gebhart/patrepeval huggingface dataset:
Surface Organometallic Chemistry of Titanium on Silica−Alumina and Catalytic Hydrogenolysis of Waxes at Low Temperature (2009)

Ti(CH2tBu)4 (1) reacts selectively with the surface silanols of a silica−alumina partially dehydroxylated at 500 °C to provide the monosiloxy species [(≡SiO)Ti(CH2tBu)3]SA (2a) and the bisiloxy species [(≡SiO)2Ti(CH2tBu)2]SA (2b) in a ca. 40:60 ratio, with concomitant evolution of 1.6 ± 0.2 equiv of neopentane per Ti. These surface complexes were characterized via the combined use of several techniques such as IR spectroscopy, 1H MAS, 13C-CP/MAS, 2D 1H−13C HETCOR, and J-resolved solid-state NMR, as well as mass balance analysis. By treatment under hydrogen at 150 °C the neopentyl ligands in complexes 2a,b undergo hydrogenolysis and a mixture of supported titanium species is obtained. IR, ESR, 1H MAS, and DQ solid-state NMR spectroscopies show the presence of ca. 3% [(≡SiO)(MsO)TiH2]SA (3a; Ms = Si, Al), 5% [(≡SiO)(MsO)Ti(Me)−H]SA (3b), 75−80% [(≡SiO)(MsO)2Ti−H]SA (3c), and 14% [(≡SiO)(MsO)2TiIII]SA (3d), along with (SiHx) and (AlHx) fragments whose formation arise from the opening of adjacent Si−O−M bridges (M = Si, Al). Species 3a−d are efficient catalysts for the hydrogenolysis of waxes with a diesel selectivity higher than 60%. Comparison with the silica-based system shows a beneficial role of the silica−alumina support on the activity of the Ti centers, attributed to a direct interaction of the surface with the active site, which possibly facilitates the β-alkyl transfer, the key C−C bond cleavage step in the proposed mechanism.
Genetic analysis of self-associating immunoglobulin G rheumatoid factors from two rheumatoid synovia implicates an antigen-driven response. (1992)

Although much has been learned about the molecular basis of immunoglobulin M (IgM) rheumatoid factors (RFs) in healthy individuals and in patients with mixed cryoglobulinemia and rheumatoid arthritis, little is known about the genetic origins of the potentially pathogenic IgG RFs in the inflamed rheumatoid synovia of patients. Recently, we generated from unmanipulated synovium B cells several hybridomas that secreted self-associating IgG RFs. To delineate the genetic origins of such potentially pathogenic RFs, we adapted the anchored polymerase chain reaction to rapidly clone and characterize the expressed Ig V genes for the L1 and the D1 IgG RFs. Then, we identified the germline counterparts of the expressed L1 IgG RF V genes. The results showed that the L1 heavy chain was encoded by a Vh gene that is expressed preferentially during early ontogenic development, and that is probably located within 240 kb upstream of the Jh locus. The overlap between this RF Vh gene and the restricted fetal antibody repertoire is reminiscent of the natural antibody-associated Vh genes, and suggests that at least part of the "potential pathogenic" IgG RFs in rheumatoid synovium may derive from the "physiological" natural antibody repertoire in a normal immune system. Indeed, the corresponding germline Vh gene for L1 encodes the heavy chain of an IgM RF found in a 19-wk-old fetal spleen. Furthermore, the comparisons of the expressed RF V genes and their germline counterparts reveal that the L1 heavy and light chain variable regions had, respectively, 16 and 7 somatic mutations, which resulted in eight and four amino acid changes. Strikingly, all eight mutations in the complementarity determining regions of the V gene-encoded regions were replacement changes, while only 6 of 11 mutations in the framework regions caused amino acid changes. Combined with L1's high binding affinity toward the Fc fragment, these results suggest strongly that the L1 IgG RF must have been driven by the Fc antigen.
Inhibition of Biofilm Formation using Newly Developed Coating Materials with Self-cleaning Properties (2008)

The purpose of this study was to evaluate the inhibition of biofilm formation on newly developed coating materials with self-cleaning properties. A series of experimental coating materials containing fluoroalkylated acrylic acid oligomer (FAAO) were applied to resin composite substrates. The surfaces of the coating materials were analyzed by X-ray photoelectron spectroscopy (XPS) and contact angle measurement. Biofilm formation on the surface was assessed using Streptococcus mutans biofilms inside an oral simulator in vitro. The results indicated that an increase in the concentration of FAAO in the coating materials enhanced surface hydrophilicity and oil-repellency. Biofilm assays demonstrated that the amount of biofilm retained on the coating materials gradually decreased when the concentration of FAAO increased in the materials. It was concluded that the coating materials incorporated with FAAO possessed self-cleaning properties and displayed signs of inhibiting biofilm formation on their surfaces.
Lipoprotein receptors and atherogenic receptor-mediated mechanisms (1994)

The liver plays a decisive role in the regulation of the plasma levels of atherogenic lipoproteins. The primary liver interaction site of chylomicron remnants and VLDL remnants (beta-VLDL) is still unidentified, whereas the subsequent cellular uptake is likely to be mediated in concert by the LDL receptor-related protein and the LDL receptor. The nature of the primary interaction site of remnants (remnant receptor) might be a liver-specific proteoglycan or a liver-specific protein. Atherogenic modified LDL can be recognized by a family of scavenger receptors. A newly identified 95 kDa protein forms the most likely candidate for mediating the in-vivo uptake of oxidized LDL from the circulation and may, therefore, protect the body against the presence of oxidized LDL in the blood compartment.
Design and Development of Three Dimensional Virtual Campus Roaming System (2011)

This paper takes an example of Taishan University to introduce the design and development of three dimensional virtual campus roaming system.According to true environment of Taishan University,we use 3Dmax for modeling,adding light,texture and material.Then we apply the software of 3D Visual scene simulation to adjust system in order to obtain the real 3D effect.Through the 3D Visual scene simulation,we set up automatic navigation system and weather system which make the information system more realistic.Finally,we develop the three dimensional virtual campus roaming system.
Mechanisms associated with resistance to tamoxifen in estrogen receptor-positive breast cancer (Review) (2014)

Anti-estrogens such as tamoxifen are widely used in the clinic to treat estrogen receptor-positive breast tumors. Patients with estrogen receptor-positive breast cancer initially respond to treatment with anti-hormonal agents such as tamoxifen, but remissions are often followed by the acquisition of resistance and, ultimately, disease relapse. The development of a rationale for the effective treatment of tamoxifen-resistant breast cancer requires an understanding of the complex signal transduction mechanisms. In the present study, we explored some mechanisms associated with resistance to tamoxifen, such as pharmacologic mechanisms, loss or modification in estrogen receptor expression, alterations in co-regulatory proteins and the regulation of the different signaling pathways that participate in different cellular processes such as survival, proliferation, stress, cell cycle, inhibition of apoptosis regulated by the Bcl-2 family, autophagy, altered expression of microRNA, and signaling pathways that regulate the epithelial-mesenchymal transition in the tumor microenvironment. Delineation of the molecular mechanisms underlying the development of resistance may aid in the development of treatment strategies to enhance response and compromise resistance.
Understanding ActiveX and OLE (1996)

David Chappell, the author of professional courses and articles on Microsoft OLE and the Common Object Model (COM), introduces readers to OLE's importance and strategic significance. He delves into how component software led to OLE and then to COM. He also covers topics such as structured storage, monikers, Uniform Data Transfer, and OLE Automation.
IRS‐1 Regulation in Health and Disease (2003)

The global incidence of diabetes is increasing at epidemic rates. Estimates suggest there are currently 150 million people with diabetes and this number is expected to double in the next 20 years. Type 2 diabetes accounts for 95% of all cases and is characterized in part by impaired sensitivity to insulin or 'insulin resistance'. Defects in the insulin signalling pathways underpin this resistance. In the current article we discuss the regulation of Insulin Receptor Substrate-1 (IRS-1), a protein that plays a pivotal role in insulin signalling and whose function is impaired in subjects with insulin resistance. Coordination of IRS-1 function is multi-faceted, involving phosphorylation of IRS-1 at multiple serine/threonine residues. This controls many aspects of IRS-1, including its interaction with the insulin receptor and subsequent tyrosine phosphorylation, as well as its subcellular distribution and targeting for degradation by the proteasome. Such tight control ensures appropriate transduction and attenuation of the insulin signal, thereby regulating insulin action in healthy individuals. Emerging evidence indicates that 'diabetogenic factors' associated with insulin resistance, such as TNFalpha and elevated circulating fatty acids, impact on insulin signalling at the level of IRS-1 serine/threonine phosphorylation. The expression and/or activity of several kinases, such as IkappaB kinase beta (IKKbeta) and salt-induced kinase 2 (SIK2), and the phosphorylation of IRS-1 at key sites, such as Ser307 and Ser789, are increased in states of insulin resistance. Identifying the pathways by which such factors activate these and other kinases, and defining the precise roles of specific serine/ threonine phosphorylation events in IRS-1 regulation, represent important goals which may eventually provide a rationale for therapeutic intervention.
[Utilizing 2-DE and MALDI-TOF MS/MS to screen differentially expressed serum proteins of silicosis]. (2007)

Complement C4, leucine-rich alpha-2-glycoprotein, alpha-1-antitrypsin, serotransferrin, plasma glutathione peroxidase, tetranectin, apolipoprotein A-I and transthyretin are differentially expressed in the silica-exposed group and phase (I) group with silicosis, and the result should be validated by other biochemical technologies.
20‐1: Invited Paper: Solution Processable Luminescent Nanomaterials for Display, Lighting and Beyond (2017)

Colloidal quantum dots (QDs) and organic‐inorganic hybrid perovskites (OIHPs) represent two key solution processable luminescent nanomaterials. We will report a recent discovery that led to green OIHP ‐ polymer composite films with high photoluminescence efficiency, color purity and unprecedented water and heat stability for LCD backlight and some current developments of ultrabright red QLEDs for lighting, sensing and photomedical applications.
Inhibition of murine macrophage nitric oxide production by synthetic oligonucleotides (2002)

Synthetic 30-mer phosphorothioate (Ps) oligonucleotides (ODN) comprised of single bases (SdA30, SdC30, SdG30, and SdT30) were assessed for their effects on nitric oxide (NO) production by murine bone marrow macrophages (BMMC) and macrophage cell lines J774 and RAW264.7. Pretreatment of these cells with any of the four Ps ODN inhibited NO production induced by CpG ODN, E. coli DNA (EC DNA), or LPS. This inhibition was time- and dose-dependent and was observed even if the Ps ODN were added as long as 12 h after stimulation. As in the case of stimulatory ODN, inhibition was dependent on backbone structure and length. Thus, all four 30-mer, single-base Ps ODN were inhibitory, and only dG30 among phosphodiester ODN was inhibitory. Together, these observations indicate that Ps ODN can inhibit macrophage production of inflammatory mediators, suggesting a role of these compounds as immunomodulatory agents.
An Effective Method for Selecting siRNA Target Sequences in Mammalian Cells (2004)

RNA interference is a gene-silencing phenomenon triggered by dsRNA (double-stranded RNA) and has been widely used for studying gene functions. The short interfering RNA (siRNA) responsible for RNA interference, however, varies markedly in its gene-silencing efficacy. Because this efficacy depends on the selected target sequences, we developed an effective selection method based on the gene degradation measure (priority score) defined by positional features of individual nucleotides. We tested this method experimentally by using it to select new siRNA target sequences in the homo sapiens cyclin B1 gene (CCNB1) and confirmed that it selected highly effective gene-silencing sequences. The proposed method will therefore be useful for selecting new siRNA target sequences in mammalian cells.
Stabilization of positive charge by .beta.-silicon (1987)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTStabilization of positive charge by .beta.-siliconJoseph B. Lambert, Gen Tai Wang, Rodney B. Finzel, and Douglas H. TeramuraCite this: J. Am. Chem. Soc. 1987, 109, 25, 7838–7845Publication Date (Print):December 1, 1987Publication History Published online1 May 2002Published inissue 1 December 1987https://pubs.acs.org/doi/10.1021/ja00259a036https://doi.org/10.1021/ja00259a036research-articleACS PublicationsRequest reuse permissionsArticle Views3389Altmetric-Citations184LEARN 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-Alertsclose Get e-Alerts
Human embryonic stem cell technologies and drug discovery (2009)

Development of new drugs is costly and takes huge resources into consideration. The big pharmaceutical companies are currently facing increasing developmental costs and a lower success-rate of bringing new compounds to the market. Therefore, it is now of outmost importance that the drug-hunting companies minimize late attritions due to sub-optimal pharmacokinetic properties or unexpected toxicity when entering the clinical programs. To achieve this, a strong need to test new candidate drugs in assays of high human relevance in vitro as early as possible has been identified. The traditionally used cell systems are however remarkably limited in this sense, and new improved technologies are of greatest importance. The human embryonic stem cells (hESC) is one of the most powerful cell types known. They have not only the possibility to divide indefinitely; these cells can also differentiate into all mature cell types of the human body. This makes them potentially very valuable for pharmaceutical development, spanning from use as tools in early target studies, DMPK or safety assessment, as screening models to find new chemical entities modulating adult stem cell fate, or as the direct use in cell therapies. This review illustrates the use of hESC in the drug discovery process, today, as well as in a future perspective. This will specifically be exemplified with the most important cell type for pharmaceutical development-the hepatocyte. We discuss how hESC-derived hepatocyte-like cells could improve this process, and how these cells should be cultured if optimized functionality and usefulness should be achieved. J. Cell. Physiol. 219: 513-519, 2009. (c) 2009 Wiley-Liss, Inc.
Intracerebroventricular Leptin Regulates Hepatic but Not Peripheral Glucose Fluxes (1998)

Acute intravenous infusions of leptin markedly alter hepatic glucose fluxes (Rossetti, L., Massillon, D., Barzilai, N., Vuguin, P., Chen, W., Hawkins, M., Wu, J., and Wang, J. (1997) J. Biol. Chem. 272, 27758-22763). Here we examine whether intracerebroventricular (ICV) leptin administration regulates peripheral and hepatic insulin action. Recombinant mouse leptin (n = 14; 0.02 or 1 microgram/kg.h) or vehicle (n = 9) were administered ICV for 6 h to conscious rats, and insulin action was determined by insulin (3 milliunits/kg.min) clamp and tracer dilution techniques. During physiologic hyperinsulinemia (approximately 65 microunits/ml), the rates of glucose uptake (Rd, 20.1 +/- 0.6 and 23.1 +/- 0.7 versus 21.7 +/- 0.6 mg/kg.min; p = NS), glycolysis and glycogen synthesis were similar in rats receiving low- and high-dose leptin versus vehicle. ICV leptin resulted in a 2-3-fold increase in hepatic phosphoenolpyruvate carboxykinase mRNA levels. Glycogenolysis and PEP-gluconeogenesis (2.1 +/- 0.3 mg/kg. min) contributed similarly to endogenous glucose production (GP) in the vehicle-infused group. However, gluconeogenesis accounted for approximately 80% of GP in both groups receiving ICV leptin, while hepatic glycogenolysis was markedly suppressed (0.7 +/- 0.3 and 1.2 +/- 0.3 versus 2.2 +/- 0.4 mg/kg.min, in rats receiving low- and high-dose leptin versus vehicle, respectively; p < 0.01). In summary, short-term ICV leptin administration: 1) failed to affect peripheral insulin action, but 2) induced a striking re-distribution of intrahepatic glucose fluxes. The latter effect largely reproduced that of leptin given systemically at much higher doses. Thus, the regulation of hepatic glucose fluxes by leptin is largely mediated via its central receptors.
Mapping of Atrial Activation During Sustained Atrial Fibrillation in Dogs with Rapid Ventricular Pacing Induced Heart Failure: Evidence for a Role of Driver Regions (2005)

Introduction: Dogs with rapid ventricular pacing (RVP)‐induced congestive heart failure (CHF) have inducible atrial tachycardia, flutter, and fibrillation (AF). We tested the hypothesis that rapid atrial activation in multiple regions and at different rates is responsible for sustained AF in this CHF model. Methods and Results: We studied 12 episodes of sustained (&gt;10 minutes) AF induced in 12 dogs with CHF produced by 3–6 weeks of RVP at 230 beats/minute. High‐density mapping of AF was performed using 382 unipolar atrial electrograms recorded simultaneously from epicardial electrodes on the right (RA) and left atria (LA) and Bachmann's bundle. AF mechanisms were based on Fast Fourier Transform (FFT) analysis and activation sequence mapping. A driver was defined as a rapid stable activation region with a single dominant frequency peak in FFT analysis. During AF, three FFT and activation patterns were seen: (1) a single LA driver (7.8 ± 1.1 Hz) near the pulmonary veins (PVs) with irregular activation in the rest of the atria (n = 4); (2) simultaneous, multisite, biatrial drivers at differing frequencies (LA vs RA dominant frequency gradient: 1.3 ± 0.8 Hz) near the PVs (8.4 ± 0.3 Hz) and high RA (8.5 ± 1.5 Hz) (n = 7); and (3) biatrial irregular activation with multiple and/or broadband frequency peaks without a dominant frequency. (LA: 7.1–11.4 Hz; RA: 5.9–7.7 Hz) (n = 1). Atrial drivers had either a focal activation pattern or were due to a macroreentrant circuit around the PVs. Conclusions: In this CHF model, FFT analysis and activation sequence mapping demonstrate that sustained AF is characterized by single and multiple, stable LA and RA drivers with predominant sources in the PVs and high RA causing fibrillatory conduction.
Gene Therapy for Restenosis (1998)

The application of gene therapy techniques to the clinical problem of coronary restenosis has generated tremendous attention and enthusiasm. Use of gene transfer technology to prevent a common intractable illness would represent a watershed event for human gene therapy. However, the time is not yet right to initiate gene therapy trials for restenosis. The biology of restenosis is incompletely understood, catheter-based gene delivery is poorly adapted to the coronary circulation, and current gene transfer vectors are ill-suited for safe and effective gene delivery to the coronary artery wall. Basic research designed to overcome these obstacles is currently more appropriate than the initiation of clinical trials.
Ultrafast Electron Transfer in the Complex between Fluorescein and a Cognate Engineered Lipocalin Protein, a So-Called Anticalin (2002)

Anticalins are a novel class of engineered ligand-binding proteins with tailored specificities derived from the lipocalin scaffold. The anticalin FluA complexes fluorescein as ligand with high affinity, and it effects almost complete quenching of its steady-state fluorescence. To study the underlying mechanism, we have applied femtosecond absorption spectroscopy, which revealed excited-state electron transfer within the FluA*Fl complex to be responsible for the strong fluorescence quenching. On the basis of a comparison of redox potentials, either tryptophan or tyrosine may serve as electron donor to the bound fluorescein group in its excited singlet state, thus forming the fluorescein trianion radical within 400 fs. The almost monoexponential rate points to a single, well-defined binding site, and its temperature independence suggests an (almost) activationless process. Applying conventional electron transfer theory to the ultrafast forward and slower back-rates, the resulting electronic interaction is rather large, with approximately 140 cm(-1) for tyrosine, which would be consistent with a coplanar arrangement of both aromatic moieties within van der Waals distance. The weak residual steady-state fluorescence originates from a small (approximately 10%) component with a time constant in the 40-60 ps range. These results demonstrate the power of time-resolved absorption spectroscopy as a diagnostic tool for the elucidation of a fluorescence quenching mechanism and the temporal profiles of the processes involved. The high structural and dynamic definition of the complexation site suggests the anticalin FluA to be a promising model in order to tailor and probe electronic interactions and energetics in proteins.
5′-C-Chain-Extended Adenosine Derivatives Related to Sinefungin. Synthesis and Biological Activity (1990)

Abstract The synthesis of four 5′-chain-extended adenosine derivatives is described. Three of these nucleosides were prepared by manipulation of lactone 6, which is derived from N6−benzoyl-2′,3′-O-isopropylideneadenosine 5′-aldehyde by chain extension through Wittig chemistry. Functional group manipulation allowed introduction of the C-6′ amide and amine groups, and the chain terminal amino or hydroxyl group. The fourth compound was prepared in five steps from the natural product sinefungin. Antiviral data and certain enzyme inhibition data are presented on the target compounds.