gebhart/patrepeval huggingface dataset:
Benoxaprofen improves psoriasis. A double-blind study (1983)

• The pathophysiologic significance of increased levels of lipoxygenase compounds in psoriatic lesions was assessed in a double-blind randomized clinical study with the 5-lipoxygenase inhibitor, benoxaprofen. Forty patients with psoriasis vulgaris were treated with 600 mg of oral benoxaprofen daily or a placebo for a period of eight weeks. Benoxaprofen therapy provided excellent treatment results in about 75% of the cases. In the placebo group, only minimal improvement occurred. Most patients receiving benoxaprofen therapy reported side effects including photosensitivity, onycholysis, milia, diarrhea, and edema. In two cases, benoxaprofen was withdrawn before completion of the treatment course because of photosensitivity. Benoxaprofen may affect psoriatic epidermis either directly by the inhibition of epidermal 5-lipoxygenase or indirectly by the inhibition of the accumulation of phagocytes in psoriatic lesions. Despite serious side effects from benoxaprofen therapy, lipoxygenase-inhibiting agents deserve further study in the treatment of psoriasis. (<i>Arch Dermatol</i>1983;119:548-552)
Human Cytomegalovirus Glycoprotein gO Complexes with gH/gL, Promoting Interference with Viral Entry into Human Fibroblasts but Not Entry into Epithelial Cells (2011)

A complex of five human cytomegalovirus virus (HCMV) proteins, gH, gL, UL128, UL130, and UL131 (gH/gL/UL128-131), is essential for virus entry into epithelial cells. We previously showed that gH/gL/UL128-131 expressed in epithelial cells interferes with subsequent HCMV entry into cells. There was no interference with only gH/gL or gB. We concluded that the expression of gH/gL/UL128-131 causes a mislocalization or downregulation of epithelial cell proteins that HCMV requires for entry. In contrast, gH/gL/UL128-131 expression in fibroblasts did not produce interference, suggesting a different mechanism for entry. Here, we show that the coexpression of another HCMV glycoprotein, gO, with gH/gL in human fibroblasts interferes with HCMV entry into fibroblasts but not epithelial cells. However, the coexpression of gO with gH/gL did not increase the cell surface expression level of gH/gL and did not enhance cell-cell fusion, a process that depends upon cell surface gH/gL. Instead, gO promoted the export of gH/gL from the endoplasmic reticulum (ER) and the accumulation of gH/gL in the trans-Golgi network. Thus, interference with gH/gL or gH/gL/gO, i.e., the mislocalization or blocking of entry mediators, occurs in cytoplasmic membranes and not in cell surface membranes of fibroblasts. Together, the results provide additional support for our hypotheses that epithelial cells express putative gH/gL/UL128-1331 receptors important for HCMV entry and that fibroblasts express distinct gH/gL receptors.
Rayleigh scattering in high-Q microspheres (2000)

The Rayleigh scattering has to be largely suppressed in high-Q whispering-gallery modes in microspheres because of restrictions imposed on scattering angles by cavity confinement. Earlier estimates of the fundamental limit for the quality factor in fused-silica microspheres are revisited, and Q≃1012 is predicted in few-millimeter-size fused-silica spheres, if the surface hydration problem is ovecome. Particular effects of surface scattering losses are analyzed, and the manifestation of scattering in the form of intermode coupling is calculated. The predominant effect of counterpropagating mode coupling (intracavity backscattering) is analyzed in the presence of a mode-matched traveling-wave coupler. As much as 100% resonance reflection regime is shown to be feasible.
Complete nucleotide sequence, molecular analysis and genome structure of bacteriophage A118 of Listeria monocytogenes : implications for phage evolution (2000)

A118 is a temperate phage isolated from Listeria monocytogenes. In this study, we report the entire nucleotide sequence and structural analysis of its 40 834 bp DNA. Electron microscopic and enzymatic analyses revealed that the A118 genome is a linear, circularly permuted, terminally redundant collection of double-stranded DNA molecules. No evidence for cohesive ends or for a terminase recognition (pac) site could be obtained, suggesting that A118 viral DNA is packaged via a headful mechanism. Partial denaturation mapping of DNA cross-linked to the tail shaft indicated that DNA packaging proceeds from left to right with respect to the arbitrary genomic map and the direction of genes necessary for lytic development. Seventy-two open reading frames (ORFs) were identified on the A118 genome, which are apparently organized in a life cycle-specific manner into at least three major transcriptional units. N-terminal amino acid sequencing, bioinformatic analyses and functional characterizations enabled the assignment of possible functions to 26 ORFs, which included DNA packaging proteins, morphopoetic proteins, lysis components, lysogeny control-associated functions and proteins necessary for DNA recombination, modification and replication. Comparative analysis of the A118 genome structure with other bacteriophages revealed local, but sometimes extensive, similarities to a number of phages spanning a broader phylogenetic range of various low G+C host bacteria, which implies relatively recent exchange of genes or genetic modules. We have also identified the A118 attachment site attP and the corresponding attB in Listeria monocytogenes, and show that site-specific integration of the A118 prophage by the A118 integrase occurs into a host gene homologous to comK of Bacillus subtilis, an autoregulatory gene specifying the major competence transcription factor.
Annexin 11 is required for midbody formation and completion of the terminal phase of cytokinesis (2004)

Annexins are Ca(2+)-binding, membrane-fusogenic proteins with diverse but poorly understood functions. Here, we show that during cell cycle progression annexin 11 translocates from the nucleus to the spindle poles in metaphase and to the spindle midzone in anaphase. Annexin 11 is recruited to the midbody in late telophase, where it forms part of the detergent-resistant matrix that also contains CHO1. To investigate the significance of these observations, we used RNA interference to deplete cells of annexin 11. A combination of confocal and video time-lapse microscopy revealed that cells lacking annexin 11 fail to establish a functional midbody. Instead, daughter cells remain connected by intercellular bridges that contain bundled microtubules and cytoplasmic organelles but exclude normal midbody components such as MKLP1 and Aurora B. Annexin 11-depleted cells failed to complete cytokinesis and died by apoptosis. These findings demonstrate an essential role for annexin 11 in the terminal phase of cytokinesis.
Polymer surface modification : relevance to adhesion (1996)

This book documents the proceedings of the Fourth International Symposium on Polymer Surface Modification: Relevance to Adhesion held under the auspices of MST Conferences, LLC in Orlando, FL, June 9-11, 2003. Polymers are used for a variety of purposes in a host of technological applications and even a cursory look at the literature will evince that currently there is tremendous interest and RD 2. Other / Miscellaneous Surface Modification Techniques; and 3. General Papers. The topics covered include: low pressure plasma surface modification of a variety of polymers using various gases; atmospheric pressure plasma treatment; improvement of stain release properties of fabrics; modification of electrostatic properties of polymers; photon-based processes for surface modification of fibers; excimer UV light treatment; excimer laser surface treatment; low-energy ion treatment; photo-grafting and photo-curing; metallization of treated polymers; chemical (wet) functionalization of polymers; adhesion of paints to thermoplastic substrates; polymer release surfaces; nanolithography in polymer films; gas barrier properties of ceramic layers on polymers; and modification of interphase layer and relevance to adhesion. This volume and its predecessors containing plentiful information should serve as a comprehensive source of latest R&D activity in the highly technologically important arena of polymer surface modification. Anyone interested a centrally or peripherallya in knowing or learning about the various ways to modify polymer surfaces should find this book of immense value.
Compressed sensing based method for ECG compression (2011)

Compressive sensing (CS) is a new approach for the acquisition and recovery of sparse signals that enables sampling rates significantly below the classical Nyquist rate. Based on the fact that electrocardiogram (ECG) signals can be approximated by a linear combination of a few coefficients taken from a Wavelet basis, we propose a compressed sensing-based approach for ECG signal compression. ECG signals generally show redundancy between adjacent heartbeats due to its quasi-periodic structure. We show that this redundancy implies a high fraction of common support between consecutive heartbeats. The contribution of this paper lies in the use of distributed compressed sensing to exploit the common sup port between samples of jointly sparse adjacent beats. Simulation results suggest that compressed sensing should be considered as a plausible methodology for ECG compression.
Screen‐printed voltammetric and amperometric electrochemical sensors for decentralized testing (1994)

Abstract This review describes the design and fabrication of screen‐printed voltommetric and amperometric electrochemical sensors, together with their applications for decentralized monitoring of several naturally occurring biomolecules, drugs, and potential environmental and industrial pollutants or toxins.
AMP-Activated Protein Kinase as a Drug Target (2006)

The AMP-activated protein kinase (AMPK) system is a regulator of energy balance at both the cellular and whole-body levels that, once activated by low energy status, effects a switch from ATP-consuming anabolic pathways to ATP-producing catabolic pathways. It now appears to be the major target for two existing classes of drug used to treat type 2 diabetes, i.e., the biguanides and thiazolidinediones. However, in both cases these activate AMPK indirectly, and an interesting question concerns whether a drug that directly activated AMPK would retain the therapeutic benefits of the existing drugs while eliminating unwanted side effects. AMPK activators also now have potential as anticancer drugs.
Pseudomonas aeruginosa Activates Human Mast Cells to Induce Neutrophil Transendothelial Migration Via Mast Cell-Derived IL-1α and β (2002)

The mechanisms of neutrophil (PMN) recruitment to Pseudomonas aeruginosa infection remain incompletely defined. Mast cells (MC) involvement in this process has not been studied previously. In this study, we demonstrate that human cord blood-derived MC phagocytose P. aeruginosa and release mediators that activate HUVEC monolayers for supporting PMN transmigration. Pretreatment of supernatants from P. aeruginosa-MC cocultures with neutralizing anti-IL-1alpha plus anti-IL-1beta Abs, or IL-1R antagonist before addition to HUVEC for stimulation completely abrogated MC-induced PMN transmigration, while anti-TNF-alpha treatment had no effect. The expression of E-selectin and ICAM-1 on HUVEC, the latter a ligand for PMN CD11/CD18, was significantly up-regulated by P. aeruginosa-induced MC mediators. Pretreatment of human PMN with anti-CD18 mAb or pretreatment of HUVEC with a combination of three mAbs (against ICAM-1, ICAM-2, and E-selectin) inhibited by 85% the MC-dependent PMN transmigration. Moreover, P. aeruginosa-induced production of IL-1alpha and IL-1beta was down-regulated by IL-10 and dexamethasone. This study demonstrates for the first time that MC may mediate P. aeruginosa-induced PMN recruitment via production of IL-1alpha and beta. These findings have important implications for diseases involving P. aeruginosa infection and suggest novel targets for modulating P. aeruginosa-induced inflammation.
Lenvatinib, an angiogenesis inhibitor targeting VEGFR/FGFR, shows broad antitumor activity in human tumor xenograft models associated with microvessel density and pericyte coverage (2014)

These results indicated that Lenvatinib inhibited VEGF- and FGF-driven angiogenesis and showed a broad spectrum of antitumor activity with a wide therapeutic window. MVD and pericyte-coverage of tumor vasculature might be biomarkers and suggest cases that would respond for lenvatinib therapy.
Magnetic Field Effects on Bow Shock Stand-Off Distance (1958)

Combined theoretical and experimental investigations have been carried out to determine the effects of applying magnetic fields to the ionized flow about a blunt body of revolution. (W.D.M.)
Ethanol inhibits insulin-like growth factor-1-mediated signalling and proliferation of C6 rat glioblastoma cells. (1994)

The data indicate that physiologically relevant concentrations of ethanol inhibit the responses of glial cells to IGF-1, including IGF-1 receptor autophosphorylation, IRS-1 and phosphatidylinositol-3 kinase activation, and cell growth.
Characterization of a factor inducing differentiation of mouse myeloid leukemic cells purified from conditioned medium of mouse Ehrlich ascites tumor cells (1984)

A factor inducing differentiation of mouse myeloid leukemic cells (MI) into macrophages was purified to apparent homogeneity from 168 1 of CM of Ehrlich ascites tumor cells. The purified factor was half-maximally active at 2 X 10(-11) M. The factor was analyzed by radioiodination, SDS-polyacrylamide gel electrophoresis and autoradiography. Its Mr was 40 000-50 000. On reduction, the factor lost activity, but showed no subunit structure. Treatment of the factor with endo-beta-N-acetylglucosaminidase F, but not endo-beta-N-acetylglucosaminidase H, gave rise to a molecule of Mr 20 000-28 000. The activity of the factor from Ehrlich cells was completely neutralized by antiserum to the factor of Mr 50 000-70 000 from mouse fibroblast L929 cells.
Overexpressed androgen receptor linked to p21WAF1 silencing may be responsible for androgen independence and resistance to apoptosis of a prostate cancer cell line. (2001)

An androgen-independent (AI) prostate cancer cell line, derived recently from an LNCaP cell line maintained in androgen-poor conditions, has properties resembling a subgroup of advanced prostate cancers in that it has an overexpressed androgen receptor (AR), undetectable levels of p21WAF1 and prostate-specific antigen, and is resistant to apoptosis. The loss of prostate-specific antigen expression but not the p21WAF1 is attributable to gene silencing by hypermethylation. The high AR and undetectable p21WAF1 of AI cells, and lower AR but highly expressed p21WAF1 of androgen-dependent parental LNCaP cells, suggest a possibility of a functional link between these two proteins. Therefore, we examined the impact the modulation of AR will have on the expression of p21WAF1. Treatment of androgen-dependent cells with an androgen agonist, R1881, increased the AR protein level, whereas it simultaneously reduced the endogenous p21WAF1-protein 8-fold and the activity of a transiently transfected p21-promoter-reporter 10-fold. The down-regulation of p21WAF1 promoter appeared to be ARE mediated, dependent on AR, and not cell-type specific. Furthermore, a reduction of the AR level in AI cells by AR-antisense oligonucleotide increased the p21WAF1 promoter-reporter activity by approximately 4-fold, confirming a functional link between these two proteins. A strong, direct induction of p21WAF1 expression achieved by treatment of AI cells with trichostatin A produced a partial reversion of the AI phenotype evidenced by increased sensitivity of these cells to paclitaxel-induced apoptosis. Moreover, a reduction of AR level by antisense treatment, which also increased p21WAF1 expression, partially restored the androgen dependence of AI cells for growth. The functional link between AR dosage and p21WAF1 expression suggests that therapeutic reduction of AR protein in advanced prostate cancers with elevated AR levels may re-establish their hormone dependence and improve therapeutic response to repeated hormonal ablation and/or induction of apoptosis.
Visible-Light-Controlled Ruthenium-Catalyzed Olefin Metathesis (2019)

Olefin metathesis is now one of the most efficient ways to create new carbon-carbon bonds. While most efforts focused on the development of ever-more efficient catalysts, a particular attention has recently been devoted to developing latent metathesis catalysts, inactive species that need an external stimulus to become active. This furnishes an increased control over the reaction which is crucial for applications in materials science. Here, we report our work on the development of a new system to achieve visible-light-controlled metathesis by merging olefin metathesis and photoredox catalysis. The combination of a ruthenium metathesis catalyst bearing two N-heterocyclic carbenes with an oxidizing pyrylium photocatalyst affords excellent temporal and spatial resolution using only visible light as stimulus. Applications of this system in synthesis, as well as in polymer patterning and photolithography with spatially resolved ring-opening metathesis polymerization, are described.
Analysis and Visualisation of Neutron-Scattering Data (1996)

Rapid data inspection and analysis for large arrays is achieved by the program LAMP which was locally written using the IDL® language. Ease of use is ensured by graphical user interfaces, and flexibility is offered by data structure which is optimised for neutron-scattering data and user-macros.
A unified approach to constrained mapping and routing on network-on-chip architectures (2005)

One of the key steps in Network-on-Chip (NoC) based design is spatial mapping of cores and routing of the communication between those cores. Known solutions to the mapping and routing problem first map cores onto a topology and then route communication, using separated and possibly conflicting objective functions. In this paper we present a unified single-objective algorithm, called Unified MApping, Routing and Slot allocation (UMARS). As the main contribution we show how to couple path selection, mapping of cores and TDMA time-slot allocation such that the network required to meet the constraints of the application is minimized. The time-complexity of UMARS is low and experimental results indicate a run-time only 20% higher than that of path selection alone. We apply the algorithm to an MPEG decoder System-on-Chip (SoC), reducing area by 33%, power by 35% and worst-case latency by a factor four over a traditional multi-step approach.
Low energy electron microscopy investigations of kinetics and energetics on clean close-packed metal surfaces (2005)

Experiments are described in which low energy electron microscopy is employed to investigate the kinetics and energetics of clean close-packed metal surfaces, using step fluctuation spectroscopy. The data contain systematic trends of surface mass diffusion and step energetics that are identified and discussed. Further experiments and equipment development have been undertaken to explore the influence of accelerated mixing on surface evolution caused by ion beams, through the resulting kinetic and energetic perturbations of surface processes.
Aberrant DNA methylation associated with aggressiveness of gastrointestinal stromal tumour (2011)

Our results suggest that GIST is not, in epigenetic terms, a uniform disease and that DNA methylation in a set of genes is associated with aggressive clinical behavior and unfavorable prognosis. The genes identified may potentially serve as biomarkers for predicting aggressive GISTs with poor survivability.
Integrated approach to 3D near surface characterization in desert regions (2008)

Andreas Laake, Claudio Strobbia and Andrew Cutts build on work previously published in First Break to show the value of an integrated approach including remote sensing data to improve near surface modelling in desert areas typical of North Africa and the Middle East.
Ultrahigh optical Q factors of crystalline resonators in the linear regime (2006)

Experimental demonstration of record optical quality factor of $(6.3\ifmmode\pm\else\textpm\fi{}0.8)\ifmmode\times\else\texttimes\fi{}{10}^{10}$ corresponding to cavity ring-down time of $\ensuremath{\tau}\ensuremath{\simeq}36\phantom{\rule{0.3em}{0ex}}\ensuremath{\mu}\mathrm{s}$ is made possible by avoiding nonlinear effects in a crystalline whispering gallery mode resonator. We discuss various loss mechanisms in $\mathrm{Ca}{\mathrm{F}}_{2}$ cavities and ways of achieving higher quality factors. Possible applications in quantum optics and photonics are discussed.
Light dosimetry in brain tissue: An in vivo model applicable to photodynamic therapy (1986)

The intensity of blue-green (488 nm) and red (633 nm) light as a function of increasing distance from an implanted laser fiberoptic source in the brains of anesthetized rats was measured. There was significant (90%) attenuation of the light intensity for both 488 nm and 633 nm at a distance of 2.5 mm from the intracerebral laser light-emitting source. At greater distances from the light-emitting source that corresponded to areas in the cerebral cortex, there was greater attenuation of light intensity for increasing distance with 488 nm than with 633 nm because of the increased vascularity of the cortical mantle and absorption of 488 nm by hemoglobin. When hematoporphyrin derivative was given intravascularly, there was increased attenuation of 633 nm through the cerebral cortex that was similar to that seen for 488 nm in normals. Direct assessment of light intensity in living tissue, which we have shown is possible in this report, will aid in our understanding and interpretation of the histological changes that occur following photodynamic therapy.
Inhibition of Epidermal Growth Factor Receptor Signaling Protects Human Malignant Glioma Cells from Hypoxia-Induced Cell Death (2004)

Epidermal growth factor receptor (EGFR) signaling has become an important target for drug development because EGFR signaling enhances tumor cell proliferation, migration, and invasion and inhibits apoptosis. However, the results of clinical trials using EGFR inhibitors in patients with solid tumors have been disappointing. Here, we report a protective effect of the EGFR inhibitors AG1478 and PD153035 against cell death induced by acute hypoxia, which contrasts with their proapoptotic effects under normoxia. Under hypoxic conditions, both agents reduced glucose consumption, delayed ATP depletion, and preserved the mitochondrial membrane potential. Exposure either to hypoxia or the EGFR inhibitors under normoxic conditions resulted in the dephosphorylation of ribosomal protein S6, a player in the energy and nutrient-sensing pathway governed by mammalian target-of-rapamycin (mTOR). Combined inhibition of phosphatidylinositol 3'-kinase (PI3K) and extracellular signal-regulated kinase-1/2 (ERK1/2) mimicked the protective effects of EGFR inhibition on hypoxia-induced cell death and protein S6 dephosphorylation. These results caution that therapies targeting EGFR signaling pathways can protect tumor cells from acute hypoxia.