gebhart/patrepeval huggingface dataset:
Early events in TNF signaling: a story of associations and dissociations (1997)

At the cellular level, the multifunctional cytokine tumor necrosis factor (TNF) modulates growth and activates genes through various intermediates, including protein kinases, protein phosphatases, reactive oxygen intermediates, phospholipases, proteases, sphingomyelinases, and transcription factors. Unlike many cytokine receptors, however, the cytoplasmic domain (CD) of the TNF receptors lacks an intrinsic protein kinase activity and yet on interaction with ligand it phosphorylates various proteins. Although the kinetics of most of these activities differ, their interactions are coordinated through the selective interplay between the CD of the receptors and the associated proteins. A unique pathway has been identified by the ability of the TNF receptors to associate with a novel family of proteins. Two distinct families of proteins have emerged, the TNF receptor-associated factors (TRAFs) and the death domain homologues. The cloning of members of these gene families and the identification of the protein-interaction motifs found within their gene products has initiated the molecular identity of factors (TRADD, FADD/MORT, RIP, FLICE/MACH, and TRAFs) associated with both of the p60 and p80 forms of the TNF receptor and with other members of the TNF receptor superfamily. In this review, we summarize these and other TNF receptor-associated proteins and their potential roles in regulating the activation of nuclear factor-kappaB and apoptosis, two major responses activated by engagement of TNF receptors by the ligand.
meso-Substitution products of ætioporphyrin I (1966)

Schiff's base derivatives have been prepared from meso-aminoætioporphyrin I. The Vilsmeier reaction with ætioporphyrin I leads to the meso-chloro-derivative but with the nickel complex of the porphin the meso-formyl compound is produced which has been characterised as its oxime, hydrazone, and Schiff's bases with aromatic aldehydes. Dehydration of the oxime yields meso-cyanoætioporphyrin I which can be hydrolysed to the meso-carboxy-derivative. The visible and n.m.r. spectra of these derivatives are summarised.
Person Re-Identification by Deep Joint Learning of Multi-Loss Classification (2017)

Existing person re-identification (re-id) methods rely mostly on either localised or global feature representation alone. This ignores their joint benefit and mutual complementary effects. In this work, we show the advantages of jointly learning local and global features in a Convolutional Neural Network (CNN) by aiming to discover correlated local and global features in different context. Specifically, we formulate a method for joint learning of local and global feature selection losses designed to optimise person re-id when using only generic matching metrics such as the L2 distance. We design a novel CNN architecture for Jointly Learning Multi-Loss (JLML) of local and global discriminative feature optimisation subject concurrently to the same re-id labelled information. Extensive comparative evaluations demonstrate the advantages of this new JLML model for person re-id over a wide range of state-of-the-art re-id methods on five benchmarks (VIPeR, GRID, CUHK01, CUHK03, Market-1501).
Inhibition of mammary carcinogenesis by systemic interleukin 12 or p185neu DNA vaccination in Her-2/neu transgenic BALB/c mice. (2001)

Because BALB/c mice transgenic for the rat Her-2/neu oncogene develop multifocal carcinomas in all mammary glands by week 33, they constitute an aggressive model for investigation of treatments designed to oppose mammary carcinogenesis. Nonspecific immune reaction elicited by systemic interleukin (IL)-12 both delayed the appearance of the first tumor and reduced the number of glands affected. However, only 5% of mice were tumor free at week 33. On the other hand, specific vaccination with plasmids encoding for the rat p185neu resulted in a further delay, so much so that 58% of mice were tumor free at week 33. No CTL response was evoked in either IL-12-treated or DNA-vaccinated mice, whereas an anti-rat p185neu antibody response was evident in the latter. Pathological examinations showed that in both IL-12-treated and DNA-vaccinated mice, the tumor growth area was infiltrated by reactive cells associated with expression of endothelial adhesion molecules and antiangiogenic proinflammatory cytokines. In the vaccinated mice, reduction of the number of cells expressing rat p185neu was combined with down-regulation of its membrane expression and even a marked inhibition in development of the terminal ductal lobular units. The reactive infiltrate in vaccinated mice contained numerous granulocytes that likely played an antiangiogenic and angiodestructive role and also joined other cells in the antibody-mediated killing of the r-p185neu+ cells. These results suggest that the elicitation of nonspecific and specific immunity could be beneficially used in individuals with a high risk of developing tumors.
Recombinant renewable polyclonal antibodies (2014)

Only a small fraction of the antibodies in a traditional polyclonal antibody mixture recognize the target of interest, frequently resulting in undesirable polyreactivity. Here, we show that high-quality recombinant polyclonals, in which hundreds of different antibodies are all directed toward a target of interest, can be easily generated in vitro by combining phage and yeast display. We show that, unlike traditional polyclonals, which are limited resources, recombinant polyclonal antibodies can be amplified over one hundred million-fold without losing representation or functionality. Our protocol was tested on 9 different targets to demonstrate how the strategy allows the selective amplification of antibodies directed toward desirable target specific epitopes, such as those found in one protein but not a closely related one, and the elimination of antibodies recognizing common epitopes, without significant loss of diversity. These recombinant renewable polyclonal antibodies are usable in different assays, and can be generated in high throughput. This approach could potentially be used to develop highly specific recombinant renewable antibodies against all human gene products.
Overexpression of protein kinase C isoenzymes alpha, beta I, gamma, and epsilon in cells overexpressing the insulin receptor. Effects on receptor phosphorylation and signaling. (1993)

Chinese hamster ovary cells overexpressing the human insulin receptor were transfected with cDNAs encoding protein kinase C isoenzymes alpha, beta I, gamma, and epsilon as well as an inactive alpha. Overexpression of these protein kinase Cs did not affect expression of the insulin receptor or insulin-stimulated tyrosine phosphorylation of the receptor. However, in response to phorbol esters, cells overexpressing isoenzymes alpha, beta I, and gamma, but not epsilon or inactive alpha, exhibited 3-4-fold higher levels of insulin receptor phosphorylation. This increased phosphorylation occurred exclusively on serines and threonine. Tryptic peptide maps indicated that this phosphorylation was primarily on serines 1305/1306 and threonine 1348 as well as several other unidentified sites. This phorbol ester-stimulated phosphorylation did not inhibit activation of the insulin receptor kinase when the receptor was activated in situ but assayed in vitro. However, in cells overexpressing protein kinase C alpha, it did inhibit an in vivo monitor of the activation of the insulin receptor kinase, the insulin-stimulated increase in anti-phosphotyrosine-precipitable phosphatidylinositol 3-kinase activity. These results indicate that increased protein kinase C alpha activity can inhibit insulin-stimulated responses and support the hypothesis that excessive protein kinase C is involved in the insulin resistance observed in non-insulin-dependent diabetics.
Case Report: Althesin in Status Epilepticus (1979)

A case of status epilepticus, resistant to conventional anti-epileptic treatment is described. Althesin rapidly abolished the epileptic activity, and control was achieved by a continuous infusion of Althesin.
Error-Correcting Codes for Ternary Content Addressable Memories (2008)

As VLSI silicon technology continues its relentless advance and memory densities increase, the problem of soft errors--bit upsets caused by alpha particles or neutron hits--demands solutions. Error-correcting codes (ECCs) are routinely used on random-access memories (RAMs) to increase soft error tolerance--codewords (CWs) (ECC bits concatenated to the data) are written to and read from memory, and the read CW is decoded to correct errors. Content addressable memories (CAMs) also demand error mitigation measures. The method employed for RAMs is also applicable to CAMs: the match-line sense amplifier is modified to function as a comparator [1], CWs are stored and searched for. We investigate the extension of this method to ternary CAMs (TCAMs). TCAMs cannot employ the efficient ECCs (known as linear block codes-LBCs) used with RAMs and CAMs. We develop the ECCs necessary to implement error-resilient TCAMs. We prove that the rate (ratio of data bits to total number of bits in the CW) of the specialized ECCs necessary for TCAMs cannot exceed 1/t, where t is the number of bit errors the code can correct (in contrast, LBCs asymptotically have rate one); simple majority codes are the best.
Adaptive transform coding of speech signals (1977)

This paper discusses speech coding systems based upon transform coding (TC). It compares several transforms and shows that the cosine transform leads to a nearly optimum performance for almost all speech sounds. Various adaptive coding strategies are then investigated, and a coding scheme is proposed that is based on a nonadaptive discrete cosine transform (DCT), on an adaptive bit assignment, and on adaptive quantization. The adaptation is controlled by a short-term basis spectrum that is derived from the transform coefficients prior to coding and transmission and that is transmitted as side information to the receiver. The main result is that this adaptive transform coder performs better than all known nonpitch-tracking coding schemes; it extends the range of speech waveform coding to lower bit rates and closes the gap between vocoders and predictive waveform coders.
Exact image theory for the Sommerfeld half-space problem, part II: Vertical electrical dipole (1984)

The exact image theory, introduced earlier by the present authors for the Sommerfeld problem with a vertical magnetic dipole above a planar interface of two dielectric media, is now extended to the more complicated problem of a vertical electric dipole. The image source is seen to be a line current which lies in complex space for best convergence. The image current function is expressable as an integral expression, easily adapted for numerical calculations and unlike for the vertical magnetic dipole, its form is dependent on the dielectric factor ratio of the two half-spaces. Series expansions are given for an easy calculation of the image current. The reflection coefficient method and Sommerfeld surface-wave expressions are obtained as limit cases of the exact image theory. The method is tested for a large grid of field points and good accuracy for a modest calculation algorithm is observed.
Three-dimensional athermal waveguides fortemperature independent lightwave devices (1994)

To realise a temperature independent narrowband optical filter, a three-demensional athermal waveguide for which optical path length is independent of temperature is developed. The temperature coefficient of the optical path length is successfully decreased to –2% of that of a conventional waveguide.
Characterization of Cytokine/Chemokine Profiles of Severe Acute Respiratory Syndrome (2005)

Induction of IP-10 is a critical event in the initiation of immune-mediated acute lung injury and lymphocyte apoptosis during the development of SARS. Superinfection after the immune injury is the main cause of death. The prompt elevation of interleukin-6, interleukin-8, and monocyte chemoattractant protein-1 is a sign of superinfection, indicating a high risk of death.
Mechanistic Studies on the Hydroxylation of Methane by Methane Monooxygenase (2003)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTMechanistic Studies on the Hydroxylation of Methane by Methane MonooxygenaseMu-Hyun Baik, Martin Newcomb, Richard A. Friesner, and Stephen J. LippardView Author Information Departments of Chemistry, Columbia University, New York, New York 10027, University of Illinois at Chicago, Chicago, Illinois 60607, and Massachusetts Institute of Technology, Cambridge, Massachusetts 02139 Cite this: Chem. Rev. 2003, 103, 6, 2385–2420Publication Date (Web):May 17, 2003Publication History Received16 December 2002Published online17 May 2003Published inissue 1 June 2003https://pubs.acs.org/doi/10.1021/cr950244fhttps://doi.org/10.1021/cr950244fresearch-articleACS PublicationsCopyright © 2003 American Chemical SocietyRequest reuse permissionsArticle Views5991Altmetric-Citations425LEARN 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 SUBJECTS:Hydrocarbons,Magnetic properties,Oxidation,Peptides and proteins,Reaction mechanisms Get e-Alerts
Resistance of human cervical carcinoma cells to tumor necrosis factor correlates with their increased sensitivity to cisplatin: evidence of a role for DNA repair and epidermal growth factor receptor. (1992)

Alterations in cellular biochemistry which are associated with the development of resistance to cytotoxic peptides, such as tumor necrosis factor (TNF), may also be responsible for changes in the response of cells to cytotoxic agents. Culturing ME-180 cervical carcinoma cells in the presence of escalating concentrations of TNF resulted in the development of an ME-180 cell variant (ME-180R) resistant to TNF but expressing a 3-5-fold increased sensitivity to cisplatin (CDDP) when measured following continuous exposure (low doses) or short-term incubation with CDDP (high doses) and clonogenic analysis. Cellular platinum uptake, efflux, and nuclear platinum content as well as the extent of DNA platination were examined and found to be identical in both ME-180 parental and ME-180R cell lines. Although ME-180R cells showed a relatively higher glutathione content than ME-180 parental cells, the effect of buthionine sulfoximine on the cellular sensitivity to CDDP and glutathione S-transferase activities of both cell lines were almost identical, suggesting that glutathione content or its metabolism did not appear to play a major role in differential CDDP cytotoxicity. Unscheduled DNA synthesis following exposure to CDDP was more inducible in ME-180 parental cells than in CDDP-sensitive ME-180R cells. Alkaline elution studies of cross-linked DNA in CDDP-treated ME-180 cells suggested that accumulation of DNA adducts reached maximal levels 10-15 h after CDDP treatment and was similar in both TNF-resistant and parental cells. Within 24 h after CDDP exposure, the extent of DNA cross-linking was markedly reduced in parental cells but remained elevated in the CDDP-sensitive ME-180R cell line. To examine the proposed regulatory role of phosphorylation in CDDP and TNF-mediated cytotoxicity, epidermal growth factor (EGF) receptor tyrosine kinase activity was measured in both TNF-resistant and parental ME-180 cells. Analysis of cell lysates demonstrated a 3-4-fold higher EGF receptor tyrosine kinase activity in ME-180R cells when compared to the parental population which correlated with increased expression of EGF receptor protein by immunoblot analysis. Based upon colony-forming assays, EGF treatment of ME-180 parental cells resulted in an increased sensitivity to CDDP (similar to ME-180R cells) and 3-fold stimulation of EGF receptor tyrosine kinase activity. Taken together, these results suggest that TNF resistance in ME-180 cervical carcinoma cells correlates with both increased EGF receptor expression and enhanced CDDP cytotoxicity.(ABSTRACT TRUNCATED AT 400 WORDS)
On the theory of Hertzian fracture (1967)

Abstract The fracture of a brittle solid under a spherical indenter is the best studied case of fracture in a strongly inhomogeneous, well defined, stress field. Two principal topics are discussed, the path of a crack in a field of non-uniformly directed stress, and the stability of cracks of various length when the prior stress on the crack path is non-uniform. For the first, it is shown that the crack growth should, to a first approximation, be orthogonal to the most tensile principal stress, and thus correspond, in a torsion-free stress field, to a surface delineated by the trajectories of the other two principal stresses: while, to a second approximation, the crack should deviate from this path by having a larger radius of curvature at every bend, thus exhibiting a pseudonertia even in slow growth. This is in accordance with the known experimental facts about the Hertzian crack, particularly the fact that the crack at the surface forms systematically outside the edge of the circle of contact, at which the maximum tensile stress occurs. On the second question, it is found that there are four crack lengths, c0, c1, c2, c3, corresponding to stationary values of energy. c0 and c2 represent unstable equilibria, and diminish with increasing load; cx and c3 represent stable equilibria and increase with increasing load. With small indenters, c0 soon becomes less than the size of pre-present surface flaws, and an unobserved shallow ring crack of depth c1 is produced: the critical condition for observed fracture is then the merging of c1 with c2, allowing unstable growth to the cone crack of depth c3. This explains Auerbach’s law, that the critical load for production of a cone crack is proportional to the radius, r, of the indenter sphere. With larger indenters, of several centimetres radius for a typical case, c1, and c2 merge and disappear before c0 exceeds the size of pre-present flaws. The critical load for cone fracture then becomes nearly propor¬tional to r2, as observed. The previous calculations of Roesler (1956 a, b) relate to the second stable crack dimension, c3, though his energy scaling principle is also applicable to the critical condition at which c1 and c2 merge. The Hertzian fracture test, within the validity range of Auerbach’s law, affords a means of measuring surface energy at the fracture surface independent of knowledge about the pre-present flaws.
Proteomic Analysis of Altered Extracellular Matrix Turnover in Bleomycin-induced Pulmonary Fibrosis (2014)

Fibrotic disease is characterized by the pathological accumulation of extracellular matrix (ECM) proteins. Surprisingly, very little is known about the synthesis and degradation rates of the many proteins and proteoglycans that constitute healthy or pathological extracellular matrix. A comprehensive understanding of altered ECM protein synthesis and degradation during the onset and progression of fibrotic disease would be immensely valuable. We have developed a dynamic proteomics platform that quantifies the fractional synthesis rates of large numbers of proteins via stable isotope labeling and LC/MS-based mass isotopomer analysis. Here, we present the first broad analysis of ECM protein kinetics during the onset of experimental pulmonary fibrosis. Mice were labeled with heavy water for up to 21 days following the induction of lung fibrosis with bleomycin. Lung tissue was subjected to sequential protein extraction to fractionate cellular, guanidine-soluble ECM proteins and residual insoluble ECM proteins. Fractional synthesis rates were calculated for 34 ECM proteins or protein subunits, including collagens, proteoglycans, and microfibrillar proteins. Overall, fractional synthesis rates of guanidine-soluble ECM proteins were faster than those of insoluble ECM proteins, suggesting that the insoluble fraction reflected older, more mature matrix components. This was confirmed through the quantitation of pyridinoline cross-links in each protein fraction. In fibrotic lung tissue, there was a significant increase in the fractional synthesis of unique sets of matrix proteins during early (pre-1 week) and late (post-1 week) fibrotic response. Furthermore, we isolated fast turnover subpopulations of several ECM proteins (e.g. type I collagen) based on guanidine solubility, allowing for accelerated detection of increased synthesis of typically slow-turnover protein populations. This establishes the presence of multiple kinetic pools of pulmonary collagen in vivo with altered turnover rates during evolving fibrosis. These data demonstrate the utility of dynamic proteomics in analyzing changes in ECM protein turnover associated with the onset and progression of fibrotic disease.
Comparative evaluation of small-molecule chemosensitizers in reversal of cisplatin resistance in ovarian cancer cells. (2012)

Cisplatin-resistance is one of the major challenges in the treatment of epithelial ovarian cancer. Small-molecule chemosensitizers provide a therapeutically feasible approach to overcome cisplatin resistance in ovarian cancer. However, proper selection of chemosensitizer is of prime importance owing to phenotypic differences in cisplatin-resistant ovarian cancers. The resistance reversal activity of chemosensitizers buthionine sulfoximine (BSO), triethylenetetramine (TETA), genistein, rapamycin and colchicine was investigated in various cisplatin-resistant ovarian cancer cells, 2008 C13, CP70 and OVCAR 8 using MTT assays. Cellular accumulation of cisplatin in the presence of chemosensitizers was analyzed by inductively-coupled plasma-mass spectroscopy (ICP-MS). Chemosensitizers exhibited resistance reversal activity in 2008 C13 and CP70 cells in the following order; colchicine> genistein>TETA> rapamycin ≥ BSO (p<0.05), which is in correlation with cellular accumulation of cisplatin. In conclusion, our study demonstrates that resistance reversal activity of chemosensitizers varies with phenotypic behavior of cisplatin-resistant ovarian cancer cells. Data from our study can be utilized to choose a specific chemosensitizer for individualized combination therapy for cisplatin-resistant ovarian cancer.
Community Outbreak Investigation of SARS-CoV-2 Transmission Among Bus Riders in Eastern China (2020)

In this cohort study and case investigation of a community outbreak of COVID-19 in Zhejiang province, individuals who rode a bus to a worship event with a patient with COVID-19 had a higher risk of SARS-CoV-2 infection than individuals who rode another bus to the same event. Airborne spread of SARS-CoV-2 seems likely to have contributed to the high attack rate in the exposed bus. Future efforts at prevention and control must consider the potential for airborne spread of the virus.
Response to changes in antiretroviral therapy after genotyping in human immunodeficiency virus-infected children (2002)

This study did not demonstrate substantial clinical benefit to HIV genotyping in antiretroviral agent-experienced pediatric patients with high viral loads. These results contrast with favorable short term clinical and virologic responses to therapeutic changes after genotyping in HIV-infected adults. However, medication history alone does not appear to be an adequate alternative to genotyping in choosing salvage regimens in antiretroviral agent-experienced children.