bluuebunny/crossref_metadata_2025_split huggingface dataset:
Coca-Cola – a model of transparency in research partnerships? A network analysis of Coca-Cola’s research funding (2008–2016)
Authors: Serôdio Paulo M , McKee Martin , Stuckler David 
Published: March 2018

AbstractObjectiveTo (i) evaluate the extent to which Coca-Cola’s ‘Transparency Lists’ of 218 researchers that it funds are comprehensive; (ii) map all scientific research acknowledging funding from Coca-Cola; (iii) identify those institutions, authors and research topics funded by Coca-Cola; and (iv) use Coca-Cola’s disclosure to gauge whether its funded researchers acknowledge the source of funding.DesignUsing Web of Science Core Collection database, we retrieved all studies declaring receipt of direct funding from the Coca-Cola brand, published between 2008 and 2016. Using conservative eligibility criteria, we iteratively removed studies and recreated Coca-Cola’s transparency lists using our data. We used network analysis and structural topic modelling to assess the structure, organization and thematic focus of Coca-Cola’s research enterprise, and string matching to evaluate the completeness of Coca-Cola’s transparency lists.ResultsThree hundred and eighty-nine articles, published in 169 different journals, and authored by 907 researchers, cite funding from The Coca-Cola Company. Of these, Coca-Cola acknowledges funding forty-two authors (<5 %). We observed that the funded research focuses mostly on nutrition and emphasizes the importance of physical activity and the concept of ‘energy balance’.ConclusionsThe Coca-Cola Company appears to have failed to declare a comprehensive list of its research activities. Further, several funded authors appear to have failed to declare receipt of funding. Most of Coca-Cola’s research support is directed towards physical activity and disregards the role of diet in obesity. Despite initiatives for greater transparency of research funding, the full scale of Coca-Cola’s involvement is still not known.
Deadbeat control based on a multipurpose disturbance observer for permanent magnet synchronous motors
Authors: Yang Haitao , Zhang Yongchang , Liang Jiejunyi , Xia Bo , Walker Paul D. , Zhang Nong 
Published: March 2018

Robustness against parameter mismatches and position‐sensorless operation are two important research topics for permanent magnet synchronous motor (PMSM) drives. Usually, the existing observers are designed for achieving a specific function. While here, both the above two functions are integrated into the proposed sliding‐mode disturbance observer: (i) if a position sensor is equipped, accurate current regulation can be achieved by deadbeat predictive current control despite mismatched motor parameters; (ii) if the position sensor is not equipped but with a good estimation of motor parameters, the observer can serve as a back electromotive force estimator. Then, the rotor position can be extracted for position‐sensorless control. Usually, a low‐pass filter is required to suppress high‐frequency noises in the conventional sliding‐mode observer. This inevitably leads to phase delay in the estimation. By comparison, a complex coefficient filter is inherently embedded in the proposed method, which can provide accurate estimation without phase delay or magnitude error. Experimental results obtained from a 2.4 kW PMSM drive platform indicate that high‐performance current control can be achieved with good robustness for position sensor‐based operation. Also, rotor position can be accurately estimated with good steady and dynamic performance for position‐sensorless operation.
Understanding the effects of peripheral vision and muscle memory on in‐vehicle touchscreen interactions
Authors: Eren Ayse Leyla , Burnett Gary , Large David R , Harvey Catherine 
Published: March 2018

It is important to gain a better understanding of how drivers interact with in‐vehicle touchscreens to help design interfaces to minimise ‘eyes‐off‐road’ time. The study investigated the relative effects of two interaction mechanisms (peripheral vision – PV, muscle memory – MM) shown to be relevant to visual behaviour when driving, on the time to press different sized buttons (small 6 × 6 cm, medium 10 × 10 cm, large 14 × 14 cm) on an in‐vehicle touchscreen. Twenty‐five participants took part in a driving simulator study and were presented with a single, white, square button on 24 successive trials. For MM conditions, participants wore a pair of glasses blocking their PV and for PV conditions, they were asked to keep their focus on the vehicle ahead. Results showed that task time gradually decreased when participants could only use MM. However, overall task time for MM conditions were significantly higher than PV conditions. Participants rated the use of MM to be more difficult than PV. In contrast, results suggest that for interfaces that utilise peripheral visual processing, the learning effect is not evident and operation times are constant over time. These findings indicate that in‐vehicle touch screens should be designed to utilise PV for making simple button selections with reduced visual demand.
General mathematical model for the calculation of economic cross sections of cables for wind farms collector systems
Authors: Đorđević Ana , Đurišić Željko 
Published: March 2018

A model for calculation of the economic cross sections of cables within the internal network of a wind farm is presented. The economic cross sections of the internal wind farm cables provide maximisation of the profit generated by the wind farm within its life‐span through an optimisation of the balance between the investment and operating costs. This study presents a practical mathematical model for determining the optimal cable cross section based on: the wind statistics at the wind turbine location, wind turbine power curve, price of the electric energy, price of the cable, and interest rate. By using the developed model in the planning phase of a wind farm project each of the connection feeders within the internal cable network can be optimised. The proposed model is demonstrated by the example of a perspective wind farm with a rated power of 25 MW located in the region of Banat, Serbia. The calculations done for the observed wind farm show that the optimisation of the interconnecting cable cross sections makes profit increase of nearly 1 million Euro, compared to the model for the calculation of cable cross sections based only on technical limitations.
Experimental validation of joint phase and amplitude wave-front sensing with coronagraphic phase diversity for high-contrast imaging
Authors: Herscovici-Schiller O. , Mugnier L. M. , Baudoz P. , Galicher R. , Sauvage J.-F. , Paul B. 
Published: March 2018

Context.The next generation of space-borne instruments dedicated to the direct detection of exoplanets requires unprecedented levels of wavefront control precision. Coronagraphic wavefront sensing techniques for these instruments must measure both the phase and amplitude of the optical aberrations using the scientific camera as a wavefront sensor.Aims.In this paper, we develop an extension of coronagraphic phase diversity to the estimation of the complex electric field, that is, the joint estimation of phase and amplitude.Methods.We introduced the formalism for complex coronagraphic phase diversity. We have demonstrated experimentally on the Très Haute Dynamique testbed at the Observatoire de Paris that it is possible to reconstruct phase and amplitude aberrations with a subnanometric precision using coronagraphic phase diversity. Finally, we have performed the first comparison between the complex wavefront estimated using coronagraphic phase diversity (which relies on time-modulation of the speckle pattern) and the one reconstructed by the self-coherent camera (which relies on the spatial modulation of the speckle pattern).Results.We demonstrate that coronagraphic phase diversity retrieves complex wavefront with subnanometric precision with a good agreement with the reconstruction performed using the self-coherent camera.Conclusions.This result paves the way to coronagraphic phase diversity as a coronagraphic wave-front sensor candidate for very high contrast space missions.
The Effect of Fibrinogen Genotype on Fibrinogen Levels after Strenuous Physical Exercise
Authors: Dhamrait S. , Moulding R. , Rumley A. , Lowe G. D. O. , World M. J. , Humphries S. E. , Montgomery H. E. , Brull D.J. 
Published: March 2018

SummaryWe have examined the effect of two f3-fibrinogen gene promoter polymorphisms (-455G>A and -854G>A) on the fibrinogen response to severe exercise in a group of male army recruits undergoing basic training. Fibrinogen was measured pre-training and again serially after severe 48 h final military exercise (FME). Out of 884 subjects, 762 completed training of whom 250 were selected for post-FME study. Fibrinogen levels (g/l) were significantly elevated over baseline levels 2, 48 and 96 h after FME, representing increases of 15.7%, 3.4% and 7.6% (p <0.005; p = 0.05 and p <0.005 respectively), with higher levels in -455A allele carriers than genotype -455GG: 3.17 ± 0.05 vs. 2.94 ± 0.05 (p <0.001), 2.86 ± 0.05 vs. 2.60 ± 0.05 (p <0.0005) and 2.98 ± 0.06 vs. 2.69 ± 0.06 (p <0.0005) at 2, 48 and 96 h respectively. There was no effect of the -854G>A polymorphism on fibrinogen, even after taking into account f3-fibrinogen -455 genotype. Thus the fibrinogen -455G>A polymorphism influences fibrinogen levels following exercise. The effect of genotype might be clinically relevant at times of hyperfibrinogenaemia such as following an acute inflammatory response.
D-Dimer as a Risk Factor for Deep Vein Thrombosis: The Leiden Thrombophilia Study
Authors: Andreescu Astrid , Rosendaal Frits , Cushman Mary 
Published: March 2018

SummaryWe studied the association of D-dimer with the risk of deep vein thrombosis (DVT). D-dimer was measured in 474 patients more than 6 months after diagnosis of a first DVT and in 474 age-and sexmatched controls. For D-dimer above the 70th percentile (130.5 ng/ml), the odds ratio (OR) for DVT was 2.2 (95% CI, 1.6-2.9). The association was unchanged with adjustment for other risk factors. Excluding participants with Factor V Leiden, prothrombin 20210A, or factors VIIIc or IX above the 90th percentile, the OR was 1.6 (95% CI, 1.1-2.3). The risks of DVT with the joint presence of high D-dimer and either factor V Leiden or prothrombin 20210A were increased 12.4-fold (95% CI 5.6-27.7) and 7.2-fold (95% CI 2.1-25.1), respectively. Higher Ddimer concentration was associated with the risk of DVT, and was supra-additive to the risks associated with factor V Leiden and the prothrombin 20210A variant. Persistence of this association in the absence of other hemostatic risk factors for DVT suggests that high D-dimer may be related to other, as yet unknown, risk factors for venous thrombosis. Confirmation of these findings is desirable.
Physical and Functional Interaction Between Cell-Surface Calreticulin and the Collagen Receptors Integrin α2β1 and Glycoprotein VI in Human Platelets
Authors: Elton Catherine , Smethurst Peter , Eggleton Paul , Farndalerd Rich 
Published: March 2018

SummaryCalreticulin is an abundant protein in the endoplasmic reticulum of most cells. In this study, flow cytometry and immunoprecipitation from surface-biotinylated platelets each provided direct evidence that calreticulin is also expressed on the surface of human platelets. Anti-calreticulin antibodies caused platelet activation, inducing Fc RIIa-independent platelet aggregation. In addition, these antibodies inhibited platelet adhesion to the integrin α2β1-specific ligands, GFOGER-GPP and monomeric collagen I, and to the glycoprotein VI-specific ligand, CRP. Inhibition of platelet adhesion to these ligands was independent of integrin αIIbβ3. In resting platelets, calreticulin was shown to interact with integrin α2β1 and glycoprotein VI. Together, these data demonstrate that surface calreticulin is associated with collagen receptors on the platelet surface, where it may play a role in the modulation of the platelet-collagen interaction.Abbreviations: BSA: bovine serum albumin; cC1qR: complement component
1q receptor; CRP: collagen-related peptide; DTSSP: 3,3’-dithiobis (sulfosuccinimidyl propionate); ER: endoplasmic reticulum; GFOGER-GPP: GPC[GPP]5GFOGER[GPP]5GPC; GpVI: glycoprotein VI; HRP: horseradish peroxidase; PDI: protein disulfide isomerase.
Erythropoietin Triggers a Signaling Pathway in Endothelial Cells and Increases the Thrombogenicity of their Extracellular Matrices In Vitro
Authors: Fusté Berta , Serradell Mireia , Escolar Ginés , Cases Aleix , Mazzara Roberto , Castillo Ricardo , Ordinas Antonio , Díaz-Ricart Maribel 
Published: March 2018

SummaryWe demonstrate that exposure of cultured human endothelial cells to rHuEPO resulted in a dose-dependent increase in the tyrosine kinase activity, with phosphorylation of JAK-2 followed by rapid phosphorylation of STAT-5. Simultaneously, rHuEPO induced long-lasting phosphorylation of MAPK p42/44. Activation of this signaling pathways was directly associated with an increase in the thrombogenic properties of the extracellular matrix generated by these cells, when they were exposed to flowing blood. The enhancement in the reactivity of the resulting extracellular matrix towards platelets was associated with a higher expression of tissue factor. All these effects were blocked by an antibody to the EPO receptor and by specific inhibitors of tyrosine phosphorylation. The observed action of rHuEPO on endothelial cells seemed to be specifically triggered by the subsequent events that follow receptor binding, and occurred even at pharmacological concentrations of the cytokine. Our results indicate that rHuEPO has a direct action on the endothelium, increasing the reactivity of the underlying extracellular matrix towards platelets, effect that may be attributed to an increase in the expression of TF.
NFκB is an Essential Intermediate in the Activation of Endothelial Cells by Anti-β2-Glycoprotein 1 Antibodies
Authors: Dunoyer-Geindre Sylvie , de Moerloose Philippe , Galve-de Rochemonteix Béatrix , Reber Guido , Kruithof Egbert 
Published: March 2018

SummaryAntiphospholipid antibodies (aPLA) are associated with thrombophilia and recurrent pregnancy loss. They bind directly to anionic phospholipids or via phospholipid-binding proteins such as β2-glycoprotein 1 (β2GP1). The underlying mechanisms by which aPLA induce a thrombophilic phenotype are not well understood.The present work was done to determine whether antibodies to β2GP1 activate endothelial cells (EC) and whether NFκB is involved in this activation. Incubation of EC with these antibodies resulted in a redistribution of NFκB from the cytoplasm to the nucleus after a delay of several hours. This was accompanied by an increased expression of tissue factor and of the leukocyte adhesion molecules ICAM-1, VCAM-1 and E-selectin. Inhibition of the nuclear translocation of NFκB abolished the response to these antibodies. In comparison to anti-β2GP1 antibodies, incubation of EC with TNF resulted in a more rapid (within 30 minutes) redistribution of NFκB and a more pronounced expression of tissue factor and of the leukocyte adhesion molecules. The slower response to the antibodies as compared to TNF suggests that the NFκB response to anti-β2GP1 antibodies is indirect.Taken together our results imply that NFκB is an essential intermediate in the activation of EC by anti-β2GP1 antibodies.
Intracranial Hemorrhage in Systemic Lupus Erythematosus Associated with an Autoantibody against Factor XIII
Authors: Velasco Pauline , Hill John , Hoffmeister Karen , Kaye Fredric , Lorand Laszlo 
Published: March 2018

SummaryIntracranial hemorrhage in a young woman with systemic lupus erythematosus necessitated two surgical evacuations. In the absence of a family history of bleeding, clot solubility in urea suggested a factor XIII (FXIII) inhibitor. The patient’s IgG bound well to the virgin and the thrombin-modified zymogen ensemble (A2B2 and A2’B2) and to the free rA2 but reacted poorly with the thrombin-modified rA2’. Since the IgG did not block the thrombin-catalyzed proteolysis of A subunits nor the dissociation of the A2’B2, its action might be to interfere with the release of activation peptides from the thrombincleaved zymogen, hindering the conformational change necessary for generating FXIIIa.Treatment with cryoprecipitate and cyclophosphamide arrested the hemorrhage and almost neutralized the antibody so that the patient’s clot became insoluble in urea and showed a close to normally cross-linked γ-γ and αn fibrin chain profile. Nevertheless, she still has detectable anti-FXIII antibody and may be at risk for hemorrhage.
The effect of ß-receptor blockade on factor VIII levels and thrombin generation in patients with venous thromboembolism
Authors: Schönauer Verena , Giannini Sandra , Christ Günter , Quehenberger Peter , Bieglmayer Christian , Stain Milena , Weltermann Ansgar , Kyrle Paul 
Published: March 2018

SummaryHigh factor VIII (FVIII) is a risk factor for venous thromboembolism (VTE). The pathomechanism by which high FVIII leads to an increased risk of VTE is unknown. Physical activity and infusion of adrenalin provoke a rise in FVIII, which can be blocked by a nonselective β-blockade. We tested the hypothesis that in patients with a VTE β-blockade decreases FVIII and inhibits coagulation activation.17 male patients with high FVIII (> 170 IU/dL, n = 7) or low FVIII (<150 IU/dL, n = 10) and a history of VTE received 40 mg of propranolol thrice daily for 14 days. FVIII and vasopressin levels were measured before and during propranolol intake and 28 days thereafter. At the same time points, haemostatic system activation was investigated by measuring prothrombin fragment f1.2 (f1.2) and thrombin antithrombin complexes (TAT) in venous blood and in blood emerging from a skin incision (shed blood).The mean FVIII level before propranolol was 192 IU/dL and 115 IU/dL in patients with high and low FVIII, respectively. During and 28 days after propranolol, no significant change in FVIII was seen in both groups. Changes in f1.2 and TAT were not detectable in either venous blood or in shed blood.β-receptor blockade did not lower FVIII or inhibit haemostatic system activation in patients with VTE and persistently high FVIII. Administration of propranolol cannot be recommended as secondary thromboprophylaxis in patients with high FVIII.
The Impact of the Glycoprotein Ia Collagen Receptor Subunit A1648G Gene Polymorphism on Coronary Artery Disease and Acute Myocardial Infarction
Authors: Gardemann Andreas , Fechter Andreas , Haberbosch Werner , Santoso Sentot , Kroll Hartmut 
Published: March 2018

SummaryPlatelet glycoprotein (GP) Ia is the major receptor for collagen and plays an important role in platelet adhesion and aggregation. Different gene polymorphisms have been identified that induce either various expression levels (C807T) or alterations of the tertiary structure (A1648G) of GPIa. Previously, we could demonstrate an association of the GPIa C807T dimorphism with nonfatal myocardial infarction. We have now analysed the influence of the GPIa A1648G (Br, HPA-5) dimorphism on the risk of coronary artery disease (CAD) and acute myocardial infarction (AMI). DNA samples from 2163 male Caucasian patients who underwent coronary angiography were genotyped by polymerase chain reaction and restriction fragment length analysis. The relation of the GPIa A1648G dimorphism to the extent of CAD was determined by multiple regression analysis with adjustment for coronary risk factors. Odds ratios (OR) as an estimate of relative risk of CAD and AMI and two-tailed p-values were calculated by multiple logistic regression. In the total study sample, no association was detected between the A1648G dimorphism and CAD or AMI. However, upon analysis of low-risk patient subgroups we found an association of the GPIa A1648G polymorphism with the risk and the extent of CAD (patients with high apoAI/apoB ratio: OR 0.59, p = 0.0090; nonand ex-smokers: OR 0.66, p = 0.0131; both inclusion criteria: OR 0.44, p = 0.0003). The relative frequency of the A1648 allele was higher in controls whereas the GG1648 genotype was overrepresented in patients with CAD. This association was also detectable when individuals with low expression levels of GPIa (C807 homozygotes) were analysed (patients with high apoAI/apoB ratio: OR 0.44, p = 0.0045; nonand ex-smokers: OR 0.61, p = 0.0370). Our findings indicate that the A1648G polymorphism of the platelet collagen receptor plays a role in CAD in well defined patient groups.
Neuroprotection by Recombinant Thrombomodulin
Authors: Taoka Yuji , Uchiba Mitsuhiro , Johno Masayoshi , Okajima Kenji 
Published: March 2018

SummaryWe examined whether recombinant human soluble thrombomodulin (rhs-TM) reduces compression trauma-induced spinal cord injury through protein C activation in rats. Administration of rhs-TM, either before or after the induction of spinal cord injury (SCI), markedly reduced the resulting motor disturbances. However, neither rhs-TM pretreated with an anti-rhs-TM monoclonal antibody (MAb) F2H5, which inhibits thrombin binding to rhs-TM, nor those pretreated with MAb R5G12, which selectively inhibits protein C activation by rhsTM, prevented the motor disturbances. Intramedullary hemorrhages, observed 24 h after trauma, were significantly reduced in animals given rhs-TM. The increase in the tissue levels of tumor necrosis factor-α (TNF-α), TNF-α mRNA expression, and the accumulation of leukocytes in the damaged segment of the spinal cord were significantly inhibited in animals receiving rhs-TM, but these effects were not observed following administration of rhs-TM pretreated with MAb R5G12 or MAb F2H5. Leukocytopenia and activated protein C all produced effects similar to those of rhs-TM.These findings suggest that rhs-TM prevents compression traumainduced SCI by inhibiting leukocyte accumulation by reducing the expression of TNF-α mRNA and such therapeutic effects of rhs-TM could be dependent on its protein C activation capacity. Findings further suggest that thrombomodulin can be implicated not only in the coagulation system but in regulation of the inflammatory response.
Rapid Change of Platelet Aggregability in Acute Hyperglycemia
Authors: Sakamoto Tomohiro , Kawano Hiroaki , Hirai Nobutaka , Miyamoto Shinzo , Takazoe Keiji , Soejima Hirofumi , Kugiyama Kiyotaka , Yoshimura Michihiro , Yasue Hirofumi , Ogawa Hisao 
Published: March 2018

SummaryWe examined the alteration of platelet aggregability in acute hyperglycemia during 75-gram oral glucose tolerance tests (OGTT). Twenty subjects underwent 75-gram OGTT and venous blood samples were obtained before (0 min), 60, 120 and 180 min postload. Platelet aggregability shown as the number of small platelet aggregates was measured with a novel laser-light scattering (LS) method. Platelet aggregability increased in parallel with both glucose and immunoreactive insulin (IRI) levels. The number of mean small aggregates at 60 min (12.30 ± 1.10 × 104) was significantly higher than the one at 0 min (8.32 ± 0.88 × 104, p <0.001), 120 min (10.63 ± 0.98 × 104, p <0.05) and 180 min (8.28 ± 0.84 × 104, p <0.001) (mean ± SEM). Small aggregates correlated positively with plasma glucose levels at 60 min postload (r = 0.67, p = 0.001) while not with IRI. It might be important to suppress transient hyperglycemia for preventing the onset of acute coronary syndromes that could be closely related to platelet hyperaggregability.