gebhart/patrepeval huggingface dataset:
New Guidelines for Applying Curable Resin-Coated Proppants (1998)

Abstract Failures of resin-coated proppants have been primarily attributed to incompatibility between fluid chemistry and the resin, insufficient closure stress, the practice of flowing the well back too aggressively, or stress cycling. This paper describes the failure mechanism that may be more predominant than any of the others: curing too fast. Proppant consolidation kinetics were studied with the use of differential scanning calorimetry and compressive-strength development. Additional studies to determine ultimate compressive-strength development and the effects of flow erosion and stress cycling on resin-coated proppants were performed. This study has determined that the temperature profile and time before proppant grains are compacted and closure stress during curing are critical factors affecting consolidation properties. The investigation also resulted in the identification of the appropriate resin-coated proppants and guidelines for their uses in proppant flowback control in hard-rock fracturing and in sand control of soft formations as in screenless fracpack completions. P. 587
Abnormal class I assembly and peptide presentation in the nonobese diabetic mouse. (1994)

Presentation of self-antigens by major histocompatibility complex (MHC) class I molecules requires the function of the MHC class II-linked genes Tap-1 and Tap-2. Evidence suggests that interruption of self-peptide presentation results in reduced cell surface expression of MHC class I molecules and the interruption correlates with progression to diabetic autoimmunity in nonobese diabetic (NOD) mice and humans. NOD mice possess a rare Tap-1 allele (Tap-1b); this is associated with reduced Tap-1 mRNA abundance in lymphocytes from diabetes-prone females and decreased conformationally correct class I molecules on the cell surface. In this study, we demonstrate that, similar to lymphoma cell lines with mutations in Tap-1 or Tap-2, the reduced expression of class I molecules on the surface of lymphocytes from diabetes-prone female NOD mice was normalized by incubation at low temperatures or by exposure to class I allele-specific peptides. As would be expected for cells that express surface class I molecules not associated with peptide, female NOD lymphocytes were resistant to lysis by class I-restricted, peptide-specific cytotoxic T lymphocytes. Furthermore, the rate of class I exit from the endoplasmic reticulum of lymphocytes from female NOD mice was delayed as demonstrated by delayed glycosylation. Male NOD mice, which are not prone to diabetes, lacked these functional defects in class I assembly and had near-normal levels of Tap-1 mRNA and exhibited normal density of class I epitopes that were peptide filled. These results are consistent with the possibility that the rare Tap-1b allele is associated with a quantitative defect in Tap-1 expression that influences disease course.
Hippocampus and contextual fear conditioning: Recent controversies and advances (2001)

Dorsal hippocampal (DH) lesions produce a severe deficit in recently, but not remotely, acquired contextual fear without impairing memory of discrete training stimuli, i.e., DH lesions produce an anterograde and time-limited retrograde amnesia specific to contextual memory. These data are consistent with the standard model which posits temporary involvement of the hippocampus in recent memory maintenance. However, three recent controversies apparently weaken the case for a selective mnemonic role for the hippocampus in contextual fear. First, although retrograde amnesia (from posttraining lesions) is severe, anterograde amnesia (from pretraining lesions) may be mild or nonexistent. Second, a performance, rather than mnemonic, account of contextual freezing deficits in hippocampal-lesioned animals has been offered. Third, damage to the entire hippocampus, including the ventral hippocampus, can produce a dramatic and temporally stable disruption of context and tone fear. These data are reviewed and explanations are offered as to why they do not necessarily challenge the standard model of hippocampal memory function in contextual fear. Finally, a more complete description of the hippocampus' proposed role in contextual fear is offered, along with new data supporting this view. In summary, the data support a specific mnemonic role for the DH in the acquisition and consolidation of contextual representations.
Protein C Inhibitor Regulates the Thrombin-Thrombomodulin Complex in the Up- and Down Regulation of TAFI Activation (2001)

Thrombin Activatable Fibrinolysis Inhibitor (TAFI) is a carboxy-peptidase B-like proenzyme that after activation by thrombin down regulates fibrinolysis. Thrombomodulin (TM) stimulates the activation of both TAFI and protein C whereas activated protein C (APC) inhibits the activation of TAFI by down regulating thrombin generation. Recently, protein C inhibitor (PCI) was identified as a potent inhibitor of thrombin bound to TM and it can thereby regulate the balance between TAFI activation, and inhibition of TAFI activation by APC. Both in a purified system and in plasma, activation of TAFI and protein C by [Ia-TM could be inhibited by PCI. Previously we found in plasma that at low concentrations (approximately 1 nM), TM predominantly stimulated the activation of TAFI whereas at higher concentrations of TM (approximately 10 nM) the activation of protein C resulted in inhibition of the activation of TAFI. In agreement with this. PCI inhibited the activation of TAFI at 1 nM TM whereas at 10 nM TM PCI inhibited the activation of protein C resulting in an increase in the activation of TAFI. This suggests that PCI can up regulate TAFI activation by inhibiting the protein C activation. PCI may therefore be an important regulator in the balance between coagulation and fibrinolysis by differentially inhibiting the activation of TAFI and of protein C. The local TM concentration plays an important role in the outcome of this process.
Neuropeptides, Via Specific Receptors, Regulate T Cell Adhesion to Fibronectin (1998)

The ability of T cells to adhere to and interact with components of the blood vessel walls and the extracellular matrix is essential for their extravasation and migration into inflamed sites. We have found that the beta1 integrin-mediated adhesion of resting human T cells to fibronectin, a major glycoprotein component of the extracellular matrix, is induced by physiologic concentrations of three neuropeptides: calcitonin gene-related protein (CGRP), neuropeptide Y, and somatostatin; each acts via its own specific receptor on the T cell membrane. In contrast, substance P (SP), which coexists with CGRP in the majority of peripheral endings of sensory nerves, including those innervating the lymphoid organs, blocks T cell adhesion to fibronectin when induced by CGRP, neuropeptide Y, somatostatin, macrophage inflammatory protein-1beta, and PMA. Inhibition of T cell adhesion was obtained both by the intact SP peptide and by its 1-4 N-terminal and its 4-11, 5-11, and 6-11 C-terminal fragments, used at similar nanomolar concentrations. The inhibitory effects of the parent SP peptide and its fragments were abrogated by an SP NK-1 receptor antagonist, suggesting they all act through the same SP NK-1 receptor. These findings suggest that neuropeptides, by activating their specific T cell-expressed receptors, can provide the T cells with both positive (proadhesive) and negative (antiadhesive) signals and thereby regulate their function. Thus, neuropeptides may influence diverse physiologic processes involving integrins, including leukocyte-mediated migration and inflammation.
Effect of Micronutrient Fortification on Nutritional and Other Properties of Nixtamal Tortillas (2008)

ABSTRACT Nixtamalization is the process of steeping dried corn in hot water with calcium hydroxide (lime) with subsequent removal of all or most of the pericarp through washing. The resulting product is called nixtamal. Approximately 60% of corn tortillas in Mexico are produced from nixtamal, with the remainder prepared from nixtamalized corn flour. Nixtamal was fortified with micronutrient premix containing iron, zinc, folic acid, niacin, riboflavin, and thiamin. Premix composition followed a proposed Mexican regulation for corn flour fortification, adjusted for moisture. Effects of premix on masa adhesiveness, hardness, and pH, as well as tortilla sensory properties, stretchability, rollability, and color were measured. Micronutrient levels were tested in the dry corn, nixtamal, masa, and tortillas. There were no significant differences in masa texture or pH, tortilla rollability, or consumer acceptance of tortillas when comparing unfortified control and fortified treatments. Added thiamin was almost entirely degraded during processing. Folic acid and riboflavin decreased 26 and 45%, respectively, through the masa‐tortilla manufacturing process. Niacin showed no significant loss. Despite processing losses, fortification resulted in significant nutrient increases compared with control tortillas. Folic acid increased 974%, riboflavin increased 300%, niacin increased 141%, iron increased 156%, and zinc increased 153% in fortified tortillas.
Oxidation of High Density Lipoproteins (1998)

The lipids of high density lipoproteins (HDL) are initially oxidized in preference to those in low density lipoprotein when human plasma is exposed to aqueous peroxyl radicals. In this work we report on the relative susceptibility of HDL protein and lipid to oxidation and on the role HDL's alpha-tocopherol (alpha-TOH) plays in modulating protein oxidation. Exposure of isolated HDL to either low fluxes of aqueous peroxyl radicals, Cu2+ ions, or soybean lipoxygenase resulted in the oxidation of apoAI and apoAII during the earliest stages of the reaction, i.e. after consumption of ubiquinol-10 and in the presence of alpha-TOH. Hydro(pero)xides of cholesteryl esters and phospholipids initially accumulated together with specific oxidized forms of apoAI and apoAII, separated by high pressure liquid chromatography. The specific oxidized forms of apoAI were 16 and 32 mass units heavier than those of the native apolipoproteins and contained 1 and 2 methionine sulfoxide residues per protein, respectively. The third methionine residue in apoAI, as well as Trp residues, remained unoxidized during the earliest stages of HDL oxidation examined. Exposure of isolated apoAI to peroxyl radicals, Cu2+, or soybean lipoxygenase resulted in nonspecific (for peroxyl radicals) or no discernible protein oxidation (Cu2+ and soybean lipoxygenase). This indicated that the formation of the specific oxidized forms of apoAI observed with native HDL was not the result of direct reaction of these oxidants with the apolipoprotein. In vitro and in vivo enrichment of HDL with alpha-TOH resulted in a dose-dependent increase in the extent of peroxyl radical-induced formation of HDL cholesteryl ester hydroperoxides (r = 0.96) and cholesteryl ester hydroxides (r = 0. 92), as well as the loss of apoAI (r = 0.96) and apoAII (r = 0.94). alpha-TOH enrichment also enhanced HDL lipid and protein oxidation induced by Cu2+ or soybean lipoxygenase. These results indicate that the earliest stages of HDL oxidation are accompanied by the oxidation of specific methionine residues in apoAI and apoAII and that in the absence of co-antioxidants, alpha-TOH can promote this process.
PbS quantum dots as additives in methylammonium halide perovskite solar cells: the effect of quantum dot capping (2019)

Colloidal PbS quantum dots (QDs) have been successfully employed as additives in halide perovskite solar cells (PSCs) acting as nucleation centers in the perovskite crystallization process. For this strategy, the surface functionalization of the QDs, controlled <i>via</i> the use of different capping ligands, is likely of key importance. In this work, we examine the influence of the PbS QD capping on the photovoltaic performance of methylammonium lead iodide PSCs. We test PSCs fabricated with PbS QD additives with different capping ligands including methylammonium lead iodide (MAPI), cesium lead iodide (CsPI) and 4-aminobenzoic acid (ABA). Both the presence of PbS QDs and the specific capping used have a significant effect on the properties of the deposited perovskite layer, which affects, in turn, the photovoltaic performance. For all capping ligands used, the inclusion of PbS QDs leads to the formation of perovskite films with larger grain size, improving, in addition, the crystalline preferential orientation and the crystallinity. Yet, differences between the capping agents were observed. The use of QDs with ABA capping had a higher impact on the morphological properties while the employment of the CsPI ligand was more effective in improving the optical properties of the perovskite films. Taking advantage of the improved properties, PSCs based on the perovskite films with embedded PbS QDs exhibit an enhanced photovoltaic performance, showing the highest increase with ABA capping. Moreover, bulk recombination <i>via</i> trap states is reduced when the ABA ligand is used for capping of the PbS QD additives in the perovskite film. We demonstrate how surface chemistry engineering of PbS QD additives in solution-processed perovskite films opens a new approach towards the design of high quality materials, paving the way to improved optoelectronic properties and more efficient photovoltaic devices.
Therapeutics against Cancer Stem Cells: Targeting the Root of Cancer (2013)

The cancer stem cell hypothesis provides a useful framework with which to investigate the mechanisms of cancer initiation, progression, and treatment. Cells with stem cell-like properties have been implicated in tumor initiation, metastatic spread and disease evolution, as well therapeutic failure. While the roles of cancer stem cells continue to be defined, known stem cell signaling pathways and stem cell niche-regulated mechanisms of survival are emerging as targets to selectively eliminate cancer stem cells. In this chapter, these mechanisms and approaches for targeting cancer stem cells through these pathways will be discussed. Strategies will also be addressed for identifying novel pathways involved in cancer stem cell survival, and requirements for the clinical evaluation of cancer stem cell-targeted therapies.
Rotary reactor for atomic layer deposition on large quantities of nanoparticles (2007)

Challenges are encountered during atomic layer deposition (ALD) on large quantities of nanoparticles. The particles must be agitated or fluidized to perform the ALD surface reactions in reasonable times and to prevent the particles from being agglomerated by the ALD film. The high surface area of nanoparticles also demands efficient reactant usage because large quantities of reactant are required for the surface reactions to reach completion. The residence time of the reactant in a fluidized particle bed reactor may be too short for high efficiency if the ALD surface reactions have low reactive sticking coefficients. To address these challenges, a novel rotary reactor was developed to achieve constant particle agitation during static ALD reactant exposures. In the design of this new reactor, a cylindrical drum with porous metal walls was positioned inside a vacuum chamber. The porous cylindrical drum was rotated by a magnetically coupled rotary feedthrough. By rotating the cylindrical drum to obtain a centrifugal force of less than one gravitational force, the particles were agitated by a continuous “avalanche” of particles. In addition, an inert N2 gas pulse helped to dislodge the particles from the porous walls and provided an efficient method to purge reactants and products from the particle bed. The effectiveness of this rotary reactor was demonstrated by Al2O3 ALD on ZrO2 particles. A number of techniques including transmission electron microscopy, Fourier transform infrared spectroscopy, and x-ray photoelectron spectroscopy confirmed that the Al2O3 ALD film conformally coats the ZrO2 particles. Combining static reactant exposures with a very high surface area sample in the rotary reactor also provides unique opportunities for studying the surface chemistry during ALD.
The Time Dimension for Scene Analysis (2005)

A fundamental issue in neural computation is the binding problem, which refers to how sensory elements in a scene organize into perceived objects, or percepts. The issue of binding is hotly debated in recent years in neuroscience and related communities. Much of the debate, however, gives little attention to computational considerations. This review intends to elucidate the computational issues that bear directly on the binding issue. The review starts with two problems considered by Rosenblatt to be the most challenging to the development of perceptron theory more than 40 years ago, and argues that the main challenge is the figure-ground separation problem, which is intrinsically related to the binding problem. The theme of the review is that the time dimension is essential for systematically attacking Rosenblatt's challenge. The temporal correlation theory as well as its special form--oscillatory correlation theory-is discussed as an adequate representation theory to address the binding problem. Recent advances in understanding oscillatory dynamics are reviewed, and these advances have overcome key computational obstacles for the development of the oscillatory correlation theory. We survey a variety of studies that address the scene analysis problem. The results of these studies have substantially advanced the capability of neural networks for figure-ground separation. A number of issues regarding oscillatory correlation are considered and clarified. Finally, the time dimension is argued to be necessary for versatile computing.
IL-6-anti-IL-6 autoantibody complexes with IL-6 activity in sera from some patients with systemic sclerosis. (1994)

Anti-IL-6 IgG autoantibodies, often found in sera from patients with systemic sclerosis, may increase to the level sufficient to bind significant amounts of IL-6 in serum. In our study of the role of anti-IL-6 autoantibodies in serum, we found that some sera with the autoantibodies possessed considerably higher IL-6 levels (more than 100 pg/ml) compared with most of sera without the autoantibodies. Size-exclusion HPLC of the sera with these autoantibodies demonstrated that a significant part of the serum IL-6 activity was attributable to circulating IL-6-anti-IL-6 autoantibody complexes. Gel filtration of IL-6-anti-IL-6 IgG complexes made in vitro by incubation of rIL-6 and IgG purified from the autoantibody-positive sera demonstrated that the complexes at 200 to 250 kDa were dominant ones and that IL-6 bound to the autoantibodies retained more than 60% of the original IL-6 activity. Moreover, IL-6-anti-IL-6 autoantibody complexes were shown to bind to recombinant soluble IL-6 receptors. Estimated affinity of anti-IL-6 IgG autoantibodies from two patients was fairly high (4.2 x 10(9) to 3.3 x 10(10) L/M). Therefore, the retention of IL-6 activity by IL-6-anti-IL-6 autoantibody complexes may be explained by intact receptor-binding sites on the autoantibody-bound IL-6 molecules. Taken together, these results suggest that the properties of anti-IL-6 autoantibodies are consistent with a potential role as specific carriers for IL-6 in the circulation.
Helicobacter pylori and gastric adaptation to repeated aspirin administration in humans. (1997)

The gastric irritant properties of nonsteroidal anti-inflammatory drugs (NSAID) are well established but the pathogenic mechanisms by which these agents damage the mucosa or delay its repair are poorly understood. The phenomenon of gastric adaptation after repeated exposures to ASA is well documented but the involvement of Helicobacter pylori (H. pylori) in NSAID-induced gastropathy and adaptation has not been elucidated. The aim of this study was 1) to compare the gastric damage in response to repeated exposures to ASA in the same subjects before and after eradication of H. pylori and 2) to examine the morphological and functional changes of gastric mucosa during the 14 day treatment with ASA in H. pylori-infected subjects before and after eradication of this bacteria: Eight healthy volunteers (age 19-28) with H. pylori infection were given ASA 1g bd during 14 days before and after H. pylori eradication. Mucosal damage was evaluated by endoscopy before and at 3, 7 and 14 days of ASA administration using modified Lanza score. During endoscopy mucosal biopsies were obtained for determination of DNA synthesis, by measuring 3H-thymidine incorporation into DNA. Prior to each endoscopy gastric microbleeding was determined in three consecutive gastric washings. Three months after successful eradication of H. pylori confirmed by 13C-urea breath test and mucosal rapid urease test, the same subjects received again 14 day treatment with ASA and underwent the same examinations as prior to the therapy. In all subjects, ASA administration induced acute gastric damage with endoscopic Lanza score reaching maximum at 3rd day. In H. pylori-positive subjects, this damage was maintained at similar level up to day 14th, whereas in H. pylori-eradicated subjects, this damage was lessened at day 14th by about 60-75%. Gastric microbleeding also reached its maximum at 3rd day of ASA treatment being significantly higher in H. pylori-eradicated subjects than in those with H. pylori infection. This microbleeding decreased to almost normal values by the end of the study in all H. pylori-negative subjects but remained significantly elevated in H. pylori-infected subjects. DNA synthesis before and following ASA administration was significantly higher in subjects after H. pylori eradication than in those with H. pylori infection. Moreover, this DNA synthesis showed significant increase at day 7 of ASA administration only in H. pylori-eradicated subjects. We conclude that: 1) gastric adaptation to ASA is impaired in H. pylori-positive subjects but eradication of H. pylori restores this adaptation, 2) the DNA synthesis and possibly also mucosal cell turnover in response to ASA are suppressed in H. pylori infection and this can be reversed by eradication of H. pylori.
Treatment of murine B cell lymphoma with bispecific monoclonal antibodies (anti-idiotype x anti-CD3) (1991)

It has previously been reported that T lymphocytes can be targeted by using bispecific antibodies consisting of anti-target antibody and anti-CD3. In the present study, a bispecific mAb was developed by somatic hybridization of mouse hybridomas, one producing a mAb against the Id determinant of the mouse B cell lymphoma 38C13 and the other a mAb against a polymorphic determinant on murine CD3. The bispecific antibody, anti-38C13 x anti-CD3, is bi-isotypic (IgG1 x IgG2a) and was purified by ion exchange and affinity chromatography. The dual specificity of the hybrid hybridoma-produced mAb could be demonstrated by flow cytometry, the induction of T cell proliferation, the induction of IL-2 secretion by polyclonal T cells, and redirected lysis of the relevant target cells. The hybrid (bi-isotypic) Fc part of the bispecific antibodies was nonfunctional in FcR-dependent redirected lysis. In vivo studies demonstrate that this bispecific mAb could efficiently target T cells towards the tumor cells, resulting in long term survival and cure of the lymphoma.
Electron thermalization in gold (1992)

We report the direct observation of the thermalization of electrons in gold following 180 fs optical pulse excitation. The evolution of the electron energy distribution from the nascent (as photoexcited) to a hot Fermi-Dirac distribution was measured by time-resolved photoemission spectroscopy. Depending on the excitation density, thermalization times as long as \ensuremath{\approxeq}1 ps were observed. A model incorporating both electron-electron and electron-phonon scattering, and using Fermi-liquid theory to properly account for screening is found to reproduce the main features of the experiment.