gebhart/patrepeval huggingface dataset:
The Selective Electrochemical Conversion of Preactivated CO2to Methane (2015)

This work reports the selective electrochemical conversion of CO_2 to methane, the reverse reaction of fossil fuel combustion. This reaction is facilitated by preactivation of the CO_2 molecule with an N-heterocyclic carbene (NHC) to form a zwitterionic species in the first step. In the presence of Ni(cyclam)^(2+) and CF_3CH_2OH, this species is shown to undergo further electrochemical reduction of the bound-CO_2 fragment at glassy carbon cathodes in dichloromethane electrolyte solution. Labeling studies confirm the origin of the carbon and protons in the methane product are the preactivated CO_2 and trifluoroethanol respectively.
Mammalian Base Excision Repair: the Forgotten Archangel (2013)

Base excision repair (BER) is a frontline repair system that is responsible for maintaining genome integrity and thus preventing premature aging, cancer and many other human diseases by repairing thousands of DNA lesions and strand breaks continuously caused by endogenous and exogenous mutagens. This fundamental and essential function of BER not only necessitates tight control of the continuous availability of basic components for fast and accurate repair, but also requires temporal and spatial coordination of BER and cell cycle progression to prevent replication of damaged DNA. The major goal of this review is to critically examine controversial and newly emerging questions about mammalian BER pathways, mechanisms regulating BER capacity, BER responses to DNA damage and their links to checkpoint control of DNA replication.
Factor IXa:Factor VIIIa Interaction (2001)

The physiologic activator of factor X consists of a complex of factor IXa, factor VIIIa, Ca(2+) and a suitable phospholipid surface. In one study, helix 330 (162 in chymotrypsin) of the protease domain of factor IXa was implicated in binding to factor VIIIa. In another study, residues 558-565 of the A2 subunit of factor VIIIa were implicated in binding to factor IXa. We now provide data, which indicate that the helix 330 of factor IXa interacts with the 558-565 region of the A2 subunit. Thus, the ability of the isolated A2 subunit was severely impaired in potentiating factor X activation by IXa(R333Q) and by a helix replacement mutant (IXa(helixVII) in which helix 330-338 is replaced by that of factor VII) but it was normal for an epidermal growth factor 1 replacement mutant (IXa(PCEGF1) in which epidermal growth factor 1 domain is replaced by that of protein C). Further, affinity of each 5-dimethylaminonaphthalene-1-sulfonyl (dansyl)-Glu-Gly-Arg-IXa (dEGR-IXa) with the A2 subunit was determined from its ability to inhibit wild-type IXa in the tenase assay and from the changes in dansyl fluorescence emission signal upon its binding to the A2 subunit. Apparent K(d(A2)) values are: dEGR-IXa(WT) or dEGR-IXa(PCEGF1) approximately 100 nm, dEGR-IXa(R333Q) approximately 1.8 micrometer, and dEGR-IXa(helixVII) >10 micrometer. In additional experiments, we measured the affinities of these factor IXa molecules for a peptide comprising residues 558-565 of the A2 subunit. Apparent K(d(peptide)) values are: dEGR-IXa(WT) or dEGR-IXa(PCEGF1) approximately 4 micrometer, and dEGR-IXa(R333Q) approximately 62 micrometer. Thus as compared with the wild-type or PCEGF1 mutant, the affinity of the R333Q mutant for the A2 subunit or the A2 558-565 peptide is similarly reduced. These data support a conclusion that the helix 330 of factor IXa interacts with the A2 558-565 sequence. This information was used to model the interface between the IXa protease domain and the A2 subunit, which is also provided herein.
Juvenile Hormone and the Physiological Basis of Insect Polymorphisms (1982)

Juvenile hormone (JH) is a developmental hormone of insects. It has become evident in recent years that JH is involved in the control of gene switching and that it exerts this control only during certain critical periods. Such JH-sensitive critical periods occur periodically during the life cycle of an insect. As a rule one or more critical periods exist during each pre-reproductive instar. The presence or absence of JH during any given critical period somehow causes the insect to "choose" between alternative developmental pathway. Using this model for the action of JH, we discuss the endocrine control of metamorphosis, phase determination in locusts and aphids, caste determination is social insects, and certain color polymorphisms.
Field induced reemission of electrons trapped in SiO2 (1979)

A new form of hot electron injection and trapping in n-channel IGFET's is described, a necessary and sufficient condition for the emission of these trapped electrons is a reset pulse of negative gate and positive drain voltages. The effect of this trapping on device characteristics, reliability, and the proposed low-temperature operation of IGFET's is discussed.
Modelbased Investigations of Gyroscopic Effect on the (Elasto‐)Kinematics of Suspension Systems (2013)

Abstract During wheel bumping caused by stochastic road excitation, the wheel performs rotational and translational movements. The bump and rebound wheel velocity leads to significant angular velocities based on the (elasto‐)kinematics of the suspension system. Based on the gyroscopic effect, moments arise about the rotating wheel induced by the angular change while bumping. Therefore it leads to undesirable wheel changes and degrades the tire contact and finally decreases the driving stability. A flexible MBS‐model of the five‐link rear axle system that includes these effects has been built up to allow a detailed investigation of the gyroscopic effect. Using the simulation results, conclusions can be drawn for refining design criteria for the kinematics, elastokinematics and topology of the suspension system to increase the active safety of the vehicle. (© 2013 Wiley‐VCH Verlag GmbH &amp; Co. KGaA, Weinheim)
Pax2 in development and renal disease (1999)

Pax genes are associated with a variety of developmental mutations in mouse and man that are gene dosage sensitive, or haploinsufficient. The Pax2 gene encodes a DNA binding, transcription factor whose expression is essential for the development of the renal epithelium. Both gain and loss of function mutants in the mouse demonstrate a requirement for Pax2 in the conversion of metanephric mesenchymal precursor cells to the fully differentiated tubular epithelium of the nephron. However, Pax2 expression is down-regulated as cells leave the mitotic cycle. Humans carrying a single Pax2 mutant allele exhibit renal hypoplasia, vesicoureteric reflux, and optic nerve colobomas. Conversely, persistent expression of Pax2 has been demonstrated in a variety of cystic and dysplastic renal diseases and correlates with continued proliferation of renal epithelial cells. Thus, Pax2 misexpresssion may be a key determinant in the initiation and progression of renal diseases marked by increased or deregulated cell proliferation.
Characterization of an immunosuppressive factor derived from colon cancer cells. (1987)

The colon cancer cell line, HT29, produces a soluble substance (HT29 factor) that blocks mitogen-induced T cell proliferation and the production of interleukin 2 (IL 2). Inhibition of T cell proliferation by the HT29 factor is reversible and is not due to a decline in cell viability or an alteration in the kinetics of T cell proliferation. It occurs even when the HT29 factor is added only 24 hr before terminating the T cell cultures, indicating that the factor affects cell division after activation of T cells has already occurred. No inhibitory activity was found in medium conditioned by human colonic epithelial cells or fibroblasts. The factor has an apparent m.w. of 56,000 and an isoelectric point of 7.9. It is sensitive to endopeptidases, heating to 56 degrees C, and extremes of pH. The HT29 factor also suppresses IL 2 production by T cells. However, low IL 2 availability alone cannot account for the suppressive effect of the factor on T cell proliferation, because the addition of exogenous IL 2 does not reverse the inhibition. This block in IL 2 responsiveness is not primarily due to a decrease in IL 2 receptors because Tac expression on activated T cells is minimally decreased during a 24-hr exposure to the HT29 factor. In addition, IL 2-induced proliferation of mitogen-activated T cells is inhibited only slightly by the HT29 factor, indicating that a block in the interaction of IL 2 with its receptor is not its main mechanism of action. Thus the inhibition of T cell proliferation is likely to be due primarily to a mechanism independent of IL 2.
Expression of src family genes during monocytic differentiation of HL-60 cells (1991)

Abstract It has been reported that src family protein-tyrosine kinases were expressed specifically in a certain lineage or differentiation stage of hematopoietic cells. To understand the molecular basis for differentiation and function of monocyte/macrophage, we investigated the expressions of src family genes by the HL-60 cells stimulated with differentiation-inducing agents. TPA and vitamin D3 (D3) were used as stimulants for monocytic development, since each agent has been known to induce phenotypically specific differentiation of HL-60 cells. The fyn, fgr, and lyn genes were characteristically expressed concomitantly with phenotypic changes and expressions of nuclear proto-oncogenes, whereas src, lck, hck, and yes genes were not. In TPA-induced differentiation of HL-60 cells, both fyn and lyn genes, but not fgr gene, were expressed. In contrast, both fgr and lyn genes, but not fyn gene, were expressed in D3-induced differentiation of the cells. The independent and characteristic expressions of these genes were observed in the further advanced differentiation of HL-60 cells induced by TPA plus D3 or D3 plus human transforming growth factor-beta 1. The granulocytic differentiation of the cells treated with retinoic acid was accompanied by intense expression of fgr, but weak or no expression of lyn and fyn gene. These data indicate that each protein-tyrosine kinase encoded by src family genes may play distinct roles in development and/or functions of monocyte/macrophage-lineage cells.
Trends in Active Pharmaceutical Ingredient Salt Selection based on Analysis of the Orange Book Database (2007)

The Orange Book database published by the U.S. Drug and Food Administration (FDA) was analyzed for the frequency of occurrence of different counterions used for the formation of pharmaceutical salts. The data obtained from the present analysis of the Orange Book are compared to reviews of the Cambridge Structural Database (CSD) and of the Martindale "The Extra Pharmacopoeia". As well as showing overall distributions of counterion usage, results are broken down into 5-year increments to identify trends in counterion selection. Chloride ions continue to be the most frequently utilized anionic counterions for the formation of salts as active pharmaceutical ingredients (APIs), while sodium ions are most widely utilized for the formation of salts starting from acidic molecules. A strong trend toward a wider variety of counterions over the past decade is observed. This trend can be explained by a stronger need to improve physical chemical properties of research and development compounds.
A Multi-Institutional Observational Study of Testosterone Levels After Testosterone Pellet (Testopel®) Insertion (2012)

Testosterone pellets (Testopel(®) , Slate Pharmaceuticals) provide sustained levels of testosterone for at least 4 months and up to 6 months in men with TDS. Implantation of ≥8 pellets achieved optimal results with respect to peak mean testosterone level and duration of effect. Testosterone pellets were generally well tolerated.
Erythrocyte dehydration in pathophysiology and treatment of sickle cell disease (1995)

A prominent feature of sickle cell disease is the presence of cells with markedly increased sickle cell hemoglobin concentration, as a consequence of the loss of potassium, chloride, and water from the erythrocyte. Because of the extreme dependency of the kinetic of polymerization on sickle cell hemoglobin concentration, these dehydrated erythrocytes have an increased tendency to polymerize and sickle. Thus blockade of the loss of potassium from the erythrocyte should prevent the increase in sickle cell hemoglobin concentration and reduce sickling. The availability of this potential therapeutic option is based on a detailed knowledge of the mechanisms leading to cell dehydration. Two ion transport pathways, the K-Cl cotransport and the Ca(2+)-activated K+ channel, play a prominent role in the dehydration of sickle erythrocytes. Possible therapeutic strategies include inhibition of K-Cl cotransport by increasing erythrocyte Mg2+ content and inhibition of the Ca(2+)-activated K channel by oral administration of clotrimazole.
Altered surfactant homeostasis and alveolar type II cell morphology in mice lacking surfactant protein D (1998)

Surfactant protein D (SP-D) is one of two collectins found in the pulmonary alveolus. On the basis of homology with other collectins, potential functions for SP-D include roles in innate immunity and surfactant metabolism. The SP-D gene was disrupted in embryonic stem cells by homologous recombination to generate mice deficient in SP-D. Mice heterozygous for the mutant SP-D allele had SP-D concentrations that were approximately 50% wild type but no other obvious phenotypic abnormality. Mice totally deficient in SP-D were healthy to 7 months but had a progressive accumulation of surfactant lipids, SP-A, and SP-B in the alveolar space. By 8 weeks the alveolar phospholipid pool was 8-fold higher than wild-type littermates. There was also a 10-fold accumulation of alveolar macrophages in the null mice, and many macrophages were both multinucleated and foamy in appearance. Type II cells in the null mice were hyperplastic and contained giant lamellar bodies. These alterations in surfactant homeostasis were not associated with detectable changes in surfactant surface activity, postnatal respiratory function, or survival. The findings in the SP-D-deficient mice suggest a role for SP-D in surfactant homeostasis.
Purification and characterization of F pili from Escherichia coli (1977)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTPurification and characterization of F pili from Escherichia coliTakayasu Date, Manabu Inuzuka, and Munemitsu TomoedaCite this: Biochemistry 1977, 16, 25, 5579–5585Publication Date (Print):December 13, 1977Publication History Published online1 May 2002Published inissue 13 December 1977https://pubs.acs.org/doi/10.1021/bi00644a030https://doi.org/10.1021/bi00644a030research-articleACS PublicationsRequest reuse permissionsArticle Views256Altmetric-Citations40LEARN 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
Interaction of BMP10 with Tcap may modulate the course of hypertensive cardiac hypertrophy (2007)

Elevated wall stress by hypertension induces an adaptive myocardial hypertrophy via releasing prohypertrophic hormones such as angiotensin II. In this study, we investigated the involvement of bone morphogenetic protein-10 (BMP10) in hypertension-induced cardiac hypertrophy. Expression of BMP10 was increased in the hypertrophied ventricles from hypertensive rats. BMP10 localized on cell surface and at stretch-sensing Z disc of cardiomyocytes, where BMP10 interacted with a protein called titin-cap (Tcap). A rare variant of the human BMP10 gene, Thr326Ile, was found to be associated with hypertensive dilated cardiomyopathy. The variant BMP10 demonstrated decreased binding to Tcap and increased extracellular secretion. Conditioned medium from cells transfected with wild-type or variant BMP10 induced hypertrophy in rat neonatal cardiomyocytes, except that medium from variant BMP10-carrying cells showed an enhanced effect reflecting the increased secretion. These observations suggested that hypertension induced expression of prohypertrophic BMP10, and the hypertrophic effect of BMP10 was modulated, at least in part, by its binding to Tcap at the Z disc.
DNA polymerase beta mutations in human colorectal cancer. (1992)

Increasing numbers of alterations have been found in protooncogenes (e.g., ras, myc), as well as tumor suppressor genes (e.g., p53, Rb) in various types of tumors. The multiple mutations cannot be explained by the spontaneous mutation rate. It has been suggested that mutator phenotypes leading to the accumulation of these mutations may be required in the early stages of tumorigenesis. To test this hypothesis, the entire coding region of DNA polymerase beta, a repair enzyme, mRNA from colorectal tumors, and corresponding normal mucosa were amplified by polymerase chain reaction, cloned, and sequenced. Mutations in the catalytic domain of DNA polymerase beta were detected in colorectal tumor specimens compared to the normal colorectal mucosa, placenta, and blood samples. Since these mutations changed the structure of polymerase beta, it is expected that the efficiency of the DNA repair system would be impaired and thus may account for the high mutation rate observed in colorectal carcinomas.
Design of a Holographic Concave Grating Used as a Multiplexer/Demultiplexer in Dense Wavelength-routed Optical Networks with Subnanometer Channel Spacing (1995)

Abstract The performance parameters of a free-space concave grating multiplexer/demultiplexer have been evaluated for applications in wavelength routed optical networks. The conditions for the stationarity of astigmatism with wavelength were rigorously derived and a novel design method was adopted to minimize the optical aberrations. The performance of this system is close to diffraction-limited over the wavelength ranges 1480–1520 nm or 1530–1570 nm. The optical isolation is better than − 30 dB for a channel spacing of 0·5 nm and the losses due to aberrations are estimated to be less than 4 dB. The results can be used to design a spectrograph suitable for wavelength cross-connection in all-optical networks.
Diphenylprolinol Silyl Ether as Catalyst of an Asymmetric, Catalytic, and Direct Michael Reaction of Nitroalkanes with α,β-Unsaturated Aldehydes (2007)

A catalytic enantioselective direct conjugate addition of nitroalkanes to alpha,beta-unsaturated aldehydes using diphenylprolinol silyl ether as an organocatalyst has been developed. Using this methodology as a key step, short syntheses of therapeutically useful compounds have also been accomplished.
X-band transhorizon measurements of CW transmissions over the sea-Part I: path loss, duration of events, and their modelling (1993)

This article presents measurements, analysis, and modelling of path loss and duration of events obtained in a transhorizon experiment over the English Channel (La Manche, operated from 1987 to 1991, totalling 3708 valid data days and using five paths with three radiofrequencies at X-band. An overview of the equipment, operation and data acquisition, and processing is first given. The study reveals that the decibel path loss is normally distributed but exhibits three distinct regions of normality: path losses with probability of occurrence greater than about 1% reflect propagation dominated by several propagation mechanism. The second region, which can be clearly identified with probabilities of path loss below about 1%, reflects the various anomalous propagation mechanisms, and these are identified and discussed. The experimental median is compared with the value derived using several prediction methods, one of which is found to agree well with only a few decibels of difference. On the other hand, the existing CCIR prediction for small time percentages under values the strongest enhancements found. The continuous reduction of path loss below a given threshold L (decibels) constitutes an event with some duration. The analysis has shown that the conditional distribution Prob (D'>or=D/L'<or=L) that events last longer than D minutes is log-normal, is very skewed, and is the same for all types of propagation conditions. It is found that the signal level can rise from the troposcatter median to above the free space value and stay there continuously for periods of time which can range from a few minutes to well over one hour. The data base and modelling of L and D are given in detail.<<ETX>>
Depth and surface normal estimation from monocular images using regression on deep features and hierarchical CRFs (2015)

Predicting the depth (or surface normal) of a scene from single monocular color images is a challenging task. This paper tackles this challenging and essentially underdetermined problem by regression on deep convolutional neural network (DCNN) features, combined with a post-processing refining step using conditional random fields (CRF). Our framework works at two levels, super-pixel level and pixel level. First, we design a DCNN model to learn the mapping from multi-scale image patches to depth or surface normal values at the super-pixel level. Second, the estimated super-pixel depth or surface normal is refined to the pixel level by exploiting various potentials on the depth or surface normal map, which includes a data term, a smoothness term among super-pixels and an auto-regression term characterizing the local structure of the estimation map. The inference problem can be efficiently solved because it admits a closed-form solution. Experiments on the Make3D and NYU Depth V2 datasets show competitive results compared with recent state-of-the-art methods.
Modification of splicing in the dystrophin gene in cultured Mdx muscle cells by antisense oligoribonucleotides (1998)

Deletions and point mutations in the gene encoding the cytoskeletal protein dystrophin and its isoforms cause either the severe progressive myopathy Duchenne muscular dystrophy (DMD) or the milder Becker muscular dystrophy (BMD), largely depending on whether the reading frame is lost or maintained respectively. Frameshift mutations tend to result in a lack of dystrophin at the sarcolemma, destabilization of the membrane and degeneration of skeletal muscle. The mdx mouse is a valuable animal model of DMD as it bears a nonsense point mutation in exon 23 of the murine DMD gene leading to an absence of dystrophin expression in the muscle sarcolemma and muscular dystrophy. This report represents a novel approach to correct dystrophin deficiency at the post-transcriptional level by transfection of muscle cells with antisense RNA. Essentially, 2'- O -methyl oligoribonucleotides (2'OMeRNA) were delivered to the nuclei of primary mdx myoblasts in culture. Dystrophin expression was observed in the sarcolemma of transfected mdx myotubes after transfection by an oligonucleotide complementary to the 3' splice site of murine dystrophin intron 22. Direct sequencing of RT-PCR products from these cells revealed precise splicing of exon 22 to exon 30, skipping the mutant exon and creating a novel in-frame dystrophin transcript. As patients with comparable in-frame internal deletions show relatively mild myopathic symptoms, this may in the future offer a therapeutic approach for DMD, as well as for other inherited disorders.