gebhart/patrepeval huggingface dataset:
Computation structures (1990)

From the Publisher:
Computation Structures integrates thorough coverage of digital logic design with a comprehensive presentation of computer architecture. It contains a wealth of information for anyone who designs computers or works with computer systems. Indeed, the authors' goal is to teach people to look at systems, as a whole, without being bound by the artificial interfaces that are often used to train specialist engineers. Ward and Halstead demystify the construction of computing hardware by illustrating how it is built up from digital circuits through higher-level components to processors and memories and emphasizing how the design of hardware is affected by its intended use. The book is firmly based in the real world, with pertinent discussions of the many trade-off decisions practicing engineers must confront. Throughout the book, the authors use the running example of the MAYBE computer--a simple microarchitecture that readers can construct and operate--to establish connections between theory and real-world practice. Among the topics addressed are the digital abstracts; combinatorial devices and circuits; the synthesis of digital systems; finite-state machines; control structures and disciplines; performance measures and trade-offs; communication; interpretation; microinterpreter architectures; microprogramming; single-sequence machines; stack, register, and memory architectures; RISC machines; processes; interrupts and priorities; and architectural horizons.
Fractal approximation of image blocks (1992)

A method for block coding of images based on a least squares fractal approximation by a self-affine system (SAS) is presented. The computational cost of the approximation is linear in the number of pixels in the image. The approximation to a rectangularly tiled block involves evaluating various low-order moments over the block, and solving a system of four linear equations for each tile. The method is applied to a standard test image and the effects of various optimizations are shown. A quantitative comparison with the adaptive discrete cosine transform at 8:1 compression is made. The fidelity of the fractal method shows promise and its greater speed and simplicity compared to other fractal transforms suggest immediate applications such as interactive browsing of remote image archives or image representation in multimedia systems.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Fault-Tolerant Topological One-Way Quantum Computation with Probabilistic Two-Qubit Gates (2010)

We propose a scalable way to construct a 3D cluster state for fault-tolerant topological one-way computation (TOWC) even if the entangling two-qubit gates succeed with a small probability. It is shown that fault-tolerant TOWC can be performed with the success probability of the two-qubit gate such as 0.5 (0.1) provided that the unheralded error probability of the two-qubit gate is less than 0.040% (0.016%). Furthermore, the resource usage is considerably suppressed compared to the conventional fault-tolerant schemes with probabilistic two-qubit gates.
Homogeneity testing by phase sampling interferometry (1985)

In diffraction-limited optical systems the number of optical components is rather high. Local changes in the refractive index of the order of 10−6 must be detected to guarantee an adequate performance of the system as a whole. Therefore, the Twyman-Perry method for the evaluation of refractive-index deviations from uniformity—further developed by Roberts and Langenbeck—has been programmed for a digital Twy-man-Green interferometer. If the glass block to be tested is slightly wedge shaped (wedge angle ~10−3 rad), the measurement can be carried out without coating the glass block. With the help of four interferograms the variations of the refractive index apart from a linear slope, as well as the thickness variations of the glass block, can be measured and displayed.
Policies and practice (2010)

NHS Evidence, a website that allows all health and social care workers to access a wide range of information on quality patient care, has a dedicated emergency and urgent care section that provides high quality and up-to-date information and resources on all aspects of emergency and urgent health care, including clinical and organisational issues.
Belagenpumatucel-L for the treatment of non-small cell lung cancer (2015)

Although the Phase III trial investigating belagenpumatucel-L in stage III/IV patients did not meet its primary end point, a survival benefit was observed in several subgroups of patients. Further studies are needed in order to select patients who may benefit from this vaccine.
Paracellular Barrier and Tight Junction Protein Expression in the Immortalized Brain Endothelial Cell Lines bEND.3, bEND.5 and Mouse Brain Endothelial Cell 4 (2013)

The blood-brain barrier (BBB) is formed by brain endothelial cells. Many immortalized brain endothelial cell lines have been established; these have been used as in vitro BBB models. The aim of the present study was to assess the paracellular barrier properties of the immortalized mouse brain endothelial cell lines bEND.3, bEND.5 cells, and mouse brain endothelial cell 4 (MBEC4), and those of the primary mouse brain endothelial cells pMBECs. bEND.3 cells showed low permeability to sodium fluorescein and obvious staining of tight junction proteins (claudin-5, occludin and ZO-1) similar to pMBECs; these barrier properties of MBEC4 and bEND.5 cells were low. In addition, bEND.3 cells expressed the highest level of claudin-5 among all cells. These results suggest that bEND.3 cells are a convenient and useful model for evaluating BBB function, especially the paracellular barrier.
Fused heterocycles from o-acylbenzenethiol derivatives (1988)

The oximes of 2-acylthioanisole derivatives may be conveniently converted into 1,2-benzisothiazoles by acetic anhydride in pyridine. 3-(2-Methylthiophenyl)-1,2-benzisothiazole, prepared by this method, has been further converted into the 1,2-benzisothiazolo[2,3-b]-1,2-benzisothiazolium system. The phenylhydrazones of certain 2-acylthioanisoles are also cyclized by polyphosphoric acid to 2-(2-methylthio)phenylindoles, which are further converted into benzo[b]thieno[3,2-b]indoles by demethylation and oxidation.
Crystal Structure ofS-Adenosylhomocysteine Hydrolase from Rat Liver, (1999)

The crystal structure of rat liver S-adenosyl-l-homocysteine hydrolase (AdoHcyase, EC 3.3.1.1) which catalyzes the reversible hydrolysis of S-adenosylhomocysteine (AdoHcy) has been determined at 2.8 Å resolution. AdoHcyase from rat liver is a tetrameric enzyme with 431 amino acid residues in each identical subunit. The subunit is composed of the catalytic domain, the NAD+-binding domain, and the small C-terminal domain. Both catalytic and NAD+-binding domains are folded into an ellipsoid with a typical α/β twisted open sheet structure. The C-terminal section is far from the main body of the subunit and extends into the opposite subunit. An NAD+ molecule binds to the consensus NAD+-binding cleft of the NAD+-binding domain. The peptide folding pattern of the catalytic domain is quite similar to the patterns observed in many methyltransferases. Although the crystal structure does not contain AdoHcy or its analogue, there is a well-formed AdoHcy-binding crevice in the catalytic domain. Without introducing any major structural changes, an AdoHcy molecule can be placed in the catalytic domain. In the structure described here, the catalytic and NAD+-binding domains are quite far apart from each other. Thus, the enzyme appears to have an “open” conformation in the absence of substrate. It is likely that binding of AdoHcy induces a large conformational change so as to place the ribose moiety of AdoHcy in close proximity to the nicotinamide moiety of NAD+. A catalytic mechanism of AdoHcyase has been proposed on the basis of this crystal structure. Glu155 acts as a proton acceptor from the O3‘-H when the proton of C3‘-H is abstracted by NAD+. His54 or Asp130 acts as a general acid−base catalyst, while Cys194 modulates the oxidation state of the bound NAD+. The polypeptide folding pattern of the catalytic domain suggests that AdoHcy molecules can travel freely to and from AdoHcyase and methyltransferases to properly regulate methyltransferase activities. We believe that the crystal structure described here can provide insight into the molecular architecture of this important regulatory enzyme.
Global survey of escape from X inactivation by RNA-sequencing in mouse (2010)

X inactivation equalizes the dosage of gene expression between the sexes, but some genes escape silencing and are thus expressed from both alleles in females. To survey X inactivation and escape in mouse, we performed RNA sequencing in Mus musculus x Mus spretus cells with complete skewing of X inactivation, relying on expression of single nucleotide polymorphisms to discriminate allelic origin. Thirteen of 393 (3.3%) mouse genes had significant expression from the inactive X, including eight novel escape genes. We estimate that mice have significantly fewer escape genes compared with humans. Furthermore, escape genes did not cluster in mouse, unlike the large escape domains in human, suggesting that expression is controlled at the level of individual genes. Our findings are consistent with the striking differences in phenotypes between female mice and women with a single X chromosome--a near normal phenotype in mice versus Turner syndrome and multiple abnormalities in humans. We found that escape genes are marked by the absence of trimethylation at lysine 27 of histone H3, a chromatin modification associated with genes subject to X inactivation. Furthermore, this epigenetic mark is developmentally regulated for some mouse genes.
Altered ligand binding by insulin-like growth factor II/mannose 6-phosphate receptors bearing missense mutations in human cancers. (1999)

The M6P/IGF2R gene, encoding the insulin-like growth factor II (IGF-II)/mannose 6-phosphate receptor (IGF2R), is frequently inactivated during carcinogenesis. M6P/IGF2R is postulated to be a tumor suppressor gene due to its ability to bind and degrade the mitogen IGF-II, promote activation of the growth inhibitor transforming growth factor beta, and regulate the targeting of lysosomal enzymes. In this study, we determined the effects of four M6P/IGF2R missense mutations associated with loss of heterozygosity in hepatocellular and breast cancers on the ligand binding properties of full-length membrane-bound receptors. Site-directed mutagenesis was used to prepare COOH-terminal, c-myc epitope-tagged human IGF2R cDNA expression constructs bearing point mutations that lead to the substitutions I1572T, G1464E, G1449V, and Q1445H, all of which are located in the receptor's extracytoplasmic domain. Ligand binding was measured in plasma membranes from 293T cells expressing full-length receptors. No binding of 125I-IGF-II to I1572T mutant receptors was observed. Binding to G1449V mutant receptors was decreased by 50% relative to wild-type (WT). However, IGF-II binding to the G1464E and Q1445H mutant receptors was equivalent to WT when plasma membranes were assayed immediately after preparation. The phosphomannosylated pseudoglycoprotein pentamannose 6-phosphate-BSA (PMP-BSA) was synthesized as a ligand for the M6P binding site. Binding of 125I-PMP-BSA was equivalent to WT for the I1572T, G1464E, and Q1445H mutations, but there was a 60% reduction in PMP-BSA binding to the G1449V mutant receptor. Thus, several missense mutations in M6P/IGF2R disrupt the ligand binding functions of the intact IGF2R, lending further support to the hypothesis that the M6P/IGF2R is a tumor suppressor gene.
A Novel Signaling Molecule for Neuropeptide Action: Activity‐dependent Neuroprotective Protein (1999)

The complete coding sequence of a novel protein (828 amino acids, pI 5.99), a potential new mediator of vasoactive intestinal peptide (VIP) activity was recently revealed. The expression of this molecule, activity-dependent neuroprotective protein (ADNP), was augmented in the presence of VIP, in cerebral cortical astrocytes. The mRNA transcripts encoding ADNP were enriched in the mouse hippocampus and cerebellum. The protein deduced sequence contained the following: (1) a unique peptide, NAPVSIPQ, sharing structural and immunological homologies with the previously reported, activity-dependent neurotrophic factor (ADNF) and exhibiting neuroprotection in vitro and in vivo; (2) a glutaredoxin active site; and (3) a classical zinc binding domain. Comparative studies suggested that the peptide, NAPVSIPQ (NAP), was more efficacious than peptides derived from ADNF. ADNP, a potential mediator of VIP-associated neuronal survival, and the new peptide, a potential lead compound for drug design, are discussed below.
Class III Antiarrhythmic Activity in Vivo by Selective Blockade of the Slowly Activating Cardiac Delayed Rectifier Potassium Current IKs by (R)-2-(2,4- Trifluoromethyl)-N-[2-oxo-5-phenyl- 1-(2,2,2-trifluoroethyl)-2,3-dihydro- 1H-benzo[e][1,4]diazepin-3-yl]acetamide (1997)

ADVERTISEMENT RETURN TO ISSUEPREVLetterNEXTClass III Antiarrhythmic Activity in Vivo by Selective Blockade of the Slowly Activating Cardiac Delayed Rectifier Potassium Current IKs by (R)-2-(2,4- Trifluoromethyl)-N-[2-oxo-5-phenyl- 1-(2,2,2-trifluoroethyl)-2,3-dihydro- 1H-benzo[e][1,4]diazepin-3-yl]acetamideHarold G. Selnick, Nigel J. Liverton, John J. Baldwin, John W. Butcher, David A. Claremon, Jason M. Elliott, Roger M. Freidinger, Stella A. King, Brian E. Libby, Charles J. McIntyre, David A. Pribush, David C. Remy, Garry R. Smith, Andrew J. Tebben, Nancy K. Jurkiewicz, Joseph J. Lynch, Joseph J. Salata, Michael C. Sanguinetti, Peter K. S. Siegl, Donald E. Slaughter, and Kamlesh VyasView Author Information Departments of Medicinal Chemistry, Pharmacology, and Drug Metabolism, Merck Research Laboratories, West Point, Pennsylvania 19486 Cite this: J. Med. Chem. 1997, 40, 24, 3865–3868Publication Date (Web):November 21, 1997Publication History Received4 August 1997Published online21 November 1997Published inissue 1 November 1997https://pubs.acs.org/doi/10.1021/jm970517uhttps://doi.org/10.1021/jm970517urapid-communicationACS PublicationsCopyright © 1997 American Chemical SocietyRequest reuse permissionsArticle Views644Altmetric-Citations86LEARN 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:Amides,Azides,Molecular structure,Potassium,Receptors Get e-Alerts
Utero-placental vascular development and placental function (1995)

The rate of fetal growth and subsequent birth weight are major determinants of postnatal survival and growth. Because the placenta is the organ through which respiratory gases, nutrients, and wastes are transported between the maternal and fetal systems, its primary function is to supply the metabolic substrates necessary to support fetal growth. Placental growth and development, therefore, are critical for normal fetal growth and development. During the last half of gestation in mammals, growth of the fetus is exponential, whereas utero-placental growth slows or ceases. Nevertheless, unless placental transport capacity keeps pace with the continually increasing demands of the fetus, fetal growth will be compromised. Studies over the last two decades have shown that placental transport capacity does indeed keep pace with fetal growth. This increase in placental function can be accounted for primarily by continual increases in placental (uterine and umbilical) blood flows, associated with increased placental vascularity. Placental vascular growth and development, in turn, are probably regulated by angiogenic factors produced by the placental tissues themselves. These placental angiogenic factors are produced primarily by the maternal placental tissues, are heparin-binding, and seem to be related to the fibroblast growth factor family. Further elucidation of the factors responsible for placental growth and vascular development is critical for an improved understanding of uteroplacental-fetal interactions, which result in delivery of a healthy offspring.
Hypoxia/reoxygenation causes inflammatory response in transgenic sickle mice but not in normal mice (2000)

In sickle cell anemia, the initiation, progression, and resolution of a vasoocclusive episode may present features of ischemia-reperfusion injury, with recurrent episodes of ischemia/hypoxia and reoxygenation promoting inflammation. Here, we have tested the hypothesis that hypoxia/reoxygenation triggers inflammation in the transgenic sickle mouse. In these mice, even at ambient air, peripheral leukocyte counts are elevated by 1.7-fold and neutrophil counts by almost 3-fold. Two hours of hypoxia, followed by reoxygenation, induced a greater than normal rolling flux and adhesion of leukocytes in these mice, but no leukocyte extravasation. When 3 hours of hypoxia was followed by reoxygenation, sickle mice, but not normal mice, showed a distinct inflammatory response characterized by an increased number of adherent and emigrated leukocytes. Because these events, which are exaggerated in sickle mice, are not seen in response to hypoxia alone, we conclude that they represent a form of reperfusion injury. Studies using an H(2)O(2)-sensitive probe revealed clear evidence of oxidant production in vascular endothelial cells after hypoxia/reoxygenation in sickle mice. Infusion of an anti-P-selectin antibody, but not an anti-E-selectin antibody, completely inhibited this inflammatory response and significantly increased wall shear rates. These findings suggest that leukocyte-endothelium interaction contribute to vasoocclusive events in the sickle mice and perhaps in human sickle disease.
Acute stress induces cardiac mast cell activation and histamine release, effects that are increased in Apolipoprotein E knockout mice (2002)

Acute restraint stress triggered cardiac histamine release in mice that was clearly derived from mast cells, as it was absent in W/W(v) mice. The high basal cardiac and serum histamine in ApoE k/o mice, along with the high number of cardiac mast cells, suggest possible ongoing cardiac mast cell activation that may participate in atherosclerosis. These results may possibly help better understand stress-related cardiovascular pathology.
Right ventricular outflow tract reconstruction: valved conduit of choice and clinical outcomes (2008)

Conduit failure and explant is inevitable. This phenomenon is worse with a longer follow-up. Mechanisms involved in conduit failure are unknown, even though they were accounted for by calcification and extensive intimal proliferation, and somatic outgrowth. Homografts are commonly used and have experienced a long history. The pulmonary homograft is the most commonly used RVOT conduit, especially in small children, due to its excellent characteristics. The newly-developed Contegra conduit has become popular due to its availability in full sizes and the acceptable results obtained at intermediate follow-up. The Hancock conduit can function sufficiently well for as long as 5-10 years, and early valve failure is relatively rare. It is admissible to use the Hancock conduit as an interim measure for future conduit reoperation due to its adequate function until subsequent operation. The application of an autologeous tissue valved conduit should be considered when other alternatives are not available.
Antigen localisation regulates immune responses in a dose‐ and time‐dependent fashion: a geographical view of immune reactivity (1997)

This review summarises experimental evidence to illustrate that induction of immune reactivity depends upon antigen reaching and being available in lymphoid organs in a dose- and time-dependent manner. If antigen reaches lymph organs in a localised staggered manner and with a concentration gradient, a response is induced in the draining lymph node. Antigen-presenting cells are of critical importance to transport antigen from the periphery to local organised lymphoid tissue. If antigen is all over the lymphoid system, then it deletes all specific cells in the thymus or induces them within a few days; because of their limited life-span they then die off, leaving the repertoire depleted of this specificity. If antigen does not reach lymphoid organs it is ignored by immune cells. Once a response is induced, activated but not resting T cells will reach antigen outside lymphoid organs, whereas activated B cells differentiate into plasma cells in an inducing environment, mostly in lymphoid tissue including bone marrow, but also in chronic lymphoid-like infiltrations in peripheral organs. In immunopathology (when the infectious agent is known) or in autoimmunity (when the triggering infectious agent is not known or not recognised) lymphoid tissue may become organised close to the antigen (e.g. in organ-specific autoimmune diseases) and may thereby maintain an autoantigen-driven disease-causing immune response for a long time. The notion that native T cells get induced or silenced in the periphery may be questioned because induction can only occur in lymphoid organs providing anatomical structures where critical cell-cell interactions are properly guided and where, therefore, cells are likely to meet sufficiently frequently and in a critical milieu. Since overall immune reactivity critically depends upon the localisation of antigens in a dose- and time-dependent manner, it seems more likely-but this remains to be shown-that activated T cells may get exhausted in non-lymphoid peripheral tissues, whereas they are usually maintained in lymphoid organs. The critical role of antigen in regulating immune responses also has relevance for our understanding of immunological defence against epithelial and mesenchymal tumours, against many infectious diseases and for understanding autoimmunity and immunological memory. Collectively the data indicate that antigen, dependent upon localisation, dose and time, seems to be the simplest regulator of immune responses.
Incorporated sarcolemmal fish oil fatty acids shorten pig ventricular action potentials (2006)

A fish oil diet increases omega3-PUFA content in the ventricular sarcolemma, decreases I(Ca,L) and I(NCX), and increases I(K1) and I(Ks), resulting in AP shortening. Incorporation of omega3-PUFAs in the sarcolemma may have consequences for arrhythmias independent of circulating omega3-PUFAs.