradation by enzymes such as 72-kD gelatinase has been implicated as an important component in tissue invasion by various types of cells. In this study, we have demonstrated that 72-kD gelatinase is induced in T cells upon adhesion to endothelial cells. We also provide evidence that the induction of 72-kD gelatinase is mediated by binding to vascular cell adhesion molecule-1 (VCAM-1). The T cells used in this study were cloned murine Th1 cells antigenic to myelin basic protein. These cells express very late antigen-4 on their cell surface and have been shown to infiltrate the brain parenchyma and cause experimental autoimmune encephalomyelitis when infused into normal mice (Baron, J. L., J. A. Madri, N. H. Ruddle, G. Hashim, and C. A. Janeway. 1993. J. Exp. Med. 177:57-68). In the experiments presented here, T cells were cocultured with VCAM-1-positive and -negative endothelial cells grown in a monolayer in order to study the expression of 72-kD gelatinase upon T cell adhesion. Additional experiments were conducted in which T cells were cocultured with VCAM-1 positive cells grown on microporous membranes suspended in transwells to study 72-kD gelatinase following T cell transmigration. T cells were also incubated with recombinant VCAM-1 in order to study the role of VCAM-1 in inducing 72-kD gelatinase. The results demonstrated that T cells adhered to both VCAM-1-positive and -negative endothelial cells. T cells that adhered to the VCAM-1-positive endothelial cells exhibited an induction in 72-kD gelatinase protein, activity, and mRNA whereas 72-kD gelatinase was not induced in the T cells that adhered to the VCAM-1-negative endothelial cells. Incubating T cells with recombinant VCAM-1 coated onto tissue culture plastic showed that T cells adhered to the molecule and that adhesion to recombinant VCAM-1 was sufficient to induce 72-kD gelatinase. Further, T cells that had transmigrated through a VCAM-1-positive endothelial cell monolayer exhibited 72-kD gelatinase activity but not mRNA expression. In addition, 72-kD gelatinase was detected on the cell surface of the transmigrated T cells by FACS analysis. In other experiments, TIMP-2 was added to the transmigration studies and was shown to reduce T cell transmigration.(ABSTRACT TRUNCATED AT 400 WORDS)
The Olefin Metathesis Approach to Epothilone A and Its Analogues (1997)

The olefin metathesis approach to epothilone A (1) and several analogues (39−41, 42−44, 51−57, 58−60, 64−65, and 67−69) is described. Key building blocks 6−8 were constructed in optically active form and were coupled and elaborated to olefin metathesis precursor 4 via an aldol reaction and an esterification coupling. Olefin metathesis of compound 4, under the catalytic influence of RuCl2(CHPh)(PCy3)2, furnished cis- and trans-cyclic olefins 3 and 48. Epoxidation of 49 gave epothilone A (1) and several analogues, whereas epoxidation of 50 resulted in additional epothilones. Similar elaboration of isomeric as well as simpler intermediates resulted in yet another series of epothilone analogues and model systems.
A Comparative Study Using Immunological and Biological Assays of the Haemostatic Responses to DDAVP Infusion Venous Occlusion and Exercise in Normal Men (1984)

In a group of six normal male volunteers, infusion of DDAVP, venous occlusion and exercise were shown to increase plasma levels of factor VIII and plasminogen activator, activity and antigen, to different extents and at differing rates. Any mechanisms suggested to explain release of these proteins by various stimuli should account for such differences. All three stimuli could also increase plasma levels of prostacyclin metabolites, although this was only significant for high doses of DDAVP. Other potential endothelial markers, such as fibronectin and thrombospondin, showed no specific increase after any of the stimuli.
Human islets of Langerhans express Fas ligand and undergo apoptosis in response to interleukin-1beta and Fas ligation. (1998)

IDDM results from a progressive loss of pancreatic beta-cells that, in humans, may be triggered by a combination of genetic and environmental factors. Recently, attention has been focused on the hypothesis that the loss of beta-cells is initiated by inappropriate induction of apoptosis. We now demonstrate that human islets of Langerhans undergo apoptosis upon exposure to interleukin-1beta. The cytokine also sharply increases the number of cells that enter apoptosis on treatment with a stimulatory anti-Fas antibody. Western blotting and immunocytochemistry clearly show for the first time that human pancreatic beta-cells normally express Fas ligand. The results suggest that human islet cells are primed to undergo apoptosis by interleukin-1beta and that this involves the close association between cell-surface Fas and its ligand.
Complex regulation of human NKG2D-DAP10 cell surface expression: opposing roles of the γc cytokines and TGF-β1 (2011)

Natural killer (NK) cells help protect the host against viral infections and tumors. NKG2D is a vital activating receptor, also expressed on subsets of T cells, whose ligands are up-regulated by cells in stress. Ligation of NKG2D leads to phosphorylation of the associated DAP10 adaptor protein, thereby activating immune cells. Understanding how the expression of NKG2D-DAP10 is regulated has implications for immunotherapy. We show that IL-2 and TGF-β1 oppositely regulate NKG2D-DAP10 expression by NK cells. IL-2 stimulation increases NKG2D surface expression despite a decrease in NKG2D mRNA levels. Stimulation with IL-2 results in a small increase of DAP10 mRNA and a large up-regulation of DAP10 protein synthesis, indicating that IL-2-mediated effects are mostly posttranscriptional. Newly synthesized DAP10 undergoes glycosylation that is required for DAP10 association with NKG2D and stabilization of NKG2D expression. TGF-β1 has an opposite and dominant effect to IL-2. TGF-β1 treatment decreases DAP10, as its presence inhibits the association of RNA polymerase II with the DAP10 promoter, but not NKG2D mRNA levels. This leads to the down-regulation of DAP10 expression and, as a consequence, NKG2D protein as well. Finally, we show that other γ(c) cytokines act similarly to IL-2 in up-regulating DAP10 expression and NKG2D-DAP10 surface expression.
An Integrated Microreactor System for Self‐Optimization of a Heck Reaction: From Micro‐ to Mesoscale Flow Systems (2010)

Aufbauen, anschalten, fertig: Die Kombination einer Rückkopplungssteuerung mit Durchflussoperationen in Mikroreaktoren (siehe Bild) ermöglicht eine vollautomatische Online-Reaktionsoptimierung. An einer Heck-Reaktion wird das Potenzial für eine schnelle Vielvariablen-Optimierung demonstriert, die mit minimalen Materialmengen auskommt. Die optimalen Bedingungen lassen sich schnell in einen 50-mal größeren Maßstab übertragen.
Idiopathic Nonspecific Interstitial Pneumonia (2008)

Idiopathic NSIP is a distinct clinical entity that occurs mostly in middle-aged women who are never-smokers. The prognosis of NSIP is very good.
Low-voltage temperature sensor for micro-power harvesters in silicon-on-sapphire CMOS (2006)

A low-voltage temperature sensor designed for MEMS power harvesting systems is fabricated. The core of the sensor is a bandgap voltage reference circuit operating with a supply voltage in the range 1–1.5 V. The prototype was fabricated on a conventional 0.5 µm silicon-on-sapphire (SOS) process. The sensor design consumes 15 µA of current at 1 V. The internal reference voltage is 550 mV. The temperature sensor has a digital square wave output the frequency of which is proportional to temperature. A linear model of the dependency of output frequency with temperature has a conversion factor of 1.6 kHz/°C. The output is also independent of supply voltage in the range 1–1.5 V. Measured results and targeted applications for the proposed circuit are reported.
Identification of 2 serine residues of MEK-1 that are differentially phosphorylated during activation by raf and MEK kinase. (1994)

The signal transduction kinase MEK (mitogen-activated protein (MAP) or extracellular signal-regulated (Erk) kinase)-1 is activated via phosphorylation by MEKK (MEK kinase) and raf kinases. We show here that these two kinases phosphorylate rat MEK-1 exclusively on two serine codons, Ser218 and Ser222. Phosphorylation of MEK-1 on serines 218 and 222 is both necessary and sufficient for MEK-1 to be activated and able to phosphorylate MAP kinase. A mutant form of MEK-1 that replaces these two codons with alanine cannot be activated, and one that substitutes glutamic acid residues in place of these 2 serines is active independent of activation by phosphorylation. These sites of activation occur in a region of MEK-1 that is similar to sites of activating phosphorylation in several other serine/threonine kinases, suggesting that this region may represent a conserved "activating domain" of many kinases. MEKK and raf display differences in site preference between these two codons, with MEKK showing preference for the amino acid at codon 218 and raf phosphorylating each residue approximately equally. This site preference might result in differences in the temporal or subsequent substrate patterns of MEK activation that result from these two activation pathways.
LXR Regulates Cholesterol Uptake Through Idol-Dependent Ubiquitination of the LDL Receptor (2009)

Cellular cholesterol levels reflect a balance between uptake, efflux, and endogenous synthesis. Here we show that the sterol-responsive nuclear liver X receptor (LXR) helps maintain cholesterol homeostasis, not only through promotion of cholesterol efflux but also through suppression of low-density lipoprotein (LDL) uptake. LXR inhibits the LDL receptor (LDLR) pathway through transcriptional induction of Idol (inducible degrader of the LDLR), an E3 ubiquitin ligase that triggers ubiquitination of the LDLR on its cytoplasmic domain, thereby targeting it for degradation. LXR ligand reduces, whereas LXR knockout increases, LDLR protein levels in vivo in a tissue-selective manner. Idol knockdown in hepatocytes increases LDLR protein levels and promotes LDL uptake. Conversely, adenovirus-mediated expression of Idol in mouse liver promotes LDLR degradation and elevates plasma LDL levels. The LXR-Idol-LDLR axis defines a complementary pathway to sterol response element-binding proteins for sterol regulation of cholesterol uptake.
Efficient generalized cross-validation with applications to parametric image restoration and resolution enhancement (2001)

In many image restoration/resolution enhancement applications, the blurring process, i.e., point spread function (PSF) of the imaging system, is not known or is known only to within a set of parameters. We estimate these PSF parameters for this ill-posed class of inverse problem from raw data, along with the regularization parameters required to stabilize the solution, using the generalized cross-validation method (GCV). We propose efficient approximation techniques based on the Lanczos algorithm and Gauss quadrature theory, reducing the computational complexity of the GCV. Data-driven PSF and regularization parameter estimation experiments with synthetic and real image sequences are presented to demonstrate the effectiveness and robustness of our method.
Radiofrequency catheter ablation of atrial arrhythmias. Results and mechanisms. (1994)

Ablation of automatic and reentrant atrial tachycardia and atrial flutter had a high success rate and caused no complications from energy application. Repeat procedures may be required for long-term success, especially in patients with atrial flutter. The mechanism by which ablation is successful is similar for atrial flutter and other forms of atrial reentry and involves severing a critical isthmus of slow conduction bounded by anatomic or structural obstacles. Automatic arrhythmias are abolished by directing lesions at the focus of abnormal impulse formation.
Apolipoprotein AIMilano. Accelerated binding and dissociation from lipids of a human apolipoprotein variant. (1985)

The lipid binding properties of apolipoprotein (apo) AIMilano, a molecular variant of human apolipoprotein AI, characterized by the Arg173----Cys substitution, was investigated by the use of dimyristoylphosphatidylcholine liposomes. Both the variant AIMilano and normal AI are incorporated to the same extent in stable complexes isolated by gel filtration, showing similar dimensions and stoichiometries. A higher affinity of apo-AIMilano for dimyristoylphosphatidylcholine is suggested by the faster association rate of the variant apoprotein compared to normal AI; similarly, apo-AIMilano is more readily displaced by guanidine hydrochloride from the isolated dimyristoylphosphatidylcholine-apoprotein complexes. When the secondary structure of apo-AIMilano was investigated by spectrofluoroscopy and circular dichroism, a higher fluorescence peak wavelength and a lower alpha-helical content were detected in the variant apoprotein compared to normal AI. The substitution Arg173----Cys in the AIMilano dramatically alters the amphipathic nature of the modified alpha-helical fragment of apoprotein AI. The association rate with lipids is accelerated by an increased exposure of hydrophobic residues. The reduced stability of the lipid-apoprotein particles is possibly mediated by a reduction in the number of helical segments involved in lipid association. The high flexibility of the AIMilano apolipoprotein in the interaction with lipids may explain its accelerated catabolism and the possibly improved uptake capacities for tissue lipids.
Proteoglycans synthesized by smooth muscle cells derived from monkey (Macaca nemestrina) aorta. (1983)

Smooth muscle cells derived from monkey aorta were cultured in medium with [35S]sulfate and [3H]glucosamine as labeling precursors. Proteoglycans in the medium and in 4 M guanidine HCl extracts of the cell layer were purified by DEAE-Sephacel and molecular sieve chromatography. Both preparations contained a predominant, large chondroitin sulfate proteoglycan (Kav = 0.30 on Sepharose CL-2B) with glycosaminoglycan chains of Mr approximately 43,000 average containing a ratio of 6-sulfate to 4-sulfate of approximately 2. Approximately 7 and 27% of the 3H label in this proteoglycan were present in N-linked and O-linked oligosaccharides, respectively. Reaggregation experiments indicated that a large proportion of these proteoglycans can form link protein-stabilized aggregates. The medium fraction also contained a smaller dermatan sulfate proteoglycan (Kav = 0.67 on Sepharose CL-2B) with glycosaminoglycan chains of Mr approximately 43,000 containing a ratio of 6-sulfate to 4-sulfate of about 0.5. This proteoglycan contained approximately the same percentage of N-linked oligosaccharides as the chondroitin sulfate proteoglycan, but few or no O-linked oligosaccharides. A smaller dermatan sulfate proteoglycan with a single chain was present only in the cell layer. Additionally, small amounts of heparan sulfate proteoglycans were synthesized by the cells.
Guest Editorial to the Special Issue on Therapeutic Ultrasound: Current Status and Future Directions (2010)

The nine papers in this special section are devoted to the topic and applicability of therapeutic ultrasound technologies and biomedical services.
Cybersecurity in the 21st Century: Applying Cyber Threat Intelligence (2015)

In the twenty-first century, the prevention of cyber attacks on critical infrastructure, key assets, and public/private sector enterprises will become a more important element of national and international security. This paper examines the extant literature published on the increasing need for a more robust, comprehensive and proactive approach to cybersecurity. Specifically, the paper explores the contemporary cyberspace environment and the current cyber threat landscape. The paper recommends the application of cyber threat intelligence (CTI) complemented by predictive analytics as an effective method for countering cyber attacks. The purpose of the paper is to advance the knowledge in this critical area, to increase the understanding of available methods for proactive detection of network security intrusions, and to highlight an emerging innovative approach to cyber threat intelligence.
Molecular epidemiology of human hepatitis A virus defined by an antigen-capture polymerase chain reaction method. (1990)

We describe an immunoaffinity-linked nucleic acid amplification system (antigen-capture/polymerase chain reaction, or AC/PCR) for detection of viruses in clinical specimens and its application to the study of the molecular epidemiology of a picornavirus, hepatitis A virus (HAV). Immunoaffinity capture of virus, synthesis of viral cDNA, and amplification of cDNA by a polymerase chain reaction (PCR) were carried out sequentially in a single reaction vessel. This approach simplified sample preparation and enhanced the specificity of conventional PCR. AC/PCR detected less than one cell culture infectious unit of virus in 80 microliters of sample. Sequencing of AC/PCR reaction products from 34 virus strains demonstrated remarkable conservation at the nucleotide level among most strains but revealed hitherto unsuspected genetic diversity among human isolates. Epidemiologically related strains were identical or closely related in sequence. Virus strains recovered from epidemics of hepatitis A in the United States and Germany were identical in sequence, providing evidence for a previously unrecognized epidemiologic link between these outbreaks.
Functional Analysis of the Cell-Specific Enhancer in the Human Proopiomelanocortin Gene by β-Galactosidase Histochemical Staining (1994)

Nucleotide sequences responsible for the cell-specific expression of the human proopiomelanocortin (POMC) gene were analyzed by histochemical staining of beta-galactosidase in culture cells transfected with chimeric genes containing the 5'-flanking regions of the human POMC gene fused to the Escherichia coli lacZ gene. The chimeric genes were stably introduced into various culture cells, including AtT-20 cells, which express the endogenous mouse POMC gene. Whereas the control gene containing the cytomegalovirus enhancer was expressed in all cell lines tested, only AtT-20 cells supported the efficient transcription of the gene containing 2.9 kb of the human POMC 5'-flanking region. These results indicate that the stable transfection-expression system utilizing the histochemical detection of the gene expression is a useful method for the analysis of cell-specific gene expression. These results have also confirmed that the trans-acting factors in mouse AtT-20 cells interact with the human POMC gene promoter region and activate the transcription of the gene. Deletion analysis has demonstrated that the profiles of the transcriptional activity of the various human POMC-lacZ fusion genes are similar to those of the rat POMC gene described previously. Comparison of the human and the rat 5'-flanking sequences revealed close homology in several regions, which might be involved in the efficient transcription of the POMC gene in AtT-20 cells.