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Archives of cardiovascular diseases. Supplements 155건

  1. [해외논문]   ours rEdaction  


    Archives of cardiovascular diseases. Supplements v.10 no.2 ,pp. i - i , 2018 , 1878-6480 ,

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  2. [해외논문]   In April 2018, the “new formula” spring of cardiology will open in Montpellier  

    Fauconnier, Jé (Corresponding author.) , ré , my , Roubille, Franç , ois
    Archives of cardiovascular diseases. Supplements v.10 no.2 ,pp. 175 - 175 , 2018 , 1878-6480 ,

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  3. [해외논문]   En avril 2018 s'ouvrira le Printemps de la Cardiologie ≪ nouvelle formule ≫ A Montpellier  

    Fauconnier, Jé (Auteur correspondant.) , ré , my , Roubille, Franç , ois
    Archives of cardiovascular diseases. Supplements v.10 no.2 ,pp. 176 - 176 , 2018 , 1878-6480 ,

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

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  4. [해외논문]   Pro-atherogenic high fat diet accelerates tumor growth in mice through activation of innate immunity  

    Tran, T. (Corresponding author.) , Montabord, M. , Esposito, B. , Mallat, Z. , Tedgui, A. , Tartour, E. , Potteaux, S.
    Archives of cardiovascular diseases. Supplements v.10 no.2 ,pp. 177 - 177 , 2018 , 1878-6480 ,

    초록

    Inflammation is a physiologic protective process triggered in response to injury or infection. When unresolved, inflammation often promotes the development of chronic pathologies such as cancer or atherosclerosis. In atherosclerosis, hypercholesterolemia-associated monocytosis drives plaque formation in mice. Epidemiologic and experimental studies have shown the involvement of dyslipidiemia and low-grade inflammation on the development of multiple cancers. Surprisingly, the link between atherosclerosis and cancer has not been studied in details. The objective of our study was to question whether a pro-atherogenic high fat diet (HFD) would modify the development of solid tumors. Our experimental approach was to feed mice susceptible to atherosclerosis with a classical HFD (15% fat, 1.25% cholesterol) or a chow diet for 2 weeks before induction of tumor development. We monitored tumor development every two days and analyzed the mechanistic events by in vitro and in vivo experiments. We found that the proatherogenic HFD accelerated the growth of several solid tumors (B16F10 and TC1) in C57Bl6 mice, independently of cholesterol levels. In contrast, the HFD induced a significant increase of myeloid cells number in circulation and in the tumor microenvironment (flow cytometry). We isolated (Miltenyi) and analyzed the phenotype (qPCR and ELISA) of tumor-infiltrating leukocytes (TILs). We found a rapid upregulation of IL-1beta and VEGFa expression and a downregulation of several inflammatory cytokines. The supernatant of TILs isolated from mice under HFD and cultured for 48hours, failed to reduce tumor cell proliferation in vitro (tritiated thymidine) and absence of IL-1beta, or selective depletion of neutrophils protected mice against tumor acceleration under HFD. These data show that in the context of a proaterogenic HFD, neutrophils accumulate in the tumor microenvironment and switch toward an immunosuppressive phenotype, thus promoting the fast growing of tumors.

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  5. [해외논문]   Exploring the role of TREM-1 receptor in experimental abdominal aortic aneurysm  

    Vandestienne, M. (Inserm U970, Paris Cardiovascular Research Center, Université) , Joffre, J. (René) , Giraud, A. (Descartes Paris 5, Paris, France ) , Potteaux, S. (Inserm U970, Paris Cardiovascular Research Center, Université) , Laurans, L. (René) , Tedgui, A. (Descartes Paris 5, Paris, France ) , Derive, M. (Inserm U970, Paris Cardiovascular Research Center, Université) , Mallat, Z. (René) , Ait Oufella, H. (Descartes Paris 5, Paris, France )
    Archives of cardiovascular diseases. Supplements v.10 no.2 ,pp. 177 - 177 , 2018 , 1878-6480 ,

    초록

    Introduction Non-syndromic Abdominal Aortic Aneurysm (AAA) is one of the leading causes of cardiovascular death in elderly men. AAA is characterized by extracellular matrix degradation, smooth muscle cell apoptosis and infiltration of inflammatory cells in the aortic wall. TREM (Triggering Receptor Expressed on Myeloid cells)-1, a receptor expressed by myeloid cells, is a key regulator of innate immune cell activity, and we hypothesized that it might be involved in AAA development. Objective We aim to decipher the role of TREM-1 in the immuno-inflammatory response associated with AAA development and rupture. Method To study the role of TREM-1 in AAA development, we used an experimental model of Angiotensin-II-induced AAA in ApoE −/− Trem-1 −/− and ApoE −/− Trem-1 +/+ mice. At day 0, 3, 7 and 28, we analyzed monocyte trafficking (flow cytometry), inflammatory cell infiltration within the aortic wall (immunostaining, qPCR), aortic wall remodeling (histology) and finally AAA development. Results Angiotensin II infusion increased TREM-1 expression on both classical and non-classical monocytes. TREM-1 deficiency limits Angiotensin II-induced monocytosis at day 3 and limits macrophage infiltration in the aorta at day 7. Trem-1 genetic deletion limits pro-inflammatory response and metalloprotease activity in the aortic wall and protects against elastin degradation. Finally, TREM-1 deficiency significantly reduced AAA rupture and severity. Conclusion We showed that TREM-1 deficiency reduced AAA development and rupture in an Angiotensin II-induced experimental mouse model.

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  6. [해외논문]   Characterisation of endogenous cardiac inflammatory cells displaying a cardiogenic potential  

    Zaouidi, S. (Corresponding author.) , Clerc, S. , Bielmann, C. , Rosenblatt-Velin, N.
    Archives of cardiovascular diseases. Supplements v.10 no.2 ,pp. 178 - 178 , 2018 , 1878-6480 ,

    초록

    During the culture of non-myocyte cells (NMCs) isolated from neonatal or adult mouse hearts, round weakly adherent cells growing on the fibroblast and endothelial cell layer appeared. The aim of this study was to identify the nature and function of these weakly adherent cardiac cells (WACs). We first characterized WACs by flow cytometry analysis. These cells were CD45+ F4/80+ CD11b+ CD206+ CD64+ cells, demonstrating their appartenance to the M2 macrophage cell subset. This was confirmed by qPCR analysis. In vivo, in neonatal or adult unmanipulated hearts, cells with the same phenotype represent about 5 to 6% of the total non-myocyte cells. We then tested the function of these cells in vitro. When cultured alone in adequate medium during 3 weeks, WACs were able to express mRNAs coding for cardiomyocyte specific markers: Nk×2.5 (×4), Troponin I (×19), beta (×4) and alpha (×9) Myosin Heavy Chain when compared to the WACs after isolation. mRNAs coding for Sca-1 (×5.5) and c-kit (×3.5) were also increased. At the protein level, some of these cells expressed CD31 or smooth muscle actin as well as Nk×2.5 or Troponin I. WAC's supernantant inhibited neonatal NMC proliferation (−25%, P P

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    회원님의 원문열람 권한에 따라 열람이 불가능 할 수 있으며 권한이 없는 경우 해당 사이트의 정책에 따라 회원가입 및 유료구매가 필요할 수 있습니다.이동하는 사이트에서의 모든 정보이용은 NDSL과 무관합니다.

    NDSL에서는 해당 원문을 복사서비스하고 있습니다. 아래의 원문복사신청 또는 장바구니담기를 통하여 원문복사서비스 이용이 가능합니다.

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  7. [해외논문]   Influence of dietary eicosapentaenoic acid on the cardiac mechanical and mitochondrial functions during early sepsis  

    Leger, T. (INRA, UMR 1019 unité) , Rigaudiè (de nutrition humaine, université) , re, J.P. (Clermont-Auvergne, France ) , Azarnoush, K. (INRA, UMR 1019 unité) , Demaison, L. (de nutrition humaine, université)
    Archives of cardiovascular diseases. Supplements v.10 no.2 ,pp. 178 - 179 , 2018 , 1878-6480 ,

    초록

    Introduction Sepsis triggers the failure of cardiac mitochondria and this deleterious effect could be prevented by omega-3 polyunsaturated fatty acids (PUFA). Objectives To evaluate the influence of eicosapentaenoic acid (C20: 5 omega-3 or EPA) on the mechanical and mitochondrial functions of the heart during early sepsis. Methods Four month-old female Wistar rats were subdivided in 4 groups ( n = 8 per group) according to: (i) the 4-week diet given (deficient in omega-3 PUFA [DEF] or enriched with EPA); (ii) the surgery performed (caecal ligation at 1cm of the apex of the heart and puncture in order to induce sepsis [CLP] or sham). The cardiac mechanical function was studied in vivo by NMR 48h after the surgery. Immediately after, part of the myocardium was used in order to extract mitochondria and another part was frozen in order to subsequently analyse the fatty acid composition of cardiac phospholipids. Results The EPA groups display a large decrease in the omega-6/omega-3 PUFA ratio of cardiac phospholipids. Sepsis increases the mRNA expression of IL-1beta in the DEF group but not in the EPA one. The mechanical function is altered neither by the diets nor by the surgeries. The DEF/CLP animals have a deficient oxidative phosphorylation compared to the DEF/Sham rats: reduced mitochondrial oxygen consumption (−42%, P P P P P Conclusion A sufficient EPA intake favours the upholding of the mitochondrial function during early sepsis, which could delay the subsequent development of heart failure. We plan to verify this beneficial effect of EPA in Humans affected by acute endocarditis.

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  8. [해외논문]   Endothelial activation and infarct size at the acute phase of myocardial infarction  

    Falque, H. (Service d'explorations fonctionnelles cardiovasculaires, France ) , Bochaton, T. (Unité) , Bernelin, H. (de soins intensifs cardiologiques, hôpital Louis-Pradel, hospices civils de Lyon, Lyon, France ) , Paccalet, A. (Unité) , Crola Da Silva, C. (de soins intensifs cardiologiques, hôpital Louis-Pradel, hospices civils de Lyon, Lyon, France ) , Baetz, D. (INSERM U1060, CarMeN laboratory, université) , Bonnefoy-Cudraz, E. (de Lyon, groupement hospitalier Est, Bron, France ) , Mewton, N. (INSERM U1060, CarMeN laboratory, université) , Ovize, M. (de Lyon, groupement hospitalier Est, Bron, France )
    Archives of cardiovascular diseases. Supplements v.10 no.2 ,pp. 178 - 178 , 2018 , 1878-6480 ,

    초록

    Introduction Acute myocardial infarction (MI) leads to an intense inflammatory response with endothelial cell activation. Vascular cell adhesion protein 1 (VCAM-1), E-selectin, intercellular adhesion molecule-1 (ICAM-1) and monocyte chemoattractant protein 1 (MCP-1) promote the adherence of leucocytes especially monocytes, in the infarcted area which may increase infarct size (IS). Objective Our objective was to evaluate the kinetic of endothelial cell activation markers at the acute phase of ST-elevated MI (STEMI) and their relationship with IS and Major Adverse Cardiac Event (MACE). Method Blood sample of 182 STEMI patients were collected at admission and four hours after reperfusion. Infarct Size (IS) was assessed in all patients using cardiac Magnetic Resonance Imaging (cMRI) one month after discharge. We performed ELISA quantification of the main markers of endothelial cell activation in serum: VCAM-1, E-selectin, ICAM-1 and MCP-1. Results Patients mean age was 58±11 years with 77% males. Median levels of each marker at admission reached 165.3ng/mL interquartile range (IQR) [127.0–193.3] for VCAM-1, 140.6ng/mL IQR [104.6–196.6] for ICAM-1, 15.3ng/mL IQR [10.2–23.3] for E-selectin and 53.8pg/mL IQR [34.7–90.5] for MCP-1. VCAM-1 and MCP-1 serum levels significantly increased four hours after admission (respectively +6% and +32%). E-selectin and ICAM-1 levels did not change four hours after admission compared to admission. Only VCAM-1 was significantly correlated with IS assessed by cMRI ( r = 0.26, P = 0.0004) and inversely correlated with left ventricular ejection fraction ( r = −0.16, P = 0.04). However, VCAM-1 level and other markers were not associated with MACE. Conclusion MI is associated with endothelial cell activation. VCAM-1 and MCP-1 significantly increased at the acute phase of MI whereas E-selectin and ICAM-1 levels are stable. Only VCAM-1 serum level was correlated with IS. However, none of these markers was associated with the occurrence of MACE.

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  9. [해외논문]   Fe-based bioresorbable alloy inhibits platelet activation  

    Verhaegen, C. (Corresponding author.) , Lepropre, S. , Octave, M. , Kautbally, S. , Thomas, A. , Reuter, S. , Scarcello, E. , Lison, D. , Bertrand, L. , Delannay, L. , Jacques, P.J. , Beauloye, C. , Horman, S. , Kefer, J.
    Archives of cardiovascular diseases. Supplements v.10 no.2 ,pp. 180 - 181 , 2018 , 1878-6480 ,

    초록

    Introduction Bioresorbable polymer stents have been used to provide a transient scaffold after coronary angioplasty. However, an increase in stent thrombosis has been observed. A current challenge is thus to develop new bioresorbable stents combining optimised mechanical and biodegradation properties together with limited thrombogenicity. Fe-based alloys are amongst the good candidates. Objective Blood compatibility of a new Fe-based alloy was studied in vitro via assessment of haemolysis and platelet activation. Methods Human whole blood was incubated for 60min with either the Fe-based alloy or the cobalt-chromium (Co-Cr) alloy composing bare metal stents. After centrifugation, optical density of the supernatant was measured at 540nm and the amount of haemolysis was calculated. For platelet activation assays, human or rat washed platelets were incubated for 60min with both alloys before measuring their reactivity to platelet agonists by flow cytometry, using CD62P and activated α2bβ3 antibodies. In addition, phosphorylation of PKC substrates was evaluated by western blot. Results No significant red cells haemolysis was induced by both alloys (0.5 and 0.3% respectively). In addition, Co-Cr alloy did not affect CD62P exposure and α2bβ3 activation at platelet surface upon thrombin (0.03 to 0.3U/ml) stimulation. In contrast, Fe alloy completely abolished their response to the agonist. A drastic inhibition of the phosphorylation state of PKC substrates was also observed after activation with thrombin, collagen (1.25 to 5μg/ml) and ADP (0.1 to 10μM). Since similar inhibitory effects were obtained when using a conditioned-reaction medium previously incubated with this Fe alloy, we postulate that its biocorrosion might release components counteracting platelet activation. Conclusion The Fe-based resorbable scaffold displays anti-thrombogenic properties and is a promising platform for next-generation stent technologies.

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  10. [해외논문]   Stent coating with a CD31 agonist improves the biocompatibility of coronary stents in vivo  

    Mesnier, J. (U1148, INSERM, France ) , Sayah, N. (U1148, INSERM, France ) , Rasser, C. (U1148, INSERM, France ) , Choqueux, C. (U1148, INSERM, France ) , Feldman, L. (Department of cardiology, university hospital X.-Bichat, Paris, France ) , Nicoletti, A. (U1148, INSERM, France ) , Gallet, R. (IMRB, université) , Ghaleh, B. (Paris Est, Créteil, France ) , Caligiuri, G. (IMRB, université)
    Archives of cardiovascular diseases. Supplements v.10 no.2 ,pp. 180 - 180 , 2018 , 1878-6480 ,

    초록

    Introduction The ideal stent coating should be able to reduce the local inflammatory reaction, as drug-eluting stents (DES) do but should also favour the rapid endothelialisation as bare-metal stents (BMS) do. Objective We aimed at combining the anti-inflammatory and pro-endothelialisation properties in a novel stent coating inspired from CD31, a transmembrane receptor critically involved in the physiologic regulation of leukocyte activation and endothelial integrity within the circulation. Method A CD31-mimetic peptide was covalently immobilized on BMS stents (Multilink ? ) by click chemistry. Uncoated stents, and everolimus-eluting made of exactly the same material (Xience ? ) were used as controls. The 3 types of stents ( n = 6/type) were implanted in the coronary arteries of farm pigs. Aspirine (75mg) and ticagrelor (180mg) were administered daily, per os. Seven days later, the stented coronary segments were carefully excised, fixed and cut longitudinally. Their luminal surface was metallized and evaluated blindly by scanning electron microscopy (). Results As shown in the figure, CD31-coated and BMS were entirely covered by a smooth endothelial cell layer whereas endothelial cells on DES were scant and non-junctional. A few round-shaped leukocytes were found adherent onto the CD31-coated and DES stents whereas BMS consistently presented areas covered by multiple spread-shaped (activated) leukocytes. Conclusion Immobilization of CD31 agonist improves the biocompatibility of coronary stents by combining the beneficial features of BMS (complete endothelialization within 7 days) and DES (reduced inflammatory reaction) without their respective drawbacks. The use of this biomimetic coating may serve to foster a more physiologic integration of coronary stents within the arterial wall.

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