58 research outputs found
Reconstruction et rĂ©Ă©quilibrage du lien social: une Ă©tude exploratoire sur les rĂŽles de lâinclusion sociale, de lâappropriation du pouvoir dâagir et de lâespoir dans le rĂ©tablissement
Le paradigme du rĂ©tablissement en santĂ© mentale remet la question de l'inclusion sociale, de l'appropriation du pouvoir d'agir et de l'espoir d'un mieux-ĂȘtre au cĆur des approches d'intervention et des services. Dans le prĂ©sent article, nous prĂ©sentons les rĂ©sultats du volet qualitatif (n = 15 participants et participantes) d'une recherche exploratoire rĂ©alisĂ©e Ă QuĂ©bec auprĂšs de personnes aux prises avec la schizophrĂ©nie ou des psychoses apparentĂ©es, vivant dans la communautĂ© et suivies dans le cadre d'un programme de traitement et de rĂ©adaptation fondĂ© sur une approche de rĂ©tablissement. Nos rĂ©sultats fournissent un Ă©clairage particulier sur les dynamiques de reconstruction et de rĂ©Ă©quilibrage des liens sociaux dans les cheminements de rĂ©tablissement de ces personnes. Ils suggĂšrent ainsi que la relation entre l'inclusion sociale et l'appropriation du pouvoir d'agir est dialectique: l'inclusion sociale est facilitĂ©e par, et contribue Ă , l'appropriation du pouvoir. De plus, cette dialectique se vit aussi dans un changement du regard portĂ© sur soi et sur son devenir, incluant l'espoir d'ĂȘtre « mieux », d'ĂȘtre « plus » et, surtout, d'ĂȘtre avec.
The recovery paradigm in mental health places social inclusion, empowerment and hope at the centre of service delivery. In this article we present results from the qualitative part (n = 15 participants) of an exploratory research project carried out in Quebec City with persons suffering from schizophrenia and related psychotic conditions, who live in the community and are served by a recovery-oriented treatment and rehabilitation centre. Our results cast light on the dynamics of reconstruction and rebalancing of social ties in the participants' recovery pathways. The results also suggest that the relationship between social inclusion and empowerment is dialectical: social inclusion is facilitated by, and contributes to, empowerment. Furthermore, this dialectic is also noted in a shift in participants' perception of self and future, including the hope to become âbetter,â to âgo further,â and, above all, to be with
Genome-wide Analyses Identify KIF5A as a Novel ALS Gene
To identify novel genes associated with ALS, we undertook two lines of investigation. We carried out a genome-wide association study comparing 20,806 ALS cases and 59,804 controls. Independently, we performed a rare variant burden analysis comparing 1,138 index familial ALS cases and 19,494 controls. Through both approaches, we identified kinesin family member 5A (KIF5A) as a novel gene associated with ALS. Interestingly, mutations predominantly in the N-terminal motor domain of KIF5A are causative for two neurodegenerative diseases: hereditary spastic paraplegia (SPG10) and Charcot-Marie-Tooth type 2 (CMT2). In contrast, ALS-associated mutations are primarily located at the C-terminal cargo-binding tail domain and patients harboring loss-of-function mutations displayed an extended survival relative to typical ALS cases. Taken together, these results broaden the phenotype spectrum resulting from mutations in KIF5A and strengthen the role of cytoskeletal defects in the pathogenesis of ALS.Peer reviewe
COVID-19 symptoms at hospital admission vary with age and sex: results from the ISARIC prospective multinational observational study
Background:
The ISARIC prospective multinational observational study is the largest cohort of hospitalized patients with COVID-19. We present relationships of age, sex, and nationality to presenting symptoms.
Methods:
International, prospective observational study of 60â109 hospitalized symptomatic patients with laboratory-confirmed COVID-19 recruited from 43 countries between 30 January and 3 August 2020. Logistic regression was performed to evaluate relationships of age and sex to published COVID-19 case definitions and the most commonly reported symptoms.
Results:
âTypicalâ symptoms of fever (69%), cough (68%) and shortness of breath (66%) were the most commonly reported. 92% of patients experienced at least one of these. Prevalence of typical symptoms was greatest in 30- to 60-year-olds (respectively 80, 79, 69%; at least one 95%). They were reported less frequently in children (â€â18 years: 69, 48, 23; 85%), older adults (â„â70 years: 61, 62, 65; 90%), and women (66, 66, 64; 90%; vs. men 71, 70, 67; 93%, each Pâ<â0.001). The most common atypical presentations under 60 years of age were nausea and vomiting and abdominal pain, and over 60 years was confusion. Regression models showed significant differences in symptoms with sex, age and country.
Interpretation:
This international collaboration has allowed us to report reliable symptom data from the largest cohort of patients admitted to hospital with COVID-19. Adults over 60 and children admitted to hospital with COVID-19 are less likely to present with typical symptoms. Nausea and vomiting are common atypical presentations under 30 years. Confusion is a frequent atypical presentation of COVID-19 in adults over 60 years. Women are less likely to experience typical symptoms than men
Le rÎle de l'interaction individu/environnement dans le fonctionnement social de personnes ùgées ayant des atteintes cognitives légÚres
Changements hémostatiques du syndrome métabolique, de l'hypertension artérielle, et de l'insuffisance cardiaque (approches physiologique et physiopathologique)
L'allongement de l'espérance de vie a fait de l'insuffisance cardiaque (IC) l'un des problÚmes majeurs de santé publique. Le syndrome métabolique (SMet) et l'hypertension sont deux facteurs conduisant à l'IC. Les modifications qui interviennent au niveau structural et cellulaire de la paroi artérielle dans le SMet, l'hypertension et l'IC pourraient entraßner des anomalies de l'hémostase qui aggravent ces tableaux cliniques. Nous avons montré au cour de ce travail les modifications du phénotype de l'hémostase dans différents modÚles animaux de pathologies impliquées dans la mise en place de l'IC. L'altération de l'hémostase précÚde les modifications de la paroi et pourrait favoriser le développement de l'IC chez le rat Zucker. Le modÚle de rat spontanément hypertendu SHR présente une hypercoagulablité de la paroi via les cellules musculaires lisses. Ces résultats ne permettent pas d'impliquer uniquement l'hypertension artérielle dans l'hypercoagulabilité plasmatique trouvée chez le rat Zucker. L'activation du récepteur à l'aldsotérone au niveau endothélial chez la souris induit un phénotype antithrombotique provoqué par une augmentation de la réactivité du systÚme anticoagulant de la protéine C, via son récepteur, l'EPCR. L'étude d'une cohorte de patients insuffisants cardiaques a permis de distinguer des paramÚtres de fonction cardiaque et de rigidité artérielle. Cette caractérisation est indispensable pour comprendre les mécanismes des événements thrombotiques associés à l'IC. La conclusion de ce travail est que les pathologies pouvant conduire à la mise en place d'une IC modifient l'hémostase vers un état d'hypercoagulabilité qui fait intervenir la paroi artérielleIncreasing life span has made heart failure (HF) a major issue for public health. The metabolic syndrome (MetS) and hypertension are two important factors which can lead to HF. Structural and cellular modification occurring in the arterial wall in the MetS, hypertension and HF may provoke hemostasis alterations that can worsen the clinical situation. We have shown in this work, hemostasis modifications in animal models of pathologies implicated in HF development. Hemostasis alterations were shown to precede functional modifications of the arterial wall and could favor HF development in Zucker rats. Spontaneously hypertensive rats showed an arterial wall hypercoagulability via smooth muscle cells. These results don't permit the implication of hypertension in the hypercoagulable state found in the Zucker rat. A mouse model with aldosterone receptor activation in the endothelium lead to a hypocoagulable state by increasing the protein C anticoagulant system via his receptor, the EPCR. Studying a human HF patient cohort permitted the measurement of cardiac function and of arterial stiffness parameters. This characterization is important to understand thrombosis events associated with HF in humans. The general conclusion of this work is that, in pathologies leading to HF, modification of hemostasis to a procoagulable state, implicates the arterial wallMETZ-SCD (574632105) / SudocNANCY1-Bib. numérique (543959902) / SudocNANCY2-Bibliotheque electronique (543959901) / SudocNANCY-INPL-Bib. électronique (545479901) / SudocSudocFranceF
Shedding Light on Hemostasis in Patients With Inflammatory Bowel Diseases
International audiencePatients with inflammatory bowel diseases (IBD) have an increased risk of thrombosis, possibly due to changes in blood cells and molecules involved in hemostasis. They have increased platelet counts and reactivity as well as increased platelet-derived large extracellular vesicles. Coagulation is continuously activated in patients with IBD, based on measured markers of thrombin generation, and the anticoagulant functions of endothelial cells are damaged. Furthermore, fibrinogen is increased and fibrin clots are denser. However, pathogenesis of thrombosis in patients with IBD appears to differ from that of patients without IBD. Patients with IBD also take drugs that might contribute to risk of thrombosis, complicating the picture. We review the features of homeostasis that are altered in patients with IBD and possible mechanisms of this relationship
Platelet aggregation impacts thrombin generation assessed by calibrated automated thrombography
A calibrated automated thrombogram (CAT) is performed usually with human platelet-free plasma (PFP) but may be more relevant with platelet-rich plasma (PRP). In this case, platelets are not stimulated by subendothelial molecules like collagen. Our aim was to assess the consequence of strong (collagen) or weak (ADP) induction of platelet release and aggregation on thrombin generation. Platelet aggregation in PRP was triggered with 10 ”g/mL collagen or 10 ”M ADP using a lumi-aggregometer. Thrombin generation curves were monitored by CAT in different conditions: PRP, PRP with activated platelets (actPRP), aggregated PRP (agPRP), aggregated platelets resuspended in autologous PFP (resPRP), PFP and PFP obtained after aggregation (agPFP). We found a 3-fold shortening of the lag time and time to peak and a marked increase in velocity and thrombin peak without changes in endogenous thrombin potential (ETP) in agPRP with both agonists compared with PRP. The same holds true in agPFP but with a marked increase in ETP compared with PFP. Similar changes in the kinetics of thrombin generation were observed with actPRP-collagen and to a lesser extent in resPRP-collagen compared with PRP. By contrast, there were no modifications of the thrombin generation curves in actPRP-ADP. Alpha-2-macroglobin-thrombin complexes were unchanged in the different PRP conditions but were increased in PFP prepared from agPFP compared to control PFP. Platelet aggregation during activation by agonists other than thrombin did not increase thrombin generation but accelerated its kinetics mainly via platelet content release and platelet-derived extracellular vesicules formation. In diseases characterized by altered platelet granule content or release as well as altered platelet activation, a platelet aggregation step prior to CAT analysis may be clinically relevant to improve laboratory estimation of the bleeding/thrombotic balance
Rivaroxaban Effects Illustrate the Underestimated Importance of Activated Platelets in Thrombin Generation Assessed by Calibrated Automated Thrombography
International audienceBackground: The direct oral anticoagulant rivaroxaban inhibiting specifically activated factor X (FXa) causes delayed thrombin generation (TG) as measured by calibrated automated thrombography (CAT). The implications of these changes for assessing bleeding or residual prothrombotic risks of patients are unclear in the absence of a better understanding of the underlying mechanism. Methods: We compared platelet rich plasma (PRP) without or with prior collagen-induced platelet aggregation (agPRP) in the CAT assay to better characterize TG in the presence of rivaroxaban. Results: In the presence of rivaroxaban, TG curves in agPRP showed a distinct profile with a rapidly ascending phase followed with a protracted phase. Inhibition of tissue factor pathway inhibitor amplified the first phase of the curve which was also modulated by procoagulant phospholipids. Inhibition of FXIIa-dependent FXI activation revealed that aggregated platelets influenced the first phase by a combination of extrinsic and intrinsic coagulation pathway initiations. Thrombin-dependent amplification of TG (even prior collagen activation) was responsible for the second phase of the TG curve. Conclusions: AgPRP fully includes platelet ability to support TG and reveal distinct TG phases in the presence of direct FXa inhibitors highlighting its potential use in an anticoagulated setting
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