gebhart/patrepeval huggingface dataset:
Beyond Porosity: 3D Leaf Intercellular Airspace Traits That Impact Mesophyll Conductance (2018)

The leaf intercellular airspace (IAS) is generally considered to have high conductance to CO<sub>2</sub> diffusion relative to the liquid phase. While previous studies accounted for leaf-level variation in porosity and mesophyll thickness, they omitted 3D IAS traits that potentially influence IAS conductance (g<sub>IAS</sub>). Here, we reevaluated the standard equation for g<sub>IAS</sub> by incorporating tortuosity, lateral path lengthening, and IAS connectivity. We measured and spatially mapped these geometric IAS traits for 19 Bromeliaceae species with Crassulacean acid metabolism (CAM) or C3 photosynthetic pathways using x-ray microcomputed tomography imaging and a novel computational approach. We found substantial variation in porosity (0.04-0.73 m<sup>3</sup> m<sup>-3</sup>), tortuosity (1.09-3.33 m<sup>2</sup> m<sup>-2</sup>), lateral path lengthening (1.12-3.19 m m<sup>-1</sup>), and IAS connectivity (0.81-0.97 m<sup>2</sup> m<sup>-2</sup>) across all bromeliad leaves. The revised g<sub>IAS</sub> model predicted significantly lower g<sub>IAS</sub> in CAM (0.01-0.19 mol m<sup>-2</sup> s<sup>-1</sup> bar<sup>-1</sup>) than in C3 (0.41-2.38 mol m<sup>-2</sup> s<sup>-1</sup> bar<sup>-1</sup>) plants due to a coordinated decline in these IAS traits. Our reevaluated equation also generally predicted lower g<sub>IAS</sub> values than the former one. Moreover, we observed high spatial heterogeneity in these IAS geometric traits throughout the mesophyll, especially within CAM leaves. Our data show that IAS traits that better capture the 3D complexity of leaves strongly influence g<sub>IAS</sub> and that the impact of the IAS on mesophyll conductance should be carefully considered with respect to leaf anatomy. We provide a simple function to estimate tortuosity and lateral path lengthening in the absence of access to imaging tools such as x-ray microcomputed tomography or other novel 3D image-processing techniques.
Immunochemical and Biosynthetic Analysis of Monoclonal Antibody-Defined Melanoma-Associated Antigen (1982)

Immunoprecipitation studies with application of monoclonal antibody F11 originally made to a partially purified spent medium antigen of melanoma cells, made it possible to delineate the molecular profiles of both the cell associated and spent medium antigens recognized on melanoma cells intrinsically labeled with glycoprotein precursors. F11 distinguishes a glycoprotein of Mr 100,000 (100 K) in the spent media of melanoma cells while a parallel analysis of detergent lysates of cells reveals a pattern of three glycoproteins of Mr 75, 77, and 100 K. Pulse-chase analysis of the biosynthesis of these antigens indicated that F11 first recognizes the 75 and 77 K antigens in the absence of a 100K component suggesting strongly that these molecules contain an antigenic site recognized by F11. The 100 K antigen appears later in the pulse-chase analysis with kinetics that suggest some of the 75 and 77 K antigens are biosynthetic precursors of the 100 K antigen. This molecule is ultimately secreted into the extracellular media and appears to be a sialoglycoprotein judging from its sensitivity to neuraminidase. A cross-reactive species with an approximate Mr 90 K is also recognized by F11 in indirect immunoprecipitation analysis of spent media from a neuroblastoma cell line indicating that a common antigenic site exists on this secreted but structurally different neuroblastoma antigen. Thus, a combination of immunochemical and biosynthetic analyses of cell-associated and secreted antigens recognized by monoclonal antibody F11 demonstrate such molecules can differ structurally when isolated from the same or different tumor cells. These findings indicate the necessity to establish molecular profiles of melanoma-associated glycoprotein antigens recognized by monoclonal antibodies to characterize and define their potential biological functions within tumor cells.
Differential engagement of Tim-1 during activation can positively or negatively costimulate T cell expansion and effector function (2007)

It has been suggested that T cell immunoglobulin mucin (Tim)-1 expressed on T cells serves to positively costimulate T cell responses. However, crosslinking of Tim-1 by its ligand Tim-4 resulted in either activation or inhibition of T cell responses, thus raising the issue of whether Tim-1 can have a dual function as a costimulator. To resolve this issue, we tested a series of monoclonal antibodies specific for Tim-1 and identified two antibodies that showed opposite functional effects. One anti-Tim-1 antibody increased the frequency of antigen-specific T cells, the production of the proinflammatory cytokines IFN-gamma and IL-17, and the severity of experimental autoimmune encephalomyelitis. In contrast, another anti-Tim-1 antibody inhibited the generation of antigen-specific T cells, production of IFN-gamma and IL-17, and development of autoimmunity, and it caused a strong Th2 response. Both antibodies bound to closely related epitopes in the IgV domain of the Tim-1 molecule, but the activating antibody had an avidity for Tim-1 that was 17 times higher than the inhibitory antibody. Although both anti-Tim-1 antibodies induced CD3 capping, only the activating antibody caused strong cytoskeletal reorganization and motility. These data indicate that Tim-1 regulates T cell responses and that Tim-1 engagement can alter T cell function depending on the affinity/avidity with which it is engaged.
Unsupervised large-vocabulary word sense disambiguation with graph-based algorithms for sequence data labeling (2005)

This paper introduces a graph-based algorithm for sequence data labeling, using random walks on graphs encoding label dependencies. The algorithm is illustrated and tested in the context of an unsupervised word sense disambiguation problem, and shown to significantly outperform the accuracy achieved through individual label assignment, as measured on standard senseannotated data sets.
Streptococcal pharyngitis (1994)

SHULMAN, S. T. MD; GERBER, M. A. MD; TANZ, R. R. MD; MARKOWITZ, M. MD Author Information
Nested linear/lattice codes for structured multiterminal binning (2002)

Network information theory promises high gains over simple point-to-point communication techniques, at the cost of higher complexity. However, lack of structured coding schemes limited the practical application of these concepts so far. One of the basic elements of a network code is the binning scheme. Wyner (1974, 1978) and other researchers proposed various forms of coset codes for efficient binning, yet these schemes were applicable only for lossless source (or noiseless channel) network coding. To extend the algebraic binning approach to lossy source (or noisy channel) network coding, previous work proposed the idea of nested codes, or more specifically, nested parity-check codes for the binary case and nested lattices in the continuous case. These ideas connect network information theory with the rich areas of linear codes and lattice codes, and have strong potential for practical applications. We review these developments and explore their tight relation to concepts such as combined shaping and precoding, coding for memories with defects, and digital watermarking. We also propose a few novel applications adhering to a unified approach.
Advanced oxidation processes. Test of a kinetic model for the oxidation of organic compounds with ozone and hydrogen peroxide in a semibatch reactor (1989)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTAdvanced oxidation processes. Test of a kinetic model for the oxidation of organic compounds with ozone and hydrogen peroxide in a semibatch reactorWilliam H. Glaze and Joon Wun KangCite this: Ind. Eng. Chem. Res. 1989, 28, 11, 1580–1587Publication Date (Print):November 1, 1989Publication History Published online1 May 2002Published inissue 1 November 1989https://pubs.acs.org/doi/10.1021/ie00095a002https://doi.org/10.1021/ie00095a002research-articleACS PublicationsRequest reuse permissionsArticle Views1087Altmetric-Citations122LEARN 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
Pak4 Induces Premature Senescence via a Pathway Requiring p16 INK4 /p19 ARF and Mitogen-Activated Protein Kinase Signaling (2005)

Exposure of primary cells to mitogenic stimuli or oncogenes often causes them to undergo premature senescence. This is most likely a protective function that prevents uncontrolled proliferation. Pak4 is a target for the Rho GTPase Cdc42. Pak4 is overexpressed in human tumor cell lines, and it is the only member of the Pak family that is highly transforming in immortalized fibroblasts. Here we show that in primary fibroblasts, activated Pak4 inhibits cell proliferation and promotes premature senescence. Furthermore, Pak4 expression levels are upregulated in response to stimuli that promote senescence. Pak4-induced arrest appears to be mediated by a pathway that requires the ERK mitogen-activated protein kinase, as well as the cell cycle inhibitors p16(INK4) and p19(ARF). These new results describing a role for Pak4 in senescence are important for understanding why this protein is associated with cancer and how it promotes transformation in immortalized cells.
STAT3 and STAT5B Are Targets of Two Different Signal Pathways Activated by Hematopoietin Receptors and Control Transcription via Separate Cytokine Response Elements (1995)

Transient transfection of expression vectors for various members of the hematopoietin receptor family and STAT proteins into COS-1 cells indicated that each receptor was capable of stimulating the DNA binding activity of STAT1, STAT3, and STAT5B. However, gp130 preferentially activated STAT1 and STAT3. Activation of STAT5B differed from that of the other two in that the box 3 sequence motif in the cytoplasmic domain of gp130 was not required. Moreover, STAT5B and STAT3 enhanced gene transcription via separate regulatory elements. This study has identified two potential signal transduction pathways by which hematopoietin receptors, including the interleukin-6 receptor, control transcription of acute phase plasma protein genes in hepatic cells.
Triglyceride-rich lipoprotein lipolysis releases neutral and oxidized FFAs that induce endothelial cell inflammation (2008)

Triglyceride-rich lipoprotein (TGRL) lipolysis products provide a pro-inflammatory stimulus that can alter endothelial barrier function. To probe the mechanism of this lipolysis-induced event, we evaluated the pro-inflammatory potential of lipid classes derived from human postprandial TGRL by lipoprotein lipase (LpL). Incubation of TGRL with LpL for 30 min increased the saturated and unsaturated FFA content of the incubation solutions significantly. Furthermore, concentrations of the hydroxylated linoleates 9-hydroxy ocatadecadienoic acid (9-HODE) and 13-HODE were elevated by LpL lipolysis, more than other measured oxylipids. The FFA fractions elicited pro-inflammatory responses inducing TNFalpha and intracellular adhesion molecule expression and reactive oxygen species (ROS) production in human aortic endothelial cells (HAECs). The FFA-mediated increase in ROS was blocked by both the cytochrome P450 2C9 inhibitor sulfaphenazole and NADPH oxidase inhibitors. Compared with linoleate, 13-HODE was found to be a more potent inducer of ROS production in HAECs, an activity that was insensitive to both NADPH oxidase and cytochrome P450 inhibitors. Therefore, although the oxidative metabolism of FFA in endothelial cells can produce inflammatory responses, TGRL lipolysis can also release preformed mediators of oxidative stress (e.g., HODEs) that may influence endothelial cell function in vivo by stimulating intracellular ROS production.
Points of View and View-points: Roggeveen's Visit Revised (1997)

Of the four expeditions known to have touched Easter Island between 1722 and 1786 many written records are available. Some reports are very scientific, including maps that show the exact landing spots. This is unfortunately not the case in regard to the Dutch visit of 1722. Although it is well known that Roggeveen's fleet came to the island on April 5, 1722, and an abstract of his journal was published in English by B.G. Corney in 1908, little importance was given to it by the general public.
Interaction of human bone marrow fibroblasts with megakaryocytes: role of the c-kit ligand (1992)

Human kit ligand (KL), also known as stem cell factor (SCF), steel factor, or mast cell growth factor, is a recently identified hematopoietic growth factor whose receptor is the product of the c-kit proto-oncogene. Alternative splicing of the pre-mRNA of KL/SCF results in secreted and membrane-bound forms of the protein. We and others have recently shown that the c-kit gene product is expressed on human megakaryocytes and that soluble KL/SCF in combination with granulocyte-macrophage colony-stimulating factor, interleukin-3 (IL-3), or IL-6 increased megakaryocyte progenitor colony formation (CFU-MEG) and stimulated mature megakaryocytes. Here we show that adhesion of human megakaryocytes to bone marrow stromal fibroblasts, which express the membrane-bound form of KL/SCF (mKL/SCF), is mediated in part by the interaction between mKL/SCF and the c-kit protein. This interaction also results in marrow fibroblast-stimulated proliferation but not an increase in ploidy of megakaryocytes; when the two cell types were separated by a transoluble membrane, proliferation did not occur. Adhesion and proliferation of human megakaryocytes to an immortalized murine stromal cell line SI/SI lacking the KL/SCF gene was impaired, whereas transfection of SI/SI cells with human mKL/SCF significantly increased both adhesion and proliferation. Marrow stromal fibroblast mKL/SCF may serve both as an adhesion structure and as a growth-potentiating factor for megakaryocytes in the bone marrow.
Human neuroblastoma cells rapidly enter cell cycle arrest and apoptosis following exposure to C-28 derivatives of the synthetic triterpenoid CDDO (2008)

Synthetic triterpenoids, such as 2-cyano-3,12-dioxoolean-1,9-dien-28-oic acid (CDDO) and its derivatives, are an extremely potent class of new anti-cancer therapeutic agents, characterized by high anti-tumor potency and low toxicity to normal tissues. This report is the first to investigate the effects of C-28 derivatives of CDDO on 22 pediatric solid tumor cell lines, including neuroblastoma, rhabdomyosarcoma, osteosarcoma, and Ewing's sarcoma. We determined IC(50)s in the range of 5-170 nM for inhibition of colony formation and DNA synthesis, and 110-630 nM for metabolic cell death and decrease in cell number, using the C-28 CDDO analogs, CDDO methyl ester (CDDO-Me), CDDO imidazolide (CDDO-Im), CDDO ethyl amide (CDDO-EA), CDDO trifluoroethyl amide (CDDO-TFEA), and CDDO diethylamide (CDDO-DE). After treatment of human neuroblastoma cells with CDDO-Me, cell cycle studies show depletion of the S-phase, while apoptosis studies show conformational activation and mitochondrial translocation of Bax protein, as well as activation of caspases -3 and -8. These data demonstrate the potential utility of CDDO analogs as promising novel therapeutic agents for high-risk pediatric solid tumors.
Interleukin‐6 in synovial fluid and serum of patients with rheumatoid arthritis and other inflammatory arthritides (1988)

Interleukin-6 (IL-6), also called 26-kd protein, hybridoma plasmacytoma growth factor, beta 2-interferon, or B cell stimulatory factor 2, is a recently described human cytokine with multiple growth and differentiation activities. Using a very sensitive bioassay based on the growth factor activity of this protein for B cell hybridomas, we found that IL-6 activity was significantly elevated in synovial fluid from patients with rheumatoid arthritis (RA) or other inflammatory arthritides, as compared with that in a group of patients with osteoarthritis. Moreover, IL-6 was detected in about one-third of the serum samples from patients with RA. In the latter group, we found a significant correlation between serum IL-6 activity and serum levels of C-reactive protein, alpha 1-acid glycoprotein, alpha 1-antitrypsin, fibrinogen, and haptoglobin, which indicates that IL-6 is related to disease activity in patients with RA.
Significant Role for Fas in the Pathogenesis of Autoimmune Diabetes (2000)

Programmed cell death represents an important pathogenic mechanism in various autoimmune diseases. Type I diabetes mellitus (IDDM) is a T cell-dependent autoimmune disease resulting in selective destruction of the beta cells of the islets of Langerhans. beta cell apoptosis has been associated with IDDM onset in both animal models and newly diagnosed diabetic patients. Several apoptotic pathways have been implicated in beta cell destruction, including Fas, perforin, and TNF-alpha. Evidence for Fas-mediated lysis of beta cells in the pathogenesis of IDDM in nonobese diabetic (NOD) mice includes: 1) Fas-deficient NOD mice bearing the lpr mutation (NOD-lpr/lpr) fail to develop IDDM; 2) transgenic expression of Fas ligand (FasL) on beta cells in NOD mice may result in accelerated IDDM; and 3) irradiated NOD-lpr/lpr mice are resistant to adoptive transfer of diabetes by cells from NOD mice. However, the interpretation of these results is complicated by the abnormal immune phenotype of NOD-lpr/lpr mice. Here we present novel evidence for the role of Fas/FasL interactions in the progression of NOD diabetes using two newly derived mouse strains. We show that NOD mice heterozygous for the FasL mutation gld, which have reduced functional FasL expression on T cells but no lymphadenopathy, fail to develop IDDM. Further, we show that NOD-lpr/lpr mice bearing the scid mutation (NOD-lpr/lpr-scid/scid), which eliminates the enhanced FasL-mediated lytic activity induced by Fas deficiency, still have delayed onset and reduced incidence of IDDM after adoptive transfer of diabetogenic NOD spleen cells. These results provide evidence that Fas/FasL-mediated programmed cell death plays a significant role in the pathogenesis of autoimmune diabetes.
Comparison of Oxygen Reduction Reaction at Silver Nanoparticles and Polycrystalline Silver Electrodes in Alkaline Solution (2012)

Adenosine 5′-triphosphate capped silver nanoparticles (ATP-Ag NPs) with diameters of 4.5 ± 1.1 nm were synthesized using a one-pot chemical reduction route. After removal of the ATP capping ligands, the electrochemical activity of these NPs for the oxygen reduction reaction (ORR) in aqueous alkaline solution (0.1 M NaOH) was studied in a single layer-by-layer (1 L LbL) film of NPs and compared with bulk polycrystalline Ag using cyclic voltammetry (CV) and rotating disk electrode (RDE) experiments. For the NPs in the 1 L LbL film, the active area of catalyst available for the ORR was calculated using the charge for the underpotential deposition (UPD) of lead (Pb) on the NPs. RDE data were analyzed to determine the ORR rate constant and the number of electrons (n-value) involved in oxygen reduction. Analysis of Koutecky–Levich (K–L) plots indicates an n-value between 3 and 4 with a higher n-value under some conditions for the NPs than for bare polycrystalline Ag. Possible origins of the variation of n-values for the Ag NPs compared to bulk Ag are discussed.
Transcription Termination (1993)

Chromosomes are organized into units of expression that are bounded by sites where transcription of DNA sequences into RNA is initiated and terminated. To allow for efficient stepwise assembly of complete transcripts, the transcribing enzyme (RNA polymerase) makes a stable complex with the DNA template until it reaches the terminator. Three general mechanisms of transcription termination have been recognized: one is by a spontaneous dissociation of the RNA at a sequence segment where RNA polymerase does not maintain its usual stable interaction with the nascent chain; another involves the action of a protein (rho factor in bacteria) on the nascent RNA to mediate its dissociation; and a third involves an action triggered by a protein that binds to the DNA at a sequence that is just downstream of the termination stop point. Transcription termination is important in the regulation of gene expression both by modulating the relative levels of various genes within a single unit of expression and by controlling continuation of transcription in response to a metabolic or regulatory signal.
Mitochondrial AKAP121 Binds and Targets Protein Tyrosine Phosphatase D1, a Novel Positive Regulator of src Signaling (2004)

A-kinase anchor protein 121 (AKAP121) and its spliced isoform AKAP84 anchor protein kinase A (PKA) to the outer membrane of mitochondria, focusing and enhancing cyclic AMP signal transduction to the organelle. We find that AKAP121/84 also binds PTPD1, a src-associated protein tyrosine phosphatase. A signaling complex containing AKAP121, PKA, PTPD1, and src is assembled in vivo. PTPD1 activates src tyrosine kinase and increases the magnitude and duration of epidermal growth factor (EGF) signaling. EGF receptor phosphorylation and downstream activation of ERK 1/2 and Elk1-dependent gene transcription are enhanced by PTPD1. Expression of a PTPD1 mutant lacking catalytic activity inhibits src and downregulates ERK 1/2 but does not affect the activity of c-Jun N-terminal kinase 1/2 and p38alpha mitogen-activated protein kinase. AKAP121 binds to and redistributes PTPD1 from the cytoplasm to mitochondria and inhibits EGF signaling. Our findings indicate that PTPD1 is a novel positive regulator of src signaling and a key component of the EGF transduction pathway. By binding and/or targeting the phosphatase on mitochondria, AKAP121 modulates the amplitude and persistence of src-dependent EGF transduction pathway. This represents the first example of physical and functional interaction between AKAPs and a protein tyrosine phosphatase.