gebhart/patrepeval huggingface dataset:
Cloning and expression of CD24 gene in human hepatocellular carcinoma: a potential early tumor marker gene correlates with p53 mutation and tumor differentiation. (1995)

To search for genes related to hepatocarcinogenesis, the differential display technique for eukaryotic mRNA was conducted. We have cloned a gene that encodes the CD24 protein from the cDNA library of human hepatocellular carcinoma (HCC). A single 2.1-kb mRNA was identified in HCC specimens and the HuH-7 HCC cell line but only rarely in small amounts in nontumor livers. In 79 unicentric HCC, CD24 mRNA was overexpressed in 52 cases (66%), found in trace amounts in 11, and not detectable in 16 (20%). In 12 cases of multicentric HCC, CD24 mRNA was overexpressed in 21 (68%) of 31 tumor nodules and was helpful for the determination of tumor clonal origin. There was an increased frequency of CD24 mRNA overexpression in patients younger than 50 years with HCC (86% versus 59%, P < 0.025), in serum hepatitis B surface antigen-positive individuals (74% versus 48%, P < 0.023), in those with an elevated serum alpha-fetoprotein level (82%, versus 56%, P < 0.04), and in HCC with alpha-fetoprotein mRNA expression (82% versus 56%, P < 0.04). There was a strong correlation of CD24 mRNA overexpression with p53 gene mutation in HCC (91% versus 46%, P < 0.0005) and poorly differentiated HCC (82% versus 53%, P < 0.0008). Despite its correlation with p53 mutation and the unfavorable outcome of HCC with p53 mutation, the CD24 mRNA expression did not correlate with tumor size, tumor invasiveness, or patient's prognosis. Thus, the CD24 gene expression appears to be a common event in HCC and may serve as an early but not prognostic biomarker for malignant transformation of hepatocytes.
Nucleotide Exchange Factor ECT2 Interacts with the Polarity Protein Complex Par6/Par3/Protein Kinase Cζ (PKCζ) and Regulates PKCζ Activity (2004)

Regulation of cell polarity is an important biological event that governs diverse cell functions such as localization of embryonic determinants and establishment of tissue and organ architecture. The Rho family GTPases and the polarity complex Par6/Par3/atypical protein kinase C (PKC) play a key role in the signaling pathway, but the molecules that regulate upstream signaling are still not known. Here we identified the guanine nucleotide exchange factor ECT2 as an activator of the polarity complex. ECT2 interacted with Par6 as well as Par3 and PKCzeta. Coexpression of Par6 and ECT2 efficiently activated Cdc42 in vivo. Overexpression of ECT2 also stimulated the PKCzeta activity, whereas dominant-negative ECT2 inhibited the increase in PKCzeta activity stimulated by Par6. ECT2 localization was detected at sites of cell-cell contact as well as in the nucleus of MDCK cells. The expression and localization of ECT2 were regulated by calcium, which is a critical regulator of cell-cell adhesion. Together, these results suggest that ECT2 regulates the polarity complex Par6/Par3/PKCzeta and possibly plays a role in epithelial cell polarity.
Observation of nanosecond laser-induced phase explosion in aluminum (2006)

The transition from normal vaporization to phase explosion during laser ablation of aluminum was investigated using a nanosecond Nd:YAG laser. The threshold nature of phase explosion was observed by a discontinuous jump in the ablation depth at approximately 5.2J∕cm2. Ablation was imaged using a shadowgraph technique that was capable of probing ablation with nanosecond exposure time and nanosecond time delay resolution with respect to laser heating. Images above the threshold captured a mixture of vapor and droplets generated by phase explosion, which began near the end of the laser pulse without a significant time lag.
.alpha.-Regioselectivity in palladium-catalyzed arylation of acyclic enol ethers (1992)

ADVERTISEMENT RETURN TO ISSUEPREVArticleNEXT.alpha.-Regioselectivity in palladium-catalyzed arylation of acyclic enol ethersWalter Cabri, Ilaria Candiani, Angelo Bedeschi, Sergio Penco, and Roberto SantiCite this: J. Org. Chem. 1992, 57, 5, 1481–1486Publication Date (Print):February 1, 1992Publication History Published online1 May 2002Published inissue 1 February 1992https://pubs.acs.org/doi/10.1021/jo00031a029https://doi.org/10.1021/jo00031a029research-articleACS PublicationsRequest reuse permissionsArticle Views2674Altmetric-Citations152LEARN 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
Liver ischemia/reperfusion injury: Processes in inflammatory networks—A review (2010)

Liver ischemia/reperfusion (IR) injury is typified by an inflammatory response. Understanding the cellular and molecular events underpinning this inflammation is fundamental to developing therapeutic strategies. Great strides have been made in this respect recently. Liver IR involves a complex web of interactions between the various cellular and humoral contributors to the inflammatory response. Kupffer cells, CD4+ lymphocytes, neutrophils, and hepatocytes are central cellular players. Various cytokines, chemokines, and complement proteins form the communication system between the cellular components. The contribution of the danger-associated molecular patterns and pattern recognition receptors to the pathophysiology of liver IR injury are slowly being elucidated. Our knowledge on the role of mitochondria in generating reactive oxygen and nitrogen species, in contributing to ionic disturbances, and in initiating the mitochondrial permeability transition with subsequent cellular death in liver IR injury is continuously being expanded. Here, we discuss recent findings pertaining to the aforementioned factors of liver IR, and we highlight areas with gaps in our knowledge, necessitating further research.
Effects of Aging and Ouabain on Left Atrial Arrhythmogenicity (2007)

Aging enhanced the LA regional electrical heterogeneity and LAPW arrhythmogenesis.
Timing of Treatment for Myocardial Reperfusion Injury (1999)

Early reperfusion of acute myocardial infarctions halts cell death due to ischemia but causes further injury, probably by oxidant mechanisms. We identified the window of opportunity during which antioxidants must be present in therapeutic concentrations to prevent reperfusion injury during 90 min of ischemia and 48 h of reperfusion in 57 dogs. We examined the effect on myocardial infarct size of intravenous infusion of N-2-mercaptopropionyl glycine (MPG), a diffusible antioxidant with a plasma half-time of 7 min, by using a series of protocols with a range of timing. Whereas infusions of MPG for > or =3 h reduced infarct size by approximately 50%, infusions for 1 h only (the first, second or third hours of reperfusion) caused only small reductions. A statistical analysis that focused on identifying components of group membership responsible for differences revealed that duration of treatment was a major determinant of infarct size. If begun any time within the first hour of reperfusion, infusions of > or =3 h markedly diminished infarct size. Because reperfusion injury proceeds for the first 3 h of reperfusion, but decreases thereafter, adequate protection is needed for > or =3 of the first 4 h of reperfusion, but more prolonged protection is not necessary.
Local Generation of Fast Ripples in Epileptic Brain (2002)

Aperiodic high-frequency oscillations (>100 Hz) reflect a short-term synchronization of neuronal electrical activity. It has been shown in the epileptic brain that spontaneous oscillations in the frequency range of 250-600 Hz reflect action potential population bursts of synchronously discharging neuronal clusters. These oscillations occur in the early stages of epileptogenesis in areas adjacent to the brain lesion and may trigger the formation of seizure-generating neuronal networks. We studied the extent of the area generating oscillations in the frequency range of 250-600 Hz [fast ripples (FRs)] in intrahippocampal kainic acid-treated rats with spontaneous seizures, by analyzing voltage versus depth profiles of FRs in hippocampal and parahippocampal areas in freely moving animals and by spatial mapping in hippocampal slice preparations in vitro. The strength of inhibition was compared in areas with and without FRs using a paired-pulse paradigm. The extent of the areas generating FRs did not exceed 1 mm(3). The areas generating FRs became broader after the application of the GABA(A) receptor antagonist bicuculline. Paired-pulse fast inhibition at 15-30 msec intervals was similar in areas generating FRs and areas not generating FRs. Our data illustrate that hypothesized clusters of highly interconnected neurons are capable of overcoming interneuron feedback inhibition, resulting in generation of epileptiform bursts, eventually leading to seizure activity.
LexA protein is a repressor of the colicin E1 gene. (1983)

LexA protein is a repressor of several chromosomal genes involved in the SOS response in Escherichia coli. In previous experiments, we found that LexA protein may also be a repressor of the colicin E1 gene. We now present evidence that the purified LexA protein strongly repressed the in vitro transcription of the colicin E1 gene. As determined in DNase I protection experiments, LexA protein bound with a high affinity to the approximately 40-base pair long sequence between the Pribnow box and the start codon of the colicin E1 gene. The sequence of the binding site was composed of two overlapped "SOS boxes" to which the LexA protein bound in a cooperative manner.
The Roles of Protein C and Thrombomodulin in the Regulation of Blood Coagulation (1989)

The coagulation process presents unusual problems with respect to control mechanisms.To limit the scope of the review, the protein C anticoagulant pathway will serve as a model to illustrate some of the biochemical mechanisms involved in control.It is perhaps worthwhile to consider initiaIly some of the fundamental observations that indicate where and how the system must be regulated.The cascade of zymogen activation events in coagulation provides the potential for explosive amplification (reviewed in Ref. 1) ultimately leading to the formation of thrombin, the serine protease responsible for clot formation, platelet activation, activation of factor XI11 with subsequent cross-linking of the fibrin network, and the feedback activation of the two regulatory proteins, factors V and VI11 (reviewed in Ref. 2).The circulating levels of the thrombin precursor, prothrombin, is at least 100 times greater than that required for rapid and complete clot formation (1, 2).This provides the potential for massive clotting in the face of a triggering event.In healthy individuals, the coagulation system is very effectively controlled, and the balance clearly lies in favor of the negative regulation of this process (3).This contrasts to the observation that when blood is shed into containers, coagulation is complete and relatively rapid.In selected disease states, especially those with an ongoing inflammatory process, the propensity to form blood clots is apparent, suggesting that these individuals might have depressed anticoagulant mechanisms.This hypothesis is supported by the observation that infants born without protein C, a component of a major anticoagulant mechanisms, often die with massive thrombotic complications in infancy (4).
ScribbleBoost: Adding Classification to Edge‐Aware Interpolation of Local Image and Video Adjustments (2008)

Abstract One of the most common tasks in image and video editing is the local adjustment of various properties (e.g., saturation or brightness) of regions within an image or video. Edge‐aware interpolation of user‐drawn scribbles offers a less effort‐intensive approach to this problem than traditional region selection and matting. However, the technique suffers a number of limitations, such as reduced performance in the presence of texture contrast, and the inability to handle fragmented appearances. We significantly improve the performance of edge‐aware interpolation for this problem by adding a boosting‐based classification step that learns to discriminate between the appearance of scribbled pixels. We show that this novel data term in combination with an existing edge‐aware optimization technique achieves substantially better results for the local image and video adjustment problem than edge‐aware interpolation techniques without classification, or related methods such as matting techniques or graph cut segmentation.
Application of Surface Reformed Thick Spin‐on‐Glass to MOS Device Planarization (1990)

A simple planarization technology is proposed, using an organosiloxane which gives a thicker film than conventional spin‐on‐glass (SOG) film. The new SOG material, HSG2200 (Hitachi Chemical Company, HSG), exhibits far better planarizing capability than the conventional one. A drawback to this film has been crack generation when it is exposed to an oxygen plasma in a resist ashing reactor. A new pretreatment, which we have named reactive glass stabilization (RGS), has been developed. RGS is the exposure of the film to an energetic plasma at low temperature using a parallel electrode sputtering reactor. The surface layer of the film is converted to an condensed state which prevents the oxygen plasma from reaching the inner unconverted layer and delays further reaction between the plasma and the organosiloxane film. Three‐layered interlevel dielectric using the RGS‐treated HSG film as a middle layer was used to planarize a two‐metal level interconnection that had superior characteristics compared to those of conventional SOGs. The resistance increase of Al‐2 lines on the HSG sandwich structure was merely 4% over 0.7 μm line and space, which is far less than that of 76% on the conventional SOG sandwich structure. MOS devices with a two‐metal level interconnection exhibited good electric characteristics and no hot carrier degradation.
Epitope-specific tolerance induction with an engineered immunoglobulin. (1996)

Isologous and heterologous immunoglobulins have been shown to be extremely effective as tolerogenic carriers for nearly 30 years. The efficacy of these proteins is due in part to their long half-life in vivo, as well as their ability to crosslink surface IgM with Fc receptors. The concept of using IgG as a carrier molecule to induce unresponsiveness in the adult immune system has been exploited for simple haptens, such as nucleosides, as well as for peptides. To further evaluate the in vivo potential of these molecules for inducing tolerance to a defined epitope, we have engineered a fusion protein of mouse IgG1 with the immunodominant epitope 12-26 from bacteriophage lambda cI repressor protein. This 15-mer, which contains both a B-cell and T-cell epitope, has been fused in-frame to the N terminus of a mouse heavy chain IgG1 construct, thus creating a "genetic hapten-carrier" system. We describe a novel in vitro and in vivo experimental system for studying the feasibility of engineered tolerogens, consisting of a recombinant flagellin challenge antigen and a murine IgG1 tolerogen, both expressing the lambda repressor epitope 12-26. Herein, we show that peptide-grafted IgG molecules injected i.v., or expressed by transfected, autologous B cells, can efficiently modulate the cellular and humoral immune responses to immunodominant epitopes. This model displays the feasibility of "tailor-designing" immune responses to whole antigens by selecting epitopes for either tolerance or immunity.
Battery Energy Storage System for Aggregated Inertia-Droop Control and a Novel Frequency Dependent State-of-Charge Recovery (2020)

To deal with the technical challenges of renewable energy penetration, this paper focuses on improving the grid voltage and frequency responses in a hybrid renewable energy source integrated power system following load and generation contingency events. A consolidated methodology is proposed to employ a battery energy storage system (BESS) to contribute to voltage regulation through droop-type control and frequency regulation by assimilated inertia emulation (IE) and droop-type control. In addition, a novel frequency-dependent state-of-charge (SOC) recovery (FDSR) is presented to regulate BESS power consumption within the FDSR constraints and recharge the battery during idle periods whenever needed. The efficacy of the proposed BESS controller is demonstrated in an IEEE-9 bus system with a 22.5% photovoltaics (PV) and wind penetration level. The simulation results obtained manifest the satisfactory performance of the proposed controller in regulating simultaneous voltage and frequency in terms of lower rate of change of frequency and better frequency nadir. Furthermore, the proposed FDSR demonstrates its superiority at the time of SOC recovery compared to the conventional approach.
Excited-State Intramolecular Proton Transfer in o-Hydroxybiaryls:  A New Route to Dihydroaromatic Compounds (2003)

An excited-state intramolecular proton transfer (ESIPT) from the phenol OH to the 7'-carbon on the naphthyl ring in o-(1-naphthyl)phenol (3) and 1-(1'-naphthyl)-2-naphthol (4) leads to efficient (Phi = 0.1-0.2) formation of the corresponding dihydrobenzoxanthenes (5 and 7) via quinone methide intermediates. This new reaction represents a clean, efficient, and high-yielding route to benzoxanthenes and dihydrobenzoxanthenes. A related ESIPT of similar efficiency has been detected at the 2'-aromatic position in these systems, by deuterium labeling studies.
Ring-Opening Metathesis Polymerization for the Preparation of Surface-Grafted Polymer Supports (1999)

A series of norbornene-based, l-valine- and l-phenylalanine-containing chiral monomers have been prepared. Starting from norborn-2-ene-5-carboxylic acid chloride and norborn-2-ene-5,6-dicarboxylic anhydride, N-(norborn-2-ene-5-carboxyl)-l-valine (I), N-(norborn-2-ene-5-carboxyl)-l-phenylalanine (II), N-(norborn-2-ene-5-carboxyl)-l-phenylalanine ethyl ester (III), the N,N-(norborn-2-ene-5,6-dicarbimid) (NBDCI)-protected amino acid derivatives NBDCI-l-valine (IV), NBDCI-l-phenylalanine (V), NBDCI-l-valine-tert-butylamide (VI), NBDCI-l-valine-anilide (VII), NBDCI-l-valine-m-nitroanilide (VIII), and NBDCI-l-valine-p-chloroanilide (IX) have been synthesized. Compounds I−IX were polymerized via ring-opening metathesis polymerization (ROMP) using initiators based on both molybdenum (Mo(N-2,6-Me2-C6H3)(CHCMe2Ph)(OCMe(CF3)2)2) (1) and ruthenium (Cl2Ru(CHPh-p-F)(PCy3)2, Cy = cyclohexyl) (2). The polymers were characterized in terms of cis/trans structure as well as optical rotation. Bromomethylated, beaded polymer supports based on poly(styrene−divinylbenzene) (PS-DVB) were prepared either via direct bromomethylation or via transhalogenation of chloromethyl-PS-DVB and subsequently surface-derivatized with norborn-2-ene groups by reaction with sodium norborn-2-ene-5-ylmethanolate. Norborn-2-ene-derivatized silica-based supports were prepared by silanization employing norborn-2-ene-5-yltrichlorosilane. Surface grafting of the norbornene-modified supports with monomers III, VI, and VII was accomplished using ROMP. Both Schrock-type and Grubbs-type initiators were found suitable for that purpose. A poly-III surface-grafted, porous 5 μm silica was found suitable for chiral HPLC separations.
210 km repeaterless 10 Gb/s transmission experiment through nondispersion-shifted fiber using partial response scheme (1995)

In order to increase the dispersion-limited propagation distance at 10 Gb/s through nondispersion-shifted fiber, a chromatic dispersion tolerant signalling technique is used, based upon a reduced optical signal bandwidth. We have achieved a 210 km repeaterless transmission distance at 10 Gb/s over nondispersion-shifted fiber with a measured bit error ratio lower than 10/sup -12/. At this distance, a receiver penalty of 1.7 dB was obtained at 10/sup -10/ bit-error ratio, while an almost penalty-free transmission has been performed through 189 km. The technique relaxes the bandwidth requirements for the optoelectronic components at the transmitter level and involves a standard 10 Gb/s receiver at the output end of the transmission link.< <ETX xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink">&gt;</ETX>
Mesoporous silicon: a platform for the delivery of therapeutics (2007)

Nanostructuring materials can radically change their properties. Two interesting examples highlighted here are nanoscale porosity inducing biodegradability, and nanoscale confinement affecting the physical form of an entrapped drug. Mesoporous silicon is under increasing study for drug-delivery applications, and is the topic of this review. The authors focus on those properties of most relevance to this application, as well as those recent studies published on small molecule and peptide/protein delivery.
Abstract 714: Targeting Coagulation Factor XII to Protect from Cardiac Ischemia Reperfusion Injury (2007)

Formation of fibrin is critical for limiting blood loss at a site of blood vessel injury (hemostasis), but may also contribute to vascular thrombosis and thus exaggerate myocardial ischemia/reperfusion injury. Hereditary deficiency of factor XII (FXII), the protease that triggers the intrinsic pathway of coagulation in vitro, is not associated with spontaneous or excessive injury-related bleeding, but can reduce thrombus formation. Therefore, we studied the contribution of FXII for myocardial ischemia reperfusion injury. Following 30 minutes of ischemia and 24 hours of reperfusion infarct size in FXII deficient mice was significantly reduced as compared to wild type controls (infarct/area at risk, WT vs. FXII−/−, 73.5%±4.4% vs. 42.3±1.6%, p&lt;0.001) despite similar area at risk (WT vs. FXII−/−, 28.3%±1.7% vs. 29.9±1.0%, p=n.s.). There was no difference in bleeding complications and bleeding time. Mice deficient in the FXII substrate factor XI were similarly protected from ischemia reperfusion injury (infarct/area at risk, FXI−/−, 16.9%±4.1%, vs. WT p&lt;0.001). The phenotype of FXII−/−mice could be rescued by intravenous application of human FXII (infarct/area at risk, FXII−/−+FXII, 77.3%±8.4%, p&lt;0.001 vs. FXIIKO). WT mice treated with the FXII inhibitor PCK (Pro-Phe-Arg-chloromethylketone) were similarly protected from myocardial ischemia/reperfusion injury (infarct/area at risk, 46.5% ±3.7%, vs. WT p&lt;0.001). The data suggest that the intrinsic pathway is crucial for pathological clotting in myocardial ischemia reperfusion injury. FXII inhibition may offer a selective and safe strategy to reduce ischemic injury.
Oral Administration of the NMDA Receptor Antagonist S-Ketamine as Add-On Therapy of Depression: A Case Series (2009)

We intended to assess safety, response to treatment and time to response of 1.25 mg/kg oral S-ketamine as add-on to standard antidepressants in four depressed patients. Two patients with melancholic depression responded early and stayed in remission, while two patients with distinct somatic symptoms, chronicity or atypical features did not respond. The limited number of patients does not allow conclusions about efficacy. Oral S-ketamine was well tolerated and could merit being studied in randomised controlled trials due to its higher practicability compared to (S-)ketamine infusion therapy. Clinical subtyping should be considered.