gebhart/patrepeval huggingface dataset:
Construction and Production of Concatameric Human TNF Receptor-Immunoglobulin Fusion Proteins (2004)

Tumor necrosis factor-a (TNF-a) and lymphotoxin-a (LT-α, TNF-β) can initiate and perpetuate human diseases such as multiple sclerosis (MS), rheumatoid arthritis (RA), and insulin-dependent diabetes mellitus (IDDM). TNFs can be blocked by the use of soluble TNF receptors. However, since monomeric soluble receptors generally exhibit low affinity or function as agonists, the use of monomeric soluble receptors has been limited in the case of cytokines such as TNF-a, TNF-β, interleukin (IL)-1, IL-4, IL-6, and IL-13, which have adapted to a multicomponent receptor system. For these reasons, very high-affinity inhibitors were created for the purpose of a TNFs antagonist to bind the TNFR and trigger cellular signal by using the multistep polymerase chain reaction method. First, recombinant simple TNFR-Ig fusion proteins were constructed from the cDNA sequences encoding the extracellular domain of the human p55 TNFR (CD120a) and the human p75 TNFR (CD120b), which were linked to hinge and constant regions of human IgG 1 heavy chain, respectively using complementary primers (CP) encoding the complementary sequences. Then, concatameric TNFR-Ig fusion proteins were constructed using recombinant PCR and a complementary primer base of recombinant simple TNFR-Ig fusion proteins. For high level expression of recombinant fusion proteins, Chinese hamster ovary (CHO) cells were used with a retroviral expression system. The transfected cells produced the simple concatameric TNFR-Ig fusion proteins capable of binding TNF and inactivating it. These soluble versions of simple concantameric TNFR-Ig fusion proteins gave rise to multiple forms such as simple dimers and concatameric homodimers. Simple TNFR-Ig fusion proteins were shown to have much more reduced TNF inhibitory activity than concatameric TNFR-Ig fusion proteins. Concatameric TNFR-Ig fusion proteins showed higher affinity than simple TNFR-Ig fusion proteins in a receptor inhibitor binding assay (RIBA). Additionally, concatameric TNFR-Ig fusion proteins were shown to have a progressive effect as a TNF inhibitor compared to the simple TNFR-Ig fusion proteins and conventional TNFR-Fc in cytotoxicity assays, and showed the same results for collagen induced arthritis (CIA) in mice in vivo.
Cloning and characterization of PTP-K1, a novel nonreceptor protein tyrosine phosphatase highly expressed in bone marrow. (1996)

A novel nonreceptor protein tyrosine phosphatase (PTP), PTP-K1, was identified using a consensus polymerase chain reaction-based approach. The full length cDNA encompasses an open reading frame of 1362 base pairs, predicting a protein of 453 amino acid residues with a molecular mass of 54 kDa. The PTP domain is located in the N-terminal portion of the molecule and shares approximately 50% amino acid identify with two other nonreceptor PTPs: PEP and PTP-PEST. PTP-K1 is preferentially expressed in mouse bone marrow with transcripts of 1.7 kb, 1.9 kb and 3.5 kb. The 1.7 kb transcript was also detected in kidney, lung and ovary. The PTP domain of PTP-K1 was expressed as a fusion protein in bacteria and had intrinsic PTP catalytic activity. Indirect immunofluorescence microscopy in COS-7 cells showed that PTP-K1 was localized to the cytoplasm. Ptp-k1 was mapped to mouse chromosome 1, and was closely linked to the interleukin-1 receptor gene. The high level expression of PTP-K1 mRNA in bone marrow suggests that PTP-K1 may be involved in signal transduction in growth and differentiation of hematopoietic cells.
Excess Heat during the Electrolysis of a Light Water Solution of K2CO3with a Nickel Cathode (1992)

Experimental results of differential heat loss calorimetry measurements during the electrolysis of light water solutions of K2CO3 and Na2CO3 with a nickel cathode are presented. A significant increase in temperature with every watt input, compared with the calibration experiment, is observed during the electrolysis of K2CO2. This effect is not observed when Na2CO3 is electrolyzed. No trivial explanation (in terms of chemical reactions, change in heat transfer properties, etc.) of this effect has been found so far. If the nontriviality of the observed overcoming of the energy breakeven barrier is further confirmed, this phenomenon may find application as an important new energy source.
Maximum Entropy Modeling of Short Sequence Motifs with Applications to RNA Splicing Signals (2004)

We propose a framework for modeling sequence motifs based on the maximum entropy principle (MEP). We recommend approximating short sequence motif distributions with the maximum entropy distribution (MED) consistent with low-order marginal constraints estimated from available data, which may include dependencies between nonadjacent as well as adjacent positions. Many maximum entropy models (MEMs) are specified by simply changing the set of constraints. Such models can be utilized to discriminate between signals and decoys. Classification performance using different MEMs gives insight into the relative importance of dependencies between different positions. We apply our framework to large datasets of RNA splicing signals. Our best models out-perform previous probabilistic models in the discrimination of human 5' (donor) and 3' (acceptor) splice sites from decoys. Finally, we discuss mechanistically motivated ways of comparing models.
Island size effects in nanoparticle-enhanced photodetectors (1998)

We report the effect of metal-island size variation in nanoparticle-enhanced photodetectors. Nanoparticle size was controlled by varying the deposition and annealing conditions used to produce the metal-island films. Increasing the size of silver-island particles fabricated onto 165 nm thick silicon-on-insulator (SOI) photodetectors resulted in a dramatic increase in the observed photocurrent. A nearly factor-of-20 photocurrent enhancement was observed for light of wavelength 800 nm, a significant improvement over previously reported results. The improvement is linked to two physical effects: the increased scattering efficiency of the larger nanoparticles and a qualitative change in the resonance characteristics of the metal-island film due to radiative coupling to the SOI waveguide modes.
Normal‐flow virus filtration: detection and assessment of the endpoint in bioprocessing (2005)

The breakthrough of a model virus, bacteriophage PhiX-174, through normal-flow virus filters was studied using both commercial process fluids and model feed streams. The results indicate that (i) PhiX-174 is a reasonable model for a mammalian parvovirus [MMV (murine minute virus)] in virus filtration studies; (ii) PhiX-174 LRV [log(reduction value)] shows a better correlation with percentage flow decline compared with volume processed under a variety of conditions; (iii) although the extent of decline in virus LRV is dependent on the mechanism of filter fouling, the fouling mechanisms operative in a viral validation study are representative of those likely to be found under actual production conditions. The mechanism of LRV decline by many process streams was proposed to be due to selective plugging of small pores. A theoretical model as well as a predictive equation for LRV decline versus flow decay was derived; experimental results from filtration studies using pore-plugging feed stocks were consistent with the equation. As protein solutions may vary in their adsorptive versus plugging behaviour during filtration, an evaluation of the LRV-versus-flow-decay relationship on a biopharmaceutical-product-specific basis may be warranted.
An 80-Tile 1.28TFLOPS Network-on-Chip in 65nm CMOS (2007)

A 275mm <sup xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">2</sup> network-on-chip architecture contains 80 tiles arranged as a 10 times 8 2D array of floating-point cores and packet-switched routers, operating at 4GHz. The 15-F04 design employs mesochronous clocking, fine-grained clock gating, dynamic sleep transistors, and body-bias techniques. The 65nm 100M transistor die is designed to achieve a peak performance of 1.0TFLOPS at 1V while dissipating 98W.
Amplification of the met gene in glioma (1995)

We have previously reported the finding of MET amplification linked to double minutes (dmins) in a human glioblastoma (TX3095). Because dmins are found in approximately 50% of glioblastomas, 18 gliomas were analyzed for MET amplification. Three grade IV glioblastomas and one grade II astrocytoma showed amplification. We could also localize the MET amplicon to dmins in glioblastoma TX3095 by fluorescence in situ hybridization.
Phase-change memory driven by poly-Si MOS transistor with low cost and high-programming gigabyte-per-second throughput (2011)

A phase-change memory (PCM) driven by poly-Si MOS transistors was fabricated. The thin phase-change-material layer deposited directly on the channel silicon layer in the PCM enables low-current reset operation (45 µA) compared to the conventional memory structure. This memory-cell configuration enables both a poly-Si MOS-driven stackable memory array and large degree programming parallelization. A contactless simple cell structure makes it possible to reduce the cell size to 4F2 and the number of process steps. Low cost and gigabyte-per-second programming throughput are thus made possible by this stackable phase-change memory.
Tetrabenazine: Spotlight on Drug Review (2016)

The intention of this review is to sum up the information regarding chemistry, mechanism of action, pharmacokinetics, interactions, contraindications, adverse effects, and clinical efficacy of TBZ in diseases other than Huntington's chorea.
Tumor necrosis factor alpha increases epithelial barrier permeability by disrupting tight junctions in Caco-2 cells (2010)

The objectives of this study were to determine the effect of tumor necrosis factor alpha (TNF-alpha) on intestinal epithelial cell permeability and the expression of tight junction proteins. Caco-2 cells were plated onto Transwell microporous filters and treated with TNF-alpha (10 or 100 ng/mL) for 0, 4, 8, 16, or 24 h. The transepithelial electrical resistance and the mucosal-to-serosal flux rates of the established paracellular marker Lucifer yellow were measured in filter-grown monolayers of Caco-2 intestinal cells. The localization and expression of the tight junction protein occludin were detected by immunofluorescence and Western blot analysis, respectively. SYBR-Green-based real-time PCR was used to measure the expression of occludin mRNA. TNF-alpha treatment produced concentration- and time-dependent decreases in Caco-2 transepithelial resistance and increases in transepithelial permeability to the paracellular marker Lucifer yellow. Western blot results indicated that TNF-alpha decreased the expression of phosphorylated occludin in detergent-insoluble fractions but did not affect the expression of non-phosphorylated occludin protein. Real-time RT-PCR data showed that TNF-alpha did not affect the expression of occludin mRNA. Taken together, our data demonstrate that TNF-alpha increases Caco-2 monolayer permeability, decreases occludin protein expression and disturbs intercellular junctions.
Generation of Human Cytolytic T Lymphocyte Lines Directed Against Prostate-Specific Antigen (PSA) Employing a PSA Oligoepitope Peptide (1998)

Prostate-specific Ag (PSA), which is expressed in a majority of prostate cancers, is a potential target for specific immunotherapy. Previous studies have shown that two 10-mer PSA peptides (designated PSA-1 and PSA-3) selected to conform to human HLA class I-A2 motifs can elicit CTL responses in vitro. A longer PSA peptide (30-mer) designated PSA-OP (oligoepitope peptide), which contains both the PSA-1 and PSA-3 HLA-A2 epitopes and an additional potential CTL epitope (designated PSA-9) for the HLA-class I-A3 allele, was investigated for the ability to induce cytotoxic T cell activity. T cell lines from different HLA-A2 and HLA-A3 donors were established by in vitro stimulation with PSA-OP; the CTL lines lysed PSA-OP as well as PSA-1- or PSA-3-pulsed C1R-A2 cells, and PSA-OP and PSA-9-pulsed C1R-A3 cells, respectively. The CTL lines derived from the PSA-OP peptide also lysed PSA-positive prostate cancer cells. PSA-OP-derived T cell lines also lysed recombinant vaccinia-PSA-infected targets but not targets infected with wild-type vaccinia. PSA-OP did not bind HLA-A2 and HLA-A3 molecules. The decrease in cytotoxicity in the presence of protease inhibitors suggests that the PSA-OP is cleaved into shorter peptides, which in turn can interact with HLA-class I molecules and, as a consequence, induce CTL-mediated lysis. We have also demonstrated that it is possible to induce CTL responses in HLA-A2.1/Kb transgenic mice by immunization with PSA-OP with adjuvant. These studies thus provide evidence that oligopeptides such as PSA-OP may be useful candidates for peptide-based cancer vaccines.
Controlled Radical Polymerization by Degenerative Transfer: Effect of the Structure of the Transfer Agent (1995)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTControlled Radical Polymerization by Degenerative Transfer: Effect of the Structure of the Transfer AgentScott G. Gaynor, Jin-Shan Wang, and Krzysztof MatyjaszewskiCite this: Macromolecules 1995, 28, 24, 8051–8056Publication Date (Print):November 1, 1995Publication History Published online1 May 2002Published inissue 1 November 1995https://pubs.acs.org/doi/10.1021/ma00128a012https://doi.org/10.1021/ma00128a012research-articleACS PublicationsRequest reuse permissionsArticle Views1694Altmetric-Citations218LEARN 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
Surface enhanced Raman scattering of nanoporous gold: Smaller pore sizes stronger enhancements (2007)

The authors report the surface enhanced Raman scattering (SERS) of nanoporous gold with nanopore sizes ranging from 5to700nm. Their comprehensive investigations prove that the strongest SERS enhancement of nanoporous gold takes place from the samples with an ultrafine nanopore size of ∼5–10nm. Both the enhancement factor and detection limit of the ultrafine nanoporous substrate are one to two orders of magnitude better than those of coarsened nonporous gold with smooth surfaces. Moreover, careful microstructure characterization reveals that the anomalous SERS enhancement of the annealed nanoporous gold arises from roughsurfaces with characteristic surface irregularities.
An Assessment of Current Brain Targets for Deep Brain Stimulation Surgery With Susceptibility-Weighted Imaging at 7 Tesla (2010)

Technical developments in MRI at 7 T have yielded improved anatomic resolution of deep brain structures, thereby holding the promise of improving anatomic-based targeting for DBS surgery. Future study is needed to validate this technique in improving the accuracy of targeting in DBS surgery.
Shared signatures between rheumatoid arthritis, systemic lupus erythematosus and Sjögren’s syndrome uncovered through gene expression meta-analysis (2014)

We define a common gene expression signature for SLE, RA and SjS. The analysis of this signature revealed relevant biological processes that may play important roles in the shared development of these pathologies.
NMR structure of a lytic polysaccharide monooxygenase provides insight into copper binding, protein dynamics, and substrate interactions (2012)

Lytic polysaccharide monooxygenases currently classified as carbohydrate binding module family 33 (CBM33) and glycoside hydrolase family 61 (GH61) are likely to play important roles in future biorefining. However, the molecular basis of their unprecedented catalytic activity remains largely unknown. We have used NMR techniques and isothermal titration calorimetry to address structural and functional aspects of CBP21, a chitin-active CBM33. NMR structural and relaxation studies showed that CBP21 is a compact and rigid molecule, and the only exception is the catalytic metal binding site. NMR data further showed that His28 and His114 in the catalytic center bind a variety of divalent metal ions with a clear preference for Cu(2+) (K(d) = 55 nM; from isothermal titration calorimetry) and higher preference for Cu(1+) (K(d) ∼ 1 nM; from the experimentally determined redox potential for CBP21-Cu(2+) of 275 mV using a thermodynamic cycle). Strong binding of Cu(1+) was also reflected in a reduction in the pK(a) values of the histidines by 3.6 and 2.2 pH units, respectively. Cyanide, a mimic of molecular oxygen, was found to bind to the metal ion only. These data support a model where copper is reduced on the enzyme by an externally provided electron and followed by oxygen binding and activation by internal electron transfer. Interactions of CBP21 with a crystalline substrate were mapped in a (2)H/(1)H exchange experiment, which showed that substrate binding involves an extended planar binding surface, including the metal binding site. Such a planar catalytic surface seems well-suited to interact with crystalline substrates.
The selective engulfment of apoptotic bodies by dendritic cells is mediated by the αvβ3 integrin and requires intracellular and extracellular calcium (1997)

Dendritic cells derived in vitro from monocytes are known to be poor phagocytes. Here we show that, unlike macrophages, monocyte-derived dendritic cells indeed fail to take up opsonized particles or necrotic cells; however, apoptotic bodies are efficiently engulfed by dendritic cells. The temperature dependence and the sensitivity to cytochalasin D indicate that the apoptotic body engulfment is representative of early stages of phagocytosis. Inhibition studies with ligands for surface molecules involved in recognition of apoptotic bodies, such as vitronectin receptor, CD36 and phosphatidylserine receptor, revealed that apoptotic body engulfment by dendritic cells is mediated preferentially by the vitronectin receptor alpha(v)beta3, while all the receptors, with different efficiency, are engaged in phagocytosis of apoptotic bodies by macrophages. The interaction between apoptotic bodies and dendritic cells elicits a rise in intracellular free calcium concentration ([Ca2+]i) which is essential for the process of engulfment. Either intra- or extracellular Ca2+ buffering inhibits apoptotic body engulfment by dendritic cells and [Ca2+]i increases, indicating the involvement of both intra- and extracellular Ca2+. In contrast, Ca2+ mobilization is dispensable for macrophage phagocytosis of apoptotic bodies. The different requirements of Ca2+ in macrophages and dendritic cells is possibly due to the differential usage of phagocytic receptors (CD36 vs. alpha(v)beta3) and might reflect different fates of apoptotic bodies in the two cell types.
Visualization Enables the Programmer to Reduce Cache Misses. (2002)

Many programs execution speed suffer from cache misses.These can be reduced on three different levels: the hardware level, the compiler level and the algorithm level.Much work has been done on the hardware level and the compiler level, however relatively little work has been done on assisting the programmer to increase the locality in his programs.In this paper, a method is proposed to visualize the locality which is not exploited by the cache hardware, based on the reuse distance metric.Visualizing the reuse distances allows the programmer to see the cache bottlenecks in its program at a single glance, which allows him to think about alternative ways to perform the same computation with increased cache efficiency.Furthermore, since the reuse distance is independent of cache size and associativity, the programmer will focus on optimizations which increase cache effectiveness for a wide range of caches.As a case study, the cache behavior of the MCF program, which has the worst cache behavior in the SPEC2000 benchmarks, is visualized.A simple optimization, based on the visualization, leads to consistent speedups from 24% to 48% on different processors and cache architectures, such as PentiumII, Itanium and Alpha.
CD22 associates with the human surface IgM-B-cell antigen receptor complex. (1993)

The B-cell surface molecule CD22, when cross-linked, modulates signaling through the surface IgM (sIgM)-B-cell receptor (BCR) complex. Here we analyzed the basis of this interaction between CD22 and the human sIgM complex. After lysis of B cells or B-cell lines in digitonin, CD22 coimmunoprecipitated a kinase activity that in vitro-phosphorylated two polypeptides of 150 and 130 kDa on tyrosine residues. By immunoblot analysis with a rabbit anti-serum specific for a synthetic peptide of CD22, we found these proteins to be CD22 itself. Furthermore, the phosphorylated 150-kDa CD22 was found in the sIgM-BCR complex maintained by digitonin, along with Ig alpha/mb-1, Ig beta/B29, and a 75-kDa polypeptide precipitated by an antiserum specific to protein-tyrosine kinase PTK72. CD22 is likely to be an important signaling partner in the sIgM-BCR complex since it is very rapidly and strikingly phosphorylated after sIgM is cross-linked and since it contains the antigen recognition homology I (ARHI) motif, present in other antigen receptor molecules.
Phosphatidylinositol 3-Kinase and Antiestrogen Resistance in Breast Cancer (2011)

Although antiestrogen therapies targeting estrogen receptor (ER) α signaling prevent disease recurrence in the majority of patients with hormone-dependent breast cancer, a significant fraction of patients exhibit de novo or acquired resistance. Currently, the only accepted mechanism linked with endocrine resistance is amplification or overexpression of the ERBB2 (human epidermal growth factor receptor 2 [HER2]) proto-oncogene. Experimental and clinical evidence suggests that hyperactivation of the phosphatidylinositol 3-kinase (PI3K) pathway, the most frequently mutated pathway in breast cancer, promotes antiestrogen resistance. PI3K is a major signaling hub downstream of HER2 and other receptor tyrosine kinases. PI3K activates several molecules involved in cell-cycle progression and survival, and in ER-positive breast cancer cells, it promotes estrogen-dependent and -independent ER transcriptional activity. Preclinical tumor models of antiestrogen-resistant breast cancer often remain sensitive to estrogens and PI3K inhibition, suggesting that simultaneous targeting of the PI3K and ER pathways may be most effective. Herein, we review alterations in the PI3K pathway associated with resistance to endocrine therapy, the state of clinical development of PI3K inhibitors, and strategies for the clinical investigation of such drugs in hormone receptor-positive breast cancer.