gebhart/patrepeval huggingface dataset:
Similitude For Thermal Scale-Up Of A Multiphase Thermolysis Reactor In The Cu-Cl Cycle Of A Hydrogen Production (2016)

The thermochemical copper-chlorine (Cu-Cl) cycle is considered as a sustainable and efficient technology for a hydrogen production, when linked with clean-energy systems such as nuclear reactors or solar thermal plants. In the Cu-Cl cycle, water is decomposed thermally into hydrogen and oxygen through a series of intermediate reactions. This paper investigates the thermal scale up analysis of the three phase oxygen production reactor in the Cu-Cl cycle, where the reaction is endothermic and the temperature is about 530 <sup>o</sup>C. The paper focuses on examining the size and number of oxygen reactors required to provide enough heat input for different rates of hydrogen production. The type of the multiphase reactor used in this paper is the continuous stirred tank reactor (CSTR) that is heated by a half pipe jacket. The thermal resistance of each section in the jacketed reactor system is studied to examine its effect on the heat balance of the reactor. It is found that the dominant contribution to the system thermal resistance is from the reactor wall. In the analysis, the Cu-Cl cycle is assumed to be driven by a nuclear reactor where two types of nuclear reactors are examined as the heat source to the oxygen reactor. These types are the CANDU Super Critical Water Reactor (CANDU-SCWR) and High Temperature Gas Reactor (HTGR). It is concluded that a better heat transfer rate has to be provided for CANDU-SCWR by 3-4 times than HTGR. The effect of the reactor aspect ratio is also examined in this paper and is found that increasing the aspect ratio decreases the number of reactors and the rate of decrease in the number of reactors decreases by increasing the aspect ratio. Finally, a comparison between the results of heat balance and existing results of mass balance is performed and is found that the size of the oxygen reactor is dominated by the heat balance rather than the material balance.
SLC7A11 expression is associated with seizures and predicts poor survival in patients with malignant glioma (2015)

Glioma is the most common malignant primary brain tumor. Its rapid growth is aided by tumor-mediated glutamate release, creating peritumoral excitotoxic cell death and vacating space for tumor expansion. Glioma glutamate release may also be responsible for seizures, which complicate the clinical course for many patients and are often the presenting symptom. A hypothesized glutamate release pathway is the cystine/glutamate transporter System xc (-) (SXC), responsible for the cellular synthesis of glutathione (GSH). However, the relationship of SXC-mediated glutamate release, seizures, and tumor growth remains unclear. Probing expression of SLC7A11/xCT, the catalytic subunit of SXC, in patient and mouse-propagated tissues, we found that ~50% of patient tumors have elevated SLC7A11 expression. Compared with tumors lacking this transporter, in vivo propagated and intracranially implanted SLC7A11-expressing tumors grew faster, produced pronounced peritumoral glutamate excitotoxicity, induced seizures, and shortened overall survival. In agreement with animal data, increased SLC7A11 expression predicted shorter patient survival according to genomic data in the REMBRANDT (National Institutes of Health Repository for Molecular Brain Neoplasia Data) database. In a clinical pilot study, we used magnetic resonance spectroscopy to determine SXC-mediated glutamate release by measuring acute changes in glutamate after administration of the U.S. Food and Drug Administration-approved SXC inhibitor, sulfasalazine (SAS). In nine glioma patients with biopsy-confirmed SXC expression, we found that expression positively correlates with glutamate release, which is acutely inhibited with oral SAS. These data suggest that SXC is the major pathway for glutamate release from gliomas and that SLC7A11 expression predicts accelerated growth and tumor-associated seizures.
Possible Roles of Partial Sequences at N- and C-termini of Amelogenin in Protein-Enamel Mineral Interaction (1989)

The purpose of this study was to assess the functional significance of homologous sequences of mammalian amelogenins at their N- and C-termini. A porcine 5-kDa fragment corresponding to the N-terminal 45 residues of amelogenins was purified from the secretory enamel. The decapeptide TDKTKREEVD corresponding to the C-terminal 10 residues of amelogenins was synthesized according to conventional solid-phase procedures. The inhibitory activity of both moieties on apatite crystal growth was determined in a supersaturated solution having an ionic composition similar to that of the fluid phase separated from porcine secretory enamel. The 5-kDa amelogenin fragment was sparingly soluble in neutral solutions and (in condensed forms because of aggregation) showed no significant inhibition of crystal growth, whereas the fragment molecules pre-adsorbed onto the seed crystals yielded modest inhibition of hydroxyapatite precipitation. However, their inhibitory activity was significantly lower than that of parent porcine amelogenin (25-kDa molecular mass). The high solubility of synthesized decapeptide allowed us to determine the adsorption isotherm onto hydroxyapatite at 37 degrees C, at an ionic strength similar to that of the enamel fluid. The obtained adsorption isotherm was described by a Langmuir model; the adsorption affinity and the maximum adsorption sites were 6.2 mL/mumol and 0.53 mumol/m2, respectively. As expected from the low adsorption affinity, the peptide showed a much weaker inhibition of apatite crystal growth than the parent amelogenin.(ABSTRACT TRUNCATED AT 250 WORDS)
Involvement of 5‐HT2A receptor and α2‐adrenoceptor blockade in the asenapine‐induced elevation of prefrontal cortical monoamine outflow (2012)

The psychotropic drug asenapine is approved for the treatment of schizophrenia and manic or mixed episodes associated with bipolar I disorder. Asenapine exhibits higher affinity for several 5-HT receptors and α(2)-adrenoceptors than for D(2) receptors. Noteworthy, blockage of both the 5-HT(2A) and α(2)-adrenergic receptors has been shown to enhance prefrontal dopamine release induced by D(2) receptor antagonists. Previous results show that asenapine, both systemically and locally, increases dopamine, noradrenaline, and serotonin release in the medial prefrontal cortex (mPFC), and that the increased dopamine release largely depends on an intracortical action. Using reverse microdialysis in freely moving rats, we here assessed the potency of low concentrations of asenapine to cause a pharmacologically significant blockage in vivo of 5-HT(2A) receptors and α(2)-adrenoceptors within the mPFC, and thus its ability to affect cortical monoamine release by these receptors. Intracortical administration of 1-(2,5-dimethoxy-4-iodophenyl)-2-aminopropane hydrochloride (DOI), a 5-HT(2A/2C) receptor agonist, increased cortical monoamine release, effects that were antagonized both by asenapine and the selective 5-HT(2A) antagonist M100907. Application of clonidine, an α(2)-adrenoceptor agonist, significantly reduced monoamine release in the mPFC. The selective α(2)-adrenoceptor antagonist idazoxan blocked, whereas asenapine partially blocked clonidine-induced cortical dopamine and noradrenaline decrease. The effects of asenapine and idazoxan on clonidine-induced serotonin decrease were less pronounced. Our results propose that low concentrations of asenapine in the mPFC exhibit a pharmacologically significant 5-HT(2A) and α(2) receptor antagonistic activity, which may contribute to enhance prefrontal monoamine release in vivo and, secondarily, its clinical effects in schizophrenia and bipolar disorder.
Engineering of Kuma030: A Gliadin Peptidase That Rapidly Degrades Immunogenic Gliadin Peptides in Gastric Conditions (2015)

Celiac disease is characterized by intestinal inflammation triggered by gliadin, a component of dietary gluten. Oral administration of proteases that can rapidly degrade gliadin in the gastric compartment has been proposed as a treatment for celiac disease; however, no protease has been shown to specifically reduce the immunogenic gliadin content, in gastric conditions, to below the threshold shown to be toxic for celiac patients. Here, we used the Rosetta Molecular Modeling Suite to redesign the active site of the acid-active gliadin endopeptidase KumaMax. The resulting protease, Kuma030, specifically recognizes tripeptide sequences that are found throughout the immunogenic regions of gliadin, as well as in homologous proteins in barley and rye. Indeed, treatment of gliadin with Kuma030 eliminates the ability of gliadin to stimulate a T cell response. Kuma030 is capable of degrading >99% of the immunogenic gliadin fraction in laboratory-simulated gastric digestions within physiologically relevant time frames, to a level below the toxic threshold for celiac patients, suggesting great potential for this enzyme as an oral therapeutic for celiac disease.
An Integrated Clinical-Genomics Approach Identifies a Candidate Multi-Analyte Blood Test for Serous Ovarian Carcinoma (2007)

Our data suggest that this assay combination warrants further investigation as a multi-analyte diagnostic test for serous ovarian adenocarcinoma.
Influence of Incision Location on Transmitter Loss, Healing, Survival, Growth, and Suture Retention of Juvenile Chinook Salmon (2011)

Abstract Fisheries research involving surgical implantation of transmitters necessitates the use of methods that minimize transmitter loss and fish mortality and optimize healing of the incision. We evaluated the effects of three incision locations on transmitter loss, healing, survival, growth, and suture retention in juvenile Chinook salmon Oncorhynchus tshawytscha . The three incision locations were (1) on the linea alba (LA incision), (2) adjacent and parallel to the LA (muscle‐cutting [MC] incision), and (3) extending from the LA towards the dorsum at a 45° angle, between the parallel lines of myomeres (muscle‐sparing [MS] incision). A Juvenile Salmon Acoustic Telemetry System acoustic transmitter (0.44 g in air) and a passive integrated transponder tag (0.10 g in air) were implanted into each fish (total N = 936 fish). The fish were held at 12°C or 20°C and were examined weekly for 98 d. The progression of healing among incision locations and the variability in transmitter loss made it difficult to identify one incision location as the best choice. The LA incisions had a much smaller wound extent (area of visible subepidermal tissue) than MC and MS incisions during the first 28 d of the study. In both temperature treatments, apposition of incisions through day 14 was better for LA incisions than for MC and MS incisions. However, MC and MS incisions were less likely than LA incisions to reopen over time and thus were less likely to allow transmitter loss through the incision.
Scale-Free Networks: A Decade and Beyond (2009)

For decades, we tacitly assumed that the components of such complex systems as the cell, the society, or the Internet are randomly wired together. In the past decade, an avalanche of research has shown that many real networks, independent of their age, function, and scope, converge to similar architectures, a universality that allowed researchers from different disciplines to embrace network theory as a common paradigm. The decade-old discovery of scale-free networks was one of those events that had helped catalyze the emergence of network science, a new research field with its distinct set of challenges and accomplishments.
DNA-Prot: Identification of DNA Binding Proteins from Protein Sequence Information using Random Forest (2009)

DNA-binding proteins (DNABPs) are important for various cellular processes, such as transcriptional regulation, recombination, replication, repair, and DNA modification. So far various bioinformatics and machine learning techniques have been applied for identification of DNA-binding proteins from protein structure. Only few methods are available for the identification of DNA binding proteins from protein sequence. In this work, we report a random forest method, DNA-Prot, to identify DNA binding proteins from protein sequence. Training was performed on the dataset containing 146 DNA-binding proteins and 250 non DNA-binding proteins. The algorithm was tested on the dataset containing 92 DNA-binding proteins and 100 non DNA-binding proteins. We obtained 80.31% accuracy from training and 84.37% accuracy from testing. Benchmarking analysis on the independent of 823 DNA-binding proteins and 823 non DNA-binding proteins shows that our approach can distinguish DNA-binding proteins from non DNA-binding proteins with more than 80% accuracy. We also compared our method with DNAbinder method on test dataset and two independent datasets. Comparable performance was observed from both methods on test dataset. In the benchmark dataset containing 823 DNA-binding proteins and 823 non DNA-binding proteins, we obtained significantly better performance from DNA-Prot with 81.83% accuracy whereas DNAbinder achieved only 61.42% accuracy using amino acid composition and 63.5% using PSSM profile. Similarly, DNA-Prot achieved better performance rate from the benchmark dataset containing 88 DNA-binding proteins and 233 non DNA-binding proteins. This result shows DNA-Prot can be efficiently used to identify DNA binding proteins from sequence information. The dataset and standalone version of DNA-Prot software can be obtained from http://www3.ntu.edu.sg/home/EPNSugan/index_files/dnaprot.htm.
Receptor‐mediated endocytosis and degradation of insulin‐like growth factor I and II in neonatal rat astrocytes (1992)

Receptor-mediated internalization and degradation of insulin-like growth factors, IGF-I and IGF-II, were studied in primary cultures of neonatal rat astrocytes. Surface-bound IGF-II was rapidly internalized, and 80% of cell-associated radioactivity was located intracellularly after 30 min. IGF-I was internalized at a slower rate, and only 40% of cell-associated radioactivity was inside the cell after 30 min. A pulse-chase experiment demonstrated that 55% and 70% of internalized IGF-I and IGF-II, respectively, was degraded to free amino acids after a 3-hr chase. Lysosomal and protease inhibitors had different effects on the binding, internalization, and processing of IGF-I and IGF-II. Inhibition of lysosomal acidification by chloroquine increased the amounts of surface-bound IGF-II and intracellular IGF-I and reduced the degradation of IGF-I. The chelating agent phenanthroline increased the surface binding of IGF-I and IGF-II and internalization of IGF-II and reduced the degradation of IGF-I and IGF-II. Finally, receptor-bound IGF-II on the cell surface was decreased with increasing cell density, whereas IGF-I binding was unaltered. Our data suggest that cell-surface expression of IGF-I receptors and IGF-II receptors is regulated by different mechanisms and that receptor-bound IGF-I and IGF-II are trafficked and processed by different intracellular pathways in neonatal rat astrocytes.
Hypothermia and cardiac arrest: the promise of intra-arrest cooling (2008)

Over the past several years, the implementation of therapeutic hypothermia has provided an exciting opportunity toward improving survival from out-of-hospital cardiac arrest. There are compelling data to support the prompt use of therapeutic hypothermia for initial survivors from out-of-hospital cardiac arrest, but animal data have suggested that initiation of therapeutic hypothermia during the intra-arrest period may significantly improve outcomes even further. In the first feasibility study in humans, Bruel and colleagues report on the implementation of this intra-arrest approach among patients suffering out-of-hospital cardiac arrest, an exciting prospect that is discussed in the present commentary.
Adoptive transfer of regulatory T cells promotes intestinal tumorigenesis and is associated with decreased NK cells and IL‐22 binding protein (2014)

High number of regulatory T cells (Tregs), both circulating and at the tumor site, often indicates a poor prognosis in CRC patient's possibly impairing natural killer (NK) cell function. To determine the role of Tregs in CRC development and their effects on NK cells, we created novel transgenic Rag-Apc mice that lack T cells and develop spontaneous intestinal tumors, and we adoptively transferred Tregs or transiently depleted NK cells during initial stages of tumorigenesis. In 6-weeks old Rag-Apc mice containing microscopic intestinal tumors adoptive transfer of Tregs or transient NK cell depletion dramatically associated with an increase in intestinal tumor multiplicity and tumor size, with significantly decreased survival rates. Importantly, Treg transfer increased small intestinal polyp formation up to 65% (P < 0.0005) and increased colon tumors multiplicities by 84% (P < 0.0001) with a significant decrease in NK cells as compared to control mice. Similarly, in NK depleted mice, colon tumor multiplicities increased up to 40% and small intestinal polyp formation up to 60% (P < 0.0001). Treg transfer or NK cell transient depletion markedly increased interleukin (IL)-22 systemically and the inflammatory signaling molecules P2X7R, and STAT3 in the tumors; and impaired production of the tumor suppressor interferon (IFN)-γ systemically. Notably, IL-22 binding protein (IL-22 BP) was associated with NKs and a significant decrease was seen at the tumor site in mice adoptively transferred with Tregs or depleted of NK cells. Our results suggest that adoptive transfer of Tregs aggressively promote intestinal tumorigenesis by decreasing NK cell number and activity by modulating IL-22 BP.
Fluorescence assay for phospholipid membrane asymmetry (1991)

Highly fluorescent 7-nitro-2,1,3-benzoxadiazol-4-yl-lipid (NBD-lipid) analogues are widely used to examine lipid transport and membrane structure. We have developed a method for chemically modifying NBD-labeled lipids in both artificial and biological membranes. This was achieved by treating fluorescently labeled membranes with dithionite (S2O4(-2)). When small unilamellar vesicles containing NBD-labeled phospholipids were reacted with dithionite, only the fluorescent lipid located on the outer leaflet of the vesicles' bilayer was reduced. Seven different NBD-lipid analogues, including a fluorescent sterol, were reduced by treatment with dithionite to nonfluorescent 7-amino-2,1,3-benzoxadiazol-4-yl-lipid derivatives. To assess the feasibility of using this reagent in biological systems, N-(7-nitro-2,1,3-benzoxadiazol-4-yl)dioleoylphosphatidylethanol ami ne was inserted into the outer leaflet of the plasma membrane of CHO-K1 cells. Subsequent incubation of these cells with a nontoxic concentration of dithionite resulted in the complete loss of fluorescence from the plasma membrane. In contrast, when cells were permitted to endocytose some of their fluorescently labeled plasma membrane and then treated with dithionite, fluorescence at the plasma membrane was eliminated, while intracellular labeling was not affected. These data suggest that dithionite reacts with NBD-labeled lipids in the outer leaflet of membrane bilayers, producing nonfluorescent derivatives. We demonstrate how reduction of NBD-lipids with dithionite can be used to prepare asymmetrically labeled liposomes and to measure transverse-membrane asymmetry in vesicles. This method should be useful in many biochemical investigations, including the measurement of phospholipid translocase activity.
Unsuitability of monoclonal antibodies to oncogene proteins for anti‐tumour drug‐targeting (1986)

Monoclonal antibodies (MAbs) to ras, sis, erb-B, src, myb and myc oncoproteins were evaluated for their potential to target anti-cancer drugs to malignant cells. Each antibody was tested for reactivity against both fixed and viable cultured human tumour cells by immunofluorescence, and all reacted against a variety of fixed tumour cell preparations. Reactions were also observed against fixed non-malignant cells. None, however, reacted significantly with viable cells. Two antibodies (against ras and myc proteins) were tested for their ability to localize to tumour xenografts in nude mice, and conjugates were constructed by linking these antibodies to methotrexate using human serum albumin as an intermediate carrier. Neither antibody localized to tumour in vivo, and the methotrexate conjugates were not significantly cytotoxic for tumour cells in vitro, in contrast to similar conjugates simultaneously prepared with a proven anti-tumour MAb (791T/36). It was concluded that currently available MAbs to oncogene proteins are not suitable vectors for targeting cytotoxic agents to tumour cells.
Data, data structures and models (2002)

In this paper travel surveys from Europe, America and Asia are compared.Besides descriptive statistics models are developed, which are based on the SEM-method respectively the MLMmethod.The models give information about the structures between the variables.Precondition for these analyses is the adaptation of the respective surveys.The adaptation consists of the preparation of a spatial, a household and a person file as well as of the harmonisation of the selected variables.
Mutational analysis of potato yellow mosaic geminivirus (1995)

Mutations have been inserted into the virion and complementary sense ORFs encoding proteins with M(r)s in excess of 9 kDa of both DNA A and DNA B of potato yellow mosaic geminivirus (PYMV). Wild-type and mutant monomeric clones were tested for their ability to replicate, produce PYMV-specific DNA, spread and cause symptoms in Nicotiana benthamiana plants following biolistic inoculation. Dimeric clones of the DNA A mutants were also investigated by agroinoculation of leaf discs. In contrast to N. benthamiana plants agroinoculated with PYMV DNA A, in which the wild-type DNA A component was capable of limited independent replication and spread, both excised DNA A and B components were required for DNA replication and symptom development in plants inoculated by the biolistic method. Mixtures of both genomic components were also infectious for potato plants following biolistic inoculation. Mutations in ORFs AL1, AL2, BR1 and BL1 resulted in clones incapable of infecting N. benthamiana plants. However, the AL2 mutation, but not the AL1 mutation, allowed viral DNA replication in leaf discs. Mutations to both the AR1 and AL3 ORFs produced clones which were infectious in plants but showed a considerable delay in the production of attenuated symptoms as compared to wild-type infections. Mutating the AL3 ORF dramatically reduced viral DNA replication in both whole plants and leaf discs. Mutations to the AL4 ORF produced clones which were as infectious for both N. benthamiana and potato plants as the wild-type clones. Our results are compared with those from mutagenesis studies on related bipartite geminiviruses.