gebhart/patrepeval huggingface dataset:
Altered subcellular location of an activated and tumour-associated epidermal growth factor receptor. (1995)

The epidermal growth factor (EGF) receptor is a membrane bound tyrosine kinase whose activity is initiated by ligand binding. The malignant brain tumour glioblastoma frequently shows amplification and rearrangements of the EGF receptor gene that are associated with the synthesis of a constitutively activated tyrosine kinase, lacking amino acids 6-273 near the protein's N-terminus. When expressed in Chinese hamster ovary (CHO) cells, this mutant receptor (p140EGFR) displays ligand-independent tyrosine kinase activity, stimulates DNA synthesis, and promotes cell proliferation. Here, we investigate the subcellular location of p140EGFR in CHO cell transfectants as well as in human glioblastoma tumours. p140EGFR had an intracellular location that contrasted sharply with the plasma membrane location of the wild-type EGF receptor. Endoglycosidase H sensitivity analysis and the pattern of p140EGFR immunoreactivity suggested that the aberrant tyrosine kinase resided primarily in the endoplasmic reticulum. The half-life of p140EGFR in the endoplasmic reticulum was extended several-fold over that of the ligand-activated wild-type receptor. The altered subcellular location of p140EGFR in combination with its prolonged half-life suggest that this activated tyrosine kinase may escape the regulatory mechanisms utilized for the attenuation of wild-type receptor signaling. Therefore, the previously reported growth stimulatory property of the ligand-independent p140EGFR may be attributed to a sustained tyrosine kinase activity resulting from an altered subcellular location.
DPSK vs. pilot-aided PSK MAP equalization for fast-fading channels (1999)

We extend our recent work in maximum a posteriori (MAP) equalization for frequency-selective fast-fading channels to the case of differentially encoded transmitted symbols. The equalizer employs an expanded trellis for the purpose of joint channel estimation and equalization. Channel estimation is performed using minimum mean square error techniques coupled with the hypothesis trellis of the MAP algorithm. Differential encoding avoids phase ambiguities associated with coherent detection of phase-shift keying (PSK) symbols. A MAP equalizer employed in an absolutely encoded PSK system avoids coherent detection, but requires additional pilot symbols in order to resolve the phase ambiguity. The pilot symbols result in lower power and bandwidth efficiencies. This paper concludes that a pilot-aided absolutely encoded binary PSK system has superior BER performance, even after the penalty in signal to noise ratio (SNR) has been take into account. However, at low SNR, the benefit in BER is not as significant, and higher pilot symbol rates are required. Thus DPSK is competitive only at low SNR.
Multiple signaling pathways induced by hexavalent, monospecific, anti-CD20 and hexavalent, bispecific, anti-CD20/CD22 humanized antibodies correlate with enhanced toxicity to B-cell lymphomas and leukemias (2010)

We have generated hexavalent antibodies (HexAbs) comprising 6 Fabs tethered to one Fc of human IgG1. Three such constructs, 20-20, a monospecific HexAb comprising 6 Fabs of veltuzumab (humanized anti-CD20 immunoglobulin G1κ [IgG1κ]), 20-22, a bispecific HexAb comprising veltuzumab and 4 Fabs of epratuzumab (humanized anti-CD22 IgG1κ), and 22-20, a bispecific HexAb comprising epratuzumab and 4 Fabs of veltuzumab, were previously shown to inhibit pro-liferation of several lymphoma cell lines at nanomolar concentrations in the absence of a crosslinking antibody. We now report an in-depth analysis of the apoptotic and survival signals induced by the 3 HexAbs in Burkitt lymphomas and provide in vitro cytotoxicity data for additional lymphoma cell lines and also chronic lymphocytic leukemia patient specimens. Among the key findings are the significant increase in the levels of phosphorylated p38 and phosphatase and tensin homolog deleted on chromosome 10 (PTEN) by all 3 HexAbs and the notable differences in the signaling events triggered by the HexAbs from those incurred by crosslinking veltuzumab or rituximab with a secondary antibody. Thus, the greatly enhanced direct toxicity of these HexAbs correlates with their ability to alter the basal expression of various intracellular proteins involved in regulating cell growth, survival, and apoptosis, with the net outcome leading to cell death.
The enhanced ethanol sensing properties of multi-walled carbon nanotubes/SnO2core/shell nanostructures (2006)

Multi-walled carbon nanotubes/SnO2 (CNT/SnO2) core/shell nanostructures were synthesized by a simple wet-chemical method. The thickness of the SnO2 shell was about 10 nm and the diameters of the SnO2 particles were 2–8 nm. Sensors based on the core/shell heterostructures exhibited enhanced ethanol sensing properties. The sensitivity to 50 ppm ethanol was up to 24.5, and the response time and recovery time were about 1 and 10 s, respectively. In addition, the fluctuation of the sensitivity was less than ± 3% on remeasurement after 3 months. These results indicate that the core/shell nanostructures are potentially new sensing materials for fabricating gas sensors.
Breathing space (2003)

Rose gallacher improved her knowledge of chronic obstructive pulmonary disease after reading a continuing professional development article
In vivo conversion of human HDL3 to HDL2 and apoE-rich HDL1 in the rat: effects of lipid transfer protein. (1987)

In this study we determined in vivo conversions of human 3H-labeled cholesteryl ester-labeled HDL3 [( 3H]CE-HDL3) in male rats and the effects of partially purified lipid transfer protein on the conversion processes. Zonal centrifugation techniques were used to prepare the [3H]CE-HDL3 and to follow the conversion processes. One hour after the injection, a complete conversion of HDL3 to the HDL2-density species was found. With time, [3H]CE separated with apoE-rich HDL1 and, by 18 hr, 35.9% of plasma radioactivity was associated with the apoE-rich HDL1 lipoprotein fraction. In vitro incubation of [3H]CE-HDL3 in rat plasma reproduced in part the HDL3----HDL2 conversion, but no movement of radioactivity to HDL1 was observed. Injection of the rats with partially purified lipid transfer proteins induced [3H]CE exchange between lipoproteins. The conversion of HDL3 to HDL2, however, was minimally affected. Formation of [3H]CE-HDL1, in contrast, was reduced to about one-half of that found in control animals. It is concluded that in vivo conditions are necessary for conversions of HDL3 (and HDL2) to HDL1, and that lipid transfer reactions delay this process.
Diastereomers of Cytolysins, a Novel Class of Potent Antibacterial Peptides (1996)

An amphipathic alpha-helical structure is considered to be a prerequisite for the lytic activity of most short linear cytolytic polypeptides that act on both mammalian cells and bacteria. This structure allows them also to exert diverse pathological and pharmacological effects, presumably by mimicking protein components that are involved in membrane-related events. In this study D-amino acid-incorporated analogues (diastereomers) of the cytolysin pardaxin, which is active against mammalian cells and bacteria, were synthesized and structurally and functionally characterized. We demonstrate that the diastereomers do not retain the alpha-helical structure, which in turn abolishes their cytotoxic effects on mammalian cells. However, they retain a high antibacterial activity, which is expressed in a complete lysis of the bacteria, as revealed by negative staining electron microscopy. The disruption of the alpha-helical structure should prevent the diastereomer analogues from permeating the bacterial wall by forming transmembrane pores but rather by dissolving the membrane as a detergent. These findings open the way for a new strategy in developing a novel class of highly potent antibacterial polypeptides for the treatment of infectious diseases, due to the increasing resistance of bacteria to the available antibacterial drugs.
Coding the displaced frame difference for video compression (2002)

Popular techniques employed to code the displaced frame difference (DFD) treat it no differently from an ordinary image for coding purposes. Since the DFD is generated by the process of motion compensation, such methods do not fully exploit the underlying redundancies. This paper proposes a DFD coding method which exploits such redundancies while incurring negligible information overhead. The key idea is to predict locations of high DFD concentration which occupy small portions of the image and use this predicted information (which is also available to the decoder without additional information transmission) to improve the quality of the decoded image. Two key features of the proposed approach are its compatibility with any transform based DFD coding scheme and negligible information overhead. Tests with a fully functional video coder show the efficacy of the proposed approach.
Interspecies homology of nitrogenase genes. (1980)

Cloned nitrogen fixation (nif) genes from Klebsiella pneumoniae hybridize to DNA from 19 out of 19 widely divergent nitrogen-fixing bacterial strains but do not hybridize to DNA from 10 different non-nitrogen-fixing species. K. pneumoniae nif DNA fragments that hybridize to DNA from other species contain part of the three structural genes that code for nitrogenase polypeptides. We have utilized this homology to clone an EcoRI restriction endonuclease fragment from Rhizobium meliloti that hybridizes to the K. pneumoniae nif structural genes. Some of the species whose DNA hybridizes with K. pneumoniae nif DNA have been postulated to have diverged from K. pneumoniae 3 x 10(9) years ago. Nitrogenase genes are the only known example of such highly conserved prokaryotic translated genes. Nitrogenase genes are either extraordinarily conserved in evolution or have been exchanged between different nitrogen-fixing species relatively recently in evolutionary time.
Tackling HIV through robust diagnostics in the developing world: current status and future opportunities (2010)

Over the last thirty years, the world has seen HIV circulate the globe, affecting 33 million people to date and killing 2 million people a year. The disease has affected developed and developing countries alike, and in the U.S., remains one of the top ten leading causes of death. Many regions of the world are highly impacted by this disease, including sub-Saharan Africa, South and South-East Asia, and Eastern Europe. Fortunately, multilateral, global efforts, along with successful developments in diagnostic tools and anti-retroviral drugs (ARVs) have successfully curbed the spread of HIV over the last ten years. In spite of this fact, access to HIV treatment and preventive healthcare is varying and limited in developing countries. A lack of healthcare infrastructure, financial support, and healthcare workers are some logistical factors that are responsible. HIV stigmatization, discrimination, and inadequate education pose additional social challenges that are hindering countries from advancing in HIV prevention. This review focuses on current technological tools that are used for HIV diagnosis and ongoing research that is aimed at addressing the conditions in low-resource settings. Recent developments in microfluidic applications and mobile health technologies are promising approaches to building a compact, portable, and robust device that can provide information-rich, real-time diagnoses. We also discuss the role that governments, healthcare workers, and even researchers can play in order to increase the acceptance of newly introduced devices and treatments in rural communities.
Murine CD8+ cytotoxic T lymphocytes lyse Toxoplasma gondii-infected cells (1991)

Studies were performed to determine whether CTL against Toxoplasma gondii-infected cells could be induced in a murine model of T. gondii infection in which CD8+ T lymphocytes have been shown to play a major role in resistance against this parasite. In 51Cr release assays, nylon wool nonadherent spleen cells from BALB/c (H-2d) mice immunized with the temperature-sensitive (ts-4) mutant strain of T. gondii were cytotoxic for T. gondii-infected P815 (H-2d) mastocytoma cells but not for uninfected cells. This cytotoxic activity was remarkably increased after in vitro stimulation with T. gondii-infected syngeneic spleen cells. The effector cells were shown to be CD8+ T lymphocytes, because the cytotoxicity was significantly inhibited by depletion of CD8+ T lymphocytes but not by depletion of CD4+ T lymphocytes. This cytotoxic activity was genetically restricted. Spleen cells from T. gondii-immune BALB/c mice were not cytotoxic for T. gondii-infected EL4 (H-2b) thymoma cells, whereas spleen cells from T. gondii-immune C57B1/6 (H-2b) mice were cytotoxic for T. gondii-infected EL4 cells but not for T. gondii-infected P815 cells. The cytolytic activity of CD8+ T lymphocytes against T. gondii-infected cells might be a mechanism whereby these cells confer resistance against T. gondii.
Intracellular Signaling Mechanisms of Acetaminophen-Induced Liver Cell Death (2005)

Acetaminophen hepatotoxicity is the leading cause of drug-induced liver failure. Despite substantial efforts in the past, the mechanisms of acetaminophen-induced liver cell injury are still incompletely understood. Recent advances suggest that reactive metabolite formation, glutathione depletion, and alkylation of proteins, especially mitochondrial proteins, are critical initiating events for the toxicity. Bcl-2 family members Bax and Bid then form pores in the outer mitochondrial membrane and release intermembrane proteins, e.g., apoptosis-inducing factor (AIF) and endonuclease G, which then translocate to the nucleus and initiate chromatin condensation and DNA fragmentation, respectively. Mitochondrial dysfunction, due to covalent binding, leads to formation of reactive oxygen and peroxynitrite, which trigger the membrane permeability transition and the collapse of the mitochondrial membrane potential. In addition to the diminishing capacity to synthesize ATP, endonuclease G and AIF are further released. Endonuclease G, together with an activated nuclear Ca2+,Mg2+-dependent endonuclease, cause DNA degradation, thereby preventing cell recovery and regeneration. Disruption of the Ca2+ homeostasis also leads to activation of intracellular proteases, e.g., calpains, which can proteolytically cleave structural proteins. Thus, multiple events including massive mitochondrial dysfunction and ATP depletion, extensive DNA fragmentation, and modification of intracellular proteins contribute to the development of oncotic necrotic cell death in the liver after acetaminophen overdose. Based on the recognition of the temporal sequence and interdependency of these mechanisms, it appears most promising to therapeutically target either the initiating event (metabolic activation) or the central propagating event (mitochondrial dysfunction and peroxynitrite formation) to prevent acetaminophen-induced liver cell death.
ato Operon: a Highly Inducible System for Acetoacetate and Butyrate Degradation in Escherichia coli (1972)

1 Growth of Escherichia coli in the presence of acetoacetate as inducer stimulates the rate of synthesis of two enzymes, an acetoacetyl-CoA: acetate CoA-transferase and a thiolase by a factor of 3000. The combined action of these enzymes allows for the degradation of acetoacetate to acetate and acetyl-CoA. 2 The structural genes for these enzymes, called ato A (CoA-transferase) and atoB (thiolase), and a regulatory gene, atoC, are closely linked, forming an operon (ato operon) with the order his…atoCAB…nalA on the bacterial chromosome. 3 The regulatory gene atoC is defined by a spontaneous mutation to the atoCc state which allows E. coli to grow on butyrate and to synthesize the enzymes of the ato operon constitutively. This mutation can only be selected for when the enzymes of the C-3 oxidation pathway are themselves formed constitutively. The atoCc state is required for butyrate degradation because this acid does not serve as inducer of the ato operon but requires the CoA-transferase for activation. 4 The evidence so far available indicates that the atoCc mutation is trans- dominant over the inducible atoC+ state suggesting a positive mechanism of control. 5 The uptake of butyrate is reduced or completely suppressed when mutational lesions prevent the further metabolism of this substrate.
Antitumor effect of vaccinia virus in glioma model. (1999)

The ability of certain viruses to lyse cancer cells suggests that they may have potential as oncolytic agents. We investigated the effect of vaccinia virus (VV) and its recombinant derivatives (recVV2, rVV-p53) on growth of C6 rat glioma cells that form fast growing tumors in athymic nude mice. VV effectively infected C6 cells in vitro, inducing high level of foreign gene expression. Most of C6 cells infected in vitro with rVV-p53 expressing the tumor suppressor p53 protein showed apoptosis specific morphological changes in DAPI-stained nuclei and DNA fragmentation pattern on gel electrophoresis; infection with VV induced low level of cell apoptosis. In an ex vivo experiment, VV-infected C6 cells were implanted s.c. in athymic nude mice and tumor development was monitored. In contrast to the control PBS group, most of mice implanted with infected cells remained tumor free until the end of the observation period. In an in vivo experiment, injection of VV or rVV-p53 after the C6 cells had been implanted in nude mice induced effective inhibition of tumor growth in comparison with control PBS groups. The oncolytic effect was greater with rVV-p53, apparently due to overexpressed p53 and p53-mediated cell apoptosis. In study of virus virulence we did not observe disease symptoms in athymic mice infected with a high dose of VV. Experimental results indicate that vaccinia virus itself and vaccinia-mediated delivery of therapeutic genes represent novel potential strategies for tumor therapy.
Sleep apnea in patients with acute myocardial infarction (1991)

This study suggests that sleep apnea is common in the setting of acute myocardial infarction. It may be a factor predisposing to, or even causing, sudden death in patients with acute phase of myocardial infarction.
Design automation tools for tile-based analogue cells (1989)

Mixed analogue-digital ASICs are becoming increasingly important as more silicon vendors provide mixed signal capability in their fabrication processes and design tools. This paper assesses the merits and limitations of the tile-based approach by comparing it to other design methods for designing analogue cells for mixed-signal ASIC. It then explores how design automation tools may be used to overcome some of the drawbacks of the tile-based method. Next the authors describe an Analogue Tile Compiler (ATC) which is currently under development at Imperial College and LSI Logic. Finally they conclude with some suggestions intended to show how such an automated design approach might influence the future of mixed signal ASIC designs.<
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Therapeutic activity of deoxyspergualin in comparison with cyclosporin A, and its combined use with cyclosporin A and prednisolone in highly allogeneic skin transplantation in the rat. (1992)

The present paper demonstrates the efficacy of a novel immunosuppressive agent, deoxyspergualin (DSG), in rat skin transplantation despite major histocompatible antigen differences, both by itself and in combination with cyclosporin A (CyA) and prednisolone (PD). DSG significantly prolonged the median survival time (MST) of WKAH skin on F344 rats, when given at daily doses of 1.5-12 mg/kg i.p. for 10 days starting from day one after grafting. A significant increase of the MST has been observed also in the rats orally receiving CyA at daily doses of 12.5-50 mg/kg according to the same dosing protocol. DSG was as effective as CyA in prolonging the MST. In contrast, when treatment started 4 days after grafting (at the time of the rejection crisis), DSG (6 mg/kg) was able to reverse the rejection, whereas CyA (50 mg/kg) was not. When DSG (1.5 mg/kg) and CyA (6.25 or 12.5 mg/kg) were given together from day one after grafting, the combined therapy was superior to each monotherapy. Similarly, when DSG (1.5 mg/kg) and PD (10 mg/kg) were given simultaneously from the rejection crisis, the combined therapy was demonstrated to have stronger activity than any of the monotherapies. Moreover, the skin-allografted rats could be switched successfully either from CyA to DSG treatment or from DSG to CyA treatment.
In Vivo Chromatin Accessibility Correlates With Gene Silencing in Drosophila (1998)

Gene silencing by heterochromatin is a well-known phenomenon that, in Drosophila, is called position effect variegation (PEV). The long-held hypothesis that this gene silencing is associated with an altered chromatin structure received direct support only recently. Another gene-silencing phenomenon in Drosophila, although similar in its phenotype of variegation, has been shown to be associated with euchromatic sequences and is dependent on developmental regulators of the Polycomb group (Pc-G) of gene products. One model proposes that the Pc-G products may cause a local heterochromatinization that maintains a repressed state of transcription of their target genes. Here, we test these models by measuring the accessibility of white or miniwhite sequences, in different contexts, to the Escherichia coli dam DNA methyltransferase in vivo. We present evidence that PEV and Pc-G-mediated repression mechanisms, although based on different protein factors, may indeed involve similar higher-order chromatin structure.
Effect of Simultaneous Existence of Two Ion-Exchangers with Opposite Charges of Lipophilic Groups (1999)

The effect of simultaneous existence in PVC membrane of both anion- and cation-exchanger taken in optimal molar ratio is shown for cation-selective membranes containing calcium (ETH 129, ETH 5234) and magnesium (ETH 5214, ETH 4030) ionophores. The presence of cation- as well as anion-exchanger is preferable for improvement of membrane selectivity. Potentiometric properties for calcium and magnesium selective membranes containing both ion-exchangers are compared to the results obtained by impedance spectroscopic method.
Controlled Growth and Photocatalytic Properties of CdS Nanocrystals Implanted in Layered Metal Hydroxide Matrixes (2005)

Layered double hydroxide Cd(1)(-)(x)()Al(x)()(OH)(2)(DS)(x)().3.0H(2)O (CdAlDS) and a related hydroxide salt compound Cd(2)(OH)(3)(DS).2.5H(2)O (CdDS), where DS stands for dodecyl sulfate sandwiched between two adjacent inorganic layers, have been synthesized and used as precursors for CdS nanoparticle growth. Through a gas/solid reaction, CdS nanocrystals implanted in the layer matrixes of the layered double hydroxides are grown, and the sizes of the nanocrystals vary in the range of 3-6 nm in diameter. The presence of trivalent Al cations in the layered double hydroxide can be taken advantage of to control the size of the CdS nanocrystals, and it also helps to prevent the formed nanocrystals from extraction from the solid matrixes. The nano-CdS implanted composite exhibits high photocatalytic activity for degradation of the nonbiodegradable rhodamine B under both UV and visible irradiations.