gebhart/patrepeval huggingface dataset:
Corneal endothelial wound closure in vitro. Effects of EGF and/or indomethacin. (1989)

In response to stress, the corneal endothelium must maintain or region its barrier function. To study cellular responses of the corneal endothelium, our laboratory has developed an in vitro model of rabbit corneal endothelial wound closure. When cells are free to divide, a 3 mm diameter wound closes within 4 days. 5-fluorouracil added to these cultures does not affect the cellular morphology or ultrastructure, but does inhibit cell division. In the presence of 5-fluorouracil, wounds close in approximately 7 days. These conditions mimic the amitotic state and general behavior of adult human corneal endothelium in vivo. Using this model, we studied the effects of epidermal growth factor (EGF) and/or indomethacin treatment on corneal endothelial wound closure in mitotically competent and inhibited cultures. EGF appeared to stimulate migration, whereas indomethacin appeared to enhance cell spreading in response to wounding, particularly in mitotically inhibited cultures. Treatment with the above agents at the time of wounding had little effect on wound closure rates, but did affect closure patterns. In contrast, pretreatment of cultures, particularly with indomethacin, significantly accelerated closure in mitotically inhibited cultures. In the presence of indomethacin, wounds closed in 3-4 days compared to 7-8 days for controls. These results indicate that the response of corneal endothelial cells to wounding can be pharmacologically manipulated, and perhaps accelerated, and suggest that the treatment of the endothelium with nonsteroidal anti-inflammatory drugs or EGF-like growth factors may be clinically useful.
Learning Programs: A Hierarchical Bayesian Approach (2010)

We are interested in learning programs for multiple related tasks given only a few training examples per task. Since the program for a single task is underdetermined by its data, we introduce a nonparametric hierarchical Bayesian prior over programs which shares statistical strength across multiple tasks. The key challenge is to parametrize this multi-task sharing. For this, we introduce a new representation of programs based on combinatory logic and provide an MCMC algorithm that can perform safe program transformations on this representation to reveal shared inter-program substructures. 1.
A survey of recent research in image database management (2002)

Research in the area of image database management is surveyed. Results with publication dates of 1984-1990 are covered. The impact of technologies such as optical disk storage, digital video, and high-speed local area networks is explored. Programming paradigms, such as object-oriented programming, rule-based systems, and constraint-based methodologies, are discussed. Research in some of the core areas of image database management is surveyed, and an overview is given of some systems. Conclusions based on the survey are given.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
1,8-Naphthalimides in Phosphorescent Organic LEDs:  The Interplay between Dopant, Exciplex, and Host Emission (2002)

Four different 1,8-naphthalimide derivatives were examined in phosphorescent organic light emitting diodes (OLEDs), i.e., 1,8-naphthalimide, N-phenyl-1,8-naphthalimide, N-2,6-dibromophenyl-1,8-naphthalimide (niBr), and bis-N,N-1,8-naphthalimide. Photoluminescence from all four naphthalimides have violet-blue fluorescence and phosphorescent bands between 550 and 650 nm (visible at 77 K). While all four compounds gave good glassy films when doped with a phosphorescent dopant, only the niBr films remained glassy for extended periods. OLED studies focused on niBr, with two different architectures. One OLED structure (type 1) had the niBr layer as a doped luminescent layer and an undoped niBr layer to act as a hole-blocking layer. The alternate structure (type 2) utilizes a doped CBP layer as the luminescent layer and the niBr layer is used as a hole-blocking layer only (CBP = 4,4'-N,N'-dicarbazolylbiphenyl). Type 1 and 2 OLEDs were prepared with green, yellow, and red emissive phosphorescent dopants (Irppy, btIr, and btpIr, respectively). The dopants were organometallic Ir complexes, previously shown to give highly efficient OLEDs. Of the three dopants, the btpIr-based OLEDs showed the best device performance in both structures (peak efficiencies for type 2: 3.2% and 2.3 lum/W at 6.3 V; type 1: 1.7% and 1.3 lm/W at 6.1 V). The green and yellow dopants gave very similar performance in both type 1 and 2 devices (peak efficiencies are 0.2-0.3%), which were significantly poorer than the btpIr-based OLEDs. The emission spectrum of the btIr- and btpIr-based devices (type 1 and 2) are the same as the solution photoluminescence spectrum of the dopant alone, while the Irppy device gives a broad red emission line (lambda(max) = 640 nm). The red Irppy.niBr emission line is assigned to an Irppy.niBr exciplex. The type 2 Irppy-based device gave a voltage-dependent spectrum, with the red emission observed at low bias (4-8 V), switching over to strong green emission as the bias was raised. All other devices showed bias-independent spectra. Estimates of HOMO, LUMO, and excited-state energies (dopant, niBr, and exciplex) were used to explain the observed spectral properties of these devices. btpIr-based devices emit efficiently from isolated dopant states (external efficiencies = 3.2 %, 2.3 lum/W). Irppy-based devices emit only from exciplex states, with low efficiency (external efficiency = 0.3%). btIr.niBr films have very similar energies for the dopant, exciplex, and niBr triplet states, such that relaxation can go through any of these states, leading to low device efficiency (external efficiency = 0.4%). High device efficiency is achieved only when dopant emission is the dominant pathway for relaxation, since exciplex and niBr triplet states give either weak or no electroluminescence.
Wide-band and gain-flattened hybrid fiber amplifier consisting of an EDFA and a multiwavelength pumped Raman amplifier (1999)

A wide-band and finely gain-flattened hybrid fiber amplifier is realized. The seamless 3.0-, 1.3-, and 1.0-dB bandwidths of 80, 76, and 69 nm with relative gain-flatness of 11.3%, 4.7%, and 3.7%, respectively, are achieved for the first time using the amplifier. The amplifier consists of an erbium-doped fiber amplifier, which has a short fluoride-based erbium-doped fiber, a discrete Raman amplifier, which has two isolated Raman fibers pumped simultaneously at three wavelengths, and a small-peak-loss gain-equalizer. The amplifier also yields optical noise figures under 6.0 dB.
Effects of Growth Regulators on the Induction of Anthocyanin Synthesis in Carrot Suspension Cultures (1986)

Journal Article Effects of Growth Regulators on the Induction of Anthocyanin Synthesis in Carrot Suspension Cultures Get access Yoshihiro Ozeki, Yoshihiro Ozeki Department of Botany, Faculty of Science, The University of TokyoHongo, Tokyo 113, Japan Search for other works by this author on: Oxford Academic Google Scholar Atsushi Komamine Atsushi Komamine Department of Botany, Faculty of Science, The University of TokyoHongo, Tokyo 113, Japan Search for other works by this author on: Oxford Academic Google Scholar Plant and Cell Physiology, Volume 27, Issue 7, October 1986, Pages 1361–1368, https://doi.org/10.1093/oxfordjournals.pcp.a077234 Published: 01 October 1986 Article history Received: 28 November 1985 Accepted: 23 July 1986 Published: 01 October 1986
Effect of menthol on cold receptor activity. Analysis of receptor processes. (1986)

The effect of menthol on the discharge pattern of feline nasal and lingual cold receptors was analyzed in order to elucidate the underlying sensory transducer mechanism. A repetitive beating activity and burst (grouped) discharges were observed in both cold receptor populations at constant temperatures and after rapid cooling. An analysis of the impulse activity revealed a cyclic pattern of impulse generation, which suggested the existence of an underlying receptor potential oscillation that initiates impulses in the afferent nerve when it exceeds a threshold value. The frequency and amplitude of the periodic impulse-inducing receptor processes were characterized by the burst frequency, which increased with warming, and by the average number of impulses generated during each cycle, which increased with cooling. Menthol at micromolar concentrations induced an acceleration of the burst frequency at higher temperatures, but reduced the burst frequency in the midtemperature range. At temperatures above 25 degrees C, menthol increased the number of impulses elicited during each cycle and induced bursting in previously repetitively discharging fibers. At low temperatures, menthol suppressed bursting and finally inhibited all cold receptor activity. The impulse pattern at constant temperatures and during the dynamic response to rapid cooling was comparably affected by menthol. Calcium application completely abolished the stimulating menthol effect. Since, in equal concentrations, menthol specifically impairs neuronal calcium currents, the results are consistent with the conjecture that in cold receptors, menthol reduces the activation of a calcium-stimulated outward current by an impeding effect on a calcium conductance, thereby inducing depolarization and a modification of bursting behavior. The data confirm the hypothesis of a calcium-controlled outward conductance being involved in the generation of cyclic afferent activity in cold receptors.
Characterization and Enrichment of Cardiomyocytes Derived From Human Embryonic Stem Cells (2002)

Cell replacement therapy is a promising approach for the treatment of cardiac diseases, but is challenged by a limited supply of appropriate cells. We have investigated whether functional cardiomyocytes can be efficiently generated from human embryonic stem (hES) cells. Cardiomyocyte differentiation was evaluated using 3 parent (H1, H7, and H9) hES cell lines and 2 clonal (H9.1 and H9.2) hES cell lines. All cell lines examined differentiated into cardiomyocytes, even after long-term culture (50 passages or approximately 260 population doublings). Upon differentiation, beating cells were observed after one week in differentiation conditions, increased in numbers with time, and could retain contractility for over 70 days. The beating cells expressed markers characteristic of cardiomyocytes, such as cardiac alpha-myosin heavy chain, cardiac troponin I and T, atrial natriuretic factor, and cardiac transcription factors GATA-4, Nkx2.5, and MEF-2. In addition, cardiomyocyte differentiation could be enhanced by treatment of cells with 5-aza-2'-deoxycytidine but not DMSO or retinoic acid. Furthermore, the differentiated cultures could be dissociated and enriched by Percoll density centrifugation to give a population containing 70% cardiomyocytes. The enriched population was proliferative and showed appropriate expression of cardiomyocyte markers. The extended replicative capacity of hES cells and the ability to differentiate and enrich for functional human cardiomyocytes warrant further development of these cells for clinical application in heart diseases.
Morphological Basis of Long-Term Habituation and Sensitization in Aplysia (1983)

The morphological basis of the persistent synaptic plasticity that underlies long-term habituation and sensitization of the gill withdrawal reflex in Aplysia californica was explored by examining the fine structure of sensory neuron presynaptic terminals (the critical site of plasticity for the short-term forms of both types of learning) in control animals and in animals whose behavior had been modified by training. The number, size, and vesicle complement of sensory neuron active zones were larger in animals showing long-term sensitization than in control animals and smaller in animals showing long-term habituation. These changes are likely to represent an anatomical substrate for the memory consolidation of these tasks.
Polymorphisms in the promoter region of the neutrophil elastase gene are associated with lung cancer development. (2002)

Neutrophil elastase (NE) is a powerful serine protease capable of degrading most protein components of the extracellular matrix. We hypothesize that this elastase may play a significant role in lung cancer development and tested our hypothesis in a study of 348 primary lung cancer cases and 299 controls. Analysis of the entire gene using denaturing high performance liquid chromatography identified two novel single nucleotide polymorphisms (SNPs) in the promoter region: -903 T or G (REP-a) and -741 G or A (REP-b). Allele frequencies of these two SNPs were compared between the cases and controls using chi(2) statistics. The estimated relative risk in association with the TT at REP-a or the GG at REP-b was measured by odds ratio. Individuals with -903TT or -741GG allele had a 2.3 and 1.4 times higher risk of developing lung cancer than those with TG or AA+AG alleles, respectively. The relative risk for the combined effects of both high-risk alleles at REP-a and REP-b, i.e., TT-GG type, was 24.8. Functional association of the two markers with cancer risk was examined by luciferase activity of the promoter containing different SNPs. We demonstrated a 1.9-fold relative luciferase activity in the promoter construct with -903T/-741G (T-G) compared with the -903G/-741A (G-A) in A549 human non-small cell lung cancer cells, providing evidence that the TT-GG type correlates with a high NE level. In conclusion, our findings support an etiological role of NE in lung cancer development.
In Vitro Degradation of Trimethylene Carbonate Based (Co)polymers (2002)

Abstract Trimethylene carbonate (TMC) was copolymerized with D , L ‐lactide (DLLA) or with ε ‐caprolactone (CL), and the degradation of melt‐pressed solid copolymer films in phosphate‐buffered saline at pH 7.4 and 37 °C was followed for a period of over two years. The parent homopolymers were used as reference materials. The degradation profile of TMC‐DLLA‐ and TMC‐CL based copolymers was similar and was best described by autocatalyzed bulk hydrolysis, preferentially of ester bonds. The hydrolysis rates varied by two orders of magnitude, depending on polymer composition and physical characteristics under the degradation conditions. TMC‐DLLA copolymers degraded faster than the parent homopolymers. The copolymers lost their tensile strength in less than five months, after which mass loss occurred. Copolymers with 50 or 80 mol‐% of TMC underwent total degradation in eleven months. For TMC‐CL copolymers, a slow and gradual decrease in molecular weight and deterioration of the mechanical performance was observed. These copolymers maintained suitable mechanical properties for seventeen months or longer. Chain scission in the semicrystalline copolymers resulted in an increase in crystallinity. In comparison with the CL homopolymer, the introduction of a small amount of TMC (10 mol‐%) significantly reduced the increase in crystallinity during degradation. Poly(TMC) specimens were dimensionally stable and showed a negligible decrease in molecular weight. A 60% decrease in the initial tensile strength of the polymer samples was observed after two years. magnified image
Binding and Action of CEM-101, a New Fluoroketolide Antibiotic That Inhibits Protein Synthesis (2010)

We characterized the mechanism of action and the drug-binding site of a novel ketolide, CEM-101, which belongs to the latest class of macrolide antibiotics. CEM-101 shows high affinity for the ribosomes of Gram-negative (Escherichia coli) and Gram-positive (Staphylococcus aureus) bacteria. The ketolide shows high selectivity in its inhibitory action and readily interferes with synthesis of a reporter protein in the bacterial but not eukaryotic cell-free translation system. Binding of CEM-101 to its ribosomal target site was characterized biochemically and by X-ray crystallography. The X-ray structure of CEM-101 in complex with the E. coli ribosome shows that the drug binds in the major macrolide site in the upper part of the ribosomal exit tunnel. The lactone ring of the drug forms hydrophobic interactions with the walls of the tunnel, the desosamine sugar projects toward the peptidyl transferase center and interacts with the A2058/A2509 cleft, and the extended alkyl-aryl arm of the drug is oriented down the tunnel and makes contact with a base pair formed by A752 and U2609 of the 23S rRNA. The position of the CEM-101 alkyl-aryl extended arm differs from that reported for the side chain of the ketolide telithromycin complexed with either bacterial (Deinococcus radiodurans) or archaeal (Haloarcula marismortui) large ribosomal subunits but closely matches the position of the side chain of telithromycin complexed to the E. coli ribosome. A difference in the chemical structure of the side chain of CEM-101 in comparison with the side chain of telithromycin and the presence of the fluorine atom at position 2 of the lactone ring likely account for the superior activity of CEM-101. The results of chemical probing suggest that the orientation of the CEM-101 extended side chain observed in the E. coli ribosome closely resembles its placement in Staphylococcus aureus ribosomes and thus likely accurately reflects interaction of CEM-101 with the ribosomes of the pathogenic bacterial targets of the drug. Chemical probing further demonstrated weak binding of CEM-101, but not of erythromycin, to the ribosome dimethylated at A2058 by the action of Erm methyltransferase.
Molecular Biology of Pseudorabies Virus: Impact on Neurovirology and Veterinary Medicine (2005)

Pseudorabies virus (PRV) is a herpesvirus of swine, a member of the Alphaherpesvirinae subfamily, and the etiological agent of Aujeszky's disease. This review describes the contributions of PRV research to herpesvirus biology, neurobiology, and viral pathogenesis by focusing on (i) the molecular biology of PRV, (ii) model systems to study PRV pathogenesis and neurovirulence, (iii) PRV transsynaptic tracing of neuronal circuits, and (iv) veterinary aspects of pseudorabies disease. The structure of the enveloped infectious particle, the content of the viral DNA genome, and a step-by-step overview of the viral replication cycle are presented. PRV infection is initiated by binding to cellular receptors to allow penetration into the cell. After reaching the nucleus, the viral genome directs a regulated gene expression cascade that culminates with viral DNA replication and production of new virion constituents. Finally, progeny virions self-assemble and exit the host cells. Animal models and neuronal culture systems developed for the study of PRV pathogenesis and neurovirulence are discussed. PRV serves asa self-perpetuating transsynaptic tracer of neuronal circuitry, and we detail the original studies of PRV circuitry mapping, the biology underlying this application, and the development of the next generation of tracer viruses. The basic veterinary aspects of pseudorabies management and disease in swine are discussed. PRV infection progresses from acute infection of the respiratory epithelium to latent infection in the peripheral nervous system. Sporadic reactivation from latency can transmit PRV to new hosts. The successful management of PRV disease has relied on vaccination, prevention, and testing.
Identification of a Novel Function of the AlphavirusCapping Apparatus (2000)

Both genomic and subgenomic RNAs of the Alphavirus have m(7)G(5')ppp(5')N (cap0 structure) at their 5' end. Previously it has been shown that Alphavirus-specific nonstructural protein Nsp1 has guanine-7N-methyltransferase and guanylyltransferase activities needed in the synthesis of the cap structure. During normal cap synthesis the 5' gamma-phosphate of the nascent viral RNA chain is removed by a specific RNA 5'-triphosphatase before condensation with GMP, delivered by the guanylyltransferase. Using a novel RNA triphosphatase assay, we show here that nonstructural protein Nsp2 (799 amino acids) of Semliki Forest virus specifically cleaves the gamma,beta-triphosphate bond at the 5' end of RNA. The same activity was demonstrated for Nsp2 of Sindbis virus, as well as for the amino-terminal fragment of Semliki Forest virus Nsp2-N (residues 1-470). The carboxyl-terminal part of Semliki Forest virus Nsp2-C (residues 471-799) had no RNA triphosphatase activity. Replacement of Lys-192 by Asn in the nucleotide-binding site completely abolished RNA triphosphatase and nucleoside triphosphatase activities of Semliki Forest virus Nsp2 and Nsp2-N. Here we provide biochemical characterization of the newly found function of Nsp2 and discuss the unique properties of the entire Alphavirus-capping apparatus.
Physiologic Effects of Pyridoxalated-Hemoglobin-Polyethylene Glycol Conjugate Solution in Exchange Transfusion (1986)

MATSUSHITA, M.; IWASHITA, Y.*; IWASAKI, K.; OHKI, H.; NASU, M.; HORIUCHI, T.; CHEN, J. F.; GOLDCAMP, J.; MURABAYASHI, S.; HARASAKI, H.; MALCHESKY, P. S.; NOSÉ, Y. Author Information
Ionotropic and Metabotropic Receptors, Protein Kinase A, Protein Kinase C, and Src Contribute to C-Fiber-Induced ERK Activation and cAMP Response Element-Binding Protein Phosphorylation in Dorsal Horn Neurons, Leading to Central Sensitization (2004)

Molecular mechanisms underlying C-fiber stimulation-induced ERK (extracellular signal-regulated kinase) activation in dorsal horn neurons and its contribution to central sensitization have been investigated. In adult rat spinal slice preparations, activation of C-fiber primary afferents by a brief exposure of capsaicin produces an eightfold to 10-fold increase in ERK phosphorylation (pERK) in superficial dorsal horn neurons. The pERK induction is reduced by blockade of NMDA, AMPA/kainate, group I metabotropic glutamate receptor, neurokinin-1, and tyrosine receptor kinase receptors. The ERK activation produced by capsaicin is totally suppressed by inhibition of either protein kinase A (PKA) or PKC. PKA or PKC activators either alone or more effectively together induce pERK in superficial dorsal horn neurons. Inhibition of calcium calmodulin-dependent kinase (CaMK) has no effect, but pERK is reduced by inhibition of the tyrosine kinase Src. The induction of cAMP response element binding protein phosphorylation (pCREB) in spinal cord slices in response to C-fiber stimulation is suppressed by preventing ERK activation with the MAP kinase kinase inhibitor 2-(2-diamino-3-methoxyphenyl-4H-1-benzopyran-4-one (PD98059) and by PKA, PKC, and CaMK inhibitors. Similar signaling contributes to pERK induction after electrical stimulation of dorsal root C-fibers. Intraplantar injection of capsaicin in an intact animal increases expression of pCREB, c-Fos, and prodynorphin in the superficial dorsal horn, changes that are prevented by intrathecal injection of PD98059. Intrathecal PD98059 also attenuates capsaicin-induced secondary mechanical allodynia, a pain behavior reflecting hypersensitivity of dorsal horn neurons (central sensitization). We postulate that activation of ionotropic and metabotropic receptors by C-fiber nociceptor afferents activates ERK via both PKA and PKC, and that this contributes to central sensitization through post-translational and CREB-mediated transcriptional regulation in dorsal horn neurons.