gebhart/patrepeval huggingface dataset:
Regulation of alpha-factor production in Saccharomyces cerevisiae: a-factor pheromone-induced expression of the MF alpha 1 and STE13 genes. (1989)

Production of the mating pheromone alpha-factor was examined in Saccharomyces cerevisiae MAT alpha cells that had been exposed to the mating pheromone a-factor. A 2-h treatment with a-factor caused a significant increase in alpha-factor concentration in the medium as demonstrated by a halo assay. MF alpha 1 is one of the two genes coding for a precursor of alpha-factor. A Northern (RNA) analysis of total RNA from a-factor-treated MAT alpha cells revealed a rapid two- to threefold increase in MF alpha 1 transcript levels, reaching maximum within 60 min of exposure to the pheromone. Pheromone induction did not require ongoing protein synthesis. a-Factor-induced MF alpha 1 expression was quantitated by analysis of an MF alpha 1::SUC2 fusion gene whose product was assayed for invertase activity. Expression of the MF alpha 1::SUC2 gene in MAT alpha cells responded to the a-factor signal like the chromosomal version of MF alpha 1. Maturation of the alpha-factor precursor involves three proteolytic activities which are encoded by the KEX1, KEX2, and STE13 genes, respectively. Two of these genes, namely, KEX2 and STE13, were examined for pheromone-induced expression. Only the STE13 gene exhibited pheromone induction at the transcriptional level.
Combustion instability modeling and analysis (1995)

It is well known that the two key elements for achieving low emissions and high performance in a gas turbine combustor are to simultaneously establish (1) a lean combustion zone for maintaining low NO{sub x} emissions and (2) rapid mixing for good ignition and flame stability. However, these requirements, when coupled with the short combustor lengths used to limit the residence time for NO formation typical of advanced gas turbine combustors, can lead to problems regarding unburned hydrocarbons (UHC) and carbon monoxide (CO) emissions, as well as the occurrence of combustion instabilities. Clearly, the key to successful gas turbine development is based on understanding the effects of geometry and operating conditions on combustion instability, emissions (including UHC, CO and NO{sub x}) and performance. The concurrent development of suitable analytical and numerical models that are validated with experimental studies is important for achieving this objective. A major benefit of the present research will be to provide for the first time an experimentally verified model of emissions and performance of gas turbine combustors.
Performance of Concurrent Tasks: A Psychophysiological Analysis of the Reciprocity of Information-Processing Resources (1983)

The resources allocated to a primary and secondary task are reciprocal. Subjects performed a tracking task in which the discrete displacements of the tracking cursor could be used to elicit event-related brain potentials. As the resource demands of the tracking task were increased, potentials elicited by the task-defined events increased in amplitude, whereas those elicited by secondary task auditory stimuli decreased.
Arginine-Ornithine Antiporter ArcD Controls Arginine Metabolism and Interspecies Biofilm Development of Streptococcus gordonii (2015)

Arginine is utilized by the oral inhabitant Streptococcus gordonii as a substrate of the arginine deiminase system (ADS), eventually producing ATP and NH3, the latter of which is responsible for microbial resistance to pH stress. S. gordonii expresses a putative arginine-ornithine antiporter (ArcD) whose function has not been investigated despite relevance to the ADS and potential influence on inter-bacterial communication with periodontal pathogens that utilize amino acids as a main energy source. Here, we generated an S. gordonii ΔarcD mutant to explore the role of ArcD in physiological homeostasis and bacterial cross-feeding. First, we confirmed that S. gordonii ArcD plays crucial roles for mediating arginine uptake and promoting bacterial growth, particularly under arginine-limited conditions. Next, metabolomic profiling and transcriptional analysis of the ΔarcD mutant revealed that deletion of this gene caused intracellular accumulation of ornithine leading to malfunction of the ADS and suppression of de novo arginine biosynthesis. The mutant strain also showed increased susceptibility to low pH stress due to reduced production of ammonia. Finally, accumulation of Fusobacterium nucleatum was found to be significantly decreased in biofilm formed by the ΔarcD mutant as compared with the wild-type strain, although ornithine supplementation restored fusobacterium biovolume in dual-species biofilms with the ΔarcD mutant and also enhanced single species biofilm development by F. nucleatum. Our results are the first direct evidence showing that S. gordonii ArcD modulates not only alkali and energy production but also interspecies interaction with F. nucleatum, thus initiating a middle stage of periodontopathic biofilm formation, by metabolic cross-feeding.
Non-Enzymatic RNA Hydrolysis Promoted by the Combined Catalytic Activity of Buffers and Magnesium Ions (1999)

Although Mg2+ is an important cofactor for the specific degradation of RNA by ribozymes, it is not considered as a typical chemical nuclease. In this study we show that in combination with common buffers such as tris(hydroxymethyl)aminomethane and sodium borate, Mg2+ is a powerful catalyst for the degradation of RNA. pH and temperature are found to be the principal factors for the efficient degradation of RNA. Whereas in Tris-HCl/Mg2+ the efficient cleavage starts at pH values higher than 7.5 and temperatures higher than 37 degrees C, in sodium borate RNA degradation begins at pH 7.0 and at 37 degrees C. RNA hydrolysis promoted under the combined catalytic activity of buffer/Mg2+ results in partially degraded RNA and negligible amounts of acid-soluble material. Reaction is insensitive to the concentration of monovalent cations but is completely prevented by chelating agents (EDTA and citrate) at concentrations exceeding that of Mg2+. Borate-magnesium reaction is inhibited also by some polyvalent alcohols (glycerol) and sugars.
Do senescence markers correlate in vitro and in situ within individual human donors? (2018)

Little is known on how well senescence markers <i>in vitro</i> and <i>in situ</i> correlate within individual donors. We studied correlations between the same and different <i>in vitro</i> markers. Furthermore, we tested correlations between <i>in vitro</i> markers with <i>in situ</i> p16INK4a positivity.From 100 donors (20-91 years), cultured dermal fibroblasts were assessed for reactive oxygen species (ROS), telomere-associated foci (TAF), p16INK4a and senescence-associated β-gal (SAβ-gal), with/ without 0.6 µM rotenone for 3 days (short-term). In fibroblasts from 40 donors, telomere shortening, ROS and SAβ-gal were additionally assessed, with/ without 20 nM rotenone for 7 weeks (long-term). In skin from 52 donors, the number of p16INK4a positive dermal cells was assessed <i>in situ</i>.More than half of the correlations of the same senescence markers <i>in vitro</i> between duplicate experiments and between short-term versus long-term experiments were significant. Half of the different senescence marker correlations were significant within the short-term and within the long-term experiments. The different senescence markers <i>in vitro</i> were not significantly correlated intra-individually with <i>in situ</i> p16INK4a positivity. In conclusion, the same and different senescence markers are frequently correlated significantly within and between <i>in vitro</i> experiments, but <i>in vitro</i> senescence markers are not correlated with p16INK4a positivity <i>in situ</i>.
Improved diagnosis of primary Toxoplasma gondii infection in early pregnancy by determination of antitoxoplasma immunoglobulin G avidity (1997)

The ability to discriminate between primary Toxoplasma gondii infection acquired in early pregnancy and infection that occurred prior to pregnancy was assessed by an enzyme immunoassay (EIA) to determine the avidity of toxoplasma-specific immunoglobulin G (IgG). The results were compared to those of the Platelia Toxo-IgM EIA and the dye test. The mean IgG avidity of 73 serum samples collected within 20 weeks after the estimated time of infection was 5.9%. Among 26 serum samples showing latent infection (toxoplasma-specific IgG positive and IgM negative) and 56 IgM-positive serum samples with a low dye test titer (<300 IU/ml), the mean avidities were 51.3 and 57.5%, respectively. A total of 72.8% of 92 IgM-positive serum samples with a high dye test titer (>300 IU/ml), suggesting a recent toxoplasma infection, had an IgG avidity of >20%, indicating that the infection started more than 20 weeks earlier. By introducing high IgG avidity as a criterion in the first half of pregnancy to exclude the possibility that toxoplasma infection was acquired during gestation, many women will avoid unnecessary examinations, treatment, and anxiety.
Stereotactic Transcranial Magnetic Stimulation: Correlation with Direct Electrical Cortical Stimulation (1997)

Our findings indicate that stereotactic TMS is feasible and can provide accurate noninvasive localization of cortical motor function. It may prove to be a useful method for presurgical planning.
4-Hydroxylation of estrogens as marker of human mammary tumors. (1996)

Estrogen is a known risk factor in human breast cancer. In rodent models, estradiol has been shown to induce tumors in those tissues in which this hormone is predominantly converted to the catechol metabolite 4-hydroxyestradiol by a specific 4-hydroxylase enzyme, whereas tumors fail to develop in organs in which 2-hydroxylation predominates. We have now found that microsomes prepared from human mammary adenocarcinoma and fibroadenoma predominantly catalyze the metabolic 4-hydroxylation of estradiol (ratios of 4-hydroxyestradiol/2-hydroxyestradiol formation in adenocarcinoma and fibroadenoma, 3.8 and 3.7, respectively). In contrast, microsomes from normal tissue obtained either from breast cancer patients or from reduction mammoplasty operations expressed comparable estradiol 2- and 4-hydroxylase activities (corresponding ratios, 1.3 and 0.7, respectively). An elevated ratio of 4-/2-hydroxyestradiol formation in neoplastic mammary tissue may therefore provide a useful marker of benign or malignant breast tumors and may indicate a mechanistic role of 4-hydroxyestradiol in tumor development.
Polarized hydroxyapatite promotes spread and motility of osteoblastic cells (2009)

Osteoblast adhesion to surfaces of implant substrates is recognized as playing a fundamental role in the process of osteoconduction. The purpose of this study was to evaluate the in vitro adhesion of osteoblasts cultured on polarized hydroxyapatite (HA), which provides two kinds of surfaces; negatively charged HA (N-HA) and positively charged HA (P-HA). Those surfaces have been proved to enhance the osteobonding capabilities. Osteoblastic cells were seeded onto normal and polarized HA; adhesion and motility of each was observed. Polarization did not affect the percentage of the spread cells against all the adhered cells, but had a significant effect on the spreading of each cell as shown by the measured elongation of the adhered cells by fluorescence observation. The elongation of each cell was especially enhanced on the N-HA and P-HA, when compared with normal HA (O-HA). In addition, the polarization affected cell motility shown by wound healing. Motility analysis showed that the same number of cells started to migrate toward the wound areas on each type of surface. However, the migration of each cell type towards the wound area was accelerated on the N-HA and P-HA. The charges induced on the HA surface accelerated the cytoskeleton reorganization of the adhered cells. The acceleration was appeared as cell shape, actin filament pattern such as stress fiber formation, and prolongation of cell motility distance.
Recombinant C1 inhibitor P5/P3 variants display resistance to catalytic inactivation by stimulated neutrophils. (1993)

Proteolytic inactivation of serine protease inhibitors (serpins) by neutrophil elastase (HNE) is presumed to contribute to the deregulation of plasma cascade systems in septic shock. Here, we report a supplementary approach to construct serpins, in our case C1 inhibitor, that are resistant to catalytic inactivation by HNE. Instead of shifting the specificity of alpha 1-antitrypsin towards the proteases of the contact activation and complement systems, we attempted to obtain a C1 inhibitor species which resists proteolytic inactivation by HNE. 12 recombinant C1 inhibitor variants were produced with mainly conservative substitutions at the cleavage sites for HNE, 440-Ile and/or 442-Val. Three variants significantly resisted proteolytic inactivation, both by purified HNE, as well as by activated neutrophils. The increase in functional half-life in the presence of FMLP-stimulated cells was found to be 18-fold for the 440-Leu/442-Ala variant. Inhibitory function of these variants was relatively unimpaired, as examined by the formation of stable complexes with C1s, beta-Factor XIIa, kallikrein, and plasmin, and as determined by kinetic analysis. The calculated association rate constants (k(on)) were reduced twofold at most for C1s, and appeared unaffected for beta-Factor XIIa. The effect on the k(on) with kallikrein was more pronounced, ranging from a significant ninefold reduction to an unmodified rate. The results show that the reactive centre loop of C1 inhibitor can be modified towards decreased sensitivity for nontarget proteases without loss of specificity for target proteases. We conclude that this approach extends the possibilities of applying recombinant serpin variants for therapeutic use in inflammatory diseases.
Collagenases in human synovial fluid (1969)

An enzyme which degrades native collagen at neutral pH has been isolated from cultures of rheumatoid synovium in vitro, but little or no collagenolytic activity has been found in homogenates of fresh rheumatoid synovium. Similar to most other mammalian collagenases this synovial enzyme is readily inhibited by serum proteins. Proteins of synovial fluid are derived largely from serum and synovial fluid from noninflamed joints was found to inhibit synovial collagenase; the inhibitor was destroyed by trypsin, but not by hyaluronidase. Inhibitory activity was reduced in approximately one-half of the fluids from patients with rheumatoid arthritis. In a total of nine synovial fluids, collagenolytic activity was detectable. This activity was not present in constant amounts in synovial fluids aspirated at different times from the same patient and tended to vary inversely with the titer of inhibitory proteins. The collagenolytic activity in the synovial fluids from different patients was variably inhibited by serum proteins. Two distinct collagenases were detected in some rheumatoid synovial fluids and separated by gel filtration. One, labeled "B" enzyme, with an estimated molecular weight 20,000-25,000 resembled the collagenase obtained from synovial cultures. The other, labeled "A" enzyme degraded collagen fibrils as well as collagen in solution. Disc electrophoresis on acrylamide gels and electron microscopy of segment long spacing (SLS) aggregates of reaction products of the enzymes at 27 degrees C demonstrated that both "A" and "B" enzymes cleaved collagen molecules at a point three-quarters from the amino terminal end of the molecule. Thus collagen degradation in rheumatoid arthritis could result from the operation of these two collagenases.
Preclinical Effects of Opioid Antagonists on Feeding and Appetite (2009)

A large component of the evidence linking the endogenous opioid system to the control of food intake and body weight has been derived from the ability of general and selective opioid antagonists to block food intake under a number of homeostatically mediated and reward-mediated conditions. This chapter will examine the role of general and specific opioid receptor subtype antagonist involvement in the mediation of (1) the palatable and hedonic aspects of food intake and food choice, including ingestion of simple sugars and fats; (2) the ingestive response to homeostatic regulatory challenges including food deprivation, glucoprivation, and lipoprivation; (3) body weight regulation in normophagic, genetically-obese, diet-obese and stressed animals; and (4) pharmacologically-induced feeding. Detailed description of the central sites of antagonist will be provided, as well as comparing opioid antagonist effects with those derived from molecular gene expression and knockout and knockdown (antisense) approaches. The pervasive effects of opioid antagonists on the different aspects of feeding behavior make the development of more selective antagonist peptide analogues and drugs attractive target systems for the treatment of obesity and diabetes and intake of macronutrients associated with these important dysfunctions.
Endothelin-1 and vasculitis. (1990)

To the Editor.— Endothelin-1 is a novel 21-residue vasoconstrictor peptide produced by vascular endothelial cells. 1 It may play important roles in the pathogenesis of hypertension 2 and has been shown recently to be a potent mitogen for vascular smooth-muscle cells. 3 Although the causes of atherosclerosis, Buerger's disease, and Takayasu's arteritis remain elusive, the vascular lesions represented by injured vascular endothelial cells associated with abnormal proliferation of the underlying vascular smooth muscle are pathological features in common among these entities. To elucidate its pathophysiological role in the development of systemic vascular diseases, we have measured basal plasma levels of immunoreactive endothelin-1 in patients with atherosclerosis, Buerger's disease, and Takayasu's arteritis. Study.— Thirty-five normal subjects (16 men and 19 women, aged 53.9 [ ± 16.3] years), 13 patients with ischemic heart disease (11 men and two women, aged 55.8 [ ± 7.0] years), 13 male patients with Buerger's disease (aged 53.8 [ ±
Scanning field emission from patterned carbon nanotube films (2000)

The investigation of the field emission (FE) properties of carbon nanotube (CNT) films by a scanning anode FE apparatus, reveals a strong dependence on the density and morphology of the CNT deposit. Large differences between the microscopic and macroscopic current and emission site densities are observed, and explained in terms of a variation of the field enhancement factor β. As a consequence, the emitted current density can be optimized by tuning the density of CNTs. Films with medium densities (on the order of 107 emitters/cm2, according to electrostatic calculations) show the highest emitted current densities.
Tissue distribution of ACE2 protein, the functional receptor for SARS coronavirus. A first step in understanding SARS pathogenesis (2004)

Severe acute respiratory syndrome (SARS) is an acute infectious disease that spreads mainly via the respiratory route. A distinct coronavirus (SARS-CoV) has been identified as the aetiological agent of SARS. Recently, a metallopeptidase named angiotensin-converting enzyme 2 (ACE2) has been identified as the functional receptor for SARS-CoV. Although ACE2 mRNA is known to be present in virtually all organs, its protein expression is largely unknown. Since identifying the possible route of infection has major implications for understanding the pathogenesis and future treatment strategies for SARS, the present study investigated the localization of ACE2 protein in various human organs (oral and nasal mucosa, nasopharynx, lung, stomach, small intestine, colon, skin, lymph nodes, thymus, bone marrow, spleen, liver, kidney, and brain). The most remarkable finding was the surface expression of ACE2 protein on lung alveolar epithelial cells and enterocytes of the small intestine. Furthermore, ACE2 was present in arterial and venous endothelial cells and arterial smooth muscle cells in all organs studied. In conclusion, ACE2 is abundantly present in humans in the epithelia of the lung and small intestine, which might provide possible routes of entry for the SARS-CoV. This epithelial expression, together with the presence of ACE2 in vascular endothelium, also provides a first step in understanding the pathogenesis of the main SARS disease manifestations.
Imaging of light emission from the expression of luciferases in living cells and organisms: a review (2002)

Luciferases are enzymes that emit light in the presence of oxygen and a substrate (luciferin) and which have been used for real-time, low-light imaging of gene expression in cell cultures, individual cells, whole organisms, and transgenic organisms. Such luciferin-luciferase systems include, among others, the bacterial lux genes of terrestrial Photorhabdus luminescens and marine Vibrio harveyi bacteria, as well as eukaryotic luciferase luc and ruc genes from firefly species (Photinus) and the sea pansy (Renilla reniformis), respectively. In various vectors and in fusion constructs with other gene products such as green fluorescence protein (GFP; from the jellyfish Aequorea), luciferases have served as reporters in a number of promoter search and targeted gene expression experiments over the last two decades. Luciferase imaging has also been used to trace bacterial and viral infection in vivo and to visualize the proliferation of tumour cells in animal models.
THE MOLECULAR STRUCTURE OF CELL ADHESION MOLECULES (1997)

Considerable advances have been made in our knowledge of the molecular structure of cell adhesion molecules, their binding sites, and adhesion complexes. For the cadherins, protein zero, and CD2, additional experimental data support the insights obtained from structural analysis of their domains and molecular models of their adhesion complexes. For neural cell adhesion molecules, L1, fibronectin, tenascin-C, integrins, and vascular cell adhesion molecules, the molecular structure of domains, and in most cases their binding sites, have been elucidated. The substrate recognition sites in some of these molecules possess rate constants for association and dissociation that permit both rapid cell migration and, through avidity, high-affinity cell-cell interactions.
Encoding Information Flow in Haskell (2006)

This paper presents an embedded security sublanguage for enforcing information-flow policies in the standard Haskell programming language. The sublanguage provides useful information-flow control mechanisms including dynamic security lattices, run-time code privileges and declassification, without modifying the base language. This design avoids the redundant work of producing new languages, lowers the threshold for adopting security-typed languages, and also provides great flexibility and modularity for using security-policy frameworks. The embedded security sublanguage is designed using a standard combinator interface called arrows. Computations constructed in the sublanguage have static and explicit control-flow components, making it possible to implement information-flow control using static-analysis techniques at run time, while providing strong security guarantees. This paper presents a concrete Haskell implementation and an example application demonstrating the proposed techniques