gebhart/patrepeval huggingface dataset:
Identification and characterization of a coronavirus packaging signal (1992)

Previously, a mouse hepatitis virus (MHV) genomic sequence necessary for defective interfering (DI) RNA packaging into MHV particles (packaging signal) was mapped to within a region of 1,480 nucleotides in the MHV polymerase gene by comparison of two DI RNAs. One of these, DIssF, is 3.6 kb in size and exhibits efficient packaging, whereas the other, DIssE, which is 2.3 kb, does not. For more precise mapping, a series of mutant DIssF RNAs with deletions within this 1,480-nucleotide region were constructed. After transfection of in vitro-synthesized mutant DI RNA in MHV-infected cells, the virus product was passaged several times. The efficiency of DI RNA packaging into MHV virions was then estimated by viral homologous interference activity and by analysis of intracellular virus-specific RNAs and virion RNA. The results indicated that an area of 190 nucleotides was necessary for packaging. A computer-generated secondary structural analysis of the A59 and JHM strains of MHV demonstrated that within this 190-nucleotide region a stable stem-loop of 69 nucleotides was common between the two viruses. A DIssE-derived DI DNA which had these 69 nucleotides inserted into the DIssE sequence demonstrated efficient DI RNA packaging. Site-directed mutagenic analysis showed that of these 69 nucleotides, the minimum sequence of the packaging signal was 61 nucleotides and that destruction of the secondary structure abolished packaging ability. These studies demonstrated that an MHV packaging signal was present within the 61 nucleotides, which are located on MHV genomic RNA 1,381 to 1,441 nucleotides upstream of the 3' end of gene 1.
Artemin, a Member of the Glial Cell Line-derived Neurotrophic Factor Family of Ligands, Is HER2-regulated and Mediates Acquired Trastuzumab Resistance by Promoting Cancer Stem Cell-like Behavior in Mammary Carcinoma Cells (2014)

Previous studies have demonstrated that Artemin (ARTN) functions as a cancer stem cell (CSC) and metastatic factor in mammary carcinoma. Herein, we report that ARTN mediates acquired resistance to trastuzumab in HER2-positive mammary carcinoma cells. Ligands that increase HER2 activity increased ARTN expression in HER2-positive mammary carcinoma cells, whereas trastuzumab inhibited ARTN expression. Forced expression of ARTN decreased the sensitivity of HER2-positive mammary carcinoma cells to trastuzumab both in vitro and in vivo. Conversely, siRNA-mediated depletion of ARTN enhanced trastuzumab efficacy. Cells with acquired resistance to trastuzumab exhibited increased ARTN expression, the depletion of which restored trastuzumab sensitivity. Trastuzumab resistance produced an increased CSC population concomitant with enhanced mammospheric growth. ARTN mediated the enhancement of the CSC population by increased BCL-2 expression, and the CSC population in trastuzumab-resistant cells was abrogated upon inhibition of BCL-2. Hence, we conclude that ARTN is one mediator of acquired resistance to trastuzumab in HER2-positive mammary carcinoma cells.
Extracellular enveloped vaccinia virus. Entry, egress, and evasion. (1998)

Vaccinia virus is a large and complex virus that produces two types of infectious virus particles, termed intracellular mature virus (IMV) and extracellular enveloped virus (EEV). EEV contains an extra lipid envelope and ten associated proteins that are absent from IMV. Although EEV represents less than 1% of infectious progeny it is very important biologically. First, it mediates virus dissemination and second, it is the virus against which protective immune responses are directed. This article reviews the genes known to encode EEV proteins and their functions, describes recent data showing that the cellular receptors for IMV and EEV are different, and demonstrates that EEV, in contrast to IMV, is resistant to neutralisation by antibody.
Buffer Capacity Computation for Throughput Constrained Streaming Applications with Data-Dependent Inter-Task Communication (2008)

Streaming applications are often implemented as task graphs, in which data is communicated from task to task over buffers. Currently, techniques exist to compute buffer capacities that guarantee satisfaction of the throughput constraint if the amount of data produced and consumed by the tasks is known at design-time. However, applications such as audio and video decoders have tasks that produce and consume an amount of data that depends on the decoded stream. This paper introduces a dataflow model that allows for data-dependent communication, together with an algorithm that computes buffer capacities that guarantee satisfaction of a throughput constraint. The applicability of this algorithm is demonstrated by computing buffer capacities for an H.263 video decoder.
Sequence of the rabbit whey acidic protein cDNA (1988)

Journal Article Sequence of the rabbit whey acidic protein cDNA Get access Eve Devinoy, Eve Devinoy Laboratoire de Physiologie de la Lactation, Institut National de la Recherche AgronomiqueF-78350 Jouy-en-Josas, France Search for other works by this author on: Oxford Academic PubMed Google Scholar Christine Hubert, Christine Hubert Laboratoire de Physiologie de la Lactation, Institut National de la Recherche AgronomiqueF-78350 Jouy-en-Josas, France Search for other works by this author on: Oxford Academic PubMed Google Scholar Esther Schaerer, Esther Schaerer 1Institut de Biochimie Université de Lausanne et Institut Suisse de Recherches Expérimentales sur le CancerCH-1066 Epalinges, Switzerland Search for other works by this author on: Oxford Academic PubMed Google Scholar Louis-Marie Houdebine, Louis-Marie Houdebine Laboratoire de Physiologie de la Lactation, Institut National de la Recherche AgronomiqueF-78350 Jouy-en-Josas, France Search for other works by this author on: Oxford Academic PubMed Google Scholar Jean-Pierre Kraehenbuhl Jean-Pierre Kraehenbuhl Laboratoire de Physiologie de la Lactation, Institut National de la Recherche AgronomiqueF-78350 Jouy-en-Josas, France Search for other works by this author on: Oxford Academic PubMed Google Scholar Nucleic Acids Research, Volume 16, Issue 16, 25 August 1988, Page 8180, https://doi.org/10.1093/nar/16.16.8180 Published: 25 August 1988 Article history Accepted: 14 July 1988 Published: 25 August 1988
Distributed Fusion Architectures and Algorithms for Target Tracking (1997)

Modern surveillance systems often utilize multiple physically distributed sensors of different types to provide complementary and overlapping coverage on targets. In order to generate target tracks and estimates, the sensor data need to be fused. While a centralized processing approach is theoretically optimal, there are significant advantages in distributing the fusion operations over multiple processing nodes. This paper discusses architectures for distributed fusion, whereby each node processes the data from its own set of sensors and communicates with other nodes to improve on the estimates, The information graph is introduced as a way of modeling information flow in distributed fusion systems and for developing algorithms. Fusion for target tracking involves two main operations: estimation and association. Distributed estimation algorithms based on the information graph are presented for arbitrary fusion architectures and related to linear and nonlinear distributed estimation results. The distributed data association problem is discussed in terms of track-to-track association likelihoods. Distributed versions of two popular tracking approaches (joint probabilistic data association and multiple hypothesis tracking) are then presented, and examples of applications are given.
Combining compiler and runtime IPC predictions to reduce energy in next generation architectures (2004)

Next generation architectures will require innovative solutions to reduce energy consumption. One of the trends we expect is more extensive utilization of compiler information directly targeting energy optimizations. As we show in this paper, static information provides some unique benefits, not available with runtime hardware-based techniques alone. To achieve energy reduction, we use IPC information at various granularities, to adaptively adjust voltage and speed, and to throttle the fetch rate in response to changes in ILP. We evaluate schemes that are based on static IPC, runtime IPC and also combined, hybrid approaches.We show that IPC-based adaptive voltage scaling schemes can reduce energy consumption significantly, but the approach that also uses static IPC information in combination with runtime IPC, better captures program ILP burstiness and helps meet applications' target performance: an important criterion in the real-time domain. We have found that static IPC-based fetch-throttling works very well, in most cases performing similarly or better than hardware-only runtime IPC-based schemes. Overall, static IPC based resource throttling alone can save up to 14% energy in the processor with less than 5\% IPC degradation. The hybrid scheme saves somewhat more energy but at the expense of higher performance degradation than the static-only approach. In fact, we obtain the lowest IPC degradation with the static IPC-based scheme.
Human Papillomavirus Type 16 E7 DNA Vaccine: Mutation in the Open Reading Frame of E7 Enhances Specific Cytotoxic T-Lymphocyte Induction and Antitumor Activity (1999)

A human papillomavirus type 16 E7 DNA vaccine with the open reading frame encoding mutations in two zinc-binding motifs expressed a rapidly degraded E7 protein. This vaccine induced a significantly stronger E7-specific cytotoxic T-lymphocyte response and better tumor protection in mice than did a wild-type E7 DNA vaccine expressing a stable E7 protein.
Selective IgA Deficiency (2010)

The genetic basis of IgA deficiency remains to be clarified. Better understanding of the production and function of IgA is essential in elucidating the disease mechanism in IgA deficiency.
Turbo and Turbo-Like Codes: Principles and Applications in Telecommunications (2007)

For decades, the de facto standard for forward error correction was a convolutional code decoded with the Viterbi algorithm, often concatenated with another code (e.g., a Reed-Solomon code). But since the introduction of turbo codes in 1993, much more powerful codes referred to collectively as turbo and turbo-like codes have eclipsed classical methods. These powerful error-correcting techniques achieve excellent error-rate performance that can closely approach Shannon's channel capacity limit. The lure of these large coding gains has resulted in their incorporation into a widening array of telecommunications standards and systems. This paper will briefly characterize turbo and turbo-like codes, examine their implications for physical layer system design, and discuss standards and systems where they are being used. The emphasis will be on telecommunications applications, particularly wireless, though others are mentioned. Some thoughts on the use of turbo and turbo-like codes in the future will also be given.
Protamine: a review of its toxicity. (1985)

The prospective human studies considered above reveal that in some patients protamine is associated with decreases in SBP and SVR, especially when administered rapidly. Cardiac output increases reflexly, except perhaps in patients with less compliant ventricles, which are more dependent on preload to maintain stroke volume. In the latter, decreases in filling volume associated with protamine can lower CO. Regardless of the rate of administration, protamine does not produce predictable, acute increases in PAP, although increases in PAP may occur during idiosyncratic reactions (see the section on idiosyncratic reactions below). Left atrial or aortic administration of protamine may not confer protection from its hemodynamic or idiosyncratic sequelae (see below). Little evidence exists to conclude that protamine directly depresses contractility of the human heart.
Synthesis and properties of the ionomer diblock copolymer poly(4‐vinylbenzyl triethyl ammonium bromide)‐b‐polyisobutene (2003)

Abstract A new amphiphilic diblock copolymer containing an ionomer segment, poly[(4‐vinylbenzyl triethyl ammonium bromide)‐ co ‐(4‐methylstyrene)‐ co ‐(4‐bromomethylstyrene)]‐ b ‐polyisobutene [poly(4‐VBTEAB)‐ b ‐PIB], was synthesized by the chemical modification of poly(4‐methylstyrene)‐ b ‐polyisobutene [poly(4‐MSt)‐ b ‐PIB]. First, the 4‐methylstyrene moiety in poly(4‐MSt)‐ b ‐PIB was brominated with azobisisobutyronitrile as an initiator at 60 °C in CCl 4 , and then the highly reactive benzyl bromide groups were ionized by a reaction with triethylamine in a toluene/isopropyl alcohol (80/20 v/v) mixture at about 85 °C to produce the ionomer diblock copolymer poly(4‐VBTEAB)‐ b ‐PIB. The solubility of the ionomer block copolymer was quite different from that of the corresponding poly[(4‐methylstyrene)‐ co ‐(4‐bromomethylstyrene)]‐ b ‐polyisobutene {poly[(4‐MSt)‐ co ‐(4‐BrMSt)]‐ b ‐PIB}. Transmission electron microscopy observations demonstrated that all three diblock copolymers had microphase‐separation structures in which polyisobutene (PIB) domains existed in the continuous phase of the poly(4‐methylstyrene) segment or its derivative segment matrix. Dynamic mechanical thermal analysis measurements showed that poly[(4‐MSt)‐ co ‐(4‐BrMSt)]‐ b ‐PIB had two glass‐transition temperatures ( T g 's), −56 °C for the PIB segment and 62 °C for the poly[(4‐MSt)‐ co ‐(4‐BrMSt)] domain, whereas poly(4‐VBTEAB)‐ b ‐PIB showed one T g at −8 °C of the PIB domain; T g of the poly[(4‐vinylbenzyl triethyl ammonium bromide)‐ co ‐(4‐methylstyrene)‐ co ‐(4‐bromomethylstyrene)] domain was not observable because of the strong ionic interactions resulting in a higher T g and a retention of modulus up to 124 °C. © 2003 Wiley Periodicals, Inc. J Polym Sci Part A: Polym Chem 41: 2755–2764, 2003
Modeling of transdermal fluorescence measurements from first-in-human clinical trials for renal function determination using fluorescent tracer agent MB-102 (2017)

The fluorescent tracer agent 3,6-diamino-2,5-bisN-[(1R)-1-carboxy-2-hydroxyethyl]carbamoylpyrazine, designated MB-102, is cleared from the body solely by the kidneys. A prototype noninvasive fluorescence detection device has been developed for monitoring transdermal fluorescence after bolus intravenous injection of MB-102 in order to measure kidney function. A mathematical model of the detected fluorescence signal was created for evaluation of observed variations in agent kinetics across body locations and for analysis of candidate instrument geometries. The model comprises pharmacokinetics of agent distribution within body compartments, local diffusion of the agent within the skin, Monte Carlo photon transport through tissue, and ray tracing of the instrument optics. Data from eight human subjects with normal renal function and a range of skin colors shows good agreement with simulated data. Body site dependence of equilibration kinetics was explored using the model to find the local vasculature-to-interstitial diffusion time constant, blood volume fraction, and interstitial volume fraction. Finally, candidate instrument geometries were evaluated using the model. While an increase in source-detector separation was found to increase sensitivity to tissue optical properties, it reduced the relative intensity of the background signal with minimal effect on the measured equilibration kinetics.
A KAS2 cDNA complements the phenotypes of the Arabidopsis fab1 mutant that differs in a single residue bordering the substrate binding pocket (2002)

The fab1 mutant of Arabidopsis is partially deficient in activity of beta-ketoacyl-[acyl carrier protein] synthase II (KAS II). This defect results in increased levels of 16:0 fatty acid and is associated with damage and death of the mutants at low temperature. Transformation of fab1 plants with a cDNA from Brassica napus encoding a KAS II enzyme resulted in complementation of both mutant phenotypes. The dual complementation by expression of the single gene proves that low-temperature damage is a consequence of altered membrane unsaturation. The fab1 mutation is a single nucleotide change in Arabidopsis KAS2 that results in a Leu337Phe substitution. The Leu337 residue is conserved among plant and bacterial KAS proteins, and in the crystal structures of E. coli KAS I and KAS II, this leucine abuts a phenylalanine whose imidazole ring extends into the substrate binding cavity causing the fatty acid chain to bend. For functional analysis the equivalent Leu207Phe mutation was introduced into the fabB gene encoding the E. coli KAS I enzyme. Compared to wild-type, the Leu207Phe protein showed a 10-fold decrease in binding affinity for the fatty acid substrate, exhibited a modified behavior during size-exclusion chromatography and was severely impaired in condensation activity. These results suggest that the molecular defect in fab1 plants is a structural instability of the KAS2 gene product induced by insufficient space for the imidazole ring of the mutant phenylalanine residue.
Acute atrial tachyarrhythmia induces angiotensin II type 1 receptor-mediated oxidative stress and microvascular flow abnormalities in the ventricles (2009)

Rapid atrial pacing induces AT(1)-receptor-mediated oxidative stress in LV myocardium that is accompanied by impaired microvascular blood flow and cTn-I release. These findings provide a plausible mechanism for the frequently observed cTn-I elevation accompanied with typical angina pectoris symptoms in patients with paroxysmal AF and normal (non-stenotic) coronary arteries.
Endoscopic management of uterine myoma (1999)

This study was undertaken to evaluate the various gynecologic endoscopic surgical techniques including resectoscopic myomectomy, laparoscopic myomectomy, and laparoscopy assisted vaginal hysterectomy (LAVH) used in the treatment of uterine myomas. The medical records of 136 cases of uterine myomas treated using one or more of the gynecologic endoscopic surgical techniques in the Department of Obstetrics and Gynecology at Yonsei University were retrospectively reviewed from March 1997 to September 1998. Of the 136 cases reviewed, there were 40 submucosal myomas and 96 intramural and subserosal myomas. For statistical analysis, Student's t-test was used. Submucosal myomectomy using the resectosope was performed in 35 cases (mean age: 39 +/- 1.5 years), laparoscopic myomecotmy in 35 cases (mean age: 36 +/- 1.9 years), and LAVH in 66 cases (mean age: 42 +/- 1.1 years). In cases of huge myomas, the GnRH agonist was used prior to surgery, and in cases of heavy uterine bleeding, angioblock of the uterine artery was undertaken before the endoscopic procedures. The mean operating time was significantly shorter in resectoscopic myomectomy (41 +/- 12 min), followed by laparoscopic myomectomy (85.0 +/- 10.3 min) and LAVH (123 +/- 5.3 min). The mean hospital stay for resectoscopic myomectomy, laparoscopic myomectomy, and LAVH was 1.9 +/- 0.5, 2.5 +/- 0.5, and 3.4 +/- 0.8 days (p < 0.001), respectively. There were 3 cases of complications including pulmonary edema and uterine perforation in the resectoscopic myomectomy group, and 4 cases of complications including bladder, ureter, and epigastric vessel injury in the LAVH group. In conclusion, the therapeutic effect of various gynecologic endoscopic surgical techniques can be maximized in terms of shorter operation time, shorter hospital stay, faster recovery, and less blood loss by the appropriate management of uterine myoma in well-chosen patients.
Complete sequencing of TP53 predicts poor response to systemic therapy of advanced breast cancer. (2000)

TP53 has been implicated in regulation of the cell cycle, DNA repair, and apoptosis. We studied, in primary breast tumors through direct cDNA sequencing of exons 2-11, whether TP53 gene mutations can predict response in patients with advanced disease to either first-line tamoxifen therapy (202 patients, of whom 55% responded) or up-front (poly)chemotherapy (41 patients, of whom 46% responded). TP53 mutations were detected in 90 of 243 (37%) tumors, and one-fourth of these mutations resulted in a premature termination of the protein. The mutations were observed in 32% (65 of 202) of the primary tumors of tamoxifen-treated patients and in 61% (25 of 41) of the primary tumors of the chemotherapy patients. TP53 mutation was significantly associated with a poor response to tamoxifen [31% versus 66%; odds ratio (OR), 0.22; 95% confidence interval (CI), 0.12-0.42; P < 0.0001]. Patients with TP53 gene mutations in codons that directly contact DNA or with mutations in the zinc-binding domain loop L3 showed the lowest response to tamoxifen (18% and 15% response rates, respectively). TP53 mutations were related, although not significantly, to a poor response to up-front chemotherapy (36% versus 63%; OR, 0.34; 95% CI, 0.09-1.24). In multivariate analysis for response including the classical parameters age and menopausal status, disease-free interval, dominant site of relapse, and levels of estrogen receptor and progesterone receptor, TP53 mutation was a significant predictor of poor response in the tamoxifen-treated group (OR, 0.29; 95% CI, 0.13-0.63; P = 0.0014). TP53-mutated and estrogen receptor-negative (<10 fmol/mg protein) tumors appeared to be the most resistant phenotype. Interestingly, the response of patients with TP53 mutations to chemotherapy after tamoxifen was not worse than that of patients without these mutations (50% versus 42%; OR, 1.35, nonsignificant). The median progression-free survival after systemic treatment was shorter for patients with a TP53 mutation than for patients with wild-type TP53 (6.6 and 0.6 months less for tamoxifen and up-front chemotherapy, respectively). In conclusion, TP53 gene mutation of the primary tumor is helpful in predicting the response of patients with metastatic breast disease to tamoxifen therapy. The type of mutation and its biological function should be considered in the analyses of the predictive value of TP53.
CD69-mediated pathway of lymphocyte activation: anti-CD69 monoclonal antibodies trigger the cytolytic activity of different lymphoid effector cells with the exception of cytolytic T lymphocytes expressing T cell receptor alpha/beta. (1991)

The effect of anti-CD69 monoclonal antibodies (mAbs) on the induction of the cytolytic activity in different types of lymphoid effector cells has been investigated. Three anti-CD69 mAbs, including the reference mAb MLR3 and two new mAbs (c227 and 31C4), have been used. All cloned CD3-CD16+ natural killer (NK) cells belonging to different subsets (as defined by the surface expression of GL183 and/or EB6 antigens) were efficiently triggered by anti-CD69 mAbs and lysed P815 mastocytoma cells in a redirected killing assay. Triggering of the cytolytic activity could also be induced in CD3-CD16- NK clones, which fail to respond to other stimuli (including anti-CD16, anti-CD2 mAbs, or phytohemagglutinin). A similar triggering effect was detected in T cell receptor (TCR) gamma/delta+ clones belonging to different subsets. On the other hand, anti-CD69 mAbs could not induce triggering of the cytolytic activity in TCR alpha/beta+ cytolytic clones. Since all thymocytes are known to express CD69 antigen after cell activation, we analyzed a series of phenotypically different cytolytic thymocyte populations and clones for their responsiveness to anti-CD69 mAb in a redirected killing assay. Again, anti-CD69 mAb triggered TCR gamma/delta+ but not TCR alpha/beta+ thymocytes. Anti-CD69 mAb efficiently triggered the cytolytic activity of "early" thymocytes lines or clones (CD3-4-8-7+), which lack all other known pathways of cell activation. Thus, it appears that CD69 molecules may initiate a pathway of activation of cytolytic functions common to a number of activated effector lymphocytes with the remarkable exception of TCR alpha/beta+ cytolytic cells.