gebhart/patrepeval huggingface dataset:
An Efficient Catalyst for Asymmetric Epoxidation of Terminal Olefins (1998)

ADVERTISEMENT RETURN TO ISSUEPREVCommunicationNEXTAn Efficient Catalyst for Asymmetric Epoxidation of Terminal OlefinsJames P. Collman, Zhong Wang, Andrei Straumanis, Mélanie Quelquejeu, and Eric RoseView Author Information Department of Chemistry, Stanford University Stanford, California 94305-5080 Laboratoire de Synthèse Organique et Organométallique UMR CNRS 7611, Tour 44, 4, Place Jussieu 75252 Paris Cedex 05, France Cite this: J. Am. Chem. Soc. 1999, 121, 2, 460–461Publication Date (Web):December 29, 1998Publication History Received29 May 1998Published online29 December 1998Published inissue 1 January 1999https://pubs.acs.org/doi/10.1021/ja9818699https://doi.org/10.1021/ja9818699rapid-communicationACS PublicationsCopyright © 1999 American Chemical SocietyRequest reuse permissionsArticle Views2632Altmetric-Citations145LEARN ABOUT THESE METRICSArticle Views are the COUNTER-compliant sum of full text article downloads since November 2008 (both PDF and HTML) across all institutions and individuals. These metrics are regularly updated to reflect usage leading up to the last few days.Citations are the number of other articles citing this article, calculated by Crossref and updated daily. Find more information about Crossref citation counts.The Altmetric Attention Score is a quantitative measure of the attention that a research article has received online. Clicking on the donut icon will load a page at altmetric.com with additional details about the score and the social media presence for the given article. Find more information on the Altmetric Attention Score and how the score is calculated. Share Add toView InAdd Full Text with ReferenceAdd Description ExportRISCitationCitation and abstractCitation and referencesMore Options Share onFacebookTwitterWechatLinked InRedditEmail Other access optionsGet e-AlertscloseSupporting Info (1)»Supporting Information Supporting Information SUBJECTS:Catalysts,Hydrocarbons,Organic reactions,Pyrroles,Stereoselectivity Get e-Alerts
Universal on-chip communication channel (2010)

On-chip communication in mixed-clock systems has become a major issue; especially when asynchronous as well as multiple-clock-domain cores are used in a single chip. This paper proposes a new on-chip communication channel which can be used as asynchronous ⇒ synchronous, synchronous ⇒ asynchronous or synchronous ⇒ synchronous (mixed-clock) communication channel, all with the same design. The synchronization issue, i.e. the metastability, is analyzed; we show that its probability of occurring is practically zero in our designed channel. Because the routers in Asynchronous Network on Chips (ANoCs) are asynchronous and they have to communicate with synchronous cores, the proposed channel is well suited in such systems. Also, other mixed-clock SoCs can equally implement this channel as the interconnection between synchronous IP cores. The proposed channel is simulated in 90nm CMOS process using Predictive Technology Model (PTM) library with accurate Spice models. The throughput, latency and power consumption of our work are analyzed and compared with existing designs.
Molecular function and biological importance of CNNM family Mg2+ transporters (2018)

Cyclin M (CNNM) family proteins are evolutionarily conserved Mg2+ transporters. They extrude Mg2+ from cells and maintain intracellular Mg2+ levels within the normal range. Moreover, they play an important role in Mg2+ (re)absorption in the intestine and kidney by mediating the directional transport of Mg2+ across epithelial tissue from the tubular lumen to the body inside. Mg2+ efflux is suppressed by the direct binding with phosphatase of regenerating liver (PRL), and the formation of the complex is dynamically regulated by cysteine phosphorylation of PRL. The dysfunction of CNNM family proteins is responsible for inherited hypomagnesemia, as well as various intractable diseases, such as cancer and hypertension. Through multiple functional analyses of CNNM family proteins, the biomedical significance of the proper regulation of Mg2+ levels has been elucidated.
Synthesis, metal-binding properties and polypeptide solubilization of ‘crowned’ arborols (1994)

The first dendritic crown ether polymers (‘crowned’ arborols: G1, G2 and G3) have been synthesized and characterized. The convergent synthetic method was found to be more convenient than the divergent synthetic method. The building block in the branch was prepared from N-benzyloxycarbonyl-1,4,10,13-tetraoxa-7,16-diazacyclooctadecane and 3,5-bis(ethoxycarbonylmethoxy)benzoyl chloride. Since the basic repeating unit is the amino dicarboxylic acid, one can utilize the methods developed for peptide synthesis. Final products were obtained in moderate yields by coupling of each generational fragment with a core (benzene-1,3,5-tricarbonyl trichloride) followed by reduction of all amide linkages to tertiary amine linkages by borane–dimethyl sulfide. The complexation ability of these ‘crowned’ arborols was estimated by two-phase solvent extraction of alkali picrate salts. We found that some of these arborols can solubilize proteins in organic solvents.
Leukopenia in Familial Mediterranean Fever: Case Series and Literature Review with Special Emphasis on Pathogenesis (2013)

Leukopenia is a blood disease in which the number of circulating white blood cells diminishes. All underlying causes of leukopenia are not yet known. The subjects of this study are 15 leukopenic patients who were assessed by a systemic workup, including physical examination, blood tests, and molecular analysis. A common and unusual cause was revealed in all patients. This cause was a disorder with a laboratory characteristic of leukocytosis, namely familial Mediterranean fever (FMF). It was discussed that leukopenia arising in the context of FMF is mainly due to autophagy and apoptosis processes. These two pathophysiological characteristics of FMF were thought to explain the particular (episodic and self-limited) leukopenia in this disorder. Based on the results of this study in conjunction with the currently existing literature data, we suggest that FMF causes leukopenia. Leukopenic cases should be investigated for FMF, particularly if the leukopenia is episodic in nature. Early recognition of FMF would help to skip unnecessary invasive procedures and to prevent the development of amyloidosis, the devastating complication of FMF.
RNA-guided retargeting of Sleeping Beauty transposition in human cells (2020)

An ideal tool for gene therapy would enable efficient gene integration at predetermined sites in the human genome. Here we demonstrate biased genome-wide integration of the <i>Sleeping Beauty</i> (SB) transposon by combining it with components of the CRISPR/Cas9 system. We provide proof-of-concept that it is possible to influence the target site selection of SB by fusing it to a catalytically inactive Cas9 (dCas9) and by providing a single guide RNA (sgRNA) against the human <i>Alu</i> retrotransposon. Enrichment of transposon integrations was dependent on the sgRNA, and occurred in an asymmetric pattern with a bias towards sites in a relatively narrow, 300 bp window downstream of the sgRNA targets. Our data indicate that the targeting mechanism specified by CRISPR/Cas9 forces integration into genomic regions that are otherwise poor targets for SB transposition. Future modifications of this technology may allow the development of methods for specific gene insertion for precision genetic engineering.
Apoptosis and Autophagy Induction As Mechanism of Cancer Prevention by Naturally Occurring Dietary Agents (2012)

Nontoxic naturally occurring compounds, especially those from dietary sources, are receiving increasing consideration for prevention and treatment of diseases including cancer. There is a growing need for innovative anticancer therapies and therefore search for natural compounds with novel biological activities or antineoplastic potential is currently an important area in drug discovery. Support for this interest also comes from increasing concern over the efficacy and safety of many conventional therapies, especially those that run over a long course of time. Laboratory studies in different in vitro and in vivo systems have shown that many natural compounds possess the capacity to regulate response to oxidative stress and DNA damage, suppress angiogenesis, inhibit cell proliferation and induce autophagy and apoptosis. This review discusses the induction of apoptosis and autophagy as a mechanism of cancer prevention by some of the most studied naturally occurring dietary compounds.
A Diode Phase Shifter for Array Antennas (1964)

The appeal of a phased array antenna is well recognized in the search for a radiator whose power is not limited by the finite capacity of its component subradiators--only their number--and whose beam may be steered at high speeds and even subdivided into multibeams. Numerous methods are proposed to control the phase of the coherently energized subradiators and thus steer their resultant beam. Microwave, two-port, electronically switchable phase shifters used in series with one or more radiator elements and using PIN switching diodes for control are frequently recommended. Previously, the problems in implementing such a device have been the achievement of high power capability and low insertion loss.
The effect of TGF-beta on the induction CD8 and NK1.1 expression in CTLL-2 cell line. (2003)

Our results indicated that these would be useful models to investigate CD8 precursor potentials in populations of CD4-CD8- (double negative) cells and the relationship of NK1.1. These results also support a role for TGF-beta in T-cell differentiation and the hypothesis that T-cells and NK cells may have the same ontogeny.
Metabolic Stress Opens K+ Channels in Hepatoma Cells through a Ca2+- and Protein Kinase Cα-dependent Mechanism (1996)

These studies of a model liver cell line evaluate the mechanisms responsible for regulated release of K+ ions during metabolic stress. Metabolic inhibition of HTC hepatoma cells by exposure to 2, 4-dinitrophenol (50 microM) and 2-deoxy-D-glucose (10 mM) stimulated outward currents carried by K+ of 974 +/- 75 pA at 0 mV (n = 20, p < 0.001). Currents were inhibited by chelation of intracellular Ca2+ or exposure to apamin (50 nM), an inhibitor of SKCa channels. In cell-attached recordings from intact cells, removal of metabolic substrates (25/28 cells) or exposure to metabolic inhibitors (32/40 cells) opened K+-selective channels with a conductance of 6.5 +/- 0. 2 pS. Channels had an open probability of 0.31 +/- 0.08 and opened in bursts averaging 3.55 +/- 0.27 ms in duration (n = 6). Metabolic stress was associated with rapid translocation of the alpha isoform of protein kinase C (PKCalpha) from cytosol to membrane; and down-regulation of PKCalpha by phorbol esters or exposure to the PKC inhibitor chelerythrine (10 microM) each inhibited currents. Moreover, intracellular perfusion with purified PKCalpha activated currents in a Ca2+- and concentration-dependent manner. These findings indicate that metabolic stress leads to opening of apamin-sensitive SKCa channels in hepatoma cells through a Ca2+- and PKC-dependent mechanism and suggest that PKCalpha may be selectively involved in the response. This mechanism functionally couples the metabolic state of cells to membrane K+ permeability and represents a potential target for modification of liver injury associated with ischemia and preservation.
Methodik (1997)

Die Auswahl der Teilnehmer an der Untersuchung für die Experimental- und Vergleichsgruppe (vgl. ROSSI et al. 1988, S.126 ff.) vollzog sich unter folgenden formalen Einschlußkriterien:
Regulation of T‐cell receptor signalling by membrane microdomains (2004)

There is now considerable evidence suggesting that the plasma membrane of mammalian cells is compartmentalized by functional lipid raft microdomains. These structures are assemblies of specialized lipids and proteins and have been implicated in diverse biological functions. Analysis of their protein content using proteomics and other methods revealed enrichment of signalling proteins, suggesting a role for these domains in intracellular signalling. In T lymphocytes, structure/function experiments and complementary pharmacological studies have shown that raft microdomains control the localization and function of proteins which are components of signalling pathways regulated by the T-cell antigen receptor (TCR). Based on these studies, a model for TCR phosphorylation in lipid rafts is presented. However, despite substantial progress in the field, critical questions remain. For example, it is unclear if membrane rafts represent a homogeneous population and if their structure is modified upon TCR stimulation. In the future, proteomics and the parallel development of complementary analytical methods will undoubtedly contribute in further delineating the role of lipid rafts in signal transduction mechanisms.
Minimum Expected Length of Fixed-to-Variable Lossless Compression Without Prefix Constraints (2011)

The minimum expected length for fixed-to-variable length encoding of an n-block memoryless source with entropy H grows as nH + O(1), where the term O(1) lies between 0 and 1. However, this well-known performance is obtained under the implicit constraint that the code assigned to the whole n-block is a prefix code. Dropping the prefix constraint, which is rarely necessary at the block level, we show that the minimum expected length for a finite-alphabet memoryless source with known distribution grows as nH-1/2 log n + O(1) unless the source is equiprobable. We also refine this result up to o(1) for those memoryless sources whose log probabilities do not reside on a lattice.
Effect of the Lipophilic o-Naphthoquinone CG 10-248 on Rat Liver Mitochondria Structure and Function (2002)

CG 10-248 (3,4-dihydro-2,2 dimethyl-9-chloro-2H-naphtho[1,2b]pyran-5,6-dione), a beta-lapachone analogue, modified the ultrastructure of rat liver mitochondria in vitro, in the absence of added oxidizable substrates. The condensed mitochondrial state was replaced by the orthodox or swollen state to a significant degree. The number of modified mitochondria depended on incubation time and quinone concentration, in the 25-100 microM range. Under the same experimental conditions, mitochondrial respiration was uncoupled as indicated by the increase in the rate of succinate oxidation by controlled mitochondria in metabolic state "4" (not in state "3"), and by the activation of latent F0F1-ATP synthase. Taking into account structural similarities, the results reported here may be valid for other o-naphthoquinones, such as beta-lapachone.
Effect of Diphenyl Ether Herbicides on Oxidation of Protoporphyrinogen to Protoporphyrin in Organellar and Plasma Membrane Enriched Fractions of Barley (1991)

In barley (Hordeum vulgare L.) root cells, activity for oxidizing protoporphyrinogen to protoporphyrin (protoporphyrinogen oxidase), a step in chlorophyll and heme synthesis, was found both in the crude mitochondrial fraction and in a plasma membrane enriched fraction separated by a sucrose gradient technique utilized for preparing plasma membranes. The specific activity (expressed as nanomoles of protoporphyrin formed per hour per milligram protein) in the mitochondrial fraction was 8 and in the plasma membrane enriched fraction was 4 to 6. The plasma membrane enriched fraction exhibited minimal cytochrome oxidase activity and no carotenoid content, indicating little contamination with mitochondrial or plastid membranes. Etioplasts from etiolated barley leaves exhibited a protoporphyrinogen oxidase specific activity of 7 to 12. Protoporphyrinogen oxidase activity in the barley root mitochondrial fraction and etioplast extracts was more than 90% inhibited by assay in the presence of the diphenyl ether herbicide acifluorfen methyl, but the activity in the plasma membrane enriched fraction exhibited much less inhibition by this herbicide (12 to 38% inhibition) under the same assay conditions. Acifluorfen-methyl inhibition of the organellar (mitochondrial or plastid) enzyme was maximal upon preincubation of the enzyme with 4 mm dithiothreitol, although a lesser degree of inhibition was noted if the organellar enzyme was preincubated in the presence of other reductants such as glutathione or ascorbate. Acifluorfen-methyl caused only 20% inhibition if the enzyme was preincubated in buffer without reductants. Incubation of barley etioplast extracts with the earlier tetrapyrrole precursor coproporphyrinogen and acifluorfen-methyl resulted in the accumulation of protoporphyrinogen, which could be converted to protoporphyrin even in the presence of the herbicide by the addition of the plasma membrane enriched fraction from barley roots. These findings have implications for the toxicity of diphenyl ether herbicides, whose light induced tissue damage is apparently caused by accumulation of the photoreactive porphyrin intermediate, protoporphyrin, when the organellar protoporphyrinogen oxidase enzyme is inhibited by herbicides. Our results suggest that the protoporphyrinogen that accumulates as a result of herbicide inhibition of the organellar enzyme can be oxidized to protoporphyrin by a protoporphyrinogen oxidizing activity that is located at sites such as the plasma membrane, which is much less sensitive to inhibition by diphenylether herbicides.
Characteristics of 42 cases of incidental discovery of pheochromocytoma (2011)

We have retrospectively analyzed the medical files of 86 consecutive patients who were diagnosed as cases of adrenal or extra-adrenal pheochromocytoma at Changhai hospital between 2001 and 2009. Patients with incidentally detected pheochromocytoma often had lower prevalence of hypertension and lower mean arterial blood pressure compared with those patients suspected of pheochromocytoma on clinical grounds.

Key words: 
Incidentally discovered pheochromocytoma;  Clinical characteristics;  Diagnosis
Enteral IGF-I enhances fetal growth and gastrointestinal development in oesophageal ligated fetal sheep (1999)

Infants with upper gut atresia often have impaired intrauterine growth and gut function. IGF-I is important in fetal growth and is contained in amniotic fluid. We therefore wanted to test the hypothesis that IGF-I infused into fetal gut would reverse the effects of an upper gut obstruction on gut structure and growth in fetal sheep. At 90 days gestation fetuses (n=6 per group) underwent oesophageal ligation, followed by continuous infusion of IGF-I (1-8 microgram/day) or saline into the gut beyond the ligation until 137 days. Controls underwent sham ligation only. Oesophageal ligation tended to reduce fetal body and organ weights. IGF-I treatment prevented this reduction and increased body length and spleen weight above those of controls. The decrease in bowel wall thickness induced by oesophageal ligation was also prevented by IGF-I treatment. Amniotic fluid IGF-I concentrations did not change over gestation and were higher in the IGF-I treated group. No change in fetal plasma IGF-I concentrations were detectable. We conclude that enterally administered IGF-I may enhance fetal growth and gut development in utero and that IGF-I in amniotic fluid may play a physiological role in gut development in the fetus.
Oxidative stress in dermatology (1993)

Oxidants, Antioxidants, and Oxidative Injury in Dermatopathology Reactive Oxygen Species in Pathology with Special Reference to the Skin, Barry Halliwell Solubility-Diffusion of Dioxygen in the Skin, M. E. Hatcher and W. Z. Plachy Evidence for UV Light as an Oxidative Stressor in Skin, Eric H. Witt, Paul Motchnik, and Lester Packer Reactive Oxidants in Skin: UV-Induced Lipid Peroxidation, Ryohei Ogura and Masayasu Sugiyama Vitamin E. Prevention of Ultraviolet-Induced Skin Damage, John R. Trevithick The Cutaneous Antioxidant System, Donald A. Vessey The Effects of UV Radiation on Skin Connective Tissue, Graeme F. Bryce Antioxidant Protection Against Ultraviolet Light-Induced Skin Damage, Edward Pelle, Kenneth Marenus, and Daniel Maes Reactive Oxidants in Photosensitized Skin Inflammations, Narendranath S. Ranadive and I. Aravind Menon Solar Ultraviolet Effects on Mammalian Cell DNA, Meyrick J. Peak, Jennifer G. Peak, and Irene E. Kochevar Oxidative Stress, Cytokines, and Lymphocyte Activation, Marie-Anne Gougerot-Pocidalo and Jean-Pierre Revillard Oxidative Stress in Skin Chemical Carcinogenesis, Rajesh Agarwal and Hasan Mukhtar The Defensive Role of Antioxidants in Skin Carcinogenesis, Homer S. Black Changes of Antioxidant Enzymes and Effects of Active Oxygens on Aged Human Skin Fibroblasts, Yasuko Shindo, Junichi Akiyama, and Yoshio Takase Electron Donor and Acceptor Properties of Melanin Pigments in the Skin, Krzysztof Reszka and Kowichi Jimbow Clinical Dermatopathology, Dermatopharmacology, and Dermatotoxicology Skin Diseases Associated with Oxidative Injury, Yoshiki Mayachi Biology of Aging Skin: Bioengineering Mensuration of Cutaneous Properties, Jeff Harvell and Howard I. Maibach Mechanism of Photosensitivity Due to Porphyrins: Chemical Species Involved and Relevance to Clinical Porphyrias, Herbert F. Haberman and I. Aravind Menon Determination of Blood Cell Chemiluminescence: A Method to Investigate Selected Skin Diseases, Klaus Holhmaier Reactive Oxygen Species in the Pathophysiology of Ischemia/Reperfusion Injury in Skin, Michael F. Angel and Paul N. Manson Dermatopharmacology of Oxidative Stress, M. B. Roberfroid and Pedro Buc Calderon Environmental Stress and Reactive Oxidants in Skin Toxicology, Jurgen Fuchs, Nanna Schurer, and Rainer Milbradt Hyperbaric Oxygenation in the Treatment of Skin Diseases, Michael Buslau and Gerd Hoffmann
A Knowledge-Based Approach to Overcome Structural Differences in Object Oriented Database Integration. (1988)

S.265-304
Glial Fibrillary Tangles and JAK/STAT-Mediated Glial and Neuronal Cell Death in a<i>Drosophila</i>Model of Glial Tauopathy (2010)

A subset of neurodegenerative tauopathies is characterized by abundant filamentous inclusions of hyperphosphorylated tau in both neurons and glia. Although the contribution of neuronal tau to behavioral changes and neuronal loss in neurodegenerative diseases has been studied extensively, the functional consequences of tau deposition in glial cells have been less well characterized. To investigate the role of abnormal tau accumulation and aggregation in glial cells, we created a Drosophila model of glial tauopathy by expressing human wild-type tau in adult fly glial cells. Glial expression of tau resulted in robust aggregation of phosphorylated tau into fibrillary inclusions similar to human glial tangles. Tangle formation was accompanied by shortened lifespan and age-dependent apoptotic cell death of both glia and neurons. Genetic manipulation of Janus kinase/signal transducer and activator of transcription (JAK/STAT) signaling modified toxicity of glial tau. We also identified a synergistic interaction of combined tau expression in neurons and glial cells. In summary, we present a genetically tractable model of glial fibrillary tau tangle formation and identify JAK/STAT signaling as mediating the death of both glia and neurons in this model.