gebhart/patrepeval huggingface dataset:
ATP binding cassette transporter ABC1 is required for the release of interleukin‐1β by P2X7‐stimulated and lipopolysaccharide‐primed mouse Schwann cells (2004)

Schwann cells are best known as myelinating glial cells of the peripheral nervous system, but they also participate actively in the sphere of immunity by producing pro-inflammatory cytokines, such as interleukin-1beta (IL-1beta). In a previous study, we demonstrated that posttranslational processing of IL-1beta by immune-challenged Schwann cells required the P2X7 receptor. Remarkably, the release of IL-1beta was not associated with cell death, indicating the involvement of an active mechanism. ATP binding cassette (ABC) transporters are known to transport leaderless secretory proteins, such as IL-1beta; therefore, we investigated whether such transporters were at work in Schwann cells. Mouse Schwann cells expressed ABC1 transporter mRNA and displayed the functional protein. Glybenclamide and diisothiocyanato-stilbene-disulfonic acid (DIDS), two blockers of chloride fluxes that drive the export activity of ABC1 transporters, inhibited IL-1beta release without altering its intracellular processing. Enhancing chloride efflux potentiated the release of IL-1beta, while decreasing it led to a strong reduction in its release. Because the stimulation of the P2X7 receptor also activates a chloride conductance, we investigated the possibility of a sole anionic pathway mobilized by the P2X7 receptor and ABC1. Glybenclamide and DIDS had no significant effects on the P2X7-activated chloride current suggesting therefore the existence of two different pathways. In summary, ABC1 transporters are required for the release of IL-1beta by mouse Schwann cells. Being associated together with chloride conductance, P2X7 receptors and ABC1 transporters delineate a subtle and complex regulation of IL-1beta production in mammalian Schwann cells. Furthermore, ABC1 transporters could be a target of therapeutic interest for regulating IL-1beta activity in neuroinflammation disorders.
Inverse reconstruction of epicardial potentials improved by vectorcardiography and realistic potentials (2013)

The inverse problem of electrocardiography is to reconstruct electrical activity at the level of the epicardium from body-surface electrograms and a patient-specific torsoheart geometry. This is complicated by the ill-posedness of the inverse problem, making the reconstruction imperfect. Previously, we have shown that the use of realistic epicardial training electrograms can improve reconstruction quality in silico. Here, we apply this method in a patient and compare the resulting computed electrograms with intracardiac measurements. Additionally, we utilize a new method that yields further improvements by incorporating characteristics of vectorcardiographic information. Patient-specific vectorcardiographic optimization combined with training data created on a patient-specific heart improves morphologies of the reconstructed epicardial potentials. This underlines the need for constraints based on real patient-specific information in the regularization of the electrocardiographic inverse problem.
Improvements in the device characteristics of amorphous indium gallium zinc oxide thin-film transistors by Ar plasma treatment (2007)

The effect of Ar plasma treatment on amorphous indium gallium zinc oxide (a-IGZO) thin films was investigated. The net electron carrier concentration (1020–1021cm−3) of the a-IGZO thin films dramatically increased upon their exposure to the Ar plasma compared to that (1014cm−3) of the as-deposited thin film. The authors attempted to reduce the contact resistance between the Pt∕Ti (source/drain electrode) and a-IGZO (channel) by using the Ar plasma treatment. Without the treatment, the a-IGZO thin film transistors (TFTs) with W∕L=50∕4μm exhibited a moderate field-effect mobility (μFE) of 3.3cm2∕Vs, subthreshold gate swing (S) of 0.25V∕decade, and Ion∕off ratio of 4×107. The device performance of the a-IGZO TFTs was significantly improved by the Ar plasma treatment. As a result, an excellent S value of 0.19V∕decade and high Ion∕off ratio of 1×108, as well as a high μFE of 9.1cm2∕Vs, were achieved for the treated a-IGZO TFTs.
The Mechanism of Isomerization of Olefins with Transition Metal Catalysts (1966)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXTThe Mechanism of Isomerization of Olefins with Transition Metal CatalystsRichard Cramer and R. V. Lindsey Jr.Cite this: J. Am. Chem. Soc. 1966, 88, 15, 3534–3544Publication Date (Print):August 1, 1966Publication History Published online1 May 2002Published inissue 1 August 1966https://pubs.acs.org/doi/10.1021/ja00967a013https://doi.org/10.1021/ja00967a013research-articleACS PublicationsRequest reuse permissionsArticle Views2860Altmetric-Citations153LEARN 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
Inflammation-promoting activity of HMGB1 on human microvascular endothelial cells (2003)

Systemic inflammation because of sepsis results in endothelial cell activation and microvascular injury. High-mobility group protein-1 (HMGB1), a novel inflammatory molecule, is a late mediator of endotoxin shock and is present in the blood of septic patients. The receptor for advanced glycation end products (RAGE) is expressed on endothelium and is a receptor for HMGB1. Here we examine the effects of HMGB1 on human endothelial cell function. Recombinant human HMGB1 (rhHMGB1) was cloned and expressed in Escherichia coli and incubated with human microvascular endothelium. rhHMGB1 caused a dose- and time-dependent increase in the expression of intercellular adhesion molecule 1 (ICAM-1), vascular cell adhesion molecule 1 (VCAM-1), and RAGE. rhHMGB1 induced the secretion of tumor necrosis factor-alpha (TNFalpha), interleukin 8 (IL-8), monocyte chemotactic protein-1 (MCP-1), plasminogen activator inhibitor 1 (PAI-1), and tissue plasminogen activator (tPA) (P <.01). rhHMGB1 stimulation resulted in transient phosphorylation of mitogen-activated protein (MAP) kinases, extracellular signal-related kinase (ERK), Jun N-terminal kinase (JNK), and p38, and in nuclear translocation of transcription factors NF-kappaB and Sp1. These effects are partially mediated by TNFalpha autocrine stimulation, as anti-TNFalpha antibodies significantly decrease chemokine and adhesion molecule responses (P </=.002). Thus, rhHMGB1 elicits proinflammatory responses on endothelial cells and may contribute to alterations in endothelial cell function in human inflammation.
Rapid Oxime and Hydrazone Ligations with Aromatic Aldehydes for Biomolecular Labeling (2008)

A high-yielding and rapid chemoselective ligation approach is presented that uses aniline catalysis to activate aromatic aldehydes toward two amine nucleophiles, namely, 6-hydrazinopyridyl and aminooxyacetyl groups. The rates of these ligations are resolved for model reactions with unprotected peptides. The resulting hydrazone and oxime conjugates are attained under ambient conditions with rate constants of 10(1)-10(3) M(-1) s(-1). These rate constants exceed those of current chemoselective ligation chemistries and enable efficient labeling of peptides and proteins at low muM concentrations, at neutral pH, without using a large excess of one of the components. The utility of the approach is demonstrated by the p-fluorobenzylation of human serum albumin and by the fluorescent labeling of an unprotected peptide with Alexa Fluor 488.
Dynamic program parallelization (1992)

Static program analysis limits the performance improvements possible from compile-time parallelization. Dynamic program parallelization shifts a portion of the analysis from complie-time to run-time, thereby enabling optimizations whose static detection is overly expensive or impossible. Lambda tagging and heap resolution are two new techniques for finding loop and non-loop parallelism in imperative, sequential languages with first-class procedures and destructive heap operations (e.g., ML and Scheme).
Structure and evolution of plant disease resistance genes. (2002)

This article reviews recent advances that shed light on plant disease resistance genes, beginning with a brief overview of their structure, followed by their genomic organization and evolution. Plant disease resistance genes have been exhaustively investigated in terms of their structural organization, sequence evolution and genome distribution. There are probably hundreds of NBS-LRR sequences and other types of R-gene-like sequences within a typical plant genome. Recent studies revealed positive selection and selective maintenance of variation in plant resistance and defence-related genes. Plant resistance genes are highly polymorphic and have diverse recognition specificities. R-genes occur as members of clustered gene families that have evolved through duplication and diversification. These genes appear to evolve more rapidly than other regions of the genome, and domains such as the leucine-rich repeat, are subject to adaptive selection
Towards a maturity model for corporate data quality management (2009)

High-quality corporate data is a prerequisite for world-wide business process harmonization, global spend analysis, integrated service management, and compliance with regulatory and legal requirements. Corporate Data Quality Management (CDQM) describes the quality oriented organization and control of a company's key data assets such as material, customer, and vendor data. With regard to the aforementioned business drivers, companies demand an instrument to assess the progress and performance of their CDQM initiative. This paper proposes a reference model for CDQM maturity assessment. The model is intended to be used for supporting the build process of CDQM. A case study shows how the model has been successfully implemented in a real-world scenario.
Requirement for Ras/Rac1-Mediated p38 and c-Jun N-Terminal Kinase Signaling in Stat3 Transcriptional Activity Induced by the Src Oncoprotein (1999)

Signal transducers and activators of transcription (STATs) are transcription factors that mediate normal biologic responses to cytokines and growth factors. However, abnormal activation of certain STAT family members, including Stat3, is increasingly associated with oncogenesis. In fibroblasts expressing the Src oncoprotein, activation of Stat3 induces specific gene expression and is required for cell transformation. Although the Src tyrosine kinase induces constitutive Stat3 phosphorylation on tyrosine, activation of Stat3-mediated gene regulation requires both tyrosine and serine phosphorylation of Stat3. We investigated the signaling pathways underlying the constitutive Stat3 activation in Src oncogenesis. Expression of Ras or Rac1 dominant negative protein blocks Stat3-mediated gene regulation induced by Src in a manner consistent with dependence on p38 and c-Jun N-terminal kinase (JNK). Both of these serine/threonine kinases and Stat3 serine phosphorylation are constitutively induced in Src-transformed fibroblasts. Furthermore, inhibition of p38 and JNK activities suppresses constitutive Stat3 serine phosphorylation and Stat3-mediated gene regulation. In vitro kinase assays with purified full-length Stat3 as the substrate show that both JNK and p38 can phosphorylate Stat3 on serine. Moreover, inhibition of p38 activity and thus of Stat3 serine phosphorylation results in suppression of transformation by v-Src but not v-Ras, consistent with a requirement for Stat3 serine phosphorylation in Src transformation. Our results demonstrate that Ras- and Rac1-mediated p38 and JNK signals are required for Stat3 transcriptional activity induced by the Src oncoprotein. These findings delineate a network of tyrosine and serine/threonine kinase signaling pathways that converge on Stat3 in the context of oncogenesis.
An update on androgen deprivation therapy for prostate cancer (2010)

Androgen deprivation therapy (ADT) with gonadal testosterone depletion is the frontline treatment for advanced prostate cancer. Other hormonal interventions have a role in the treatment of prostate cancer. We sought to examine systematically the evidence for hormonal interventions in prostate cancer, risks of ADT, and interventions that mitigate these risks. Search results for therapeutic studies were focused primarily on randomized controlled clinical trials, and the Jadad scale criteria were used to evaluate the quality of these studies. Four trials of the efficacy of intermittent ADT versus continuous ADT were included. One randomized study analysis and six postrandomization analyses were included on the effects of ADT on cardiovascular mortality. Seven randomized controlled trials of pharmacologic interventions were included for the treatment of metabolic effects due to ADT. One randomized trial of GnRH antagonist versus GnRH agonist was included. Six phase I/II clinical trials of secondary hormonal therapies with novel mechanisms of action were included. Randomized studies completed to date indicate that intermittent ADT might be equivalent to continuous ADT. Although adverse effects of ADT include risk factors for cardiovascular disease, effects on cardiovascular mortality are uncertain. Bone loss and increased risk of fracture may be effectively treated with pharmacologic interventions. Benefits of ADT must be balanced with a consideration of the risks.
The Unstable Structure, 1900–1914 (1999)

Why did the Russian Imperial monarchy crumble to the ground in February 1917? Soviet historians claimed that it was a collapse waiting to happen. The tsarist state, according to the precepts of Marxism-Leninism, served the interests of the upper and middle classes of town and countryside and placed the instruments of a mediaeval autocracy at their disposal — and the inevitable result was political and national oppression, economic exploitation and cultural backwardness. Supposedly the unique effective counter-measure was to form a party committed to the doctrines of Marx and Engels and to the mobilisation of the Russian working class in an age of European socialist revolution. This party needed to have a highly centralised, clandestine organisation if it was ever to destabilise the Imperial regime. It also had to have a leader of genius. Official historical textbooks asserted that just such a genius was present in the person of Vladimir Lenin [22]. There was an attempt by a few communist scholars in the last decades of the USSR's existence to query the details of this analysis. In particular, they indicated that the Russian Empire had a predominantly agrarian and traditionalist society and that there was nothing inevitable about a successful revolution led by urban socialists [31]. But these doubters were overruled by the party leadership and orthodox party historians, whose mantra was that Marxism, Lenin and the working class predetermined tsarism's downfall.
Biological Tuning of Synthetic Tactics in Solid-Phase Synthesis:  Application to Aβ(1−42) (2004)

The beta-amyloid(1-42) sequence has long been recognized as a challenging target for solid-phase peptide synthesis. We found that the known disaggregating role of Met-35 sulfoxide could be capitalized during stepwise solid-phase assembly of the A beta(1-42) peptide chain to mitigate on-resin peptide chain aggregation, a presumed major source of synthetic difficulties. Furthermore, we demonstrate a hitherto-unreported on-resin reduction of the sulfoxide "aggregation protecting group" to allow for standard cleavage protocols, obviating a separate solution-phase sulfoxide reduction step.
Ketone bodies as substrates (1990)

KB, acetoacetate (AcAc), P-hydroxybutyrate (BHB) and acetone were first recognized as components of human plasma in diabetics in 1865 (Gerhardt, 1865). This unfortunate connection has persisted and the role of KB as substrates has tended to be obscured because of their association as a danger signal in diabetes.
Supramolecular Hydrogel Formation Based on Inclusion Complexation Between Poly(ethylene glycol)‐Modified Chitosan and α‐Cyclodextrin (2004)

Supramolecular hydrogels have been prepared on the basis of polymer inclusion complex (PIC) formation between poly(ethylene glycol) (PEG)-modified chitosans and alpha-cyclodextrin (alpha-CD). A series of PEG-modified chitosans were synthesized by coupling reactions between chitosan and monocarboxylated PEG using water-soluble carbodiimide (EDC) as coupling agent. With simple mixing, the resultant supramolecular assembly of the polymers and alpha-CD molecules led to hydrogel formation in aqueous media. The supramolecular structure of the PIC hydrogels was confirmed by differential scanning calorimetry (DSC), X-ray diffraction, and (13)C cross-polarized/magic-angle spinning (CP/MAS) NMR characterization. The PEG side-chains on the chitosan backbones were found to form inclusion complexes (ICs) with alpha-CD molecules, resulting in the formation of channel-type crystalline micro-domains. The IC domains play an important role in holding together hydrated chitosan chains as physical junctions. The gelation property was affected by several factors including the PEG content in the polymers, the solution concentration, the mixing ratio of host and guest molecules, temperature, pH, etc. All the hydrogels in acidic conditions exhibited thermo-reversible gel-sol transitions under appropriate conditions of mixing ratio and PEG content in the mixing process. The transitions were induced by supramolecular association and dissociation. These supramolecular hydrogels were found to have phase-separated structures that consist of hydrophobic crystalline PIC domains, which were formed by the host-guest interaction between alpha-CD and PEG, and hydrated chitosan matrices below the pK(a).The formation of inclusion complexes between alpha-cyclodextrin and PEG-modified chitosan leads to the formation of hydrogels that can undergo thermo-reversible supramolecular dissociation.
60 nm planarized ultra-thin body solid phase epitaxy MOSFETs (2002)

The continuous scaling of MOSFET technology into the deep sub-micron regime poses considerable challenge to the conventional MOSFET structure. To suppress short-channel effects such as DIBL and V/sub t/ roll-off, extremely high levels of channel doping are required, but these result in increased leakage and degraded mobility. Simulation shows that the ultra-thin body MOSFET is a promising alternative structure that effectively suppresses DIBL and other short channel effects. The channel film thickness required is typically 30% of the gate length. The most difficult step for fabrication of the ultra-thin body FET is the formation of a uniform thin channel film. Oxidation and etch back have been proposed, but are limited by thickness uniformity of the starting SOI wafers and by process-induced variation. On the other hand, deposited films can be well controlled and have good uniformity, so finding ways to deposit highly uniform channel material is very plausible. Solid phase epitaxy (SPE) has been reported for fabrication of sub-100 nm devices (Subramanian et al, 1999). In SPE, the thin film is formed by lateral crystallization of an amorphous deposited silicon film, giving precise control over channel thickness. In this paper, 60 nm planarized SPEFETs with excellent performance are reported. The effect of different trench sizes is investigated. Both single sided and two sided crystallization on the channel film is also studied.
Ghrelin inhibits leptin- and activation-induced proinflammatory cytokine expression by human monocytes and T cells (2004)

Ghrelin, a recently described endogenous ligand for the growth hormone secretagogue receptor (GHS-R), is produced by stomach cells and is a potent circulating orexigen, controlling energy expenditure, adiposity, and growth hormone secretion. However, the functional role of ghrelin in regulation of immune responses remains undefined. Here we report that GHS-R and ghrelin are expressed in human T lymphocytes and monocytes, where ghrelin acts via GHS-R to specifically inhibit the expression of proinflammatory anorectic cytokines such as IL-1β, IL-6, and TNF-α. Ghrelin led to a dose-dependent inhibition of leptin-induced cytokine expression, while leptin upregulated GHS-R expression on human T lymphocytes. These data suggest the existence of a reciprocal regulatory network by which ghrelin and leptin control immune cell activation and inflammation. Moreover, ghrelin also exerts potent anti-inflammatory effects and attenuates endotoxin-induced anorexia in a murine endotoxemia model. We believe this to be the first report demonstrating that ghrelin functions as a key signal, coupling the metabolic axis to the immune system, and supporting the potential use of ghrelin and GHS-R agonists in the management of disease-associated cachexia.
Inhibition of connexin 43 synthesis by antisense RNA in rat glioma cells. (1997)

The 9L rat glioma cells communicate via gap junctions which are formed of connexin 43. The gap junctional communication was inhibited in these cells by transfecting them with an antisense Cx43 DNA construct, and its effect on their growth rate was investigated. This construct was induced by a Zn(2+)-inducible metallothionein promoter. Results showed that the induction of antisense RNA expression in rat 9L glioma cells produced the loss of gap junctions which was reflected in the loss of gap junctional communication. By inducing the antisense construct with zinc acetate, and using specific antibodies to connexin 43, the synthesis of this connexin was inhibited in the transfected cells and gap junctions were lost on the cell-cell appositions. There was no such effect on the untransfected cells. The loss of gap junctions at cell-cell appositions also correlated with the loss of Lucifer yellow fluorescent dye transfer between the cells. The effect of loss of gap junctions on the growth rate of the cells was assessed. In spite of the drastic decrease in the number of gap junctions between cells, their growth rate was only approximately 20% less than that of the transfected but non-induced cells. Therefore, gap junction communication is not negatively related to the rate of growth of these cells.
Virulent strains of Streptococcus suis serotype 2 and highly virulent strains of Streptococcus suis serotype 1 can be recognized by a unique ribotype profile (1997)

The ribotype profiles of 42 different Streptococcus suis strains were studied. These strains belonged to five serotypes and differed in their virulence for pigs as well as in the expression of the muramidase-released protein and the extracellular protein factor. For the ribotyping, chromosomal DNAs were digested with EcoRI and were hybridized with a 1,066-bp ribosomal DNA probe. The hybridization patterns showed genetic heterogeneity within and between the serotypes. Pathogenic strains of serotype 2 and highly pathogenic strains of serotype 1 could be recognized by their unique ribotype profiles. Nonpathogenic strains showed a high degree of genetic heterogeneity. Moreover, by comparing the 16S ribosomal DNA sequences of a number of S. suis strains, we were able to design two DNA probes which specifically hybridized with S. suis strains.