517 research outputs found
Access to Physician Services: Does Supplemental Insurance Matter? Evidence from France
In France, public health insurance is universal but incomplete, with private payments accounting for roughly 25 percent of all spending. As a result, most people have supplemental private health insurance. We investigate the effects of such insurance on the utilization of physician services using data from the 1998 EnquËte Santâ Protection Sociale, a nationally representative survey of the French population. Our results indicate that insurance has a strong and significant effect on the utilization of physician services. Individuals with supplemental coverage have substantially more physician visits than those without. In a context where patients are free to choose their provider, we find no evidence that adults with supplemental insurance are more likely to visit a specialist than a general practitioner.
Concurrence et antisĂ©lection en assurance maladie : lâexpĂ©rience des Pays-Bas
Quels sont les bĂ©nĂ©fices mais aussi les Ă©cueils attendus du renforcement de la concurrence sur le marchĂ© de lâassurance maladie ? Lâintervention de lâEtat demeure-t-elle justifiĂ©e ? Quelles sont les modalitĂ©s optimalesdâune telle intervention ? Autant dâinterrogations auxquelles le prĂ©sent article tente dâapporter des Ă©clairages Ă partir de la confrontation des rĂ©sultats de la thĂ©orie microĂ©conomique de lâassurance Ă lâexpĂ©rience pratique du systĂšme de santĂ© des Pays-Bas dans ce domaine.Which are the benefits but also the pitfalls to be expected from strengthening competition in the health insurance markets ? Is State intervention still legitimate ? Which are the optimal forms it should take ? These are some of the questions addressed in this paper whixh confronts the theorical predictions from insurance economics with the practical experience of the Dutch health care system
Concurrence et antisĂ©lection en assurance maladie : lâexpĂ©rience des Pays-Bas
Quels sont les bĂ©nĂ©fices mais aussi les Ă©cueils attendus du renforcement de la concurrence sur le marchĂ© de lâassurance maladie ? Lâintervention de lâEtat demeure-t-elle justifiĂ©e ? Quelles sont les modalitĂ©s optimalesdâune telle intervention ? Autant dâinterrogations auxquelles le prĂ©sent article tente dâapporter des Ă©clairages Ă partir de la confrontation des rĂ©sultats de la thĂ©orie microĂ©conomique de lâassurance Ă lâexpĂ©rience pratique du systĂšme de santĂ© des Pays-Bas dans ce domaine.Which are the benefits but also the pitfalls to be expected from strengthening competition in the health insurance markets ? Is State intervention still legitimate ? Which are the optimal forms it should take ? These are some of the questions addressed in this paper whixh confronts the theorical predictions from insurance economics with the practical experience of the Dutch health care system
Fzd7 (Frizzled-7) Expressed by Endothelial Cells Controls Blood Vessel Formation Through Wnt/ÎČ-Catenin Canonical Signaling.
Abstract OBJECTIVE: Vessel formation requires precise orchestration of a series of morphometric and molecular events controlled by a multitude of angiogenic factors and morphogens. Wnt/frizzled signaling is required for proper vascular formation. In this study, we investigated the role of the Fzd7 (frizzled-7) receptor in retinal vascular development and its relationship with the Wnt/ÎČ-catenin canonical pathway and Notch signaling. APPROACH AND RESULTS: Using transgenic mice, we demonstrated that Fzd7 is required for postnatal vascular formation. Endothelial cell (EC) deletion of fzd7 (fzd7ECKO) delayed retinal plexus formation because of an impairment in tip cell phenotype and a decrease in stalk cell proliferation. Dvl (dishevelled) proteins are a main component of Wnt signaling and play a functionally redundant role. We found that Dvl3 depletion in dvl1-/- mice mimicked the fzd7ECKO vascular phenotype and demonstrated that Fzd7 acted via ÎČ-catenin activation by showing that LiCl treatment rescued impairment in tip and stalk cell phenotypes induced in fzd7 mutants. Deletion of fzd7 or Dvl1/3 induced a strong decrease in Wnt canonical genes and Notch partners' expression. Genetic and pharmacological rescue strategies demonstrated that Fzd7 acted via ÎČ-catenin activation, upstream of Notch signaling to control Dll4 and Jagged1 EC expression. CONCLUSIONS: Fzd7 expressed by EC drives postnatal angiogenesis via activation of Dvl/ÎČ-catenin signaling and can control the integrative interaction of Wnt and Notch signaling during postnatal angiogenesis
Adjustment and Characterization of an Original Model of Chronic Ischemic Heart Failure in Pig
We present and characterize an original experimental model to create a chronic ischemic heart failure in pig. Two ameroid constrictors were placed around the LAD and the circumflex artery. Two months after surgery, pigs presented a poor LV function associated with a severe mitral valve insufficiency. Echocardiography analysis showed substantial anomalies in radial and circumferential deformations, both on the anterior and lateral surface of the heart. These anomalies in function were coupled with anomalies of perfusion observed in echocardiography after injection of contrast medium. No demonstration of myocardial infarction was observed with histological analysis. Our findings suggest that we were able to create and to stabilize a chronic ischemic heart failure model in the pig. This model represents a useful tool for the development of new medical or surgical treatment in this field
Vascular endothelial cell expression of JAK2V617F is sufficient to promote a pro-thrombotic state due to increased P-selectin expression
Thrombosis is the main cause of morbidity and mortality in patients with JAK2V617F myeloproliferative neoplasms. Recent studies have reported the presence of JAK2V617F in endothelial cells of some patients with myeloproliferative neoplasms. We investigated the role of endothelial cells that express JAK2V617F in thrombus formation using an in vitro model of human endothelial cells overexpressing JAK2V617F and an in vivo model of mice with endothelial-specific JAK2V617F expression. Interestingly, these mice displayed a higher propensity for thrombus. When deciphering the mechanisms by which JAK2V617F-expressing endothelial cells promote thrombosis, we observed that they have a pro-adhesive phenotype associated with increased endothelial P-selectin exposure, secondary to degranulation of Weibel-Palade bodies. We demonstrated that P-selectin blockade was sufficient to reduce the increased propensity of thrombosis. Moreover, treatment with hydroxyurea also reduced thrombosis and decreased the pathological interaction between leukocytes and JAK2V617F-expressing endothelial cells through direct reduction of endothelial P-selectin expression. Taken together, our data provide evidence that JAK2V617F-expressing endothelial cells promote thrombosis through induction of endothelial P-selectin expression, which can be reversed by hydroxyurea. Our findings increase our understanding of thrombosis in patients with myeloproliferative neoplasms, at least those with JAK2V617F-positive endothelial cells, and highlight a new role for hydroxyurea. This novel finding provides the proof of concept that an acquired genetic mutation can affect the pro-thrombotic nature of endothelial cells, suggesting that other mutations in endothelial cells could be causal in thrombotic disorders of unknown cause, which account for 50% of recurrent venous thromboses
Cost-effectiveness of screening of coronary artery disease in patients with type 2 DIABetes at a very high cardiovascular risk (SCADIAB study) rational and design
Background: Screening for coronary artery disease (CAD) remains broadly performed in patients with type 2 diabetes (T2DM), although the lack of evidence. We conduct a real-world evidence (RWE) study to assess the risk of major clinical outcomes and economic impact of routine CAD screening in T2DM individuals at a very high cardiovascular risk. Methods: SCADIAB is a comparative nationwide cohort study using data from the French National Health Data System. The main inclusion criteria are: ageââ„â40 years, DT2 diagnosed forââ„â7 years, withââ„â2 additional cardiovascular risk factors plus a history of microvascular or macrovascular disease, except CAD. We estimatedââ„â90,000 eligible participants for our study. Data will be extracted from 01/01/2008 to 31/12/2019. Eligible participants will be identified during a first 7-year selection period (2008â2015). Each participant will be assigned either in experimental (CAD screening procedure during the selection period) or control group (no CAD screening) on 01/01/2015, and followed for 5 years. The primary endpoint is the incremental cost per life year saved over 5 years in CAD screening group versus no CAD screening. The main secondary endpoints are: total 5-year direct costs of each strategy; incidence of major cardiovascular (acute coronary syndrome, hospitalization for heart failure, coronary revascularization or all-cause death), cerebrovascular (hospitalization for transient ischemic attack, stroke, or carotid revascularization) and lower-limb events (peripheral artery disease, ischemic diabetic foot, lower-limb revascularization or amputation); and the budget impact for the French Insurance system to promote the cost-effective strategy. Analyses will be adjusted for a high-dimension propensity score taking into account known and unknown confounders. SCADIAB has been funded by the French Ministry of Health and the protocol has been approved by the French ethic authorities. Data management and analyses will start in the second half of 2021. Discussion: SCADIAB is a large and contemporary RWE study that will assess the economic and clinical impacts of routine CAD screening in T2DM people at a very high cardiovascular risk. It will also evaluate the clinical practice regarding CAD screening and help to make future recommendations and optimize the use of health care resources
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