gebhart/patrepeval huggingface dataset:
Transient electroluminescence of polymer light emitting diodes using electrical pulses (1999)

Detailed experimental and theoretical analysis of the pulsed excitation of polymer light emitting diodes is presented. We find a set of universal transient features for a variety of device configurations (different polymers/cathodes) which can be reproduced using our phenomenological numerical model. We find that the temporal evolution of the electroluminescence in response to a step voltage pulse is characterized by: (i) a delay followed by; (ii) a fast initial rise at turn-on followed by; (iii) a slow rise (slower by at least one order of magnitude). The large mobility mismatch between holes and electrons in conjugated polymers allows us to separately time resolve the motion of holes and electrons. We suggest a method for extracting mobility values that takes into account the possible field-induced broadening of carrier fronts, and which is found to be compatible with mobilities determined from constant wave measurements. By using appropriate device configurations it is possible to determine the mobilities of both holes and electrons from a single device. Mobilities for holes and electrons are extracted for a poly(p-phenylenevinylene) copolymer and poly(di-octyl fluorene).
A single amino acid substitution converts a carboxylesterase to an organophosphorus hydrolase and confers insecticide resistance on a blowfly (1997)

Resistance to organophosphorus (OP) insecticides is associated with decreased carboxylesterase activity in several insect species. It has been proposed that the resistance may be the result of a mutation in a carboxylesterase that simultaneously reduces its carboxylesterase activity and confers an OP hydrolase activity (the "mutant ali-esterase hypothesis"). In the sheep blowfly, Lucilia cuprina, the association is due to a change in a specific esterase isozyme, E3, which, in resistant flies, has a null phenotype on gels stained using standard carboxylesterase substrates. Here we show that an OP-resistant allele of the gene that encodes E3 differs at five amino acid replacement sites from a previously described OP-susceptible allele. Knowledge of the structure of a related enzyme (acetylcholinesterase) suggests that one of these substitutions (Gly137 --> Asp) lies within the active site of the enzyme. The occurrence of this substitution is completely correlated with resistance across 15 isogenic strains. In vitro expression of two natural and two synthetic chimeric alleles shows that the Asp137 substitution alone is responsible for both the loss of E3's carboxylesterase activity and the acquisition of a novel OP hydrolase activity. Modeling of Asp137 in the homologous position in acetylcholinesterase suggests that Asp137 may act as a base to orientate a water molecule in the appropriate position for hydrolysis of the phosphorylated enzyme intermediate.
Management of solitary pulmonary nodules. An organized approach based on growth rate and statistics (1974)

Too many patients with benign pulmonary nodules are subjected to lung resection. Based on tumor growth rate and statistics, a method of treatment for patients with pulmonary nodules is proposed that relies on serial chest x-ray films when a definite diagnosis cannot be made by sputum analysis in patients 30 to 45 years old and evaluation by sputum analysis and needle or brush biopsy in patients over 45 years old. Patients less than 30 years of age require serial films only. This approach should spare most patients with benign nodules from surgery while maintaining present survival rates in malignant solitary pulmonary nodules.
The Phosphorylation of Ribosomal Protein S6 in Hamster Fibroblasts Infected with Pseudorabies Virus Inactivated by Ultraviolet Radiation (1984)

Infection of baby hamster fibroblasts with pseudorabies virus at high multiplicities resulted in a substantial increase in the phosphorylation of ribosomal protein S6. However, the phosphorylation was still observed with virus that had been completely inactivated by u.v. irradiation. We therefore conclude that expression of the viral genome is not required for the virus to elicit this effect.
Isolation and characterization of a chicken homolog of the c-ret proto-oncogene. (1995)

The c-ret proto-oncogene encodes a receptor tyrosine kinase that plays important roles in human disease and in normal mammalian development. Mutations in the human RET gene are associated with multiple endocrine neoplasia syndromes and Hirschsprung's disease in humans, while targeted mutagenesis of murine c-ret resulted in severe developmental abnormalities affecting the excretory and peripheral nervous systems. To examine the evolutionary conservation of the ret protein sequence and its developmental expression pattern, we isolated and sequenced cDNA clones of chicken c-ret and examined its expression in chick embryos and adult tissues. The cytoplasmic domains of chicken and human ret were relatively well conserved (91% similar), but the extracellular domains were more divergent (68% similar), although the conservation of cysteine residues in this region suggests a conserved secondary structure. As in mouse and human, chicken c-ret encodes two protein isoforms. The number and sizes of the transcripts were similar to those in human and mouse cells, and during chick embryogenesis, c-ret mRNA was observed in many of the same sites as in the mouse, including the Wolffian duct and ureteric bud, the enteric, dorsal root, sympathetic and facioacoustic ganglia, and the ventral spinal cord. Evolutionary differences in expression were observed in the trigeminal ganglion, the ventral roots of the spinal cord, the mesenchymal cells of the branchial arches and the adult testes. The results are discussed with regard to the role of the ret receptor in normal development and disease.
Tailoring Galvanic Replacement Reaction for the Preparation of Pt/Ag Bimetallic Hollow Nanostructures with Controlled Number of Voids (2012)

Here we report the synthesis of Pt/Ag bimetallic nanostructures with controlled number of void spaces via a tailored galvanic replacement reaction (GRR). Ag nanocubes (NCs) were employed as the template to react with Pt ions in the presence of HCl. The use of HCl in the GRR caused rapid precipitation of AgCl, which grew on the surface of Ag NCs and acted as a removable secondary template for the deposition of Pt. The number of nucleation sites for AgCl was tailored by controlling the amount of HCl added to the Ag NCs or by introducing PVP to the reaction. This strategy led to the formation of Pt/Ag hollow nanoboxes, dimers, multimers, or popcorn-shaped nanostructures consisting of one, two, or multiple hollow domains. Due to the presence of large void space and porous walls, these nanostructures exhibited high surface area and improved catalytic activity for methanol oxidation reaction.
Use of specific fluorescent antibodies for the identification of hemoglobin C in erythrocytes (1977)

Antibodies against hemoglobulin C (alpha2beta2 6Glu leads to Lys) were produced by immunizing horses and were purified by affinity chromatography. As expected from the bivalency of both the antibody and the antigen, the purified antibodies failed to produce immunoprecipitates upon reaction with the corresponding antigens. Identification of hemoglobin C in individual erythrocytes was achieved by reacting the fluorescein isothiocyanate-conjugated antibodies with the hemoglobin antigen in fixed smears of peripheral blood. Red cells from persons having a hemoglobin C gene were labeled strongly upon reaction with anti-Hb C-FITC; there was no labeling of red cells containing normal hemoglobins or Hb S, suggesting that the anti-Hb C antibodies recognize only the amino-terminal segment of the beta chains that contain lysine in position beta6.
Preassembled capsids of type D retroviruses contain a signal sufficient for targeting specifically to the plasma membrane (1990)

The capsids of Mason-Pfizer monkey virus (M-PMV), an immunosuppressive type D retrovirus, are preassembled in the infected cell cytoplasm and are then transported to the plasma membrane, where they are enveloped in a virus glycoprotein-containing lipid bilayer. The role of viral glycoprotein in intracellular transport of M-PMV capsids was investigated with a spontaneous mutant (5A) of M-PMV, which we show here to be defective in envelope glycoprotein biosynthesis. DNA sequence analysis of the env gene of mutant 5A reveals a single nucleotide deletion in the middle of the gene, which results in the synthesis of a truncated form of the envelope glycoprotein. Evidence is presented showing that the mutant glycoprotein is not expressed at the cell surface but is retained in the endoplasmic reticulum. Normal levels of gag-pro-pol precursor polyproteins are made and processed in mutant genome-transfected cells, and high levels of noninfectious particles lacking viral glycoprotein are released with normal kinetics into the culture medium. No intracisternal budding of capsids is observed. We conclude that viral glycoprotein is required neither for targeting preassembled capsids of M-PMV to the plasma membrane for final maturation nor for the budding process. Since the presence or absence of M-PMV glycoprotein at the site of budding does not affect the efficiency or kinetics of the targeting process, the preassembled capsid of M-PMV, in contrast to those of intracisternal type A particles, appears to have an intrinsic signal for intracellular transport to the plasma membrane.
Immunosuppression by Glucocorticoids: Inhibition of NF-κB Activity Through Induction of IκB Synthesis (1995)

Glucocorticoids are among the most potent anti-inflammatory and immunosuppressive agents. They inhibit synthesis of almost all known cytokines and of several cell surface molecules required for immune function, but the mechanism underlying this activity has been unclear. Here it is shown that glucocorticoids are potent inhibitors of nuclear factor kappa B (NF-kappa B) activation in mice and cultured cells. This inhibition is mediated by induction of the I kappa B alpha inhibitory protein, which traps activated NF-kappa B in inactive cytoplasmic complexes. Because NF-kappa B activates many immunoregulatory genes in response to pro-inflammatory stimuli, the inhibition of its activity can be a major component of the anti-inflammatory activity of glucocorticoids.
Highly Efficient Cross‐Dehydrogenative‐Coupling between Ethers and Active Methylene Compounds (2006)

An unlikely couple: CC bonds can be formed between ethers and methylene compounds by cross-dehydrogenative-coupling (see scheme; DDQ=2,3-dichloro-5,6-dicyanobenzoquinone). This straightforward reaction employs mild conditions and simple catalysts and allows reasonably high yields. Supporting information for this article is available on the WWW under http://www.wiley-vch.de/contents/jc_2002/2006/z503255_s.pdf or from the author. Please note: The publisher is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.
Life Below the Gum Line: Pathogenic Mechanisms ofPorphyromonas gingivalis (1998)

Porphyromonas gingivalis, a gram-negative anaerobe, is a major etiological agent in the initiation and progression of severe forms of periodontal disease. An opportunistic pathogen, P. gingivalis can also exist in commensal harmony with the host, with disease episodes ensuing from a shift in the ecological balance within the complex periodontal microenvironment. Colonization of the subgingival region is facilitated by the ability to adhere to available substrates such as adsorbed salivary molecules, matrix proteins, epithelial cells, and bacteria that are already established as a biofilm on tooth and epithelial surfaces. Binding to all of these substrates may be mediated by various regions of P. gingivalis fimbrillin, the structural subunit of the major fimbriae. P. gingivalis is an asaccharolytic organism, with a requirement for hemin (as a source of iron) and peptides for growth. At least three hemagglutinins and five proteinases are produced to satisfy these requirements. The hemagglutinin and proteinase genes contain extensive regions of highly conserved sequences, with posttranslational processing of proteinase gene products contributing to the formation of multimeric surface protein-adhesin complexes. Many of the virulence properties of P. gingivalis appear to be consequent to its adaptations to obtain hemin and peptides. Thus, hemagglutinins participate in adherence interactions with host cells, while proteinases contribute to inactivation of the effector molecules of the immune response and to tissue destruction. In addition to direct assault on the periodontal tissues, P. gingivalis can modulate eucaryotic cell signal transduction pathways, directing its uptake by gingival epithelial cells. Within this privileged site, P. gingivalis can replicate and impinge upon components of the innate host defense. Although a variety of surface molecules stimulate production of cytokines and other participants in the immune response, P. gingivalis may also undertake a stealth role whereby pivotal immune mediators are selectively inactivated. In keeping with its strict metabolic requirements, regulation of gene expression in P. gingivalis can be controlled at the transcriptional level. Finally, although periodontal disease is localized to the tissues surrounding the tooth, evidence is accumulating that infection with P. gingivalis may predispose to more serious systemic conditions such as cardiovascular disease and to delivery of preterm infants.
Thermodynamic studies of DNA‐dye complexes, 2. DNA‐methylene blue and DNA‐thionine systems (1981)

Abstract The interaction between DNA and various dyes (methylene blue ( 1 ), and thionine ( 2 )) was studied by means of the heat of mixing. From the results, the thermodynamic quantities were estimated for the DNA‐dye system by an intercalation process. The free energy change of the system DNA‐ 2 was found to be nearly equal to that of the system DNA‐ 1 , but the absolute value of the heat of interaction of the system DNA‐ 2 , which has amino groups, is higher than that of the system DNA‐ 1 . These facts are comparable with those previously found for the systems DNA‐proflavine and DNA‐acridine orange. However, the locations of 1 and 2 intercalated into DNA may be different from those of acridine orange and proflavine because the enthalpy changes for the systems DNA‐ 1 and DNA‐ 2 are higher than those of the systems DNA‐acridine orange and DNA‐proflavine, respectively. These facts showed that the location of the intercalated dye depends on the presence of amino groups in 3‐position of the dye.
Molecular Features of the Transition from Prostatic Intraepithelial Neoplasia (PIN) to Prostate Cancer (2004)

To characterize the molecular feature in prostate carcinogenesis and the putative transition from prostatic intraepithelial neoplasia (PIN) to invasive prostate cancer (PC), we analyzed gene-expression profiles of 20 PCs and 10 high-grade PINs with a cDNA microarray representing 23,040 genes. Considering the histological heterogeneity of PCs and the minimal nature of PIN lesions, we applied laser microbeam microdissection to purify populations of PC and PIN cells, and then compared their expression profiles with those of corresponding normal prostatic epithelium also purified by laser microbeam microdissection. A hierarchical clustering analysis separated the PC group from the PIN group, except for three tumors that were morphologically defined as one very-high-grade PIN and two low-grade PCs, suggesting that PINs and PCs share some molecular features and supporting the hypothesis of PIN-to-PC transition. On the basis of this hypothesis, we identified 21 up-regulated genes and 63 down-regulated genes commonly in PINs and PCs compared with normal epithelium, which were considered to be involved in the presumably early stage of prostatic carcinogenesis. They included AMACR, OR51E2, RODH, and SMS. Furthermore, we identified 41 up-regulated genes and 98 down-regulated genes in the transition from PINs to PCs; those altered genes, such as POV1, CDKN2C, EPHA4, APOD, FASN, ITGB2, LAMB2, PLAU, and TIMP1, included elements that are likely to be involved in cell adhesion or the motility of invasive PC cells. The down-regulation of EPHA4 by small interfering RNA in PC cells lead to attenuation of PC cell viability. These data provide clues to the molecular mechanisms underlying prostatic carcinogenesis, and suggest candidate genes the products of which might serve as molecular targets for the prevention and treatment of PC.
Conversion of lacZ Enhancer Trap Lines to GAL4 Lines Using Targeted Transposition in Drosophila melanogaster (1999)

Since the development of the enhancer trap technique, many large libraries of nuclear localized lacZ P-element stocks have been generated. These lines can lend themselves to the molecular and biological characterization of new genes. However they are not as useful for the study of development of cellular morphologies. With the advent of the GAL4 expression system, enhancer traps have a far greater potential for utility in biological studies. Yet generation of GAL4 lines by standard random mobilization has been reported to have a low efficiency. To avoid this problem we have employed targeted transposition to generate glial-specific GAL4 lines for the study of glial cellular development. Targeted transposition is the precise exchange of one P element for another. We report the successful and complete replacement of two glial enhancer trap P[lacZ, ry+] elements with the P[GAL4, w+] element. The frequencies of transposition to the target loci were 1.3% and 0.4%. We have thus found it more efficient to generate GAL4 lines from preexisting P-element lines than to obtain tissue-specific expression of GAL4 by random P-element mobilization. It is likely that similar screens can be performed to convert many other P-element lines to the GAL4 system.
Gefitinib for the first-line treatment of locally advanced or metastatic non-small cell lung cancer (2010)

This paper presents a summary of the evidence review group (ERG) report into the clinical effectiveness and cost-effectiveness of gefitinib for the first-line treatment of locally advanced or metastatic non-small cell lung cancer, in accordance with the licensed indication, based upon the manufacturer’s submission to the National Institute for Health and Clinical Excellence (NICE) as part of the single technology appraisal process. The submitted clinical evidence consisted of the IRESSA Pan-ASian Study (IPASS); a phase III open-label randomised controlled trial conducted in 87 centres in East Asia which compared the use of gefitinib with paclitaxel/carboplatin in 1217 chemotherapy (CTX)-naive patients with stage IIIB/IV pulmonary adenocarcinoma. The manufacturer’s submission focused on a subgroup of patients in IPASS who were epidermal growth factor receptor (EGFR) gene mutation-positive (M+) ( n = 261; 21% of the total IPASS population). The primary clinical outcome was progression-free survival (PFS). Secondary outcomes included overall survival, clinically relevant improvement in quality of life and adverse events (AEs). Cost-effectiveness was measured in terms of incremental cost per quality-adjusted life-year (QALY). In the overall population, PFS was significantly longer in patients treated with gefitinib than in those treated with paclitaxel/carboplatin (hazard ratio 0.74, 95% confidence interval 0.65 to 0.85; p &lt; 0.0001). The manufacturer reported an incremental cost-effectiveness ratio (ICER) of £20,744 per QALY gained for the target population. The probabilistic sensitivity analysis illustrated that for patients who are EGFR M+, gefitinib compared with doublet CTX was not likely to be cost-effective at what would usually be considered standard levels of willingness to pay for an additional QALY; the mean ICER for gefitinib EGFR M+ versus doublet CTX EGFR M+ was reported as £35,700 per QALY. Additional analysis by the ERG included amendments to the base-case analysis, including an alternative approach to projecting survival, inclusion of two important additional comparators, sensitivity to EGFR M+ prevalence, and AE costs and disutilities. The manufacturer’s submission provides clinical evidence to support the use of gefitinib in EGFR M+ patients with adenocarcinoma histology only. Before patients can be offered first-line treatment with gefitinib they must undergo EGFR mutation status testing which is currently not routinely available in the NHS. At the time of writing, the guidance document issued by NICE on 28 July 2010 states that ‘Gefitinib is recommended as an option for the first-line treatment of people with locally advanced or metastatic non-small-cell lung cancer (NSCLC) if they test positive for the epidermal growth factor receptor tyrosine kinase (EGFR-TK) mutation and the manufacturer provides gefitinib at the fixed price agreed under the patient access scheme’.
<title>Color measurements based on a color camera</title> (1997)

The domain of color camera applications is increasing all time due to recent progress in color machine vision research. Colorimetric measurement tasks are quite complex as the purpose of color measurement is to provide a quantitative evaluation of the phenomenon of colors as perceived by human vision. A proper colorimetric calibration of the color camera system is needed in order to make color a practical tool in machine vision. This paper discuses two approaches to color measurements based on a color camera and includes an overview of practical approaches to color camera calibration under unstable illumination conditions.
Mutational Analysis of the Chicken Progesterone Receptor (1989)

Oligonucleotide-directed site mutagenesis was used to prepare a series of chicken progesterone receptor deletion mutants in an attempt to elucidate structure-function relationships of the receptor. These mutants spanned the entire 659-amino acid coding region of the A form of the receptor. The ability of these mutants to bind progesterone was analyzed following in vitro transcription and translation. Results obtained indicate that a large portion of the protein ranging from amino acid 420 to the extreme carboxyl terminus is necessary to maintain the protein in a conformation which is capable of binding hormone. Following transient cotransfection of mutant receptor proteins into CV-1 cells along with a reporter gene containing an authentic GRE/PRE (PRE-TK-CAT), our results indicated that any deletion throughout the entire molecule results in a decrease in transcriptional activation. Most of these decreases result from an inability of the mutant receptor proteins to bind DNA or hormone. However, two areas of the receptor have been identified which are unrelated to either DNA or hormone binding but markedly affect the ability of the receptor to transactivate target genes.
Early Increase of von Willebrand Factor Predicts Adverse Outcome in Unstable Coronary Artery Disease (1998)

In patients with unstable angina or non-Q-wave myocardial infarction, the acute-phase proteins increase over the first 2 days despite medical treatment. The early rise of von Willebrand factor is an independent predictor of adverse clinical outcome at 14 days and at 30 days. Enoxaparin provides protection as evidenced by the reduced release of von Willebrand factor, which represents a favorable prognostic finding.