gebhart/patrepeval huggingface dataset:
The role of CD40 in CD40L- and antibody-mediated platelet activation (2005)

Our initial finding that CD40- and CD40 ligand (CD40L)-deficient mice displayed prolonged tail bleeding and platelet function analyzer (PFA-100) closure times prompted us to further investigate the role of the CD40-CD40L dyad in primary hemostasis and platelet function. Recombinant human soluble CD40L (rhsCD40L), chemical cross-linking of which suggested a trimeric structure of the protein in solution, activated platelets in a CD40-dependent manner as evidenced by increased CD62P expression. CD40 monoclonal antibody (mAb) M3, which completely blocked rhsCD40L-induced platelet activation, also prolonged PFA-100 closure times of normal human blood. In contrast, CD40 mAb G28-5 showed less potential in blocking rhsCD40L-induced CD62P expression and did not affect PFA-100 closure times. However, when added to the platelets after rhsCD40L, G28-5 significantly enhanced the platelet response by causing clustering of, and signaling through, FcgammaRII. Similarly, higher order multimeric immune complexes formed at a 1/3 molar ratio of M90, a CD40L mAb, to rhsCD40L induced strong Fcgamma RII-mediated platelet activation when translocated to the platelet surface in a CD40-dependent manner, including the induction of morphological shape changes, fibrinogen binding, platelet aggregation, dense granule release, microparticle generation and monocyte-platelet-conjugate formation. The results suggest that CD40 may play a role in primary hemostasis and platelet biology by two independent mechanisms: First, by functioning as a primary signaling receptor for CD40L and, second, by serving as a docking molecule for CD40L immune complexes. The latter would also provide a potential mechanistic explanation for the unexpected high incidence of CD40L mAb-associated thrombotic events in recent human and animal studies.
5-Hydroxytryptamine (5-HT)<sub>1A</sub> Autoreceptor Adaptive Changes in Substance P (Neurokinin 1) Receptor Knock-Out Mice Mimic Antidepressant-Induced Desensitization (2001)

Antagonists at substance P receptors of the neurokinin 1 (NK1) type have been shown to represent a novel class of antidepressant drugs, with comparable clinical efficacy to the selective serotonin (5-HT) reuptake inhibitors (SSRIs). Because 5-HT(1A) receptors may be critically involved in the mechanisms of action of SSRIs, we examined whether these receptors could also be affected in a model of whole-life blockade of NK1 receptors, i.e. knock-out mice lacking the latter receptors (NK1-/-). 5-HT(1A) receptor labeling by the selective antagonist radioligand [(3)H]N-[2-[4-(2-methoxyphenyl)1-piperazinyl]-ethyl]-N-(2-pyridinyl)-cyclohexanecarboxamide (WAY 100635) and 5-HT(1A)-dependent [(35)S]GTP-gamma-S binding at the level of the dorsal raphe nucleus (DRN) in brain sections, as well as the concentration of 5-HT(1A) mRNA in the anterior raphe area were significantly reduced (-19 to -46%) in NK1-/- compared with NK1+/+ mice. Furthermore, a approximately 10-fold decrease in the potency of the 5-HT(1A) receptor agonist ipsapirone to inhibit the discharge of serotoninergic neurons in the dorsal raphe nucleus within brainstem slices, and reduced hypothermic response to 8-OH-DPAT, were noted in NK1-/- versus NK1+/+ mice. On the other hand, cortical 5-HT overflow caused by systemic injection of the SSRI paroxetine was four- to sixfold higher in freely moving NK1-/- mutants than in wild-type NK1+/+ mice. Accordingly, the constitutive lack of NK1 receptors appears to be associated with a downregulation/functional desensitization of 5-HT(1A) autoreceptors resembling that induced by chronic treatment with SSRI antidepressants. Double immunocytochemical labeling experiments suggest that such a heteroregulation of 5-HT(1A) autoreceptors in NK1-/- mutants does not reflect the existence of direct NK1-5-HT(1A) receptor interactions in normal mice.
Relationship between systemic inflammation and rhythmicity of acute exacerbations of COPD (2021)

There is a close relationship between acute exacerbations (AE) of COPD, systemic inflammation and lung function decline. <b>Aim:</b> To determine the relationship between a high CRP level during AE-COPD and the rhythmicity of occurrence of these acute events. <b>Methods:</b> It is a retrospective single center study including COPD patients admitted to our hospital between 2005 and 2017. We included patients with an available CRP value during at least 3 AE. We considered moderate and severe AE. We calculated the mean CRP value for each patient. We compared two groups of patients: G1: mean CRP<50 mg/L (287 patients, 44%), G2: mean CRP≥50 mg/L (363, 56%). <b>Results:</b> A total of 650 COPD patients were included in the study. The time period between the AE1-AE2, AE2-AE3, AE3-AE4, AE4-AE5 was respectively 202, 133, 128, and 117 days. The time to next event is shorter in G2 (192, 126, 123, and 115 days) compared to G1 (221, 137, 132, and 124 days) without a significant difference. <b>Conclusions:</b> Time period between AE-COPD is becoming shorter over time. The time to next event is earlier in patient with a higher systemic inflammation. The latter is a major determinant of the perpetuation of AE and should be considered while managing COPD patients.
Objective video quality measurement using various degradation factors (2006)

Abstract:- In this paper, we propose a new video quality measurement method which is based on several degradation factors. The proposed method assumes that reference videos are available. In the proposed algorithm, the VQM (Video Quality Metric) is calculated as a weighted sum of seven features which represent sources of various video degradations. In particular, the degradation factors include PSNR in the lowest frequency band of the wavelet transform, PSNR in edge areas, edge error ratio, degradation ratio of edge images, a blocking coefficient, PSNR in visible chrominance signals and a contrast attenuation ratio. Experimental results show that the proposed method consistently provides satisfactory performances. Key-Words:- video quality, objective video quality measurement, degradation factors. 1
Identification of CD34+ subsets after glycoprotease selection: engraftment of CD34+Thy-1+Lin- stem cells in fetal sheep. (1996)

Epitopes on the CD34 molecule detected by some CD34 antibodies can be cleaved by a unique glycoprotease from Pasteurella haemolytica, which cleaves only glycoproteins rich in O-linked glycans. A method to isolate CD34+ cells from adult bone marrow was developed subsequently, in which CD34+ cells were isolated in high purity and yield following immunomagnetic bead selection and detachment with the glycoprotease. Using a variety of other cell-surface markers shown here to be insensitive to glycoprotease, committed progenitors of T lymphoid, B lymphoid, monomyeloid, megakaryoblastic, or erythroid lineages could be identified. Significantly, candidate hematopoietic stem cells (HSC) that are contained within a CD34+Lin- (CD2-, CD14-, CD15-, CD16-, CD19-) (or CD34+CD38-) subset expressing the Thy-1 antigen (CDw90), c-kit receptor (CD117), and CDw109 but lacking expression of CD71 and HLA-DR antigens also were detected. Functionally distinct subsets of glycoprotease-selected CD34+ cells were identified and subfractionated using flow cytometry and fluorescence-activated cell sorting (FACS). These subsets included candidate HSCs expressing the CD34+Thy-1+Lin- phenotype, which were sorted from a CD34+ fraction of a mobilized peripheral blood (MPB) sample. In a fetal sheep model, when CD34+Thy-1+Lin- cells were injected intraperitoneally, they were capable of homing to the marrow, where they generated long-term multilineage hematopoiesis and maintained human CD34+ cells, indicating that candidate HSC subsets of CD34+ cells selected with this highly specific enzyme were capable of engraftment in vivo. The ability to identify and purify virtually any phenotypically defined subset of glycoprotease-selected CD34+ stem/progenitor cells should facilitate the study of hematopoiesis in vitro and in animal models in vivo as well as the development of novel genetic techniques for the correction of specific blood cell disorders in humans.
Detecting context sensitive hot spots in standard cell libraries (2009)

Advances in lithography patterning have been the primary driving force in microelectronics manufacturing processes. With the increasing gap between the wavelength of the optical source and feature sizes, the accompanying strong diffraction effects have a significant impact on the pattern fidelity of on-silicon layout shapes. Layout patterns become highly sensitive to those context shapes lying within the optical radius of influence. Under such optical proximity effects, manufacturability hot spots such as necking and bridging may occur. Studies have shown that manufacturability hot spots are pattern dependent in nature and should be considered at the design stage [1]. It is desirable to detect these hot spots as early as possible in the design flow to minimize the costs for correction. In this work, we propose a hot spot prediction method based on a support vector machine technique. Given the location of a hot spot candidate and its context patterns, the proposed method is capable of efficiently predicting whether a candidate would become a hot spot. It takes just seconds to classify thousands of samples. Due to its computational efficiency, it is possible to use this method in physical design tools to rapidly assess the quality of printed patterns. We demonstrate one such application in which we evaluate the layout quality in the boundary region of standard cells. In the conventional standard cell layout optimization process, lithography simulation is the main layout verification method. Since it is a very time-consuming process, the iterative optimization approach between simulation and layout correction [2] takes a long time and only a limited number of context patterns can be explored. We show that with the proposed hot spot prediction method, for each standard cell, a much greater context pattern space can be explored, and the context sensitivity of a hot spot candidate located near a cell boundary can be estimated.
Reversal of Acute Paraplegia with Cerebrospinal Fluid Drainage After Endovascular Thoracic Aortic Aneurysm Repair (2001)

ALTHOUGH data from animal studies of acute polycythemia show that this condition is associated with a decreased cardiac output and increased systemic vascular resistance (SVR) because of an increased blood viscosity, 1-3 this is not confirmed in man. In contrast to polycythemia, acute isovolemic hemodilution leads to an increase in cardiac output, a decrease in SVR, and an increase in the oxygen extraction. However, there is no report in the literature on the effects of acute isovolemic hemodilution in a polycythemic individual. We describe the treatment and the effects of acute hemodilution in a patient with chronic polycythemia undergoing surgery for an erythropoietinproducing renal tumor.
MPSoC memory optimization using program transformation (2007)

Multiprocessor system-on-a-chip (MPSoC) architectures have received a lot of attention in the past years, but few advances in compilation techniques target these architectures. This is particularly true for the exploitation of data locality. Most of the compilation techniques for parallel architectures discussed in the literature are based on a single loop nest. This article presents new techniques that consist in applying loop fusion and tiling to several loop nests and to parallelize the resulting code across different processors. These two techniques reduce the number of memory accesses. However, they increase dependencies and thereby reduce the exploitable parallelism in the code. This article tries to address this contradiction. To optimize the memory space used by temporary arrays, smaller buffers are used as a replacement. Different strategies are studied to optimize the processing time spent accessing these buffers. The experiments show that these techniques yield a significant reduction in the number of data cache misses (30%) and in processing time (50%).
Detecting Primary User Emulation Attacks in Cognitive Radio Networks via Physical Layer Network Coding (2013)

Primary user emulation (PUE) attacks on cognitive radio networks pose a serious threat to the deployment of this technique. Previous approaches usually depend on individual or combined received signal strength (RSS) measurements to detect emulators. In this paper, we propose a new mechanism based on physical layer network coding to detect the emulators. When two signal sequences interfere at the receiver, the starting point of collision is determined by the distances among the receiver and the senders. Using the signal interference results at multiple receivers and the positions of reference senders, we can determine the position of the ‘claimed’ primary user. We can then compare this localization result with the known position of the primary user to detect the PUE attack. We design a PUE detection mechanism for wireless networks with trustworthy reference senders. We analyze the overhead of the proposed approach and study its detection accuracy through simulation.
Record linkage with uniqueness constraints and erroneous values (2010)

Many data-management applications require integrating data from a variety of sources, where different sources may refer to the same real-world entity in different ways and some may even provide erroneous data. An important task in this process is to recognize and merge the various references that refer to the same entity. In practice, some attributes satisfy a uniqueness constraint---each real-world entity (or most entities) has a unique value for the attribute ( e.g. , business contact phone, address, and email). Traditional techniques tackle this case by first linking records that are likely to refer to the same real-world entity, and then fusing the linked records and resolving conflicts if any. Such methods can fall short for three reasons: first, erroneous values from sources may prevent correct linking; second, the real world may contain exceptions to the uniqueness constraints and always enforcing uniqueness can miss correct values; third, locally resolving conflicts for linked records may overlook important global evidence. This paper proposes a novel technique to solve this problem. The key component of our solution is to reduce the problem into a k -partite graph clustering problem and consider in clustering both similarity of attribute values and the sources that associate a pair of values in the same record. Thus, we perform global linkage and fusion simultaneously, and can identify incorrect values and differentiate them from alternative representations of the correct value from the beginning. In addition, we extend our algorithm to be tolerant to a few violations of the uniqueness constraints. Experimental results show accuracy and scalability of our technique.
Improved Adhesion of Acrylic Restorative Materials to Dental Enamel by Precoating with Monomers Containing Phosphonate Groups (1977)

The adhesion of acrylic composite restorative materials to etched dental enamel is increased by a factor of two or more when the enamel is coated with a thin layer of vinyl-benzyl phosponic acid (VBPA) prior to forming the enamel-restorative bond. The present results support the suggestion that the enhanced adhesion is attributable to bonding between calcium ions in the enamel surface and phosphonate groups in the VBPA.
Domain 1 of the urokinase receptor (uPAR) is required for uPAR‐mediated cell binding to vitronectin (2000)

In the present paper we have analyzed uPAR-mediated cellular binding to vitronectin using the murine erythroid progenitor cell line 32D. We show that expression of uPAR in 32D cells promotes cellular binding to vitronectin, but fails to support cell spreading. The strength of binding is correlated to the expression level of uPAR and is strongly stimulated by the presence of uPAR ligands. Using a truncated variant of uPAR lacking domain 1 and by antibody inhibition experiments, we demonstrate that domain 1 plays a crucial role in uPAR-mediated cellular binding. The failure of the mutant uPAR to promote cellular binding is paralleled by a strong reduction in the affinity for vitronectin in vitro.
Metal ion binding by amino acids: Strontium and barium <scp>l</scp>‐aspartate trihydrate Sr/Ba(<scp>l</scp>‐Asp) · 3 H<sub>2</sub>O (1990)

Abstract Strontium and barium l ‐aspartate are obtained by neutralization of aqueous solutions of l ‐aspartic acid with strontium or barium hydroxide, respectively. Slow crystallization from hot water affords the crystalline trihydrates, saturated solutions of which show pH values of 11.0 and 10.8 at ambient temperature. – The crystal structure of the two compounds has been determined by single crystal X‐ray diffraction. The compounds are isomorphous (orthorhombic, space group P 2 1 2 1 2 1 ), and the structural parameters are very similar as expected from the small differences in the ionic radii of the two metals. – The cations are arranged in double strings parallel to the b axis. The l ‐aspartate dianions are bridging these double strings by chelating contacts of the two carboxylate groups with the metal atoms of different strings to give layers. While the α‐carboxylate groups are only bidentate and associated with one metal atom each, the β‐carboxylate oxygen atoms are also each bridging two adjacent metals of the neighbouring string. The three water molecules are all coordinated to the metal atoms, which attain coordination number 9 . The amino groups are not engaged in metal coordination, but are part of a system of hydrogen bonds cross‐linking the layers.
Standing stabilizability and stepping maneuver in planar bipedalism based on the best COM-ZMP regulator (2009)

The goal of this paper is to answer (i) how the stabilization performance of a biped controller can be evaluated on a certain invariant supporting region, (ii) how the standing stabilizer which performs the best on a given supporting region can be designed, (iii) how the system can be judged if it is stabilizable by the best standing stabilizer without deforming the current supporting region, and (iv) how the supporting region should be deformed if it is judged to be necessary. In order to answer these question, the stable standing region is defined. It gives a criterion to design the best standing stabilizer, to judge if the deformation of the supporting region is necessary to stabilize the system, and to maneuver the stepping motion in accordance with the standing stabilizability condition, which is also defined in the paper. It is found that the best standing stabilizer can be designed by a simple pole-assignment technique. This framework unifies the standing stability and the stepping stability of bipedalism, which have been separately considered in conventional studies. The discussion goes on an approximate planar COM-ZMP model, in which the total mass is concentrated at the center of mass, and the position of ZMP is regarded as the input. Though it is the simplest dynamical model of bipeds, it can conceal differences of body constitutions and represent the macroscopic dynamics. Therefore, this paper contributes to not only the biped robot controller design but also the biomechanical analyses.
Roles for fibrinogen, immunoglobulin and complement in platelet activation promoted by <i>Staphylococcus aureus</i> clumping factor A (2005)

Staphylococcus aureus is an important cause of infective endocarditis (IE) in patients without a history of prior heart valve damage. The ability to stimulate the activation of resting platelets and their subsequent aggregation is regarded as an important virulence factor of bacteria that cause IE. Clumping factor A is the dominant surface protein responsible for platelet activation by S. aureus cells in the stationary phase of growth. This study used Lactococcus lactis as a surrogate host to study the mechanism of ClfA-promoted platelet activation. Expression of ClfA from a nisin-inducible promoter demonstrated that a minimum level of surface-expressed ClfA was required. Using platelets that were purified from plasma, the requirement for both bound fibrinogen and immunoglobulin was demonstrated. The immunoglobulin G (IgG) requirement is consistent with the potent inhibition of platelet activation by a monoclonal antibody specific for the platelet FcgammaRIIa receptor. Furthermore the IgG must contain antibodies specific for the ClfA A domain. A model is proposed whereby bacterial cells armed with a sufficient number of surface-bound fibrinogen molecules can engage resting platelet glycoprotein GPIIb/IIIa, aided by bound IgG molecules, which encourages the clustering of FcgammaRIIa receptors. This can trigger activation of signal transduction leading to activation of GPIIb/IIIa and aggregation of platelets. In addition, analysis of a mutant of ClfA totally lacking the ability to bind fibrinogen revealed a second, although less efficient, mechanism of platelet activation. The fibrinogen-independent pathway required IgG and complement deposition to trigger platelet aggregation.
A functional screening of the kinome identifies the Polo‐like kinase 4 as a potential therapeutic target for malignant rhabdoid tumors, and possibly, other embryonal tumors of the brain (2017)

Our findings indicate that rhabdoid tumor cell proliferation is highly dependent on PLK4 and suggest that targeting PLK4 with small-molecule inhibitors may hold a novel strategy for the treatment of MRT and possibly other embryonal tumors of the brain. This is the first time that PLK4 has been described as a potential target for both brain and pediatric tumors.
Clopidogrel with or without Omeprazole in Coronary Artery Disease (2010)

Among patients receiving aspirin and clopidogrel, prophylactic use of a PPI reduced the rate of upper gastrointestinal bleeding. There was no apparent cardiovascular interaction between clopidogrel and omeprazole, but our results do not rule out a clinically meaningful difference in cardiovascular events due to use of a PPI. (Funded by Cogentus Pharmaceuticals; ClinicalTrials.gov number, NCT00557921.).
Efficacy of B16 Melanoma Cells Exposed <i>In Vitro</i> to Long-Term IFN-α Treatment (B16α Cells) as a Tumor Vaccine in Mice (1998)

B16 melanoma cells exposed to >2 weeks of in vitro interferon-alpha (IFN-alpha) treatment (B16alpha cells) were UV inactivated and used for vaccination. This vaccination was efficacious against challenge with parental B16 cells in the absence of adjuvant therapy. Vaccinations based on parental cells and B16 cells exposed to short-term in vitro IFN-alpha treatment were not effective. The efficacy of B16alpha vaccination was evaluated using three B16 tumor models. Using intraperitoneal (i.p.) tumor challenge given after vaccination, vaccination efficacy depended on the concentration of IFN-alpha to which B16alpha cells were exposed, the number of inactivated B16alpha cells inoculated, the number of inoculations administered, and the amount of tumor burden. A significant fraction (30%) of vaccinated mice surviving initial challenge had durable immunity against a second parental tumor challenge. This immunity increased to 92% with administration of a single booster vaccination. Using metastatic tumor challenge given after vaccination, vaccination reduced lung metastases by approximately 67%. Using vaccination begun 3 days after subcutaneous (s.c.) tumor challenge, regression of established tumor occurred when vaccination was given i.p. (39%) or contralaterally s.c. (53%). Taken together, the results suggest that vaccination with inactivated B16alpha cells may serve as a model for induction of host tumor immunity against primary or secondary tumors.