gebhart/patrepeval huggingface dataset:
Carbohydrates in protein (1938)

Research Article| September 01 1938 Carbohydrates in protein: The carbohydrate component of crystalline egg albumin A. Neuberger A. Neuberger 1 1The Department of Pathological Chemistry, University College Hospital Medical School, London Search for other works by this author on: This Site PubMed Google Scholar Biochem J (1938) 32 (9): 1435–1451. https://doi.org/10.1042/bj0321435 Views Icon Views Article contents Figures & tables Video Audio Supplementary Data Peer Review Share Icon Share Facebook Twitter LinkedIn MailTo Cite Icon Cite Get Permissions Citation A. Neuberger; Carbohydrates in protein: The carbohydrate component of crystalline egg albumin. Biochem J 1 September 1938; 32 (9): 1435–1451. doi: https://doi.org/10.1042/bj0321435 Download citation file: Ris (Zotero) Reference Manager EasyBib Bookends Mendeley Papers EndNote RefWorks BibTex toolbar search Search Dropdown Menu toolbar search search input Search input auto suggest filter your search All ContentAll JournalsBiochemical Journal Search Advanced Search This content is only available as a PDF. © 1938 CAMBRIDGE UNIVERSITY PRESS1938 Article PDF first page preview Close Modal You do not currently have access to this content.
Strand-specific mismatch correction in nuclear extracts of human and Drosophila melanogaster cell lines. (1990)

Nuclear extracts derived from HeLa and Drosophila melanogaster KC cell lines have been found to correct single base-base mispairs within open circular DNA heteroduplexes containing a strand-specific, site-specific incision located 808 base pairs from the mismatch. Correction in both extract systems is strand specific, being highly biased to the incised DNA strand. Different mispairs within a homologous set of heteroduplexes were processed with different efficiencies (G.T greater than G.G approximately equal to A.C greater than C.C), and correction was accompanied by mismatch-dependent DNA synthesis localized to the region spanning the mispair and the strand break, thus demonstrating that mismatch recognition is associated with the repair reaction. Correction of each of these heteroduplexes was abolished by aphidicolin but was relatively insensitive to the presence of high concentrations of ddTTP, indicating probable involvement of alpha and/or delta class DNA polymerase(s). These findings suggest that higher eukaryotic cells possess a general, strand-specific mismatch repair system analogous to the Escherichia coli mutHLS and the Streptococcus pneumoniae hexAB pathways, systems that contribute in a major way to the genetic stability of these bacterial species.
Gap misrepair mutagenesis: efficient site-directed induction of transition, transversion, and frameshift mutations in vitro. (1982)

Short single-stranded gaps can be constructed by limited exonuclease action at single-stranded breaks (nicks) placed at predetermined sites on closed circular DNA molecules. As efficient primer-templates for DNA polymerase, single-stranded gaps can be repaired in vitro to regenerate an intact DNA duplex. In this report two in vitro reaction schemes are described that produce a high frequency of errors during repair ("misrepair") of gaps and thereby allow the efficient recovery of mutations limited to the nucleotide sequence at or near the original gap. In the first of these misrepair schemes, nucleotide misincorporations are stimulated by omission of one of the four deoxynucleoside triphosphates; the misincorporations are trapped by the presence of excess DNA ligase in the reaction mixture. The second misrepair scheme involves the misincorporation of an excision-resistant alpha-thiophosphate nucleotide, followed by gap filling in the presence of all four conventional deoxynucleoside triphosphates. When applied to short gaps constructed at one of several unique restriction sites on the small plasmid pBR322, both gap misrepair methods yielded mutations within the targeted restriction site at high frequency (6--42%). A majority of the sequence changes identified were base substitutions; transversions and transitions are approximately equally represented. The remaining sequence changes were an insertion of a single base pair and deletions of one to four base pairs.
A large-scale survey of the novel 15q24 microdeletion syndrome in autism spectrum disorders identifies an atypical deletion that narrows the critical region (2010)

From the current and previous studies, deletions in the 15q24 region represent rare causes of ASDs with an estimated frequency of 0.1 to 0.2% in individuals ascertained for ASDs, although the proportion might be higher in sporadic cases. These rates compare with a frequency of about 0.3% in patients ascertained for unexplained intellectual disability and congenital anomalies. This atypical deletion reduces the minimal interval for the syndrome from 1.75 Mb to 766 kb, implicating a reduced number of genes (15 versus 38). Sequencing of genes in the 15q24 interval in large ASD and intellectual disability samples may identify mutations of etiologic importance in the development of these disorders.
Normalization and Subtraction of Cap-Trapper-Selected cDNAs to Prepare Full-Length cDNA Libraries for Rapid Discovery of New Genes (2000)

In the effort to prepare the mouse full-length cDNA encyclopedia, we previously developed several techniques to prepare and select full-length cDNAs. To increase the number of different cDNAs, we introduce here a strategy to prepare normalized and subtracted cDNA libraries in a single step. The method is based on hybridization of the first-strand, full-length cDNA with several RNA drivers, including starting mRNA as the normalizing driver and run-off transcripts from minilibraries containing highly expressed genes, rearrayed clones, and previously sequenced cDNAs as subtracting drivers. Our method keeps the proportion of full-length cDNAs in the subtracted/normalized library high. Moreover, our method dramatically enhances the discovery of new genes as compared to results obtained by using standard, full-length cDNA libraries. This procedure can be extended to the preparation of full-length cDNA encyclopedias from other organisms.
Static scattering in filled nematic: new liquid crystal display technique (1991)

A new bistable liquid crystal display is described that uses a nematic phase in which solid particles are dispersed. The display effects rely on direct static light scattering so that no polarisers are required. A two-frequency addressing scheme provides, in principle, a method for electrical control.
Optical Properties and Electronic Structure of Amorphous Germanium (1966)

Abstract The optical constants of amorphous Ge are determined for the photon energies from 0.08 to 1.6 eV. From 0.08 to 0.5 eV, the absorption is due to k ‐conserving transitions of holes between the valence bands as in p‐type crystals; the spin‐orbit splitting is found to be 0.20 and 0.21 eV in non‐annealed, and annealed samples respectively. The effective masses of the holes in the three bands are 0.49 m (respectively 0.43 m ); 0.04 m , and 0.08 m . An absorption band is observed below the main absorption edge (at 300 °K the maximum of this band is at 0.86 eV); the absorption in this band increases with increasing temperature. This band is considered to be due to excitons bound to neutral acceptors, and these are presumably the same ones that play a decisive role in the transport properties and which are considered to be associated with vacancies. The absorption edge has the form: ω 2 ϵ 2 ∼(hω− E g ) 2 ( E g = 0.88 eV at 300 °K). This suggests that the optical transitions conserve energy but not k vector, and that the densities of states near the band extrema have the same energy‐dependence as in crystalline Ge. A simple theory describing this situation is proposed, and comparison of it with the experimental results leads to an estimate of the localization of the conduction‐band wavefunctions.
Dose ranging study of the oxytocin antagonist atosiban in the treatment of preterm labor (1996)

Atosiban's effect on uterine activity in preterm labor was enhanced by bolus infusion and was similar to the effect of ritodrine, but with fewer side effects.
Chimeric Anti-CD20 (IDEC-C2B8) Monoclonal Antibody Sensitizes a B Cell Lymphoma Cell Line to Cell Killing by Cytotoxic Drugs (1997)

More than 50% of patients with aggressive B lymphomas and the majority of patients with low grade lymphomas are not cured by current therapeutic strategies. The lymphomas express the B cell antigen CD20 on the cell surface and this antigen serves as target for antibody-directed therapies. Clinical studies with encouraging results have been underway with the use of a chimeric anti-CD20 antibody (IDEC-C2B8), consisting of human IgG1-6 constant regions and variable regions from the murine monoclonal anti-CD20 antibody IDEC-2B8. This study investigated the potential anti-tumor therapeutic value of combination treatment with anti-C2B8 and cytotoxic drugs. The in vitro study examined the sensitizing effect of C2B8 antibody on the DHL-4 B lymphoma line to various cytotoxic agents. Cytotoxicity was determined by the MTT assay. Surface and cytoplasmic proteins were determined by flow cytometry. Pretreatment of DHL-4 with C2B8 resulted in inhibition of cell proliferation and cell death and a fraction of the cells underwent apoptosis. While the DHL-4 tumor cells were relatively resistant to several cytotoxic drugs, pretreatment with C2B8 rendered the cells sensitive to TNF-alpha, ricin, diphtheria toxin (DTX), adriamycin and cisplatin but not to VP-16. Chemosensitization of DHL-4 tumor cells was not due to downmodulation of either the MDR-1 or bcl-2 gene products. However, treatment of DHL-4 with C2B8 inhibited TNF-alpha secretion. These findings demonstrate that C2B8 antibody potentiates the sensitivity of DHL-4 tumor cells to several cytotoxic agents. Further, the findings suggest that combination treatments with C2B8 antibody and drugs may be of clinical benefit in the treatment of patients with resistant aggressive B lymphomas.
Cloning and transcriptional regulation of a novel adipocyte-specific gene, FSP27. CAAT-enhancer-binding protein (C/EBP) and C/EBP-like proteins interact with sequences required for differentiation-dependent expression. (1992)

We have reported previously the cloning of several cDNAs whose mRNAs are induced during differentiation of the adipogenic cell line TA1. Here we characterize an adipocyte-specific gene, which we refer to as FSP27 (formerly clone 47), that encodes a protein of 27 kDa, the sequence of which is unrelated to any in the current data banks. The FSP27 promoter confers adipocyte-specific expression to a heterologous reporter gene in transfected adipogenic cell lines, e.g. TA1 and 3T3-L1. Analysis of regulatory elements in the FSP27 promoter region indicates the presence of (a) a proximal palindromic sequence that is necessary for adipocyte-specific expression; and (b) a distal differentiation-independent enhancer-like element. The palindromic sequence TTCGAAA is protected from digestion by DNase I using nuclear extracts from TA1 preadipocytes and adipocytes. Heated rat liver nuclear extract, a very abundant source of the transcription factor CAAT-enhancer-binding protein (C/EBP) and related proteins, generates an equivalent footprint over the palindrome. However, C/EBP can account for only a portion of the protein-DNA complexes in TA1 cells because preadipocytes as well as adipocytes contain proteins distinct from C/EBP which interact with the same sequence. We suggest that C/EBP and other C/EBP-like proteins play a critical role in regulating the transcription of the fat-specific gene FSP27.
Adaptive feedback active noise control headset: implementation, evaluation and its extensions (2005)

In this paper, we present design and real-time implementation of a single-channel adaptive feedback active noise control (AFANC) headset for audio and communication applications. Several important design and implementation considerations, such as the ideal position of error microphone, training signal used, selection of adaptive algorithms and structures will be addressed in this paper. Real-time measurements and comparisons are also carried out with the latest commercial headset to evaluate its performance. In addition, several new extensions to the AFANC headset are described and evaluated.
Synthetic route to benzo[c]thiophene and the naphtho[c]thiophenes (1971)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTSynthetic route to benzo[c]thiophene and the naphtho[c]thiophenesM. P. Cava, N. M. Pollack, O. A. Mamer, and M. J. MitchellCite this: J. Org. Chem. 1971, 36, 25, 3932–3937Publication Date (Print):December 1, 1971Publication History Published online1 May 2002Published inissue 1 December 1971https://pubs.acs.org/doi/10.1021/jo00824a019https://doi.org/10.1021/jo00824a019research-articleACS PublicationsRequest reuse permissionsArticle Views781Altmetric-Citations120LEARN 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-Alertsclose Get e-Alerts
Lubricin/Proteoglycan 4 binds to and regulates the activity of Toll-Like Receptors In Vitro (2016)

Proteoglycan 4 (PRG4/lubricin) is secreted by cells that reside in articular cartilage and line the synovial joint. Lubricin may play a role in modulating inflammatory responses through interaction with CD44. This led us to examine if lubricin could be playing a larger role in the modulation of inflammation/immunity through interaction with Toll-like receptors (TLRs). Human Embryonic Kidney (HEK) cells overexpressing TLRs 2, 4 or 5 and surface plasmon resonance were employed to determine if full length recombinant human lubricin was able to bind to and activate TLRs. Primary human synovial fibroblasts were also examined using flow cytometry and Luminex multiplex ELISA. A rat destabilization model of osteoarthritis (OA) was used to determine if lubricin injections were able to regulate pain and/or inflammation in vivo. Lubricin can bind to and regulate the activity of TLRs, leading to downstream changes in inflammatory signalling independent of HA. We confirmed these findings in vivo through intra-articular injections of lubricin in a rat OA model where the inhibition of systemic inflammatory signaling and reduction in pain were observed. Lubricin plays an important role in regulating the inflammatory environment under both homeostatic and tissue injury states.
Learning a Discriminative Null Space for Person Re-identification (2016)

Most existing person re-identification (re-id) methods focus on learning the optimal distance metrics across camera views. Typically a person's appearance is represented using features of thousands of dimensions, whilst only hundreds of training samples are available due to the difficulties in collecting matched training images. With the number of training samples much smaller than the feature dimension, the existing methods thus face the classic small sample size (SSS) problem and have to resort to dimensionality reduction techniques and/or matrix regularisation, which lead to loss of discriminative power. In this work, we propose to overcome the SSS problem in re-id distance metric learning by matching people in a discriminative null space of the training data. In this null space, images of the same person are collapsed into a single point thus minimising the within-class scatter to the extreme and maximising the relative between-class separation simultaneously. Importantly, it has a fixed dimension, a closed-form solution and is very efficient to compute. Extensive experiments carried out on five person re-identification benchmarks including VIPeR, PRID2011, CUHK01, CUHK03 and Market1501 show that such a simple approach beats the state-of-the-art alternatives, often by a big margin.
Activating Transcription Factor 3 Induces DNA Synthesis and Expression of Cyclin D1 in Hepatocytes (2001)

Activating transcription factor 3 (ATF3) is an early response gene that is induced rapidly during in vivo situations of cellular growth such as liver regeneration. However, neither the physiological function nor the potential target genes of this transcription factor related to cellular proliferation have been identified in the liver or other tissues. We demonstrate here that endogenous ATF3 mRNA expression is rapidly induced up to 4-fold upon mitogenic stimulation of quiescent Hepa 1-6 mouse hepatoma cells. Overexpression of exogenous ATF3 results in a significant, dose-dependent increase in DNA synthesis of up to 140% over control cells. ATF3-transfected cells also display significantly higher rates of [(3)H]thymidine incorporation in comparison with nontransfected controls in the presence of serum. Northern blot analysis and co-transfection experiments demonstrate that overexpression of ATF3 enhances cyclin D1 mRNA expression and activates the cyclin D1 promoter 2.5-fold when activating protein-1 (AP-1) and cyclic AMP response element (CRE) sites within the promoter are intact. ATF3-mediated promoter activation is reduced to 1.3-fold and 1.6-fold respectively when the AP-1 or CRE sites are mutated, and mutation of both sites simultaneously leads to the complete abrogation of promoter activation. Furthermore, DNA-binding studies demonstrate that ATF3 binds directly to the AP-1 site within the cyclin D1 promoter. These results indicate that ATF3 expression stimulates hepatocellular proliferation, suggesting that this effect is mediated, at least in part, by the ATF3-dependent activation of cyclin D1 transcription.
Direct electron transfer catalysed by enzymes: application for biosensor development (2000)

The ability to catalyse an electrode reaction via direct (mediatorless) electron transfer has been demonstrated for a number of redox enzymes. In the case of mediatorless electron transfer, the electron is transferred directly from the electrode to the substrate molecule via the active site of the enzyme, or vice versa. The electron itself is the second substrate for the reaction. An important point characterizing bioelectrocatalysis is the catalytic removal of the reaction over-voltage. Therefore the enzyme attached to the electrode is able to catalyse electrode reaction and forms a 'molecular transducer'. The substrate can be detected by potentiometric measurement of the removal of reaction over-voltage. The enzyme laccase is able to catalyse the reaction of oxygen electroreduction. Therefore a laccase molecular layer attached to the electrode surface forms an oxygen transducer. The formation of the layer results in a change of the electrocatalytic feature of the electrode. Laccase label coupled with either ligand or receptor allows the detection of ligand-receptor complex formation/dissociation on the electrode surface. The detection is virtually reagentless. The substrates for the reaction are molecular oxygen and the electron itself. Numerous reagentless immunosensors of different formats (competitive, displacement and sandwich) have been developed, as well as the reagentless detection system for immunofiltration/immunochromatography.
X-linked lymphoreticular disease in the scurfy (sf) mutant mouse. (1991)

Scurfy (sf) is a spontaneous, sex-linked, recessive mutation that maps to the extreme proximal portion of the X chromosome, about 2 centimorgans from sparse fur (spf). Hemizygotes for sf manifest several clinical disorders, evident at 14 days of age, including scaliness and crusting of the eyelids, ears, and tail, runting, reddening and swelling of the genital papilla, anemia, cachexia, and early death (average, 24 days). Our studies indicate that the phenotype of hemizygous scurfy is not, as has been suggested, a model for human X-linked ichthyosis, but appears to be a disease primarily affecting the lymphoreticular, and possibly the hematopoietic, systems. Gross lesions include marked splenomegaly, hepatomegaly, enlarged lymph nodes, and variable thickening of the ears. The characteristic histologic lesion is a lymphohistiocytic proliferation and infiltration of peripheral lymph nodes, spleen, liver, and skin. In routine hematoxylin and eosin-stained sections, these lesions efface lymph node architecture, thicken the dermis, and form nodular portal infiltrates in the liver. Scurfy lesions characteristically contain a population of large blastlike cells with round to oval nuclei, a vesicular chromatin pattern, and prominent single nucleoli. Mixed perivascular infiltrates of lymphocytes, macrophages, and granulocytes sometimes are found in kidney, heart, pancreas, lung, and mesenteries. There is excessive hematopoiesis in the liver and spleen. Cells expressing B220 or Thy-1 antigens localize to appropriate areas in the lymph nodes and spleen, but are rare in the portal infiltrates and are absent from the skin. There is a marked, polyclonal increase in serum IgG, severe Coombs'-positive anemia, and leukocytosis with atypical mononuclear cells. Scurfy mice are negative for antinuclear antibodies. Despite their morphologically aberrant lymphoreticular system, scurfy mice can exist in a conventional environment without evidence of opportunistic infection. Raising scurfy mice in a specific-pathogen-free environment does not alter disease expression. Thus, while our findings indicate that scurfy disease may be the result of immune dysfunction, it is not a classic immunodeficiency.
Influence of heart rate increase on uncorrected pre-ejection period/left ventricular ejection time (PEP/LVET) ratio in normal individuals. (1976)

In 26 normal volunteers, increase in heart rate from mean 73-94 +/- 1-97 to 103-61 +/- 2-72/min, by either intravenous atropine administration or rapid right atrial pacing, produced definite changes in the uncorrected systolic time intervals. As expected, total electromechanical systole (QS2) and left ventricular ejection time (LVET) were shortened, while the pre-ejection period (PEP) was unaffected. There was a consistent and significant increase of the PEP/LVET ratio (P less than 0-001). It is postulated that when this ratio is taken to express left ventricular contractility, it should probably be corrected for heart rate. Appropriate regression equations for such a correction were calculated (PEP/LVET=0-249 + 0-0168 HR).