gebhart/patrepeval huggingface dataset:
Homotaurine (3 aminopropanesulfonic acid; 3APS) protects from the convulsant and cytotoxic effect of systemically administered kainic acid (1982)

Pretreatment of rats with homotaurine (3 aminopropanesulfonic acid; 3APS), a synthetic gamma-aminobutyric acid (GABA) analog, protected from the convulsant and cytotoxic action of systemically injected kainic acid (KA). Wet dog shaking (WDS) behavior was significantly reduced. Taurine, an inhibitory non-GABA-mimetic amino acid, and muscimol (another direct GABA-agonist) reduced the number of seizures and lesions in the brain but were less effective than homotaurine. Progabide (a GABA-agonist) did not modify kainic acid effects. The neurotoxicity of kainic acid could have been due to repetitive convulsive activity. Activation of GABA-mediated inhibition is an effective, but not the determinant means of preventing KA-induced abnormalities.
Automatic feature extraction from spectrograms for acoustic-phonetic analysis (2003)

Proposes a new approach for automatic feature extraction from spectrograms, which is an essential component of acoustic-phonetic analysis in automatic continuous speech recognition. The method comprised four levels: segmentation, pattern classification, feature recognition and labelling, and a post-processor. There were three types of patterns: fuzzy, formant and silence. The extracted features included voice bar, stripes, cut-off and transitions of the first four formants. Some techniques are presented, such as two special distortion functions used in segmentation, and a peak-iterate function to detect the stripes feature. This software has been implemented as part of a speech knowledge interface, which was an expert system for speech analysis for speaker-independent, continuous speech recognition. It has been tested with a set of data chosen from a spectrogram database; the correct detection rate for most features was over 89%, and in some cases was as high as 98%.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
DNA import competence and mitochondrial genetics (2014)

To understand the mechanism(s) underlying mitochondrial competence for DNA uptake and to exploit these pathways for the development of in vivo models of gene therapy. Methods. DNA uptake into isolated mitochondria from plant or from mutant Saccharomyces cerevisiae defective for mitochondrial proteins and carriers, biochemical approaches and transfection of mammalian cells with DNA bound to mitochondriotropic liposomes. Results. Special focus on the inner membrane showed the involvement of isoforms of the adenine nucleotide translocator and the contribution of proteins controlling mitochondrial morphology in DNA uptake into yeast organelles. Transfection assays led to significant incorporation of a mitochondrial construct into mammalian cells and expression of a marker gene. Conclusions. The data imply that there are multiple mitochondrial DNA import pathways. On the other hand, preliminary results suggest that mitochondriotropic liposomes can deliver DNA to mitochondria in live mammalian cells.
Rupture of Multiple Parallel Molecular Bonds under Dynamic Loading (2000)

Biological adhesion often involves several pairs of specific receptor-ligand molecules. Using rate equations, we study theoretically the rupture of such multiple parallel bonds under dynamic loading assisted by thermal activation. For a simple generic type of cooperativity, both the rupture time and force exhibit several different scaling regimes. The dependence of the rupture force on the number of bonds is predicted to be either linear, like a square root, or logarithmic.
Energy Hypometabolism in Posterior Cingulate Cortex of Alzheimer's Patients: Superficial Laminar Cytochrome Oxidase Associated with Disease Duration (2001)

Among brain regions affected in Alzheimer's disease (AD), the posterior cingulate shows the earliest and largest decrement in energy metabolism. Positron emission tomography (PET) studies have shown that these decrements appear before the onset of memory deficits or other symptoms in persons at genetic risk for AD. This study compares in vivo imaging results and in situ postmortem analyses by examining the posterior cingulate (area 23) in 15 AD patients and 13 age-matched nondemented controls using quantitative cytochrome oxidase histochemistry as an intracellular measure of oxidative energy metabolic capacity. Each of the six layers of the posterior cingulate demonstrated a decline in cytochrome oxidase activity in AD relative to controls, whereas adjacent motor cortex showed no significant differences. This decrement did not appear to be mainly secondary to nonspecific decrement in mitochondrial enzymes, oxidative stress, cell loss, or histopathology. The cytochrome oxidase decrement was most severe in the superficial layer I (-39%), which demonstrated a correlation to disease duration. Covariance analyses suggest that superficial laminas undergo a functional uncoupling from the deeper layers of posterior cingulate cortex in AD, whereas no such effects are found in motor cortex or controls. These findings expand on previous results from PET studies by illuminating the layer-specific cytochrome oxidase contributions to energy hypometabolism. The findings suggest a decrement of cytochrome oxidase in posterior cingulate cortex, with progressive reduction within the superficial laminas linked to disease duration. Such decrement could contribute to some of the behavioral symptoms displayed by AD patients. This decrement appeared greater in women.
Adoptive cell therapy with tumor-infiltrating lymphocytes supported by checkpoint inhibition across multiple solid cancer types (2021)

NCT03296137, and EudraCT No. 2017-002323-25.
Electron Transport in Dye-Sensitized Solar Cells Based on ZnO Nanotubes: Evidence for Highly Efficient Charge Collection and Exceptionally Rapid Dynamics (2009)

Dye-sensitized solar cells based on ordered arrays of polycrystalline ZnO nanotubes, 64 mum in length, are shown to exhibit efficient electron collection over the entire photoanode array length. Electrochemical impedance spectroscopy, open-circuit photovoltage decay analysis, and incident-photon-to-current efficiency spectra are used to quantify charge transport and lifetimes. Despite the relatively thick photoanode, the charge extraction time is found to be faster than observed in traditional TiO(2) nanoparticle photoanodes. If the extraction dynamics are interpreted as diffusive, effective electron diffusion coefficients of up to 0.4 cm(2) s(-1) are obtained, making these pseudo-1D photoanodes the fastest reported for an operating DSC to date. Rapid electron collection is of practical significance because it should enable alternative redox shuttles, which display relatively fast electron-interception dynamics, to be employed without significant loss of photocurrent.
A common mechanism controls the life cycle and architecture of plants (1998)

The overall aerial architecture of flowering plants depends on a group of meristematic cells in the shoot apex. We demonstrate that the Arabidopsis TERMINAL FLOWER 1 gene has a unified effect on the rate of progression of the shoot apex through different developmental phases. In transgenic Arabidopsis plants which ectopically express TERMINAL FLOWER 1, both the vegetative and reproductive phases are greatly extended. As a consequence, these plants exhibit dramatic changes in their overall morphology, producing an enlarged vegetative rosette of leaves, followed by a highly branched inflorescence which eventually forms normal flowers. Activity of the floral meristem identity genes LEAFY and APETALA 1 is not directly inhibited by TERMINAL FLOWER 1, but their upregulation is markedly delayed compared to wild-type controls. These phenotypic and molecular effects complement those observed in the tfl1 mutant, where all phases are shortened. The results suggest that TERMINAL FLOWER 1 participates in a common mechanism underlying major shoot apical phase transitions, rather than there being unrelated mechanisms which regulate each specific transition during the life cycle.
An 18 kW solar array research facility for fault detection experiments (2016)

Monitoring utility-scale solar arrays was shown to minimize cost of maintenance and help optimize the performance of the array under various conditions. In this paper, we describe the design of an 18 kW experimental facility that consists of 104 panels fitted with smart monitoring devices. Each of these devices embeds sensors, wireless transceivers, and relays that enable continuous monitoring, fault detection, and real-time connection topology changes. The facility enables networked data exchanges via the use of wireless data sharing with servers, fusion and control centers, and mobile devices. Research planned at this stage includes developing machine learning methods for fault detection. Preliminary simulation results on fault detection using machine learning are given in this paper.
Lipopolysaccharide-driven Th2 Cytokine Production in Macrophages Is Regulated by Both MyD88 and TRAM (2009)

Gram-negative bacterial lipopolysaccharide (LPS) activates macrophages by interacting with Toll-like receptor 4 (TLR4) and triggers the production of various pro-inflammatory Th1 type (type 1) cytokines such as IFNgamma, TNFalpha, and IL8. Though some recent studies cited macrophages as potential sources for Th2 type (type 2) cytokines, little however is known about the intracellular events that lead to LPS-induced type 2 cytokines in macrophages. To understand the mechanisms by which LPS induces type 2 cytokine gene expression, macrophages were stimulated with LPS, and the expression of IL-4 and IL-5 genes were examined. LPS, acting through TLR4, activates both type 1 and type 2 cytokine production both in vitro and in vivo by using macrophages from C3H/HeJ or C3H/HeOuJ mice. Although the baseline level of both TNFalpha and IL-4 protein was very low, TNFalpha was released rapidly after stimulation (within 4 h); however, IL-4 was released after 48 h LPS stimulation in secreted form. Silencing of myeloid differentiation protein (MyD88) and TRIF-related adaptor molecule (TRAM), using small interfering RNA abolished IL-4 induction induced by LPS whereas silencing of TRAM has no effect on TNFalpha induction, thereby indicating that LPS-induced TNFalpha is MyD88-dependent but IL-4 is required both MyD88 and TRAM. These findings suggest a novel function of LPS and the signaling pathways in the induction of IL-4 gene expression.
A chromosomal gene required for killer plasmid expression, mating, and spore maturation in Saccharomyces cerevisiae. (1976)

"Killer" strains of Saccharomyces cerevisiae are those that harbor a double-stranded RNA plasmid and secrete a toxin that kills only strains not carrying this plasmid (sensitives). Two chromosomal genes (kex1 and kex2) are required for the secretion of toxin by plasmid-carrying strains. The kex2 gene, which maps at a site distinct from the mating-type locus, is also required for normal mating by alpha strains and meiotic sporulation in all strains. Strains that are alpha mating-type and kex2 fail to secrete the pheromone alpha-factor or to respond to the alpha-factor II pheromone which causes a morphological change, but they do respond to alpha-factor I which causes G1 arrest in alpha cells. Strains that are alpha mating-type and kex2 show no defect in mating; pheromone secretion, or response to alpha-factor. Diploids that are homozygous for the kex2 mutation, unlike wildtype or heterozygous diploids, fail to undergo sporulation, with the defect occurring in the final spore maturation stage. These same defects in the sexual cycle are present in all kex2 mutants independent of the presence of the "killer" plasmid.
Three‐dimensional myocardial scar characterization from the endocardium: Usefulness of endocardial unipolar electroanatomic mapping (2019)

Epicardial ablation may be required to eliminate ventricular tachycardia (VT) in patients with underlying structural heart disease. The decision to gain epicardial access is frequently based on the suspicion of an epicardial origin for the VT and/or presence of an arrhythmogenic substrate. Epicardial pathology and VT is frequently present in patients with nonischemic right and/or left cardiomyopathies even in the setting of modest or no endocardial bipolar voltage substrate. In this setting, unipolar voltage mapping from the endocardium serves to help identify midmyocardial and/or epicardial VT substrate. The additional value of endocardial unipolar mapping includes its usefulness to predict the clinical outcome after VT ablation, to determine the irreversibility of myocardial disease, and to guide endomyocardial biopsy procedures to specific areas of intramural scarring. In this review, we aim to provide a guide to the use of endocardial unipolar mapping and its appropriate interpretation in a variety of clinical situations.
Protein Kinase C-β and Oxygen Deprivation (2000)

Fibrin deposition is a salient feature of hypoxemic vasculature and results from induction of tissue factor. Such tissue factor expression in an oxygen deficient environment is driven by the transcription factor Early Growth Response (Egr)-1. Using homozygous null mice for the protein kinase C beta-isoform gene (PKCbeta null), PKCbeta is shown to be upstream of Egr-1 in this oxygen deprivation-mediated pathway for triggering procoagulant events. Whereas wild-type mice exposed to hypoxia (6%) displayed a robust increase in tissue factor transcripts and antigen, and vascular fibrin deposition, PKCbeta null animals showed a markedly blunted response. Consistent with a central role for Egr-1 in hypoxia-induced expression of tissue factor, PKCbeta null mice subjected to oxygen deprivation displayed at most a minor elevation in Egr-1 transcripts, antigen, and intensity of the gel shift band by electrophoretic mobility shift assay, compared with normoxic animals. These data firmly establish PKCbeta as a trigger for events leading to induction of Egr-1 and tissue factor under hypoxic conditions, and provide insight into a biologic cascade whereby oxygen deprivation recruits targets of PKCbeta and Egr-1, thereby amplifying the cellular response.
Anti-T antibody in malignant melanoma patients. Influence of response and survival following chemotherapy—changes in serum levels followingC parvum, BCG immunization (1980)

The level of anti-T antibodies directed towards the precursor T antigen of the MN blood group system was measured in the sera of 55 patients with disseminated melanoma, before and during chemoimmunotherapy. The anti-T titer was subnormal in patients before therapy; patients who responded to therapy had significantly higher titers than did nonresponders in sera taken before therapy, at regression/progression of disease, and during the last pulse of treatment. Higher pretreatment titers were associated with a significntly longer survival time. A single infusion of Corynebacterium parvum was given to 14 other melanoma patients and significant elevation of preimmunization titers was observed on days 14, 21, and 28 after infusion; Bacillus Calmette-Guerin, vaccination of 9 patients did not significantly alter the anti-T titer. The expression of the normally cryptic T antigen on melanoma cells would absorb naturally circulating anti-T antibodies. Less dense expression of T antigen on melanoma cells that were responsive to therapy, i.e., less "malignant," would explain the better prognosis for patients with higher titers. The increase in anti-T antibodies following administration of C parvum but not of BCG is of possible clinical relevance when C parvum is used as an immunotherapeutic agent.
KRAS-mutated non-small cell lung cancer cells are responsive to either co-treatment with erlotinib or gefitinib and histone deacetylase inhibitors or single treatment with lapatinib (2011)

The epidermal growth factor receptor (EGFR) tyrosine kinase inhibitors erlotinib and gefitinib provide significant clinical benefit for non-small cell lung cancer (NSCLC) patients whose tumors bear EGFR mutations/amplifications. However, anti-EGFR therapy is largely ineffective in NSCLC with activating KRAS mutations. In this study, we investigated the treatment efficacy of erlotinib and gefitinib in combination with the histone deacetylase inhibitors (HDACi) vorinostat and sodium butyrate in the KRAS-mutated NSCLC cell line A549. For comparison, we tested the combination of HDACi with the dual tyrosine kinase inhibitor lapatinib. A549 cells proved to be resistant to erlotinib and gefitinib, but could be sensitized by cotreatment with HDACi, as assessed by flow cytometric analyses of cell death and mitochondrial depolarization. In contrast, A549 cells were a priori responsive to lapatinib treatment, but responsiveness to lapatinib could not be enhanced by HDACi cotreatment. These divergent effects of the different combination regimens may be explained by dissimilar types of cell death induced by the treatments: The use of the pan-caspase inhibitor z-VAD-fmk in the cell death and mitochondrial depolarization assays as well as fluorescence microscopy analyses indicated that erlotinib or gefitinib combined with HDACi elicited apoptosis, whereas lapatinib treatment induced a non-apoptotic type of cell death. Our study suggests that both HDACi/EGFR inhibitor-combination treatment and lapatinib-single treatment may be effective options for the therapy of NSCLC with KRAS mutations.
Hepatitis C virus infection and non‐hodgkin lymphoma: Results of the NCI‐seer multi‐center case‐control study (2004)

Several studies have noted elevated hepatitis C virus (HCV) prevalence among patients with non-Hodgkin lymphoma (NHL), suggesting that HCV infection increases NHL risk through chronic immune stimulation. Population-based data from the U.S. are lacking. In a population-based case-control study of NHL in the United States, we identified HCV infection using an enzyme immunoassay, confirmed by recombinant immunoblot assay or HCV RNA detection. The association between HCV and NHL was assessed using logistic regression, adjusting for demographic factors, illicit drug use or medical history. Thirty-two of 813 (3.9%) NHL cases and 14 of 684 (2.1%) controls were HCV-infected [odds ratio (OR) 1.96, 95%CI 1.07-4.03]. For separate NHL subtypes, numbers were limited. Nonetheless, positive associations were noted for follicular (OR 2.46, 95%CI 1.01-5.81), marginal zone (3.99, 0-13.6) and mucosa-associated lymphoid tissue (2.04, 0-7.20) NHLs. For all NHLs combined, the HCV-NHL association changed little after adjustment for sex, age, race and study center (OR 1.89, 95%CI 1.00-4.00). HCV was common in controls who had injected drugs (40%) or used other illicit drugs (6.5%), but adjustment for drug use did not affect the HCV-NHL association (OR 1.87, 95%CI 0.95-4.10). Transfusion history was unrelated to HCV status, and adjustment for this exposure did not attenuate the HCV-NHL association (OR 2.15, 95%CI 1.12-4.76). Excluding 4 subjects with a history of hemodialysis or 3 subjects with organ transplants also did not affect the results. Our study demonstrates an association between HCV infection and NHL in the United States. HCV infection may be a cause of NHL.
The diffusion of oxygen and lactic acid through tissues (1928)

Abstract The diffusion of dissolved substances through cells and tissues is a determining factor in many vital processes. The slowness of diffusion on the scale of ordinary sensible objects gives to the unaided imagination an imperfect realisation of its speed and importance in systems of the dimensions of the living cell. The diffusion constant k is expressed in terms of the number of unit quantities of substance which diffuse per minute across an area of 1 sq. cm. in a gradient of concentration per cm. of 1 unit quantity per c. c. For aqueous solutions of ordinary substances k is usually of the order of 2 to 10 times 10-4. The diffusion constant is of the dimensions L2T-1, 2 in length, -1 in time. Expressing it in units of 1μ (0·0001 cm.) instead of 1 cm., and of 1σ (0·001 sec.) instead of minutes, k is of the order of unity, instead of multiple of 10-4. Thus the diffusion constant is a fairly large quantity for systems involving distances of the order of 1μ and times of the order of 1σ. A cylinder 1 cm. in diameter composed of material similar to frog's nerve, if suddenly placed in oxygen, would take 185 minutes to attain 90 per cent. of is full saturation with that gas. An actual nerve 0·7 mm. thick would take 54 seconds for the same stage of saturation to be reached. A single nerve fiber 7μ thick would take only 5·4 σ. Again, the rapidity of diffusion attainable in systems of small dimensions is the basis of the capillary circulation, and therewith of the whole design of the larger animals; and the rate at which diffusion an supply oxygen to a fatigued muscle for the removal of lactic acid is an important factor in determining the speed at which recovery can occur.
Enhanced Chemical Ordering and Coercivity in FePt Alloy Nanoparticles by Sb‐Doping (2005)

Sb doping stabilizes the chemically ordered tetragonal L10 structure in FePt alloy nanoparticles, yielding higher coercivities (Hc) at lower annealing temperatures (see Figure) than previously reported. Upon annealing to ∼ 300 °C, nanoparticles yield coercivities more than ten times those previously reported for FePt nanoparticles of similar sizes annealed to the same temperature. These findings are of importance for ultrahigh-density memory device applications.
Comparative studies of the serum half-life extension of a protein via site-specific conjugation to a species-matched or -mismatched albumin (2018)

Human serum albumin (HSA) has been investigated as a serum half-life extender of therapeutic proteins thanks to its unusually long serum half-life. However, in mice, the serum half-life of a HSA-conjugated protein was much shorter than that of HSA in humans, likely due to the species-dependent nature of albumin-FcRn interactions. Herein, we investigated species-dependent albumin-FcRn interactions using species-matched albumin (mouse serum albumin) and species-mismatched albumin (HSA) in non-transgenic mice. We site-specifically introduced a clickable non-natural amino acid to a target protein followed by conjugation to an albumin species via a hetero-bifunctional linker. Using in vitro binding assays, we showed that both HSA- and MSA-conjugated proteins bound mouse FcRns. Conjugation of HSA led to very limited extension of the serum half-life of sfGFP in mice (16.3 h), compared to that of HSA in transgenic mice harboring an allele of mouse FcRn knock-out and expressing humn FcRn (67 h) reported previously. These results suggest that the FcRn-mediated recycling of HSA is not effective in mice. However, conjugation of mouse serum albumin (MSA) resulted in a serum half-life of sfGFP (27.7 h) comparable to that of MSA in mice (28.8 h). Altogether, our study supported that albumin-FcRn interactions are species dependent in vivo.