gebhart/patrepeval huggingface dataset:
M(DM): an open framework for interoperation of multimodel multidatabase systems (2003)

The authors present M(DM), an extensible metalevel system in which the syntax and the semantics of data models, schemas, and databases can be uniformly represented. M(DM) consists primarily of a set of metatypes that capture and express data-model constructs in second-order logic: a data model is represented as a collection of M(DM) metatypes. To achieve extensibility, M(DM)'s metatypes are organized into an inheritance lattice. The robustness and openness of the approach are demonstrated by expressing a variety of data models in M(DM), and the authors show how to exploit M(DM)'s metalevel capabilities for hiding representational heterogeneities in multimodel multidatabase systems.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Arsenic removal from aqueous solutions by adsorption onto iron oxide/activated carbon magnetic composite (2014)

In this work the adsorption features of activated carbon and the magnetic properties of iron oxides were combined in a composite to produce magnetic adsorbent. Batch experiments were conducted to study the adsorption behavior of arsenate onto the synthetic magnetic adsorbent. The effects of initial solution pH, contact time, adsorbent dosage and co-existing anionic component on the adsorption of arsenate were investigated. The results showed that the removal percentage of arsenate could be over 95% in the conditions of adsorbent dosage 5.0 g/L, initial solution pH 3.0-8.0, and contact time 1 h. Under the experimental conditions, phosphate and silicate caused greater decrease in arsenate removal percentage among the anions, and sulfate had almost no effect on the adsorption of arsenate. Kinetics study showed that the overall adsorption rate of arsenate was illustrated by the pseudo-second-order kinetic model. The applicability of the Langmuir and Freundlich models for the arsenate adsorption data was tested. Both the models adequately describe the experimental data. Moreover, the magnetic composite adsorbent could be easily recovered from the medium by an external magnetic field. It can therefore be potentially applied for the treatment of water contaminated by arsenate.
Molecular genetic analysis of silencing in two lines of Triticum aestivum transformed with the reporter gene construct pAHC25 (2005)

Summary Unpredictable silencing of foreign genes introduced into wheat by particle bombardment transformation has been previously observed. To investigate the cause of this silencing, we selected two independent wheat lines that had been transformed via the particle gun with plasmid pAHC25 containing the genes uid A (GUS) and bar (BASTA herbicide‐resistance) each controlled by the maize ubiquitin promoterintron ( Ubil ). One of these lines (WT2) had shown progressive reductions in transgenic phenotype in successive generations until GUS activity and herbicide‐resistance were undetectable in all progeny of the T 3 generation tested. A second line, (WT1) exhibited the expected levels of GUS expression and herbicide‐resistance up to the T 3 generation except for the loss of transgenic phenotype in a single T 1 segregant. Transgene stability, silencing and integration locus was investigated in three generations in both lines. The silencing observed in the WT2 line was found to be acting at the transcription level for both the uid A and bar genes. Analysis of transgene promoter methylation in selected T 1 , T 2 and T 3 individuals revealed a positive link between methylation status and gene silencing. The silenced T1 individual from line WT1 was also linked to promoter methylation and insertion locus rearrangement. Fluorescence in situ hybridisation (FISH) revealed highly divergent transgene insertion loci for WT1 and WT2. WT1 was detected close to the telomere whereas the WT2 insertion was located in the region of the centromere. The effect of these findings on transgene silencing and stability are discussed.
Role of DNA methylation in the development of Epstein–Barr virus‐associated gastric carcinoma (2012)

The frequencies of DNA methylation of certain tumor-related genes are higher in Epstein-Barr virus (EBV)-associated gastric carcinomas than in EBV-negative gastric carcinomas. EBV-associated gastric carcinomas have distinct clinicopathological features; however, there are no case-control studies comparing methylation frequency between EBV-associated gastric carcinomas and controls that have been adjusted according to the clinicopathological features of EBV-associated gastric carcinomas. This study evaluated 25 EBV-associated gastric carcinomas that were positive for EBV-encoded small RNA 1 (EBER-1) by in situ hybridization and 50 EBV-negative gastric carcinomas that were matched with the EBV-associated gastric carcinomas by age, sex, histology, depth of tumor invasion, and stage. Methylation status of 16 loci associated with tumor-related genes was analyzed by methylation-specific polymerase chain reaction (PCR) to identify genes in which DNA methylation specifically occurred in EBV-associated gastric carcinomas. Methylation frequencies of 12 of the 16 genes were higher in EBV-associated gastric carcinomas than in EBV-negative controls, and the frequency of methylation of 6 specific loci (MINT2, MINT31, p14, p16, p73, and RUNX3) was significantly higher in EBV-associated gastric carcinomas than in EBV-negative controls. There were no significant differences in the methylation frequencies of the other genes. The mean methylation index in EBV-associated gastric carcinomas was significantly higher than that in EBV-negative controls. DNA methylation of tumor suppressor genes that regulate the cell cycle and apoptosis specifically occurred in EBV-associated gastric carcinomas. Aberrant DNA methylation might lead to the development and progression of EBV-associated gastric carcinoma.
Amino-terminal protein-protein interaction motif (POZ-domain) is responsible for activities of the promyelocytic leukemia zinc finger-retinoic acid receptor-alpha fusion protein. (1996)

Promyelocytic leukemia zinc finger-retinoic acid receptor a (PLZF-RARalpha), a fusion receptor generated as a result of a variant t(11;17) chromosomal translocation that occurs in a small subset of acute promyelocytic leukemia (APL) patients, has been shown to display a dominant-negative effect against the wild-type RARalpha/retinoid X receptor alpha (RXRalpha). We now show that its N-terminal region (called the POZ-domain), which mediates protein-protein interaction as well as specific nuclear localization of the wild-type PLZF and chimeric PLZF-RARalpha proteins, is primarily responsible for this activity. To further investigate the mechanisms of PLZF-RARalpha action, we have also studied its ligand-receptor, protein-protein, and protein-DNA interaction properties and compared them with those of the promyelocytic leukemia gene (PML)-RARalpha, which is expressed in the majority of APLs as a result of t(15;17) translocation. PLZF-RARalpha and PML-RARalpha have essentially the same ligand-binding affinities and can bind in vitro to retinoic acid response elements (RAREs) as homodimers or heterodimers with RXRalpha. PLZF-RARalpha homodimerization and heterodimerization with RXRalpha were primarily mediated by the POZ-domain and RARalpha sequence, respectively. Despite having identical RARalpha sequences, PLZF-RARalpha and PML-RARalpha homodimers recognized with different affinities distinct RAREs. Furthermore, PLZF-RARalpha could heterodimerize in vitro with the wild-type PLZF, suggesting that it may play a role in leukemogenesis by antagonizing actions of not only the retinoid receptors but also the wild-type PLZF and possibly other POZ-domain-containing regulators. These different protein-protein interactions and the target gene specificities of PLZF-RARalpha and PML-RARalpha may underlie, at least in part, the apparent resistance of APL with t(11;17) to differentiation effects of all-trans-retinoic acid.
Structure and Interactions of the Human Programmed Cell Death 1 Receptor (2013)

PD-1, a receptor expressed by T cells, B cells, and monocytes, is a potent regulator of immune responses and a promising therapeutic target. The structure and interactions of human PD-1 are, however, incompletely characterized. We present the solution nuclear magnetic resonance (NMR)-based structure of the human PD-1 extracellular region and detailed analyses of its interactions with its ligands, PD-L1 and PD-L2. PD-1 has typical immunoglobulin superfamily topology but differs at the edge of the GFCC' sheet, which is flexible and completely lacks a C" strand. Changes in PD-1 backbone NMR signals induced by ligand binding suggest that, whereas binding is centered on the GFCC' sheet, PD-1 is engaged by its two ligands differently and in ways incompletely explained by crystal structures of mouse PD-1 · ligand complexes. The affinities of these interactions and that of PD-L1 with the costimulatory protein B7-1, measured using surface plasmon resonance, are significantly weaker than expected. The 3-4-fold greater affinity of PD-L2 versus PD-L1 for human PD-1 is principally due to the 3-fold smaller dissociation rate for PD-L2 binding. Isothermal titration calorimetry revealed that the PD-1/PD-L1 interaction is entropically driven, whereas PD-1/PD-L2 binding has a large enthalpic component. Mathematical simulations based on the biophysical data and quantitative expression data suggest an unexpectedly limited contribution of PD-L2 to PD-1 ligation during interactions of activated T cells with antigen-presenting cells. These findings provide a rigorous structural and biophysical framework for interpreting the important functions of PD-1 and reveal that potent inhibitory signaling can be initiated by weakly interacting receptors.
Stimulation of all epithelial elements during skin regeneration by keratinocyte growth factor. (1994)

Keratinocyte growth factor (KGF), a recently discovered 18.9 kD member of the fibroblast growth factor family has been shown to selectively induce keratinocyte proliferation and differentiation in tissue culture. To explore its potential stimulating keratinocyte growth and differentiation in vivo, we analyzed for the influence of KGF on epithelial derived elements within a wound created through the cartilage on the rabbit ear. KGF accelerated reepithelialization (p = 0.004) and increased the thickness of the epithelium (p = 0.0005) when 4-40 micrograms/cm2 recombinant KGF was added at the time of wounding. The regenerating epidermis showed normal differentiation as detected by cytokeratin immunostaining. Remarkably, however, KGF stimulated proliferation and differentiation of early progenitor cells within hair follicles and sebaceous glands in the wound bed and adjacent dermis. There was a transient but highly significant increase in specific labeling of cycling cells in both basal and suprabasal layers that extended into the spinous layer of the regenerating epidermis. As an indication of specificity, the inflammatory cells and fibroblasts within the wound were not influenced by KGF. The results indicate that KGF is unique in its ability to accelerate reepithelialization and dermal regeneration by targeting multiple epithelial elements within the skin. These results suggest that KGF may induce specific epithelial progenitor cell lineages within the skin to proliferate and differentiate, and thus may be a critical determinant of regeneration of skin. Furthermore, these findings illustrate the potential capacity of this system to analyze epithelial differentiation programs and disorders of epidermis, dermal glandular elements, and hair follicles.
Astrogliosis in culture. IV. Effects of basic fibroblast growth factor (1995)

Previous studies have shown that the mechanical wounding of 3-week-old cultured rat astrocytes results in cell proliferation and hypertrophy resembling astrocyte responses to a brain injury in vivo. We now report the effects of basic fibroblast growth factor (bFGF) and an anti-bFGF antibody on astrocyte morphology, proliferation, and migration following in vitro wounding of confluent secondary cultures. Addition of bFGF (20 ng/ml) to wounded cultures induced morphological changes characteristic of differentiation in wounded and nonwounded areas of the culture. Combined treatment with bFGF and an anti-bFGF antibody (100 micrograms/ml) prevented this effect. Astrocyte proliferation along the edges of a scratch wound was at maximum 24 hr after wounding in cells growing in Eagle's minimum essential medium (EMEM) containing 10% serum. Low serum concentration and treatment with dibutyryl cyclic adenosine monophosphate (dbc-AMP) reduced injury-associated astrocyte proliferation. Addition of bFGF to cultures in EMEM with serum increased astrocyte proliferation at 18 and 24 hr after wounding. This effect was reduced considerably by treatment of cultures with bFGF in combination with an anti-bFGF antibody. The combined treatment and the antibody alone reduced cell division to a level lower than in control cultures. Twenty-four hr following wounding, astrocytes along the edges of the wound exhibited extension of thick, flat processes into the wound area. At 3 and 5 days after wounding, a bodily migration of astrocytes into the wounded area was observed. Addition of bFGF significantly increased astrocyte migration 1 day after wounding, with maximum effect on day 3 and no subsequent increase on day 5. A combination of bFGF and anti-bFGF antibody as well as the antibody alone reduced astrocyte migration to a level lower than in controls. Immunohistochemical localization and isoform pattern of bFGF in astrocytes did not change with dbc-AMP treatment or wounding. We conclude that mechanically wounded confluent astrocytes respond to bFGF added to the culture medium by enhancing cell division, differentiation, and migration. In addition, the results of the antibody treatment also suggest a role for endogenous bFGF in astrocyte proliferation and migration elicited by wounding in vitro. These results support the notion that in vivo, both bFGF released by injury and endogenous bFGF synthesized by astrocytes, contribute to the cellular responses that lead to astrogliosis.
Mechanisms of cell death and neuroprotection by poloxamer 188 after mechanical trauma (2005)

The mechanisms of cell death and the progressive degeneration of neural tissue following traumatic brain injury (TBI) have come under intense investigation. However, the complex interactions among the evolving pathologies in multiple cell types obscure the causal relationships between the initial effects of the mechanical trauma at the cellular level and the long-term dysfunction and neuronal death. We used an in vitro model of neuronal injury to study the mechanisms of cell death in response to a well-defined mechanical insult and found that the majority of dead cells were apoptotic. We have previously reported that promotion of membrane repair acutely with the non-ionic surfactant poloxamer 188 (P188) restored cell viability to control values at 24 h postinjury. Here, we showed that P188 significantly inhibits apoptosis and prevents necrosis. We also examined the role of mitogen-activated protein kinases (MAPKs) in cell death. There was a rapid, transient activation of extracellular signal-regulated kinases, c-Jun N-terminal kinase, and p38s after mechanical insult. Of these, activation of the proapoptotic p38 was the greatest. Treatment with P188 inhibited p38 activation; however, direct inhibition of p38 by SB203580, which selectively inhibits the activity of the p38 MAPK, provided only partial inhibition of apoptosis and had no effect on necrosis. These data suggest that multiple signaling pathways may be involved in the long-term response of neurons to mechanical injury. Furthermore, that the membrane resealing action of P188 provides such significant protection from both necrosis and apoptosis suggests that acute membrane damage due to trauma is a critical precipitating event that is upstream of the many signaling cascades contributing to the subsequent pathology.
POLYPEPTIDE GROWTH FACTORS (1984)

The Hippo pathway was initially discovered in Drosophila melanogaster as a key regulator of tissue growth. It is an evolutionarily conserved signaling cascade regulating numerous biological processes, including cell growth and fate decision, organ size ...Read More
Network-Based Drug-Target Interaction Prediction with Probabilistic Soft Logic (2014)

Drug-target interaction studies are important because they can predict drugs' unexpected therapeutic or adverse side effects. In silico predictions of potential interactions are valuable and can focus effort on in vitro experiments. We propose a prediction framework that represents the problem using a bipartite graph of drug-target interactions augmented with drug-drug and target-target similarity measures and makes predictions using probabilistic soft logic (PSL). Using probabilistic rules in PSL, we predict interactions with models based on triad and tetrad structures. We apply (blocking) techniques that make link prediction in PSL more efficient for drug-target interaction prediction. We then perform extensive experimental studies to highlight different aspects of the model and the domain, first comparing the models with different structures and then measuring the effect of the proposed blocking on the prediction performance and efficiency. We demonstrate the importance of rule weight learning in the proposed PSL model and then show that PSL can effectively make use of a variety of similarity measures. We perform an experiment to validate the importance of collective inference and using multiple similarity measures for accurate predictions in contrast to non-collective and single similarity assumptions. Finally, we illustrate that our PSL model achieves state-of-the-art performance with simple, interpretable rules and evaluate our novel predictions using online data sets.
The digital signature standard (1992)

his standard specifies a Digital Signature Algorithm (DSA) appropriate for applications requiring a digital rather than written signature. The DSA digital signature is a pair of large numbers represented in a computer as strings of binary digits. .................
Advances in computer architecture (1978)

From the Publisher:
A completely updated edition of this overview of modern computer architecture. Examines alternatives to classical low-level von Neumann computer architecture, discussing the problems of classical architecture and new solutions to these problems. Illustrates new concepts through in-depth case studies of the Intel APX 432, IBM's SWARD, and other machines. State-of-the-art concepts covered include tagged storage, capability-based addressing, process management, protection domains, and error detection.
Automated UAV-based mapping for airborne reconnaissance and video exploitation (2009)

Airborne surveillance and reconnaissance are essential for successful military missions. Such capabilities are critical for force protection, situational awareness, mission planning, damage assessment and others. UAVs gather huge amount of video data but it is extremely labour-intensive for operators to analyse hours and hours of received data. At MDA, we have developed a suite of tools towards automated video exploitation including calibration, visualization, change detection and 3D reconstruction. The on-going work is to improve the robustness of these tools and automate the process as much as possible. Our calibration tool extracts and matches tie-points in the video frames incrementally to recover the camera calibration and poses, which are then refined by bundle adjustment. Our visualization tool stabilizes the video, expands its field-of-view and creates a geo-referenced mosaic from the video frames. It is important to identify anomalies in a scene, which may include detecting any improvised explosive devices (IED). However, it is tedious and difficult to compare video clips to look for differences manually. Our change detection tool allows the user to load two video clips taken from two passes at different times and flags any changes between them. 3D models are useful for situational awareness, as it is easier to understand the scene by visualizing it in 3D. Our 3D reconstruction tool creates calibrated photo-realistic 3D models from video clips taken from different viewpoints, using both semi-automated and automated approaches. The resulting 3D models also allow distance measurements and line-of- sight analysis.
Tetragonal Chicken Egg White Lysozyme Solubility in Sodium Chloride Solutions (1999)

The solubility of chicken egg white lysozyme crystallized in the tetragonal form was measured in sodium chloride solutions from 1.6 to 30.7 °C, using a miniature column solubility apparatus. Sodium chloride solution concentrations ranged from 1 to 7% (w/v). The solutions were buffered with 0.1 M sodium acetate buffer, with the solubility being measured at pH values in 0.2 pH unit increments in the pH range 4.0−5.4, with data also included at pH 4.5. Lysozyme solubility was found to increase with increasing in temperature and decreasing salt concentration. Solution pH has a varied and unpredictable effect on solubility.
Hemoglobin Is a Co-Factor of Human Trypanosome Lytic Factor (2007)

Trypanosome lytic factor (TLF) is a high-density lipoprotein (HDL) subclass providing innate protection to humans against infection by the protozoan parasite Trypanosoma brucei brucei. Two primate-specific plasma proteins, haptoglobin-related protein (Hpr) and apolipoprotein L-1 (ApoL-1), have been proposed to kill T. b. brucei both singularly or when co-assembled into the same HDL. To better understand the mechanism of T. b. brucei killing by TLF, the protein composition of TLF was investigated using a gentle immunoaffinity purification technique that avoids the loss of weakly associated proteins. HDL particles recovered by immunoaffinity absorption, with either anti-Hpr or anti-ApoL-1, were identical in protein composition and specific activity for T. b. brucei killing. Here, we show that TLF-bound Hpr strongly binds Hb and that addition of Hb stimulates TLF killing of T. b. brucei by increasing the affinity of TLF for its receptor, and by inducing Fenton chemistry within the trypanosome lysosome. These findings suggest that TLF in uninfected humans may be inactive against T. b. brucei prior to initiation of infection. We propose that infection of humans by T. b. brucei causes hemolysis that triggers the activation of TLF by the formation of Hpr-Hb complexes, leading to enhanced binding, trypanolytic activity, and clearance of parasites.