bluuebunny/crossref_metadata_2025_split huggingface dataset:
H2chemistry in interstellar ices: the case of CO ice hydrogenation in UV irradiated CO:H2ice mixtures
Authors: Chuang K.-J. , Fedoseev G. , Qasim D. , Ioppolo S. , van Dishoeck E. F. , Linnartz H. 
Published: July 2018

Context.In dense clouds, hydrogenation reactions on icy dust grains are key in the formation of molecules, like formaldehyde, methanol, and complex organic molecules (COMs). These species form through the sequential hydrogenation of CO ice. Although molecular hydrogen (H2) abundances can be four orders of magnitude higher than those of free H-atoms in dense clouds, H2surface chemistry has been largely ignored; several laboratory studies show that H2does not actively participate in “non-energetic” ice chemistry because of the high activation energies required.Aims.For the example of CO ice hydrogenation, we experimentally investigated the potential role of H2molecules on the surface chemistry when energetic processing (i.e., UV photolysis) is involved. We test whether additional hydrogenation pathways become available upon UV irradiation of a CO:H2ice mixture and whether this reaction mechanism also applies to other chemical systems.Methods.Ultra-high vacuum (UHV) experiments were performed at 8–20 K. A pre-deposited solid mixture of CO:H2was irradiated with UV-photons. Reflection absorption infrared spectroscopy (RAIRS) was used as an in situ diagnostic tool. Single reaction steps and possible isotopic effects were studied by comparing results from CO:H2and CO:D2ice mixtures.Results.After UV-irradiation of a CO:H2ice mixture, two photon-induced products, HCO and H2CO, are unambiguously detected. The proposed reaction mechanism involves electronically excited CO in the following reaction steps: CO + hν→CO*, CO*+ H2→HCO + H where newly formed H-atoms are then available for further hydrogenation reactions. The HCO formation yields have a strong temperature dependence for the investigated regime, which is most likely linked to the H2sticking coefficient. Moreover, the derived formation cross section reflects a cumulative reaction rate that mainly determined by both the H-atom diffusion rate and initial concentration of H2at 8–20 K and that is largely determined by the H2sticking coefficient. Finally, the astronomical relevance of this photo-induced reaction channel is discussed.
Le respect des obligations légales et règlementaires du chirurgien-dentiste
Authors: Aknine B. 
Published: July 2018

Le chirurgien-dentiste est soumis au respect des dispositions légales et réglementaires dans l’exercice de sa profession, puis au sein du cabinet dentaire proprement-dit et enfin en sa qualité d’employeur.
Aussi, le respect des obligations est-il pour tout professionnel de santé une obligation morale, éthique, déontologique et légale, dont le manquement est source de contentieux.
Afin de mieux appréhender les obligations du chirurgien-dentiste dans sa sphère d’activité, un exercice utilisant la qualité comme un outil permet d’adapter le mieux possible les obligations légales et réglementaires qui nous sont imposées dans notre exercice quotidien tout en stimulant le plaisir du travail bien fait et bien pensé.
Transformer vos processus ressources humaines pour améliorer votre prise en charge du patient, votre qualité et vos résultats
Authors: Boukhobza A. , Etchebarne T. 
Published: July 2018

L’objectif de cet article est d’identifier quels sont les processus ressources humaines à mettre en place au sein des cabinets d’orthodontie pour à la fois améliorer la prise en charge des patients, mais aussi la rentabilité de la structure tant en termes d’organisation que financièrement.
Le travail sur la cohésion des équipes va créer un engagement collectif qui dépend d’une part de la qualité du recrutement des collaborateurs, et ensuite des leviers de motivation mis en place au sein des équipes et entretenus dans le temps. Dans les équipes la collaboration intergénérationnelle doit être gérée et optimisée.
D’autre part l’orthodontiste dirigeant doit avoir une stratégie et des objectifs clairs pour pouvoir communiquer efficacement. Il doit par ailleurs connaître les outils de communication selon les circonstances pour faire passer les messages dont il a besoin.
Binding of Heparin Fractions to von Willebrand Factor: Effect of Molecular Weight and Affinity for Antithrombin III
Authors: Baruch D , Ajzenberg Nadine , Denis Cécile , Legendre Paulette , Lormeau Jean-Claude , Meyer Dominique 
Published: July 2018

SummaryTo investigate the influence of the structure of heparin on its binding to vWF, we compared heparin fractions of different molecular weight (MW) or affinity for antithrombin III (ATIII). We studied the interaction of purified 125I-vWF or plasma vWF, labeled with a pool of 125I-monoclonal antibodies to vWF, with unfractionated heparin immobilized on agarose beads. Fractions were compared as competitors of these interactions and their effect was quantitated by their half-maximal inhibition (IC50). When the MW of the fractions decreased, especially below 7500, their IC50 increased, indicating that the affinity of the fractions for vWF decreased with their MW. Using heparin-derived oligosaccharides, we also demonstrated that a minimal chain length of 18 monosaccharides was required for heparin binding to vWF. In addition, different fractions with low affinity for ATIII were compared as competitors of 125-vWF binding to heparin-agarose. Despite a very low content of ATIII binding sites, some fractions retained a low IC50. Thus, heparin interaction with vWF is independent of the presence of the ATIII binding site and is mostly dependent on the length of the heparin chain. These data suggest that unfractionated heparin is a more potent inhibitor of vWF-dependent functions than low MW heparin fractions.
Fibrinogen, D-Dimer and Thrombin-Antithrombin Complexes in a Random Population Sample: Relationships with Other Cardiovascular Risk Factors
Authors: Giansante Carlo , Fiotti Nicola , Cattin Luigi , Col Paolo Giovanni Da , Calabrese Salvatore 
Published: July 2018

SummaryFibrinogen is an independent risk factor for cardiovascular disease and both D-Dimer and Thrombin-Antithrombin complexes may be suitable as laboratory markers of deep venous thrombosis and are becoming more widespread in clinical practice. The aim of our study was to evaluate their normal range and to examine their correlation with various cardiovascular risk factors. Fibrinogen, D-Dimer and Thrombin-Antithrombin complexes were assessed in 516 normal subjects randomly selected from the National Health Service register of Trieste (Italy). In our community the mean value of fibrinogen was 283 ± 71 mg/dl. Fibrinogen increases with age in males and was significantly higher in male smokers. In non-smokers, females had significantly higher fibrinogen values than males. The mean value of D-Dimer was 306 ± 130 ng/ml. In females it is significantly higher. The fibrinogen and D-Dimer correlation coefficient was 0.20 (p < 0.001). The mean level of Thrombin-Antithrombin complexes was 6.25 ±6.8 ng/ml with a distribution markedly skewed towards the left; males had lower concentration than females (p = 0.047). Multiple regression analysis for fibrinogen as a dependent variable showed that D-Dimer, LDL- eholesterol, Body-Mass Index and Thrombin-Antithrombin complexes were poor predictors for fibrinogen plasma levels (R2 = 0.23) and that fibrinogen, ApoAl and age can explain only about 10% of the observed variability in D-Dimer.
Haemostatic Abnormalities Persist Despite Glycaemic Improvement by Insulin Therapy in Lean Type 2 Diabetic Patients
Authors: Knöbl Paul , Schernthaner Guntram , Schnack Christoph , Pietschmann Peter , Proidl Sylvia , Prager Rudolf , Vukovich Thomas 
Published: July 2018

SummaryDiabetes mellitus is associated with disturbances of the haemostatic system, which might contribute to the development of diabetic vascular disease. We investigated the effect of metabolic improvement by insulin therapy on the haemostatic system in 61 patients with type 2 diabetes mellitus and secondaxy sulfunyluiea failure compared with 45 healthy control subjects matched for age, sex and BMI. Median age was 65, median diabetes duration 10 years. Median HbA1c (10%) and fructosamine (4.0 mM) levels were elevated before induction of therapy and decreased significantly within 6 months of insulin treatment to 7.5% and 3.0 mM, respectively (p <0.0001). Compared with control subjects, median plasma levels of fibrinogen (317 vs 286 mg/dl), coagulation factor VII activity (1.1 vs 0.89 U/1), von Willebrand factor (1.6 vs 1.3 U/1), D-dimer (105 vs 86 jug/1), protein C:Ag (1.24 vs 0.95 U/1), total protein S:Ag (1.15 vs 0.91 U/1), and antithrombin III activity (1.17 vs 1.08 U/1) were significantly elevated. Levels of free protein S were not different from control values. No significant decline of coagulation parameters could be recorded during insulin therapy. Patients with diabetic vasculopathy had higher levels of D-dimer than those without (133 vs 76 μg/1 before, 109 vs 88 μg/1 during therapy), whereas the other haemostatic parameters were not different. Our data indicate a significant activation of the coagulation system in diabetic patients with secondary failure to sulfonylurea drugs, with signs of a prethrombotic state and endothelial cell disturbance. Induction of insulin therapy results in a significant improvement of glycaemic and lipid metabolism, but the persisting enhanced activity state of the haemostatic system might contribute to the increased cardiovascular mortality of type 2 diabetic patients.
Hereditary Protein C-Deficiency: Laboratory Values in Transmitters and Guidelines for the Diagnostic Procedure Report on a Study of the SSC Subcommittee on Protein C and Protein S
Authors: Pabinger I , Allaart C F , Hermans J , Briët E , Bertina R M ,   The Protein C Transmitter Study Group
Published: July 2018

SummaryA multicenter study on protein C-antigen and -activity values was carried out in transmitter patients with hereditary protein C deficiency (diagnosis established by pedigree analysis) and in normal controls in order to (1) establish the range of protein C levels in genetically determined heterozygotes and (2) to evaluate the usefulness of statistical procedures to discriminate between protein C deficient patients and controls. In transmitters absolute protein C activity values ranged from 19 to 82% and antigen values from 22 to 88.5%. Most transmitter patients could clearly be differentiated from the control group. However, in some transmitter patients values of protein C were within the range of the control group. The discrimination between transmitters and controls could be improved by statistical procedures. Using tolerance ellipses the overlapping area of the two groups was smallest when (factor II antigen + factor X antigen)/2 was plotted against protein C antigen. To specify the degree of uncertainty likelihood ratios were calculated to obtain the posterior probability for an individual for being deficient or not. In quadratic discriminant analysis the best discrimination between transmitters and controls was obtained using protein C activity versus factor X antigen and protein C antigen versus factor X antigen. Based on these analysis an equation was derived, which allows the calculation of the likelihood ratio favouring deficiency or non-deficiency in an individual.
Influence on Platelet Function by Heparin in Men with Unstable Coronary Artery Disease
Authors: Berglund Ulf , Wallentin Lars 
Published: July 2018

SummaryNinetyseven men with unstable coronary artery disease (CAD), i.e. unstable angina or a non Q-wave myocardial infarction, entered a double-blind placebo-controlled study with heparin intravenously 30,000-40,000 U daily. Platelet function was evaluated as ex vivo aggregation toward collagen and ADP and as the platelet inhibitory effect of prostacyclin, before and after 5 days of treatment. Heparin increased aggregation induced by ADP 1 εM from 39.6 ± 3.1% to 52.1 ± 4.1% (p = 0.014) and reduced the inhibition of aggregation by prostacyclin 1.0 ng/ml from 59.6 ± 3.7% to 39.3 ± 5.6% (p <0.001). No changes occurred in the placebo group.Thus, treatment with heparin enhances the platelet sensitivity to ADP and decreases the platelet inhibitory effect of prostacyclin in men with unstable CAD. Concomitant treatment with acetylsalicylic acid abolishes the increased reponse to ADP, but does not seem to influence the interaction between heparin and prostacyclin.
Antithrombin III: A Database of Mutations
Authors: Lane D A , Ireland H , Olds R J , Thein S L , Perry D J , Aiach M 
Published: July 2018

SummaryElucidation of the molecular defects reponsible for antithrombin III deficiency is proceeding rapidly. In order that a record is kept of the new and duplicated mutations that are found, we have compiled a database that we plan to update annually. In this, the first report of the database, we list 6 antithrombin III locus sequence polymorphisms and 94 recorded mutations causing functional deficiency of the protein, 38 of which are novel. As is the case with mutations affecting other protein genes, most mutations of antithrombin III involve a CG to TG or CA change.
Ticlopidine Selectively Inhibits Human Platelet Responses to Adenosine Diphosphate
Authors: Cattaneo Marco , Akkawat Benjaporn , Lecchi Anna , Cimminiello Claudio , Capitanio Anna M , Mannucci Pier Mannuccio 
Published: July 2018

SummaryPlatelet aggregation and fibrinogen binding were studied in 15 individuals before and 7 days after the oral administration of ticlopidine (250 mg b.i.d.). Ticlopidine significantly inhibited platelet aggregation induced by adenosine diphosphate (ADP), the endoperoxide analogue U46619, collagen or low concentrations of thrombin, but did not inhibit platelet aggregation induced by epinephrine or high concentrations of thrombin. Ticlopidine inhibited 125I-fibrinogen binding induced by ADP, U46619 or thrombin (1 U/ml). The ADP scavengers apyrase or CP/CPK, added in vitro to platelet suspensions obtained before ticlopidine, caused the same pattern of aggregation and 125I-fibrihogen binding inhibition as did ticlopidine. Ticlopidine did not inhibit further platelet aggregation and 125I-fibrinogen binding induced in the presence of ADP scavengers. After ticlopidine administration, thrombin or U46619, but not ADP, increased the binding rate of the anti-GPIIb/IIIa monoclonal antibody 7E3 to platelets. Ticlopidine inhibited clot retraction induced by reptilase plus ADP, but not that induced by thrombin or by reptilase plus epinephrine, and prevented the inhibitory effect of ADP, but not that of epinephrine, on the PGE1-induced increase in platelet cyclic AMP. The number of high- and low-affinity binding sites for 3H-ADP on formalin-fixed platelets and their K
d were not modified by ticlopidine. These findings indicate that ticlopidine selectively inhibits platelet responses to ADP.
Comparison of Factor VIII Levels after Adrenalin in Classic Hemophilia and von Willebrand’s Disease (vWd)
Authors: Eyster M Elaine , Ballard James O , Prager David 
Published: July 2018

SummaryThe factor VIII response to adrenalin was compared in 5 patients with von Willebrand’s disease (vWd) and 10 hemophiliacs with baseline factor VIII procoagulant activity (VIIIAHF) of 0.01 u/ml or greater. Patients with vWd showed a two-fold VIII AHF increase, while those with hemophilia showed no significant change 1 hr following the subcutaneous injection of adrenalin. These results suggest that the adrenalin stimulation test may be of value in distinguishing certain patients with mild hemophilia from those with vWd.
Platelet Adhesion to Collagen in Subtypes of Type I von Willebrand’s Disease Is Dependent on Platelet von Willebrand Factor
Authors: d'Alessio Patrizia , Zwaginga Jaap Jan , de Boer Hetty C , Federici Augusto B , Rodeghierio Francesco , Castaman Giancarlo , Mariani Guglielmo , Msnnucci P Mannuccio , de Groot Phillip G , Sixma Jan J 
Published: July 2018

SummaryVon Willebrand’s disease type I, characterized by low levels of factor VIII coagulant activity (VTII :C), von Willebrand factor antigen (vWF:Ag) and ristocetin cofactor activity (RiCof) (1), can be subdivided on the basis of platelet von Willebrand factor into subtype platelet normal, platelet discordant, and platelet low (2). We have investigated the contribution of platelet von Willebrand factor in these various subtypes to platelet adhesion using the rectangular perfusion chamber of Sakariassen et al. (3) with fibrillar collagen or a fibroblast matrix as adhesive surfaces. Platelet adhesion to fibrillar collagen was decreased in all subtypes of von Willebrand’s disease, but not as low as in severe von Willebrand’s disease. A close correlation was observed between platelet adhesion to collagen and plasma vWF:Ag in severe von Willebrand’s disease, subtype platelet low, subtype platelet discordant, and normal controls. The platelet adhesion in subtype platelet normal was higher than expected from the plasma vWF: Ag level. Perfusions in which washed platelets were added to a human albumin solution together with red blood cells gave similar adhesion values in subtype platelet normal and normal controls; adhesion was decreased in subtype platelet discordant, and the lowest values were found in subtype platelet low and in severe von Willebrand’s disease. These data indicate that platelet von Willebrand factor may contribute to platelet adhesion, when plasma von Willebrand factor is low. Perfusion studies over a fibroblast matrix gave similar low adhesion values for subtype platelet low and platelet normal, indicating that the contribution of platelet von Willebrand factor can only be observed on a strongly activating surface such as fibrillar collagen.
Purification and Properties of Prothrombin Modified by Asbestos Filtration of Human Plasma
Authors: Izuchi Y , Boffa M C , Soulier J P 
Published: July 2018

SummaryFiltration through asbestos filter (Seitz) of human plasma modified the prothrombin molecule as previously shown. Factor II could no longer be activated by physiological activators (Ca++ + phospholipid + V and Xa) but reacted readily with staphylocoagulase. The separation and purification of the modified prothrombin allowed the preparation of two fractions:A small slightly modified accessory fraction, “prothrombin-asbestos- 1”, lost its ability to be activated by physiological activators, and its ability to be adsorbed by barium citrate, but retained the immunological reactivity of fragment 1, as well as the mobility and molecular weight of unmodified prothrombin.A main fraction, “prothrombin-asbestos-2” appeared to be a modified prothrombin which has lost its N-terminal extremity. It was not adsorbed by barium citrate and could not be activated by physiological activators. It possessed a reduced electrophoretic mobility, as well as a reduced molecular weight (39,000), which are properties similar to those of thrombin. Both fractions 1 and 2 were devoid of thrombin activity.Asbestos was thus able to break the prothrombin molecule non enzymatically, the amputation of the N terminal extremity being responsible for the new functional and physicochemical properties of the molecule.Staphylocoagulase appeared not to need the N terminal extremity of the molecule of prothrombin to form the active thrombin-coagulase complex.
Haemostatic Factors and Inhibitors and Coronary Artery Bypass Grafting: Preoperative Alterations and Relations to Graft Occlusion
Authors: Moor Elisabeth , Hamsten Anders , Blombäck Margareta , Herzfeld Istvan , Wiman Björn , Rydén Lars 
Published: July 2018

SummaryGraft closure remains a major problem after coronary artery bypass surgery. While a number of graft characteristics influencing the risk of occlusion have been defined, the role of haemostatic factors and inhibitors has not been studied in detail. The present study examined the time course of changes in blood coagulation and fibrinolytic function after coronary artery bypass grafting in 20 consecutive patients. Pre- and postoperative determinations of haemostatic factors and inhibitors were also related to the presence of graft occlusion assessed by angiography at three months after surgery. A broad panel of haemostatic tests was used preoperatively, on the first, third and eight postoperative days, and at three months after surgery. A particular emphasis was placed on fibrinogen, factor VII activity, von Willebrand factor (vWF), plasminogen activator inhibitor-1 (PAI-1) activity, anticoagulant proteins C and S, thrombin-antithrombin complex and D-dimer. A marked activation of the coagulation cascade was noted postoperatively along with enhanced degradation of cross-linked fibrin. The degree of activation of blood coagulation and fibrinolysis differed widely between individuals and appeared to relate only partly to the acute phase reaction produced by the surgical trauma. Preoperative values of haemostatic factors and inhibitors showed fairly weak associations with the levels of postoperative determinations. Basal tPA and factor VIII levels, fibrinogen and TAT concentrations on the third and eighth postoperative day, and factor VII amidolytic activity on the third postoperative day differed (p <0.05) between patients with and without occluded grafts at reangiography. Accordingly, combined pre- and postoperative assessment of haemostatic function may contribute to the identification of individuals at risk for early graft closure after coronary artery bypass grafting.
Neutrophil but not Monocyte Activation Inhibits P-Selectin-Mediated Platelet Adhesion
Authors: Rinder Henry M , Tracey Jayne L , Rinder Christine S , Leitenberg David , Smith Brian R 
Published: July 2018

SummarySelectins are Ca2+-dependent glycoprotein receptors that mediate the adhesion of activated platelets or endothelial cells to unstimulated leukocytes. Using purified cell fractions, we examined activated neutrophil adhesion to P-selectin-expressing platelets and found that phorbol 12-myristate 13-acetate (PMA), platelet activating factor C16 (PAF), and n-formyl-met-leu-phe (fMLP) pretreatment of neutrophils inhibited activated platelet adhesion. Furthermore, PMA and PAF were capable of dissociating established resting neutrophil-activated platelet conjugates. Since L-selectin is downregulated after leukocyte activation and has been postulated as a ligand for P-selectin, we preincubated resting neutrophils with Dreg-2 and Dreg-56, blocking monoclonal antibodies (MoAb) to L-selectin; these MoAb failed to inhibit activated platelet adhesion. To more closely approximate in vivo conditions of leukocyte and platelet activation, we also employed a whole blood (WB) model of leukocyte-platelet adhesion. We found that simultaneous activation of both platelets and leukocytes by PMA caused an immediate rise in the % of P-selectin-positive platelets accompanied by a rapid increase in monocyte-platelet and neutrophil-platelet conjugates; however, the % of neutrophil-platelet conjugates subsequently declined over 30-60 min to baseline levels while monocyte-platelet adhesion remained elevated over 90 min. By contrast, selective platelet activation in WB by thrombin resulted in an increase in platelet P-selectin expression accompanied by a sustained (90 min) elevation in both monocyte- and neutrophil-platelet conjugates. This increase in leukocyte-platelet conjugates after thrombin was not inhibited by preincubation of WB with Dreg-2 or Dreg-56. We conclude that neutrophil activation decreases the expression of the ligand for platelet P-selectin within 30-60 min resulting in inhibition of neutrophil-platelet adhesion and dissociation of existing neutrophil-platelet conjugates. By contrast, monocyte activation over 90 min does not affect monocyte adhesion to activated platelets in whole blood.