gebhart/patrepeval huggingface dataset:
Continuous monitoring of receptor-mediated changes in the metabolic rates of living cells. (1990)

Activation of beta-adrenergic or muscarinic acetylcholine receptors expressed in transfected cells or epidermal growth factor receptors in human keratinocytes produces 15% to 200% changes in cellular metabolic rates. Changes in cell metabolism were monitored continuously with a previously described silicon-based microphysiometer that detects small changes in extracellular pH. The amplitude and kinetics of the metabolic changes depend upon several factors including pretreatment of the cells prior to receptor stimulation, the dose of hormone/neurotransmitter used, and the receptor complement of the cells. Responses are receptor specific; cells transfected with receptor genes respond only to the appropriate hormone/transmitter, whereas control (nontransfected) cells or cells transfected with different receptors exhibit no response. The specificity of the responses was further documented by using pharmacological antagonists. In Chinese hamster ovary (CHO) cells transfected with human beta 2-adrenergic receptors, isoproterenol produces a 20-60% increase in the rate of extracellular acidification with an EC50 of 4 nM, a response that is competitively antagonized by (-)-propranolol. The EC50 for the isoproterenol response is shifted from 4 nM to 100 nM in the presence of 3 nM (-)-propranolol. The kinetics of the metabolic response induced by beta-adrenergic receptor stimulation are markedly slower than those elicited by muscarinic receptor agonists. The maximal metabolic response in cells transfected with beta-adrenergic receptors peaks at approximately 12 min as compared with less than 30 sec in cells transfected with muscarinic receptors, perhaps reflecting activation of different second-messenger pathways. These findings illustrate an alternative means of studying cellular responses to hormones and neurotransmitters and suggest that metabolic changes will be generally useful for detecting the consequences of receptor-ligand interactions.
Distinct tachykinin NK1 receptor function in primate nucleus tractus solitarius neurons is dysregulated after second‐hand tobacco smoke exposure (2011)

The contribution of NK(1) receptors to cell excitability depended on firing phenotype of primate NTS neurons and was disrupted by SHS exposure, specifically in DS neurons. Our findings reveal a novel NK(1) receptor function in the primate brainstem and support the hypothesis that chronic exposure to SHS in children causes tachykinin-related neuroplastic changes in the CNS.
Integration of femtosecond laser written optical waveguides in a lab-on-chip (2008)

We use direct femtosecond laser writing to integrate optical waveguides into a commercial fused silica lab-on-chip (LOC). We fabricate high quality waveguides intersecting the microfluidic channels and use them to optically address with high spatial selectivity their content. Fluorescence from the photoexcited volume is efficiently collected at a 90 degrees angle by a high numerical aperture fiber, resulting in a compact and portable setup. Our approach is quite powerful because it allows the integration of photonic functionalities, by simple post-processing, into commercial LOCs, fabricated with standard techniques. By taking advantage of the unique three-dimensional capabilities of femtosecond laser writing, more complex functionalities, such as splitters or Mach-Zehnder interferometers, can be implemented.
Human immunodeficiency virus type 1 DNA synthesis, integration, and efficient viral replication in growth-arrested T cells (1993)

Human immunodeficiency virus type 1 (HIV-1) replicates efficiently in nonproliferating monocytes and macrophages but not in resting primary T lymphocytes. To determine the contribution of cell division to the HIV-1 replicative cycle in T cells, we evaluated HIV-1 expression, integration of proviral DNA, and production of infectious progeny virus in C8166 T-lymphoid cells blocked in cell division by treatment with either mitomycin, a DNA cross-linker, or aphidicolin, a DNA polymerase alpha inhibitor. The arrest of cell division was confirmed by assay of [3H]thymidine uptake; the nondividing cells remained viable for at least 3 days after treatment. HIV-1 was expressed and replicated equally well in nondividing and dividing C8166 cells, as judged by the comparison of the levels of p24 core antigens in culture supernatants, the proportion of cells expressing HIV-1 specific antigens, the pattern and quantity of HIV-1 DNA present in the extrachromosomal and total cellular DNA fractions, and the biological activity of progeny viruses. A polymerase chain reaction-based viral DNA integration assay indicated that HIV-1 provirus was integrated in C8166 cells treated with either of the two inhibitors of cell division. Similar results were obtained by using growth-arrested Jurkat T-lymphoid cells. We conclude that cell division and cellular DNA synthesis are not required for efficient HIV-1 expression in T cells.
A Highly Active Well-Defined Rhenium Heterogeneous Catalyst for Olefin Metathesis Prepared via Surface Organometallic Chemistry (2001)

International audience
A Novel Microwave Coaxial Slot Antenna for Liver Tumor Ablation (2014)

This paper is on the effect of a T-ring shape structure to enhance the capability of a microwave coaxial slot antenna (MCA) in the treatment of liver cancer. The MCA is composed of an interstitial coaxial line that is enclosed in a catheter. The T-ring shape structure is wrapped on the outer conductor of the MCA. Thanks to the new structure, the backward heating problem appearing in many coaxial antennas is reduced and the generated heat in front of the slot is higher than those for a classical MCA.
[Effect of phenol ring polymers on the release of plasminogen activators]. (1984)

The effects of synthetic and natural phenol polymers on the release of plasminogen activator were examined on an isolated vascular preparation of the pig ear. Of the synthetic phenol polymers, the products of caffeine acid and 3,4-dihydroxyphenylacetic acid were found to raise the activity of plasminogen activator. As far as the natural polymers of phenol are concerned, only sodium humate was found to produce an action similar to that of the products of caffeinic acid and 3,4-dihydroxyphenylacetic acid.
Platelet receptor polymorphisms and thrombotic risk. (2001)

Plaque rupture and/or endothelial damage lead to exposure of von Willebrand factor and collagen which facilitate the adhesion of circulating platelets via glycoprotein Ib-IX-V and the integrin alpha2 beta1, respectively, to the damaged vessel wall. This process activates the platelet and leads to a conformational change of a second integrin alphaIIb beta3 that facilitates fibrinogen binding and platelet aggregation. Thrombin generated at the blood-plaque interface converts fibrinogen to fibrin, which stabilizes thrombus growth. Therefore, any genetic differences that might alter surface expression or activity of these receptors could influence risk for adverse outcomes as a result of the haemostatic process. In the last 5 years, there has been a rapid accumulation of the literature concerning the relationship between genetic variations in platelet glycoproteins and risk for coronary heart disease. In this chapter, we present a comprehensive review of the impact of platelet receptor polymorphisms and thrombotic risk.
Point mutation of a conserved arginine (104) to lysine introduces hypersensitivity to inhibition by glyphosate in the 5‐enolpyruvylshikimate‐3‐phosphate synthase of Bacillus subtilis (1995)

The role of a conserved arginine (R104) in the putative phosphoenol pyruvate binding region of 5-enolpyruvyl shikimate-3-phosphate synthase of Bacillus subtilis has been investigated. Employing site directed mutagenesis arginine was substituted by lysine or glutamine. Native and mutant proteins were expressed and purified to near homogeneity. Estimation of Michaelis and inhibitor constants of the native and mutant proteins exhibited altered substrate-inhibitor binding mode and constants. Mutation R104K hypersensitized the enzyme reaction to inhibition by glyphosate. The role of R104 in discriminating between glyphosate and phosphoenol pyruvate is discussed.
Target-Accelerated Combinatorial Synthesis and Discovery of Highly Potent Antibiotics Effective Against Vancomycin-Resistant Bacteria (2000)

Biological activity can be predicted at a prescreening stage by using a target-accelerated combinatorial synthesis. The rate of dimerization of vancomycin analogues (see picture, X=CH=CH2, SAc) in the presence of vancomycin's targets Ac-D-Ala-D-Ala and Ac2-L-Lys-D-Ala-D-Ala correlated well with the observed biological activity. From this study three highly potent antibacterial agents effective against both vancomycin-susceptible and vancomycin-resistant bacteria strains were identified.
Liver fibrosis (2005)

Liver fibrosis is the excessive accumulation of extracellular matrix proteins including collagen that occurs in most types of chronic liver diseases. Advanced liver fibrosis results in cirrhosis, liver failure, and portal hypertension and often requires liver transplantation. Our knowledge of the cellular and molecular mechanisms of liver fibrosis has greatly advanced. Activated hepatic stellate cells, portal fibroblasts, and myofibroblasts of bone marrow origin have been identified as major collagen-producing cells in the injured liver. These cells are activated by fibrogenic cytokines such as TGF-β1, angiotensin II, and leptin. Reversibility of advanced liver fibrosis in patients has been recently documented, which has stimulated researchers to develop antifibrotic drugs. Emerging antifibrotic therapies are aimed at inhibiting the accumulation of fibrogenic cells and/or preventing the deposition of extracellular matrix proteins. Although many therapeutic interventions are effective in experimental models of liver fibrosis, their efficacy and safety in humans is unknown. This review summarizes recent progress in the study of the pathogenesis and diagnosis of liver fibrosis and discusses current antifibrotic strategies.
Guanidinoglycosides:  A Novel Family of RNA Ligands (2000)

ADVERTISEMENT RETURN TO ISSUEPREVCommunicationNEXTGuanidinoglycosides: A Novel Family of RNA LigandsNathan W. Luedtke, Tracy J. Baker, Murray Goodman, and Yitzhak TorView Author Information Department of Chemistry and Biochemistry University of California, San Diego La Jolla, California 92093-0358 Cite this: J. Am. Chem. Soc. 2000, 122, 48, 12035–12036Publication Date (Web):November 17, 2000Publication History Received5 July 2000Published online17 November 2000Published inissue 1 December 2000https://pubs.acs.org/doi/10.1021/ja002421mhttps://doi.org/10.1021/ja002421mrapid-communicationACS PublicationsCopyright © 2000 American Chemical SocietyRequest reuse permissionsArticle Views1314Altmetric-Citations96LEARN 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 optionsGet e-AlertscloseSupporting Info (1)»Supporting Information Supporting Information SUBJECTS:Carbohydrates,Fluorescence,Genetics,Magnetic properties,Selectivity Get e-Alerts
Woodchuck Hepatitis Virus Posttranscriptional Regulatory Element Enhances Expression of Transgenes Delivered by Retroviral Vectors (1999)

The expression of genes delivered by retroviral vectors is often inefficient, a potential obstacle for their widespread use in human gene therapy. Here, we explored the possibility that the posttranscriptional regulatory element of woodchuck hepatitis virus (WPRE) might help resolve this problem. Insertion of the WPRE in the 3' untranslated region of coding sequences carried by either oncoretroviral or lentiviral vectors substantially increased their levels of expression in a transgene-, promoter- and vector-independent manner. The WPRE thus increased either luciferase or green fluorescent protein production five- to eightfold, and effects of a comparable magnitude were observed with either the immediate-early cytomegalovirus or the herpesvirus thymidine kinase promoter and with both human immunodeficiency virus- and murine leukemia virus-based vectors. The WPRE exerted this influence only when placed in the sense orientation, consistent with its predicted posttranscriptional mechanism of action. These results demonstrate that the WPRE significantly improves the performance of retroviral vectors and emphasize that posttranscriptional regulation of gene expression should be taken into account in the design of gene delivery systems.
A molecular model of membrane excitability (1974)

Abstract Alamethicin, monazomycin, or EIM induce electrical excitability in lipid bilayers. The voltage‐dependent gating displays all the characteristics observed in excitable cells and its basic features can be quantitatively described by the Hodgkin‐Huxley equations. A common molecular mechanism of membrane excitation has been postulated. It assumes that in the absence of an electrical field the channel‐forming molecules lie at the surface of the membrane. An applied potential tilts them from the surface into the hydrocarbon region of the bilayer. Once in this position the molecules diffuse laterally and form aggregates which act as channels for the flow of ions. In the case of alamethicin we assume that the molecule forms an elongated ellipsoid with two glutamic residues at one end, and a metal ion in four‐ or five‐fold coordination with peptide carbonyl oxygens at the other. An applied field pulls the cationic end through the membrane to the other side, while the glutamic residues hold the other end attached to the original surface. The molecules now span the membrane and aggregate, forming oligomeric channels in which most of the peptide carbonyls face toward the center, and the methyl groups outward. Monomers and dimers do not conduct and an individual channel can have different conductance values depending on the number of monomers in the aggregate and the resulting channel diameter. A quantitative description of this process matches observed gating kinetics, gating currents, and the single channel conductance increments. Without additional assumptions, inactivation follows directly from the aggregation process because with proper rate constants, the average degree of polymerization and therefore number of open channels goes through a maximum in time. The model may also apply to the excitation process of higher cells.
Biodegradable alginate microspheres as a delivery system for naked DNA. (1999)

Sodium alginate is a naturally occurring polysaccharide that can easily be polymerized into a solid matrix to form microspheres. These biodegradable microspheres were used to encapsulate plasmid DNA containing the bacterial beta-galactosidase (LacZ) gene under the control of either the cytomegalovirus (CMV) immediate-early promoter or the Rous sarcoma virus (RSV) early promoter. Mice inoculated orally with microspheres containing plasmid DNA expressed LacZ in the intestine, spleen and liver. Inoculation of mice with microspheres containing both the plasmid DNA and bovine adenovirus type 3 (BAd3) resulted in a significant increase in LacZ expression compared to those inoculated with microspheres containing only the plasmid DNA. Our results suggest that adenoviruses are capable of augumenting transgene expression by plasmid DNA both in vitro and in vivo.
KEGG for representation and analysis of molecular networks involving diseases and drugs (2009)

Most human diseases are complex multi-factorial diseases resulting from the combination of various genetic and environmental factors. In the KEGG database resource (http://www.genome.jp/kegg/), diseases are viewed as perturbed states of the molecular system, and drugs as perturbants to the molecular system. Disease information is computerized in two forms: pathway maps and gene/molecule lists. The KEGG PATHWAY database contains pathway maps for the molecular systems in both normal and perturbed states. In the KEGG DISEASE database, each disease is represented by a list of known disease genes, any known environmental factors at the molecular level, diagnostic markers and therapeutic drugs, which may reflect the underlying molecular system. The KEGG DRUG database contains chemical structures and/or chemical components of all drugs in Japan, including crude drugs and TCM (Traditional Chinese Medicine) formulas, and drugs in the USA and Europe. This database also captures knowledge about two types of molecular networks: the interaction network with target molecules, metabolizing enzymes, other drugs, etc. and the chemical structure transformation network in the history of drug development. The new disease/drug information resource named KEGG MEDICUS can be used as a reference knowledge base for computational analysis of molecular networks, especially, by integrating large-scale experimental datasets.
Population-based risk of complications following transthoracic needle lung biopsy of a pulmonary nodule (2011)

Background
Because pulmonary nodules are found in up to 25% of patients undergoing chest computed tomography, the question of whether to biopsy is becoming increasingly common. Data on complications following transthoracic needle lung biopsy are limited to case series from selected institutions.
Segank: A Distributed Mobile Storage System (2004)

This paper presents a distributed mobile storage system designed for storage elements connected by a network of non-uniform quality. Flexible data placement is crucial, and it leads to challenges for locating data and keeping it consistent. Our system employs a locationand topology-sensitive multicast-like solution for locating data, lazy peer-to-peer propagation of invalidation information for ensuring consistency, and a distributed snapshot mechanism for supporting sharing. The combination of these mechanisms allows a user to make the most of what a non-uniform network has to offer in terms of gaining fast access to fresh data, without incurring the foreground penalty of keeping distributed elements on a weak network consistent.
Image Restoration Using Convolutional Auto-encoders with Symmetric Skip Connections (2016)

Image restoration, including image denoising, super resolution, inpainting, and so on, is a well-studied problem in computer vision and image processing, as well as a test bed for low-level image modeling algorithms. In this work, we propose a very deep fully convolutional auto-encoder network for image restoration, which is a encoding-decoding framework with symmetric convolutional-deconvolutional layers. In other words, the network is composed of multiple layers of convolution and de-convolution operators, learning end-to-end mappings from corrupted images to the original ones. The convolutional layers capture the abstraction of image contents while eliminating corruptions. Deconvolutional layers have the capability to upsample the feature maps and recover the image details. To deal with the problem that deeper networks tend to be more difficult to train, we propose to symmetrically link convolutional and deconvolutional layers with skip-layer connections, with which the training converges much faster and attains better results.
Antitumor effect of parathyroid hormone-related protein neutralizing antibody in human renal cell carcinoma in vitro and in vivo (2005)

Functional inactivation of the von Hippel-Lindau (VHL) tumor suppressor gene occurs in 40-80% of human conventional renal cell carcinomas (RCCs). We showed recently that VHL-deficient RCCs expressed large amounts of parathyroid hormone-related protein (PTHrP), and that PTHrP, acting through the PTH1 receptor (PTH1R), plays an essential role in tumor growth. We also showed that PTHrP expression is negatively regulated by the VHL gene products (pVHL). Our goal was to determine whether blocking the PTHrP/PTH1R system might be of therapeutic value against RCC, independent of VHL status and PTHrP expression levels. The antitumor activity of PTHrP neutralizing antibody and of PTH1R antagonist were evaluated in vitro and in vivo in a panel of human RCC lines expressing or not pVHL. PTHrP is upregulated compared with normal tubular cells. In vitro, tumor cell growth and viability was decreased by up to 80% by the antibody in all cell lines. These effects resulted from apoptosis. Exogenously added PTHrP had no effect on cell growth and viability, but reversed the inhibitory effects of the antibody. The growth inhibition was reproduced by a specific PTH1R antagonist in all cell lines. In vivo, the treatment of nude mice bearing the Caki-1 RCC tumor with the PTHrP antibody inhibited tumor growth by 80%, by inducing apoptosis. Proliferation and neovascularization were not affected by the antiserum. Anti-PTHrP treatment induced no side effects as assessed by animal weight and blood chemistries. Current therapeutic strategies are only marginally effective against metastatic RCC, and adverse effects are common. This study provides a rationale for evaluating the blockade of PTHrP signaling as therapy for human RCC in a clinical setting.
Diverse roles for the Eph family of receptor tyrosine kinases in carcinogenesis (2002)

The Eph family of receptor tyrosine kinases and their cell-presented ligands, the ephrins, are frequently overexpressed in a wide variety of cancers, including breast, small-cell lung and gastrointestinal cancers, melanomas, and neuroblastomas. In particular, one Eph family member, EphA2, is overexpressed in many cancers, including 40% of breast cancers. EphA2 can also transform breast epithelial cells in vitro to display properties commonly associated with the development of metastasis. Remarkably, the oncogenic properties of EphA2 contravene traditional dogma with regard to the oncogenic properties of a growth factor and its receptor tyrosine kinase: while stimulation of EphA2 by its ligand (ephrin-A1) results in EphA2 autophosphorylation, the stimulation reverses the oncogenic transformation. As will be discussed in this review, the apparent dependence of oncogenicity on the dephosphorylated state of EphA2 most probably reflects the unique nature of Eph signaling. In particular, oncogenecity may depend on the capacity of unactivated EphA2 to interact with a variety of signaling molecules. As well as acting in oncogenic transformation, a growing body of evidence supports the importance of the concerted actions of ephrins and Eph molecules in tumor angiogenesis. Genetic studies, using targeted mutagenesis in mice, reveal that ephrin-B1, ephrin-B2, and EphB4 are essential for the normal morphogenesis of the embryonic vasculature into a sophisticated network of arteries, veins, and capillaries. Initial studies indicate that these molecules are also angiogenic in tumors, and as such represent important new targets for the development of chemotherapeutic treatments.
The AM (Armenia) Domain (1996)

This memo provides information for the Internet community.This memo does not specify an Internet standard of any kind.