gebhart/patrepeval huggingface dataset:
Potentiation of human lymphokine-activated killer cell activity by swainsonine, an inhibitor of glycoprotein processing. (1989)

Interleukin 2 (IL-2) is a secreted glycoprotein which acts as an activation and proliferative signal for lymphocytes expressing membrane-bound glycoprotein IL-2 receptors. We have recently established that swainsonine (SW), an inhibitor of mannosidase II during N-linked glycoprotein processing, augmented mitogen-induced mononuclear leukocyte IL-2 receptor expression and IL-2-induced proliferation. The objective of the present investigation was to examine the effect of SW on lymphokine-activated killer (LAK) cell induction. Human mononuclear leukocytes were treated with various concentrations of SW (0.1-10 micrograms/ml) and IL-2 (1-100 units/ml) for up to 72 h. SW augmented IL-2-induced LAK activity directed against human lung carcinoma, melanoma, and leukemia cells 2-3-fold. LAK activity generated in the presence of SW at suboptimal doses of IL-2 (10 units/ml) was similar to that observed with higher concentrations of IL-2 (100 units/ml) alone. SW treatment alone or in combination with IL-2 increased the percentage of IL-2 receptor-positive cells. Furthermore, pretreatment with SW subsequently enhanced IL-2-induced lymphocyte proliferation. SW-treated mononuclear leukocytes exhibited an increase in high-mannose type glycoproteins based upon [3H]mannose labeling, susceptibility to alpha-mannosidase, and binding to concanavalin A-Sepharose. These results indicate that modulators of glycoprotein processing may be useful in lowering the concentrations of IL-2 required for LAK induction and maintenance.
In Situ Interfacial Mass Detection with Piezoelectric Transducers (1990)

The converse piezoelectric effect, in which an electric field applied across a piezoelectric material induces a stress in that material, has spurred many recent developments in mass measurement techniques. These methods commonly rely on the changes in the vibrational resonant frequency of piezoelectric quartz oscillators that result from changes in mass on the surface of the oscillator. The dependence of frequency on mass has been exploited extensively for mass measurements in vacuum or gas phase, for example, thickness monitors for thin-film preparation and sensors for chemical agents. Advances in piezoelectric methodology in the last decade now allow dynamic measurements of minute mass changes (< 10(-9) grams per square centimeter) at surfaces, thin films, and electrode interfaces in liquid media as well. Mass measurements associated with a diverse collection of interfacial processes can be readily performed, including chemical and biological sensors, reactions catalyzed by enzymes immobilized on surfaces, electron transfer at and ion exchange in thin polymer films, and doping reactions of conducting polymers.
GNU MP 6.0 Multiple Precision Arithmetic Library (2015)

GNU MP is a portable library written in C for arbitrary precision arithmetic on integers, rational numbers, and floating-point numbers. It aims to provide the fastest possible arithmetic for all applications that need higher precision than is directly supported by the basic C types.
Protective effects of idebenone and α‐tocopherol on β‐amyloid‐(1–42)‐induced learning and memory deficits in rats: implication of oxidative stress in β‐amyloid‐induced neurotoxicity in vivo (1999)

Amyloid beta-peptide (A beta), the major constituent of the senile plaques in the brains of patients with Alzheimer's disease, is cytotoxic to neurons and has a central role in the pathogenesis of the disease. Previous studies have suggested that oxidative stress is involved in the mechanisms of A beta-induced neurotoxicity in vitro. In the present study, we examined whether oxidative stress contributes to learning and memory deficits caused by continuous intracerebroventricular infusion of A beta-(1-42). In the A beta-(1-42)-infused rats, spontaneous alternation behaviour in a Y-maze and spatial memory in a water maze task were significantly impaired, as compared with A beta-(40-1)-infused control rats. The retention of passive avoidance learning was also significantly impaired by treatment with A beta-(1-42). Potent antioxidants idebenone and alpha-tocopherol prevented the behavioural deficits in Y-maze and water maze, but not passive avoidance, tasks in A beta-(1-42)-infused rats when they were repeatedly administered by mouth once a day from 3 days before the start of A beta infusion to the end of behavioural experiments. Lipid peroxide levels in the hippocampus and cerebral cortex of A beta-(1-42)-infused rats did not differ from those in control animals, and neither idebenone nor alpha-tocopherol affected the lipid peroxide levels. These results suggest that treatment with antioxidants such as idebenone and alpha-tocopherol prevents learning and memory deficits caused by A beta.
Expression of wild-type p53 in human A673 cells suppresses tumorigenicity but not growth rate. (1991)

The p53 gene has been found to be mutated in many different kinds of human cancers. In a previous study, expression of exogenous wild-type p53 in human osteosarcoma cells by retrovirus-mediated gene transfer resulted in marked enlargement of cell size, reduced growth rate in culture and loss of tumorigenicity in nude mice. Here we examine the effects of expression of wild-type or mutated p53 on human peripheral neuroepithelioma (PNET) A673 cells; these cells contained apparently normal alleles of the p53 gene but did not express a detectable quantity of p53 protein. Various characteristics of the p53-expressing cells were examined including morphology, growth rate, soft-agar colony formation, and tumorigenicity in nude mice. In contrast to osteosarcoma Saos-2 cells, expression of wild-type or mutant p53 protein in A673 cells had no effect on morphology or growth characteristics. However, clones expressing wild-type p53 protein had reduced ability to form colonies in soft agar and tumors in nude mice. To substantiate the genotype of wild-type p53-expressing cells, the proviral p53-encoding DNA of one cell clone was amplified by the polymerase chain reaction and sequenced. We concluded that expression of a single allele of the wild-type p53 gene was sufficient to suppress PNET A673 tumorigenicity but had no detectable effect on growth rate in culture.
Low-Power ECG-Based Processor for Predicting Ventricular Arrhythmia (2015)

This paper presents the design of a fully integrated electrocardiogram (ECG) signal processor (ESP) for the prediction of ventricular arrhythmia using a unique set of ECG features and a naive Bayes classifier. Real-time and adaptive techniques for the detection and the delineation of the P-QRS-T waves were investigated to extract the fiducial points. Those techniques are robust to any variations in the ECG signal with high sensitivity and precision. Two databases of the heart signal recordings from the MIT PhysioNet and the American Heart Association were used as a validation set to evaluate the performance of the processor. Based on application-specified integrated circuit (ASIC) simulation results, the overall classification accuracy was found to be 86% on the out-of-sample validation data with 3-s window size. The architecture of the proposed ESP was implemented using 65-nm CMOS process. It occupied 0.112- ${\rm mm}^{2}$ area and consumed 2.78- $\mu \text{W}$ power at an operating frequency of 10 kHz and from an operating voltage of 1 V. It is worth mentioning that the proposed ESP is the first ASIC implementation of an ECG-based processor that is used for the prediction of ventricular arrhythmia up to 3 h before the onset.
Analysis of the mouse and human acyl‐CoA thioesterase (ACOT) gene clusters shows that convergent, functional evolution results in a reduced number of human peroxisomal ACOTs 1 (2006)

The maintenance of cellular levels of free fatty acids and acyl-CoAs, the activated form of free fatty acids, is extremely important, as imbalances in lipid metabolism have serious consequences for human health. Acyl-coenzyme A (CoA) thioesterases (ACOTs) hydrolyze acyl-CoAs to the free fatty acid and CoASH, and thereby have the potential to regulate intracellular levels of these compounds. We previously identified and characterized a mouse ACOT gene cluster comprised of six genes that apparently arose by gene duplications encoding acyl-CoA thioesterases with localizations in cytosol (ACOT1), mitochondria (ACOT2), and peroxisomes (ACOT3-6). However, the corresponding human gene cluster contains only three genes (ACOT1, ACOT2, and ACOT4) coding for full-length thioesterase proteins, of which only one is peroxisomal (ACOT4). We therefore set out to characterize the human genes, and we show here that the human ACOT4 protein catalyzes the activities of three mouse peroxisomal ACOTs (ACOT3, 4, and 5), being active on succinyl-CoA and medium to long chain acyl-CoAs, while ACOT1 and ACOT2 carry out similar functions to the corresponding mouse genes. These data strongly suggest that the human ACOT4 gene has acquired the functions of three mouse genes by a functional convergent evolution that also provides an explanation for the unexpectedly low number of human genes.
A Simulation Study Examining Smartphone Destination Entry while Driving (2014)

A driving simulation study was performed to compare visual-manual (touch screen based) destination entry using a Samsung Galaxy S4 smartphone with the standard voice command based interface and a voice based "Hands-Free mode" that appears to be intended for use while driving (i.e. has a steering wheel icon adjacent to the mode selection menu and the voice interface menu screen is visually austere when compared with the standard voice mode). The performance of 24 drivers on an alphanumeric street address entry task was assessed with respect to subjective workload, task duration, standard deviation of lateral lane position, response to a detection response task (DRT), and heart rate. With the exception of heart rate, all evaluation measures indicate that the voice interfaces provide significant advantages over the touch interface. Furthermore, subjective workload ratings and task duration measures imply that the "Hands-Free" voice based mode may have some costs relative to the standard voice command based interface. Lastly, all destination entry methods were associated with an increased DRT reaction time and higher miss-rates compared to a baseline driving condition.
Toxins-antitoxins: diversity, evolution and function (2011)

Genes for toxin-antitoxin (TA) complexes are widespread in prokaryote genomes, and species frequently possess tens of plasmid and chromosomal TA loci. The complexes are categorized into three types based on genetic organization and mode of action. The toxins universally are proteins directed against specific intracellular targets, whereas the antitoxins are either proteins or small RNAs that neutralize the toxin or inhibit toxin synthesis. Within the three types of complex, there has been extensive evolutionary shuffling of toxin and antitoxin genes leading to considerable diversity in TA combinations. The intracellular targets of the protein toxins similarly are varied. Numerous toxins, many of which are sequence-specific endoribonucleases, dampen protein synthesis levels in response to a range of stress and nutritional stimuli. Key resources are conserved as a result ensuring the survival of individual cells and therefore the bacterial population. The toxin effects generally are transient and reversible permitting a set of dynamic, tunable responses that reflect environmental conditions. Moreover, by harboring multiple toxins that intercede in protein synthesis in response to different physiological cues, bacteria potentially sense an assortment of metabolic perturbations that are channeled through different TA complexes. Other toxins interfere with the action of topoisomersases, cell wall assembly, or cytoskeletal structures. TAs also play important roles in bacterial persistence, biofilm formation and multidrug tolerance, and have considerable potential both as new components of the genetic toolbox and as targets for novel antibacterial drugs.
PV string per-module maximum power point enabling converters (2003)

Many grid connected PV installations consist of a single series string of PV modules and a single DC-AC inverter. This efficiency of this topology can be enhanced with additional low power, low cost per panel converter modules. Most current flows directly in the series string which ensures high efficiency. However parallel Cúk or buck-boost DC-DC converters connected across each adjacent pair of modules now support any desired current difference between series connected PV modules. Each converter “shuffles” the desired difference in PV module currents between two modules and so on up the string. Spice simulations show that even with poor efficiency, these modules can make a significant improvement to the overall power which can be recovered from partially shaded PV strings.
Chemical chaperones increase the cellular activity of N370S β-glucosidase: A therapeutic strategy for Gaucher disease (2002)

Gaucher disease is a lysosomal storage disorder caused by deficient lysosomal beta-glucosidase (beta-Glu) activity. A marked decrease in enzyme activity results in progressive accumulation of the substrate (glucosylceramide) in macrophages, leading to hepatosplenomegaly, anemia, skeletal lesions, and sometimes CNS involvement. Enzyme replacement therapy for Gaucher disease is costly and relatively ineffective for CNS involvement. Chemical chaperones have been shown to stabilize various proteins against misfolding, increasing proper trafficking from the endoplasmic reticulum. We report herein that the addition of subinhibitory concentrations (10 microM) of N-(n-nonyl)deoxynojirimycin (NN-DNJ) to a fibroblast culture medium for 9 days leads to a 2-fold increase in the activity of N370S beta-Glu, the most common mutation causing Gaucher disease. Moreover, the increased activity persists for at least 6 days after the withdrawal of the putative chaperone. The NN-DNJ chaperone also increases WT beta-Glu activity, but not that of L444P, a less prevalent Gaucher disease variant. Incubation of isolated soluble WT enzyme with NN-DNJ reveals that beta-Glu is stabilized against heat denaturation in a dose-dependent fashion. We propose that NN-DNJ chaperones beta-Glu folding at neutral pH, thus allowing the stabilized enzyme to transit from the endoplasmic reticulum to the Golgi, enabling proper trafficking to the lysosome. Clinical data suggest that a modest increase in beta-Glu activity may be sufficient to achieve a therapeutic effect.
l-Lactide Polymerization Utilizing a Hydroxy-Functionalized 3,6-Bis(2-pyridyl)pyridazine as Supramolecular (Co)initiator:  Construction of Polymeric [2 × 2] Grids (2003)

A hydroxy-functionalized 3,6-bis(2-pyridyl)pyridazine ligand was synthesized from 3,6-bis(2-pyridyl)tetrazine and 5-hexyn-1-ol. This ligand was subsequently polymerized with l-lactide utilizing a controlled aluminum alkoxide-based polymerization. The resulting poly(l-lactide) macroligands were characterized with 1H NMR spectroscopy, IR spectroscopy, gel permeation chromatography, and MALDI-TOF-MS, revealing the successful incorporation of the ligand into the polymer chains. Complexation studies of both the hydroxy-functionalized ligand and the macroligands were performed by UV−vis spectroscopic investigations, demonstrating the exclusive formation of metallo-supramolecular gridlike architectures. In addition, AFM measurements also revealed the existence of the defined polymeric species.
Biologic significance of angiopoietin-2 expression in human hepatocellular carcinoma (1999)

Human hepatocellular carcinoma (HCC) is generally a highly vascular tumor, but the mechanisms of neovascularization that permit rapid growth have not been defined. Angiopoietins (Ang) recently have been identified as ligands for vascular endothelial-specific Tie2 receptor tyrosine kinase and may be important growth factors in the generation of new blood vessels. We investigated Ang expression in 23 samples of HCC and paired adjacent uninvolved liver samples to determine if these genes have a potential role in the growth and spread of this disease. The full coding sequence of a variant angiopoietin-2 (Ang2) cDNA was obtained from HCC specimens, and the biologic consequences of overexpression on tumor formation and hemorrhage were determined in an animal model system. Angiopoietin-1 (Ang1) was equally expressed in HCC and adjacent noncarcinomatous liver tissue. Surprisingly, Ang2 was found to be highly expressed only in tumor tissue. In addition, Ang2 was expressed in 10 of 12 hypervascular HCC, but only in 2 of 11 hypovascular HCC. Ectopic expression of Ang2 in nonexpressing HCC cells promotes the rapid development of human hepatomas and produces hemorrhage within tumors in nude mice. These results suggest a role for Ang2 in the neovascularization of HCC. This enhanced gene expression may contribute to the clinical hypervascular phenotype, as well as tumor formation and progression.
Memory persistency (2014)

Emerging nonvolatile memory technologies (NVRAM) promise the performance of DRAM with the persistence of disk. However, constraining NVRAM write order, necessary to ensure recovery correctness, limits NVRAM write concurrency and degrades throughput. We require new memory interfaces to minimally describe write constraints and allow high performance and high concurrency data structures. These goals strongly resemble memory consistency. Whereas memory consistency concerns the order that memory operations are observed between numerous processors, persistent memory systems must constrain the order that writes occur with respect to failure. We introduce memory persistency, a new approach to designing persistent memory interfaces, building on memory consistency. Similar to memory consistency, memory persistency models may be relaxed to improve performance. We describe the design space of memory persistency and desirable features that such a memory system requires. Finally, we introduce several memory persistency models and evaluate their ability to expose NVRAM write concurrency using two implementations of a persistent queue. Our results show that relaxed persistency models accelerate system throughput 30-fold by reducing NVRAM write constraints
Hemodialysis Vascular Access Dysfunction (2006)

Hemodialysis vascular access dysfunction is a major cause of morbidity and hospitalization in the hemodialysis population. The major cause of hemodialysis vascular access dysfunction is venous stenosis as a result of neointimal hyperplasia. Despite the magnitude of the clinical problem, however, there has been a paucity of novel therapeutic interventions in this field. This is in marked contrast to a recent plethora of targeted interventions for the treatment of arterial neointimal hyperplasia after coronary angioplasty. The reasons for this are two-fold. First there has been a relative lack of cellular and molecular research that focuses on venous neointimal hyperplasia in the specific setting of hemodialysis vascular access. Second, there have been inadequate efforts by the nephrology community to translate the recent advances in molecular and interventional cardiology into therapies for hemodialysis vascular access. This review therefore (1) briefly examines the different forms of hemodialysis vascular access that are available, (2) describes the pathology and pathogenesis of hemodialysis vascular access dysfunction in both polytetrafluoroethylene grafts and native arteriovenous fistulae, (3) reviews recent concepts about the pathogenesis of vascular stenosis that could potentially be applied in the setting of hemodialysis vascular access dysfunction, (4) summarizes novel experimental and clinical therapies that could potentially be used in the setting of hemodialysis vascular access dysfunction, and, finally, (5) offers some broad guidelines for future innovative translational and clinical research in this area that hopefully will reduce the huge clinical morbidity and economic costs that are associated with this condition.
Interactions Between Ca2+and H+and Functional Consequences in Vascular Smooth Muscle (2000)

Ca(2+) and H(+) ions can profoundly alter vascular tone. In many physiological and pathological processes, changes in the concentration of both ions occur. Thus, to understand the processes and mechanisms that modify force, it is necessary to understand what changes occur in these ions and, importantly, how they interact with each other. In this minireview, we highlight the quantitatively important mechanisms involved in the contractile responses of vascular tissues to pH change and discuss the cellular and molecular reasons underlying these responses.
Reduction of  CO 2 on n ‐ GaAs Electrodes and Selective Methanol Synthesis (1984)

Faradaic efficiencies and current voltage characteristics for the reduction of to on (111 As) single‐crystal electrodes have been determined. The yield of is ∼ 100% for current densities of ∼ 140 μA/cm2 at −1.2 to −1.4V vs. SCE. The excess current due to was found to have a threshold at and a maximum at . The current also exhibited a rotation‐independent j/v characteristic that is interpreted as a rate‐determining surface chemical combination step involving adsorbed H atoms and a carbon containing intermediate. The pH dependence of the saturation current is modeled with a kinetic scheme involving the parallel reduction of H+ and .
Oxazolidinone Resistance Mutations in 23S rRNA of Escherichia coli Reveal the Central Region of Domain V as the Primary Site of Drug Action (2000)

Oxazolidinone antibiotics inhibit bacterial protein synthesis by interacting with the large ribosomal subunit. The structure and exact location of the oxazolidinone binding site remain obscure, as does the manner in which these drugs inhibit translation. To investigate the drug-ribosome interaction, we selected Escherichia coli oxazolidinone-resistant mutants, which contained a randomly mutagenized plasmid-borne rRNA operon. The same mutation, G2032 to A, was identified in the 23S rRNA genes of several independent resistant isolates. Engineering of this mutation by site-directed mutagenesis in the wild-type rRNA operon produced an oxazolidinone resistance phenotype, establishing that the G2032A substitution was the determinant of resistance. Engineered U and C substitutions at G2032, as well as a G2447-to-U mutation, also conferred resistance to oxazolidinone. All the characterized resistance mutations were clustered in the vicinity of the central loop of domain V of 23S rRNA, suggesting that this rRNA region plays a major role in the interaction of the drug with the ribosome. Although the central loop of domain V is an essential integral component of the ribosomal peptidyl transferase, oxazolidinones do not inhibit peptide bond formation, and thus these drugs presumably interfere with another activity associated with the peptidyl transferase center.
Numerical evaluation of current paths in disordered media (1994)

We present numerical results for the current flowing though a disordered block of material. The results show the current flowing in well-defined channels with a disorder and energy dependent width. The correlation of the current shows a negative dip at short separations.