gebhart/patrepeval huggingface dataset:
Peptide binding to soluble HLA-DR4 molecules produced by insect cells (1992)

HLA-DR4Dw4 molecules were expressed in insect Sf9 cells. The transmembrane and cytoplasmic domains of the DR4 alpha- and beta-chains were replaced by the carboxy terminal sequence of decay accelerating factor, leading to a phosphatidyl inositol glycan membrane anchor. This structure contains a cleavage site for phosphatidyl inositol-specific phospholipase C, allowing efficient solubilization of the rDR4 molecules. We present evidence that infected insect cells express properly associated surface heterodimers and are able to present antigenic peptides to DR4Dw4-restricted T cell clones. Phosphatidyl inositol-specific phospholipase-cleaved recombinant molecules exhibited in vitro binding characteristics similar to DR4 molecules purified from lymphoblastoid cells. In terms of peptide specificity, pH optimum, kinetics, and affinity they were indistinguishable within the limits of our assay system. However, the peptide binding capacity of the recombinant molecules was higher than that of native DR4 molecules.
Atenolol in Secondary Prevention after Stroke (1995)

This study investigated the effect of 50 mg atenolol in reducing the risk of death, stroke and myocardial infarction after stroke and transient ischaemic attacks (TIA). The study was designed as a Swedish multicentre, randomised, double-blind, parallel group study with randomisation stratified according to age and prognostic score. Seven hundred and twenty patients aged over 40 years who had no contraindications to beta-blockers were included within 3 weeks of a stroke or TIA, with 372 patients (mean age 70.7 years) randomised to the treatment and 348 patients (mean age 70.1 years) to the placebo group. Major strokes made up the index events in 81% of patients in the treatment and 79% of those in the placebo group. The two groups were similar in respect to baseline characteristics. The index event was classified as an ischaemic stroke in 86.8 and 86.3% of patients in the treatment and placebo groups, respectively. Side effects of atenolol and placebo caused 17 and 10% of patients to withdraw from allocated treatment. During the follow-up period (mean 28 months) 51 patients in the treatment group died compared to 60 in the placebo group [relative risk with 95% confidence interval 0.79 (0.54–1.16)] and 74 patients in the treatment group suffered a further major stroke compared to 69 in the placebo group. Twenty-six and 29 patients, respectively, suffered an acute myocardial infarction. Calculations using survival techniques and Cox''s proportional hazard model indicated a reduced risk of death (21%) and myocardial infarction (7%) in the treatment group with no reduction in the risk of further stroke. None of these reductions was statistically significant. Thus the study failed to confirm a statistically significant reduction in death, stroke or myocardial infarction after major stroke or TIA by 50 mg atenolol. However, the results do not exclude a possible secondary prophylactic effect of atenolol in secondary prophylaxis after stroke and TIA.
Kinetics and regulation of cell-free alkaline phosphatase synthesis (1980)

Regulation of alkaline phosphatase (EC 3.1.3.1) synthesis in a cell-free system from Escherichia coli has been observed. Synthesis from transducing phage deoxyribonucleic acid templates carrying phoA+ occurred in S30 fractions from wild-type or alkaline phosphatase-constitutive mutants. It did not occur in S30) fractions from alkaline phosphatase-negative mutants (phoB). The hybrid gene phoA-lacZ was also subject to phoB control, implying that phoA transcription is regulated. The yield of active alkaline phosphatase per phoA+ gene copy from cell-free synthesis was similar to that of beta-galactosidase. Alkaline phosphatase activity took longer to appear than beta-galactosidase activity. Synthesis of alkaline phosphatase subunits was not delayed, suggesting that a minimum number of subunits are synthesized before formation of active alkaline phosphatase occurs.
A procedure for selective DNA alkylation and detection by mass spectrometry (1995)

A method which improves the detectability of DNA by mass spectrometry is presented. By quantitatively alkylating the backbone of phosphorothioate oligonucleotides the problems of gas phase ion generation by matrix assisted laser desorption ionization can be controlled. We have developed a selective alkylating protocol for phosphorothioate oligonucleotides which is a facile way of generating non-ionic nucleic acids. A variety of alkylating agents was studied and their kinetics were monitored in a gel electrophoretic assay and by mass spectrometry.
Towards Using Structural Events To Assess Non-native Speech (2010)

We investigated using structural events, e.g., clause and disfluency structure, from transcriptions of spontaneous non-native speech, to compute features for measuring speaking proficiency. Using a set of transcribed audio files collected from the TOEFL Practice Test Online (TPO), we conducted a sophisticated annotation of structural events, including clause boundaries and types, as well as disfluencies. Based on words and the annotated structural events, we extracted features related to syntactic complexity, e.g., the mean length of clause (MLC) and dependent clause frequency (DEPC), and a feature related to disfluencies, the interruption point frequency per clause (IPC). Among these features, the IPC shows the highest correlation with holistic scores (r = −0.344). Furthermore, we increased the correlation with human scores by normalizing IPC by (1) MLC (r = −0.386), (2) DEPC (r = −0.429), and (3) both (r = −0.462). In this research, the features derived from structural events of speech transcriptions are found to predict holistic scores measuring speaking proficiency. This suggests that structural events estimated on speech word strings provide a potential way for assessing nonnative speech. 1
6-[2-(Phosphonomethoxy)alkoxy]pyrimidines with Antiviral Activity (2002)

6-Hydroxypyrimidines substituted at positions 2 and 4 by hydrogen, methyl, amino, cyclopropylamino, dimethylamino, methylsulfanyl, or hydroxyl group afford by the reaction with diisopropyl 2-(chloroethoxy)methylphosphonate in the presence of NaH, Cs(2)CO(3), or DBU a mixture of N(1)- and O(6)-[2-(diisopropylphosphorylmethoxy)ethyl] isomers which were converted to the free phosphonic acids by treatment with bromotrimethylsilane followed by hydrolysis. Analogously, 2,4-diamino-6-hydroxypyrimidine gave on reaction with [(R)- and (S)-2-(diisopropylphosphorylmethoxy)propyl] tosylate, followed by deprotection, the enantiomeric 6-[2-(phosphonomethoxy)propoxy]pyrimidines. 2,4-Diamino-6-sulfanylpyrimidine gave, on treatment with diisopropyl 2-(chloroethoxy)methylphosphonate in the presence of NaH and subsequent deprotection, 2,4-diamino-6-[[2-(phosphonomethoxy)ethyl]sulfanyl]pyrimidine. 2-Amino-4-hydroxy-6-[2-(phosphonomethoxy)ethyl]pyrimidine was obtained from the appropriate 2-amino-4-chloropyrimidine derivative by alkaline hydrolysis and ester cleavage. Direct alkylation of 2-amino-4,6-dihydroxypyrimidine afforded a mixture of 2-amino-4,6-bis[2-(phosphonomethoxy)ethyl]- and 2-amino-1,4-bis[2-(phosphonomethoxy)ethyl]pyrimidine. None of the N(1)-[2-(phosphonomethoxy)ethyl] isomers exhibited any antiviral activity against DNA viruses or RNA viruses tested in vitro. On the contrary, the O(6)-isomers, namely the compounds derived from 2,4-diamino-, 2-amino-4-hydroxy-, or 2-amino-4-[2-(phosphonomethoxy)ethoxy]-6-hydroxypyrimidine, inhibited the replication of herpes viruses [herpes simplex type 1 (HSV-1) and type 2 (HSV-2), varicella-zoster virus (VZV), and cytomegalovirus (CMV)] and retroviruses [Moloney sarcoma virus (MSV) and human immunodeficiency virus type 1 (HIV-1) and type 2 (HIV-2)], their activity being most pronounced against the latter. The antiviral activity was lower if the oxygen at the position 6 was replaced by a sulfur atom, as in 2,4-diamino-6-[2-(phosphonomethoxy)ethylsulfanyl]pyrimidine. In analogy to N(9)-[2-(phosphonomethoxy)propyl]-2,6-diaminopurine (PMPDAP), solely the (R)-2,4-diamino-6-[2-(phosphonomethoxy)propoxy]pyrimidine exerted antiviral activity, whereas its (S)-enantiomer was essentially inactive.
Antifungal peptides: Origin, activity, and therapeutic potential. (2000)

Antifungal peptides have been identified in a wide range of life forms which include plants, mammals, and microorganisms. Their structures are as varied as their antifungal properties. Semisynthetic and fully synthetic analogs have been developed from a few of these natural peptides that are superior to the parent compound. A few of these peptides hold promise in combating fungal infections and have entered clinical trials.
A retrovirus expressing the 12S adenoviral E1A gene product can immortalize epithelial cells from a broad range of rat tissues. (1988)

An epithelial cell-transforming virus could be of great use, both in the culture of epithelial cell lines and in the study of carcinogenesis. Since the adenoviral E1A gene has been shown to partially transform some epithelial cells from primary rat cell cultures, we constructed retrovirus vectors containing either the 12S or 13S E1A cDNA sequences to facilitate the transfer of these genes into a variety of primary cell types. The 12S E1A virus induced proliferation and immortalization of epithelial cells in rat kidney, liver, heart, pancreas, and thyroid primary cultures. In the two cases tested, heart and liver cultures, E1A-immortalized cells were nontumorigenic, but could be completely transformed by subsequent introduction of the ras oncogene. To our surprise, the 13S virus had a greatly reduced immortalization potential. We discuss these data in light of the model of Spindler et al. (K. R. Spindler, C. Y. Eng, and A.-J. Berk, J. Virol. 53:742-750, 1985), in which the 12S E1A protein is required for the complete induction of the cellular DNA replication machinery in the quiescent human epithelial cells in which adenoviruses normally replicate.
Homogeneity of Political Elites in Korea: An Analysis of Regional and Educational Backgrounds of Cabinet Members, 1961-1990 (1995)

A collection of papers presented at the Fifth Academic Conference of the Korean American University Professors Association, ... held at the Sheraton Century Center Hotel of Atlanta, Georgea on October 21-23, 1994.
5-Substituted Pyrimidine and 7-Substituted 7-Deazapurine dNTPs as Substrates for DNA Polymerases in Competitive Primer Extension in the Presence of Natural dNTPs (2016)

A complete series of 5-substituted uracil or cytosine, as well as 7-substituted 7-deazaadenine and 7-deazaguanine 2'-deoxyribonucleoside triphosphates (dNTPs) bearing substituents of increasing bulkiness (H, Me, vinyl, ethynyl, and phenyl) were systematically studied in competitive primer extension in the presence of their natural counterparts (nonmodified dNTPs), and their kinetic data were determined. The results show that modified dNTPs bearing π-electron-containing substituents (vinyl, ethynyl, Ph) are typically excellent substrates for DNA polymerases comparable to or better than natural dNTPs. The kinetic studies revealed that these modified dNTPs have higher affinity to the active site of the enzyme-primer-template complex, and the calculations (semiempirical quantum mechanical scoring function) suggest that it is due to the cation-π interaction of the modified dNTP with Arg629 in the active site of Bst DNA polymerase.
Rational design of coagulation factor VIIa variants with substantially increased intrinsic activity (2001)

A trace amount of coagulation factor VII (FVII) circulates in the blood in the activated form, FVIIa (EC 3.4.21.21), formed by internal proteolysis. To avoid disseminated thrombus formation, FVIIa remains in a conformation with zymogen-like properties. Association with tissue factor (TF), locally exposed upon vascular injury, is necessary to render FVIIa biologically active and initiate blood clotting. We have designed potent mutants of FVIIa by replacing residues believed to function as determinants for the inherent zymogenicity. The TF-independent rate of factor X activation was dramatically improved, up to about 100-fold faster than that obtained with the wild-type enzyme and close to that of the FVIIa-soluble TF complex. The mutants appear to retain the substrate specificity of the parent enzyme and can be further stimulated by TF. Insights into the mechanism behind the increased activity of the mutants, presumably also pertinent to the TF-induced, allosteric stimulation of FVIIa activity, were obtained by studying their calcium dependence and the accessibility of the N terminus of the protease domain to chemical modification. The FVIIa analogues promise to offer a more efficacious treatment of bleeding episodes especially in hemophiliacs with inhibitory antibodies precluding conventional replacement therapy.
Hydrophobic Nanocrystals Coated with an Amphiphilic Polymer Shell:  A General Route to Water Soluble Nanocrystals (2004)

A general strategy is described which allows for transferring hydrophobically capped nanocrystals from organic to aqueous solution by wrapping an amphiphilic polymer around the particles. In particular, high quality CoPt3, Au, CdSe/ZnS, and Fe2O3 nanocrystals have been water-solubilized in this way. Analysis with transmission electron microscopy, gel electrophoresis, and fluorescence correlation spectroscopy demonstrates that monodispersity of the particles is conserved upon phase transfer to aqueous solution.
Effect of Zeta Potential on the Properties of Nano-Drug Delivery Systems - A Review (Part 2) (2013)

The zeta potential (ZP) of colloidal systems and nano-medicines, as well as their particle size exert a major effect on the various properties of nano-drug delivery systems. Not only the stability of dosage forms and their release rate are affected but also their circulation in the blood stream and absorptioninto body membranes are dramatically altered by ZP. In this paper the effect of ZP on the various properties of nano-medicines are reviewed. Furthermore, the ability of employing zeta potential to target drug delivery systems to, and drug release at specific sites of the body are discussed.Keywords: Nano-medicines, Zeta potential, Drug targeting, Site-specific release, Dosage form stability
Coping with the epidemic. The impact of proximal femoral fractures upon the acute orthopaedic services in northeast Scotland. (1999)

Increasing health care costs and an aging population have made hip fractures one of the most pressing concerns for developed nations in the latter half of the twentieth century. Using data collected in 1970 and in 1993, the extent of the hip fracture problem in the northeast of Scotland is assessed. The results demonstrate a 101% increase in the number of patients admitted with hip fractures, and an increase in the proportion of patients aged 75 years and over by 158%. Although there has been no change in the number of acute orthopaedic beds in the region, the increase in patient numbers have been managed by approximately halving the in-patient stay through the provision of rural convalescent/rehabilitation beds. Through this approach considerable savings can be made by the health service without reducing the standard of care that is required by the elderly patient later in the post-operative period. In addition, this approach will help focus local community services upon the long-term placement of the patient, in keeping with current government policy.
Two distinct endothelial lineages in ontogeny, one of them related to hemopoiesis (1996)

We have shown previously by means of quail/chick transplantations that external and visceral organs, i.e., somatopleural and splanchnopleural derivatives, acquire their endothelial network through different mechanisms, namely immigration (termed angiogenesis) versus in situ emergence of precursors (or vasculogenesis). We have traced the distribution of QH1-positive cells in chick hosts after replacement of the last somites by quail somites (orthotopic grafts) or lateral plate mesoderm (heterotopic grafts). The results lead to the conclusion that the embryo becomes vascularized by endothelial precursors from two distinct regions, splanchnopleural mesoderm and paraxial mesoderm. The territories respectively vascularized are complementary, precursors from the paraxial mesoderm occupy the body wall and kidney, i.e., they settle along with the other paraxial mesoderm derivatives and colonize the somatopleure. The precursors from the two origins have distinct recognition and potentialities properties: endothelial precursors of paraxial origin are barred from vascularizing visceral organs and from integrating into the floor of the aorta, and are never associated with hemopoiesis; splanchnopleural mesoderm grafted in the place of somites, gives off endothelial cells to body wall and kidney but also visceral organs. It gives rise to hemopoietic precursors in addition to endothelial cells.
Algorithms for trie compaction (1984)

The trie data structure has many properties which make it especially attractive for representing large files of data. These properties include fast retrieval time, quick unsuccessful search determination, and finding the longest match to a given identifier. The main drawback is the space requirement. In this paper the concept of trie compaction is formalized. An exact algorithm for optimal trie compaction and three algorithms for approximate trie compaction are given, and an analysis of the three algorithms is done. The analysis indicate that for actual tries, reductions of around 70 percent in the space required by the uncompacted trie can be expected. The quality of the compaction is shown to be insensitive to the number of nodes, while a more relevant parameter is the alphabet size of the key.
Variable-rate variable-power MQAM for fading channels (1997)

We propose a variable-rate and variable-power MQAM modulation scheme for high-speed data transmission over fading channels. We first review results for the Shannon capacity of fading channels with channel side information, where capacity is achieved using adaptive transmission techniques. We then derive the spectral efficiency of our proposed modulation. We show that there is a constant power gap between the spectral efficiency of our proposed technique and the channel capacity, and this gap is a simple function of the required bit-error rate (BER). In addition, using just five or six different signal constellations, we achieve within 1-2 dB of the maximum efficiency using unrestricted constellation sets. We compute the rate at which the transmitter needs to update its power and rate as a function of the channel Doppler frequency for these constellation sets. We also obtain the exact efficiency loss for smaller constellation sets, which may be required if the transmitter adaptation rate is constrained by hardware limitations. Our modulation scheme exhibits a 5-10-dB power gain relative to variable-power fixed-rate transmission, and up to 20 dB of gain relative to nonadaptive transmission. We also determine the effect of channel estimation error and delay on the BER performance of our adaptive scheme. We conclude with a discussion of coding techniques and the relationship between our proposed modulation and Shannon capacity.
Dexamethasone−Methotrexate:  An Efficient Chemical Inducer of Protein DimerizationIn Vivo (2000)

ADVERTISEMENT RETURN TO ISSUEPREVCommunicationNEXTDexamethasone−Methotrexate: An Efficient Chemical Inducer of Protein Dimerization In VivoHening Lin, Wassim M. Abida, Robert T. Sauer, and Virginia W. CornishView Author Information Department of Chemistry, Columbia University New York, New York 10027 Department of Biology Massachusetts Institute of Technology Cambridge, Massachusetts 02139 Cite this: J. Am. Chem. Soc. 2000, 122, 17, 4247–4248Publication Date (Web):April 13, 2000Publication History Received29 November 1999Published online13 April 2000Published inissue 1 May 2000https://doi.org/10.1021/ja9941532Copyright © 2000 American Chemical SocietyRIGHTS & PERMISSIONSArticle Views1688Altmetric-Citations79LEARN 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 InReddit Read OnlinePDF (91 KB) Get e-AlertsSupporting Info (1)»Supporting Information Supporting Information SUBJECTS:Assays,Dimerization,Fungi,Peptides and proteins,Receptors Get e-Alerts
Frequency of RAS Mutations (KRAS, NRAS, HRAS) in Human Solid Cancer (2017)

RAS oncogene affects numerous cellular functions including growth, proliferation, apoptosis, migration, division and differentiation of the cells. It has 3 known isoforms as Harvey- RAS (HRAS), Kirsten - RAS (KRAS) and Neuroblastoma- RAS (NRAS). RAS has an intrinsic GTPase activity. It encodes proteins binding the guanine nucleotides. KRAS and HRAS were discovered in studies carried out on viruses leading to cancer. Retroviral oncogenes related to murine sarcoma virus genes (Kristen Rat Sarcoma Virus and Murine Sarcoma Virus) were discovered in 1982. These two oncogenes are similar to human KRAS. Approximately 30% of all human cancers have ras genes. Mutations in KRAS account for about 85% for all RAS mutations in human tumors, NRAS is about 11–15%, and HRAS is about 1%.
An abundantly expressed mucin-like protein from Toxocara canis infective larvae: the precursor of the larval surface coat glycoproteins. (1996)

Evasion of host immunity by Toxocara canis infective larvae is mediated by the nematode surface coat, which is shed in response to binding by host antibody molecules or effector cells. The major constituent of the coat is the TES-120 glycoprotein series. We have isolated a 730-bp cDNA from the gene encoding the apoprotein precursor of TES-120. The mRNA is absent from T. canis adults but hyperabundant in larvae, making up approximately 10% of total mRNA, and is trans-spliced with the nematode 5' leader sequence SL1. It encodes a 15.8-kDa protein (after signal peptide removal) containing a typical mucin domain: 86 amino acid residues, 72.1% of which are Ser or Thr, organized into an array of heptameric repeats, interspersed with proline residues. At the C-terminal end of the putative protein are two 36-amino acid repeats containing six Cys residues, in a motif that can also be identified in several genes in Caenorhabditis elegans. Although TES-120 displays size and charge heterogeneity, there is a single copy gene and a homogeneous size of mRNA. The association of overexpression of some membrane-associated mucins with immunosuppression and tumor metastasis suggests a possible model for the role of the surface coat in immune evasion by parasitic nematodes.