gebhart/patrepeval huggingface dataset:
CAD for HERMES antennas (2003)

During the launch, landing and orbit phases of the proposed HERMES spacecraft, telecommand data (10 kb/s) and telemetry data (25 kb/s) are transmitted between HERMES and the ground by a relay satellite. An analysis of operational requirements resulted in the selection of four switched antennas, integrated within the plane structure, each of which may comprise several antennas. The two software packages used assess the performance of these antennas are briefly reviewed. The first package is for implementing the boundary element method (BEM). The program is executed on a DEC VAX 8600 and the linear system, whose matrix is complex, symmetrical and complete, is solved on an array processor, FPS 164/MAX. The electromagnetic characteristics (radiation patterns, surface currents, etc.) of the antenna are displayed graphically. The other package, SARGASSES, is an interactive simulator for antennas on structures such as aircraft or spacecraft.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Computer-assisted Fluoroscopic Targeting System for Pedicle Screw Insertion (2000)

Our data indicate that this first-generation fluoroscopy-based targeting system can significantly assist the surgeon in pedicle screw placement. The overall accuracy is comparable to an IGS, especially in the region of T9-L5. A second-generation system with a faster end-effector and user-friendly interface should significantly reduce the operating and fluoroscope time.
Correction to Targeting the Binding Function 3 (BF3) Site of the Human Androgen Receptor through Virtual Screening (2011)

ADVERTISEMENT RETURN TO ISSUEPREVAddition/CorrectionORIGINAL ARTICLEThis notice is a correctionCorrection to Targeting the Binding Function 3 (BF3) Site of the Human Androgen Receptor through Virtual ScreeningNathan A. Lack, Peter Axerio-Cilies, Peyman Tavassoli, Frank Q. Han, Ka Hong Chan, Clementine Feau, Eric LeBlanc, Emma Tomlinson Guns, R. Kiplin Guy, Paul S. Rennie, and Artem Cherkasov*Cite this: J. Med. Chem. 2012, 55, 1, 565Publication Date (Web):December 28, 2011Publication History Published online28 December 2011Published inissue 12 January 2012https://pubs.acs.org/doi/10.1021/jm201689yhttps://doi.org/10.1021/jm201689ycorrectionACS PublicationsCopyright © 2011 American Chemical Society. This publication is available under these Terms of Use. Request reuse permissions This publication is free to access through this site. Learn MoreArticle Views5657Altmetric-Citations3LEARN 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 PDF (112 KB) Get e-Alertsclose Get e-Alerts
Production Of PGI2 By Cultured Endothelial Cells And Smooth Muscle Cells (1981)

Prostacyclin (PGI2) is the main product of the cyclooxygenase pathway in endothelial cells and is a short-lived vasodilator and inhibitor of platelet aggregation. Cultured endothelial cells (EC) make PGI2 from exogenous arachidonic acid (AA) and the unstable endoperoxide PGH2. EC have also been shown to make PGI2 from endogenous AA when stimulated by the calcium ionophore A23187, thrombin, histamine, bradykinin, trypsin, platelet derived growth factor, and uremic plasma. PGI2 synthesis in EC is blocked by aspirin, indomethacin, or 15-HPAA. PGI2 synthesis is partially self-controlled and self-limiting at least in vitro since PGI2 elevates EC cAMP levels and elevated cAMP levels decrease EC PGI2 production. While the proteolytic site of thrombin (and trypsin) is involved in the stimulation of PGI2 production, high affinity binding of thrombin to endothelial cells appears not to be necessary. Alteration of the fatty acid composition of EC by manipulation of the culture media can decrease PGI2 production in response to thrombin or A23187 by 60-751. Cultured aortic smooth muscle cells (SMC) also synthesize PGI2 but at significantly lower levels than EC. SMC PGI2 production is stimulated by PDGF and in some SMC lines by thrombin. SMC grown from atherosclerotic rabbit aortas produce considerably less PGI2 from exogenous AA than do SMC from noimal aortas. Future investigations into this area will further clarify normal biochemical and physiologic pathways and perhaps suggest means by which PGI2 production in EC and SMC may be modulated in order to treat human disease.
Chronic Calcineurin Inhibitor Nephrotoxicity—Lest We Forget (2011)

Calcineurin inhibitor (CNI) nephrotoxicity was recognized in Cambridge in the late 1970s. The vasoconstrictor impact of cyclosporine (CsA) and to a lesser extent tacrolimus, in both acute and chronic settings, results from a decrease in vasodilators and increase in vasconconstrictors while direct tubular toxicity results from blockade of mitochondrial permeability transition pores and inhibition of prolyl isomerase. A biopsy of native kidneys of recipients of CNIs reveals nephrotoxicity as the most common pathological diagnosis with chronic CNI toxicity and hypertension the primary problems. A long-term study of randomized clinical trials with up to 20 years of follow-up shows inferiority of both renal function and graft survival for continuous CsA compared to either CsA withdrawal or continuous azathioprine and prednisolone. Pathological hallmarks of chronic CNI nephrotoxicity include stripped interstitial fibrosis, arteriolar hyalinosis and glomerular sclerosis, but with the exception of nodular arteriolar hyalinosis the findings are non specific. The model for chronic renal allograft loss must be multifactorial with both immune and nonimmune factors operating dependent upon an individual's risk factors for cell and/or antibody-mediated rejection, CNI nephrotoxicity and recurrent disease. Better outcomes will require early diagnosis and individualization of therapy dependent upon the dominant mechanisms impacting each patient. The revisionist view put forward by some senior, experienced and thoughtful individuals, challenges the concept of chronic CNI nephrotoxicity as an important clinical entity. By implication, the view that appears to be promoted is as follows: we need not fear-prolonged exposure to CNIs, and in seeking better long-term solutions for transplant recipients, we have forgotten alloimmunity. It is thus apparent that we must revisit the data and again question the basis for chronic CNI nephrotoxicity in current clinical practice. This contribution to the debate will focus on the evidence that CNIs are nephrotoxic and that their impact needs to be limited if we are to improve long-term outcomes after transplantation, leaving others to promote the contrary perspective and perhaps also to reflect on the largely unproven impact of the steroid avoidance and other minimization strategies so prevalent today.
Calcium ionophore A23187 induces expression of glucose-regulated genes and their heterologous fusion genes. (1985)

Using two cDNA clones which encode hamster genes specifically induced by glucose starvation, we demonstrated that an 8- and 30-fold increase, respectively, in the transcription rates of these genes was coordinately effected by calcium ionophore A23187 treatment, resulting in a similar increase in the steady-state levels of their mRNAs. This response was observed within several hours of ionophore treatment in several mammalian cell types and appeared to be specifically mediated by A23187 but not by other ionophores in general. To define the regulatory sequence which mediates this Ca2+-induced response, we showed by gene transfection techniques that the 5' flanking sequence of a rat glucose-regulated gene contained the region for induction by A23187. The system reported here offers attractive features for the study of specific gene regulation by Ca2+.
Preparation of Bispecific Antibodies by Chemical Recombination of Monoclonal Immunoglobulin G 1 Fragments (1985)

Preparation of bispecific antibodies by the chemical reassociation of monovalent fragments derived from monoclonal mouse immunoglobulin G1 is inefficient because of side reactions during reoxidation of the multiple disulfide bonds linking the heavy chains. These side reactions can be avoided by using specific dithiol complexing agents such as arsenite and effecting disulfide formation with a thiol activating agent such as 5,5'-dithiobis(2-nitrobenzoic acid). In this way bispecific antibodies were obtained in high yield and free of monospecific contaminants from monoclonal mouse immunoglobulin G1 fragments. The bispecific antibodies were used as agents for the selective immobilization of enzymes.
Protospacer recognition motifs (2013)

Protospacer adjacent motifs (PAMs) were originally characterized for CRISPR-Cas systems that were classified on the basis of their CRISPR repeat sequences. A few short 2-5 bp sequences were identified adjacent to one end of the protospacers. Experimental and bioinformatical results linked the motif to the excision of protospacers and their insertion into CRISPR loci. Subsequently, evidence accumulated from different virus- and plasmid-targeting assays, suggesting that these motifs were also recognized during DNA interference, at least for the recently classified type I and type II CRISPR-based systems. The two processes, spacer acquisition and protospacer interference, employ different molecular mechanisms, and there is increasing evidence to suggest that the sequence motifs that are recognized, while overlapping, are unlikely to be identical. In this article, we consider the properties of PAM sequences and summarize the evidence for their dual functional roles. It is proposed to use the terms protospacer associated motif (PAM) for the conserved DNA sequence and to employ spacer acqusition motif (SAM) and target interference motif (TIM), respectively, for acquisition and interference recognition sites.
Learning to Disentangle Factors of Variation with Manifold Interaction (2014)

Many latent factors of variation interact to gen-erate sensory data; for example, pose, morphol-ogy and expression in face images. In this work, we propose to learn manifold coordinates for the relevant factors of variation and to model their joint interaction. Many existing feature learning algorithms focus on a single task and extract fea-tures that are sensitive to the task-relevant factors and invariant to all others. However, models that just extract a single set of invariant features do not exploit the relationships among the latent fac-tors. To address this, we propose a higher-order Boltzmann machine that incorporates multiplica-tive interactions among groups of hidden units that each learn to encode a distinct factor of vari-ation. Furthermore, we propose correspondence-based training strategies that allow effective dis-entangling. Our model achieves state-of-the-art emotion recognition and face verification perfor-mance on the Toronto Face Database. We also demonstrate disentangled features learned on the CMU Multi-PIE dataset. 1.
Hereditary overexpression of adenosine deaminase in erythrocytes: studies in erythroid cell lines and transgenic mice (1994)

Overexpression of adenosine deaminase (ADA) in red blood cells is characterized by a marked, tissue-specific increase in levels of structurally normal ADA mRNA and enzymatic activity in the erythrocytes of affected individuals, leading to adenosine triphosphate (ATP) depletion and hemolytic anemia. This autosomal dominant trait is linked to the ADA gene. To investigate the molecular mechanism responsible for this disorder, we examined relative reporter gene activity using constructs containing 10.6 kb of 5′ flanking sequence and 12.3 kb of the first intron of the ADA gene from the normal and mutant alleles. No differences in chloramphenicol acetyltransferase (CAT) activity were found in transient transfection experiments using erythroleukemia cell lines. Transgenic mice containing the ADA constructs expressed CAT in the appropriate tissue-specific fashion, with 10(2)- to 10(4)-fold higher activity in the thymus. However, CAT activities in erythrocytes and bone marrow of mice containing high transgene copy numbers did not differ between the normal and mutant alleles. These results indicate that the mutation responsible for ADA overexpression is unlikely to reside in the 5′ and promoter regions or in the regulatory regions of the first intron. It is possible that the erythroid-specific overexpression of ADA results from a mutation at some distance from the gene or requires an interaction of a proximal mutation with more distal DNA elements.
Cytokine dysregulation and acute graft-versus-host disease (1992)

Abstract We suggest that acute GVHD after marrow transplantation reflects (1) host injury due to the conditioning regimen followed by the production of inflammatory cytokines; (2) stimulation of mature donor T cells in the milieu of increased cell surface expression of leukocyte adhesion molecules and HLA molecules, followed by the autocrine production of IL- 2; and, finally, (3) recruitment and activation of additional mononuclear effector cells from donor marrow progenitors, which produce additional inflammatory cytokines, thus sustaining the response. The second step is critical for the amplification of the systemic inflammatory response, and it is absence in autologous, syngeneic, and T-cell-depleted transplants. These T cells may also contribute to the inflammatory cytokine network. Acute GVHD can occur in the absence of primary tissue injury in such settings as transfusion-related GVHD; however, it is likely that a greater HLA disparity between donor and host is required. We propose that inflammatory cytokine production is the final common pathway of acute GVHD. If this model is correct, control of cytokine dysregulation at any of several points should control GVHD. Further studies of GVHD and investigations of cytokine antagonists (eg, IL-4 or IL-10) or combinations of antagonists such as IL-1ra and soluble TNF receptor or pentoxifylline will allow us to determine the validity of this hypothesis.
Proteic toxin-antitoxin, bacterial plasmid addiction systems and their evolution with special reference to the pas system of pTF-FC2 (1999)

Genes encoding toxin-antitoxin proteins are frequently found on plasmids where they serve to stabilize the plasmid within a bacterial population. The toxin-antitoxin proteins do not increase the likelihood of a progeny cell receiving a plasmid but rather function as post-segregational killing mechanisms which decrease the proportion of cells that survive after losing the plasmid. These toxin-antitoxin couples therefore act as plasmid addiction systems. Several new proteic toxin-antitoxin systems have been identified and these systems appear to be ubiquitous on the chromosomes of bacteria and archaea. When placed on plasmids, these chromosomal systems also have the ability to stabilize plasmids and in at least one case, chromosomal- and plasmid-based toxin-antitoxin systems have been shown to interact. Recent findings regarding toxin-antitoxin systems and questions that have arisen as a result of these findings are reviewed. Copyright (C) 1999 Federation of European Microbiological Societies.
The HBZ Factor of Human T-cell Leukemia Virus Type I Dimerizes with Transcription Factors JunB and c-Jun and Modulates Their Transcriptional Activity (2003)

The human T-cell leukemia virus type I (HTLV-I)-encoded Tax protein activates transcription from the viral promoter via association with the cellular basic leucine zipper factor cAMP-response element-binding protein-2. Tax is also able to induce cellular transformation of T lymphocytes probably by modulating transcriptional activity of cellular factors, including nuclear factor-kappaB, E2F, activator protein-1 (AP-1), and p53. Recently, we characterized in HTLV-I-infected cells the presence of a novel viral protein, HBZ, encoded by the complementary strand of the HTLV-I RNA genome (Gaudray, G., Gachon, F., Basbous, J., Biard-Piechaczyk, M., Devaux, C., and Mesnard, J.-M. (2002) J. Virol. 76, 12813-12822). HBZ is a nuclear basic leucine zipper protein that down-regulates Tax-dependent viral transcription by inhibiting the binding of cAMP-response element-binding protein-2 to the HTLV-I promoter. In searching for other cellular targets of HBZ, we identified two members of the Jun family, JunB and c-Jun. Co-immunoprecipitation and cellular colocalization confirmed that HBZ interacts in vivo with JunB and c-Jun. When transiently introduced into CEM cells with a reporter gene containing the AP-1 site from the collagenase promoter, HBZ suppressed transactivation by c-Jun. On the other hand, the combination of HBZ with Jun-B had higher transcriptional activity than JunB alone. Consistent with the structure of its basic domain, we demonstrate that HBZ decreases the DNA-binding activity of c-Jun and JunB. Last, we show that c-Jun is no longer capable of activating the basal expression of the HTLV-I promoter in the presence of HBZ in vivo. Our results support the hypothesis that HBZ could be a negative modulator of the Tax effect by controlling Tax expression at the transcriptional level and by attenuating activation of AP-1 by Tax.
The application of short-time memory devices to compensator design (1954)

IN FIG. 1 is shown a compensator cascaded with a control system. The combination will be called the compensated system. In this paper the transfer function of the control system is assumed to be linear and that for the compensator is at least piecewise linear. Each compensator discussed in the paper has incorporated, within its structure, a delay line or short-time memory unit, Fig. 2, into which information is inserted and from which the same information is extracted at various short intervals of time thereafter. The extracted information at each location is multiplied by a suitable constant and the results are summed to form rx(t).
TGF beta suppresses casein synthesis in mouse mammary explants and may play a role in controlling milk levels during pregnancy. (1993)

Mammary explants from 14-15-d-pregnant mice synthesize and secrete milk proteins in culture in response to insulin, hydrocortisone, and prolactin. Here we demonstrate that transforming growth factor beta (TGF beta) treatment suppresses, in a dose dependent and reversible manner, the ability of explants to synthesize and secrete milk caseins. TGF beta does not affect the level of casein mRNA within explants but inhibits casein synthesis posttranscriptionally. We also show increased expression of TGF beta 2 and TGF beta 3 in intact mammary gland as pregnancy progresses, with reduced expression of all three TGF betas at the onset of lactation. These findings suggest that endogenously produced TGF beta may limit the accumulation of milk caseins that are produced in the mammary gland during pregnancy.
High luminous fluorescence generation using Ce:YAG transparent ceramic excited by blue laser diode (2018)

Solid-state laser lighting is an emerging technology, whereby high-brightness white light can be generated using blue laser diodes combined with a yellow-emitting phosphor. In this study, Ce:YAG transparent ceramic wafers with different cerium concentrations and thicknesses are prepared and their optical characteristics are measured. A transmission mode is used, wherein the phosphor ceramic is fixed onto an oxygen-free copper sink, whose temperature is accurately controlled, and excited using the blue laser diode. The recorded spectrum shows that blue laser light is completely converted to yellow light with a wavelength of 565 nm and width of 200 nm. Moreover, with varied temperatures of 10-80 &amp;deg;C, the luminous flux, spectrum, and color coordinates exhibit relatively stable. More importantly, the luminous flux is highest (2690 lm) when irradiated by a 19.5-W blue laser (with a center wavelength of 454 nm) for a Ce&lt;sup&gt;3+&lt;/sup&gt; dopant concentration of 0.5 mol% and a Ce:YAG thickness of 1.6 mm. Based on these results, the Ce:YAG transparent ceramic can be used as a potential phosphor material in applications of high-power solid-state laser lighting and laser display.&lt;br/&gt; &amp;copy; 2018 Optical Society of America.
Five recombinant fragments of human serum albumin—tools for the characterization of the warfarin binding site (2000)

Human serum albumin (HSA) interacts with a vast array of chemically diverse ligands at specific binding sites. To pinpoint the essential structural elements for the formation of the warfarin binding site on human serum albumin, a defined set of five recombinant proteins comprising combinations of domains and/or subdomains of the N-terminal part were prepared and characterized by biochemical standard procedures, tryptophanyl fluorescence, and circular dichroic measurements, indicating well-preserved secondary and tertiary structures. Affinity constants for binding to warfarin were estimated by fluorescence titration experiments and found to be highest for HSA-DOM I-II and HSA, followed by HSA-DOM IB-II, HSA-DOM II, and HSA-DOM I-IIA. In addition, ultraviolet difference spectroscopy and induced circular dichroism experiments were carried out to get an in depth understanding of the binding mechanism of warfarin to the fragments as stand-alone proteins. This systematic study indicates that the primary warfarin binding site is centered in subdomain IIA with indispensable structural contributions of subdomain IIB and domain I, while domain III is not involved in this binding site, underlining the great potential that lies in the use of combinations of recombinant fragments for the study and accurate localization of ligand binding sites on HSA.
Reduced contact-inhibition and substratum adhesion in epithelial cells expressing GlcNAc-transferase V. (1995)

Malignant transformation of fibroblast and epithelial cells is accompanied by increased beta 1-6 N-acetylglucosaminyltransferase V (GlcNAc-TV) activity, a Golgi N-linked oligosaccharide processing enzyme. Herein, we report that expression of GlcNAc-TV in Mv1Lu cells, an immortalized lung epithelial cell line results in loss of contact-inhibition of cell growth, an effect that was blocked by swainsonine, an inhibitor of Golgi processing enzyme alpha-mannosidase II. In serum-deprived and high density monolayer cultures, the GlcNAc-TV transfectants formed foci, maintained microfilaments characteristic of proliferating cells, and also experienced accelerated cell death by apoptosis. Injection of the GlcNAc-TV transfectants into nude mice produced a 50% incidence of benign tumors, and progressively growing tumors in 2:12 mice with a latency of 6 mo, while no growth was observed in mice injected with control cells. In short term adhesion assays, the GlcNAc-TV expressing cells were less adhesive on surfaces coated with fibronectin and collagen type IV, but no changes were observed in levels of cell surface alpha 5 beta 1 or alpha v beta 3 integrins. The larger apparent molecular weights of the LAMP-2 glycoprotein and integrin glycoproteins alpha 5, alpha v and beta 1 in the transfected cells indicates that their oligosaccharide chains are substrates for GlcNAc-TV. The results suggest that beta 1-6GlcNAc branching of N-linked oligosaccharides contributes directly to relaxed growth controls and reduce substratum adhesion in premalignant epithelial cells.