Publications by authors named "Lecoffre C"

Objectives: We aimed to study trends in stroke unit (SU) admission during a period of their deployment in France and to assess whether this led to better and more equitable access to this specialised care.

Design: Analysis of records from the national hospital database.

Setting: All acute care hospitals in metropolitan France for the period 2009-2014.

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Objective: The aim of this study was to assess regional variations of the hospital management of stroke patients during acute and post-acute phases in France in 2015.

Material And Methods: Hospitalized patients coded with stroke as their main diagnosis or, if hospitalized in several different wards, any main ward diagnosis were identified in the 2015 French national hospital discharge database for acute care. Rates of hospitalization in stroke units (SUs) were assessed at a national level and in all metropolitan and overseas regions.

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Background And Purpose: Stroke is the leading cause of death in women and the third leading cause in men in France. In young adults (ie, <65 years old), an increase in the incidence of ischemic stroke was observed at a local scale between 1985 and 2011. After the implementation of the 2010 to 2014 National Stroke Action Plan, this study investigates national trends in patients hospitalized by stroke subtypes, in-hospital mortality, and stroke mortality between 2008 and 2014.

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The decline in children's Blood Lead Levels (BLL) raises questions about the ability of current lead poisoning screening criteria to identify those children most exposed. The objectives of the study were to evaluate the performance of current screening criteria in identifying children with blood lead levels higher than 50 µg/L in France, and to propose new criteria. Data from a national French survey, conducted among 3831 children aged 6 months to 6 years in 2008-2009 were used.

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Background: The exposure of children to lead has decreased in recent years, thanks notably to the banning of leaded gasoline. However, lead exposure remains a matter of public health concern, because no toxicity threshold has been observed, cognitive effects having been demonstrated even at low levels. It is therefore important to update exposure assessments.

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Health scares have entailed an increasing concern about environmental risks for populations. Authorities' response was to set up a system for the analysis, surveillance and management of environmental risks. Practitioners have an important role to play in this system, as primary actors of surveillance and as a close source of information about the environmental risks for the population.

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SSR182289A competitively inhibits human thrombin (K(i) = 0.031 +/- 0.002 microM) and shows good selectivity with respect to other human proteases, e.

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We studied the antithrombotic activity of a mixed micellar formulation containing 14 mg/ml argatroban administered by the subcutaneous (s.c.) route in rat and rabbit models of venous thrombosis.

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We have studied the anticoagulant properties of a novel mixed micellar formulation containing 14 mg/ml argatroban administered by the sub-cutaneous (s.c.) route to rats, rabbits, dogs and primates.

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Clot-associated thrombin retains amidolytic activity, and is resistant to inhibition by heparin, but not to low molecular weight thrombin inhibitors. We show that clot-associated thrombin induces platelet aggregation, is resistant to heparin:antithrombin III, less so to recombinant hirudin (rHV2Lys47) but not to argatroban, an active-site directed thrombin inhibitor. Fibrin clots prepared with human fibrinogen and thrombin were used to aggregate rabbit washed platelets assessed by single platelet counting, thromboxane B2 (TXB2) immunoassay and scanning electron microscopy.

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1. The antithrombotic action of argatroban, a synthetic thrombin inhibitor, was studied in three models of thrombosis in the rat, and in the tail transection bleeding time test. Heparin was studied as a reference anticoagulant.

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The inhibitory effects of argatroban on clot- or fibrin-bound human thrombin were studied using the thrombin-specific chromogenic substrate S2238 (200 microM). These effects were compared to those of recombinant hirudin (rHV2 Lys 47) and the heparin/antithrombin III complex. Argatroban concentration-dependently inhibited the cleavage of S2238 by a thrombin solution, which had been titrated to give the same change in OD405 nm as fibrin-bound thrombin, with an IC50 of 1.

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The endotracheal deposition of pancreatic porcine elastase (EPP) at 40 u X kg-1 body weight provokes a typical pulmonary emphysema (alveoli disruption) in rats. This emphysema is significant (p less than 0.001) when quantitatively compared to a placebo (100% increase of the mean linear intercept, ILM).

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