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Marjan Haghi - One of the best experts on this subject based on the ideXlab platform.

  • Supra hepatic inferior vena cava and right atrial thrombosis following a traffic car crash
    Journal of injury & violence research, 2016
    Co-Authors: Feridoun Sabzi, Hossein Karim, Marjan Haghi
    Abstract:

    We present a case of nephrotic syndrome associated with right atrial and supra hepatic vein part of inferior vena caval thrombosis. This patient presented with dyspena, lower extremity edema and back pain after a vehicle accident and blunt trauma to the abdomen. Trauma should be considered not only as a thrombophilic pre-disposition, but also as a predisposing factor to IVC Endothelium Injury and thrombosis formation. Echocardiography revealed supra hepatic vein IVC thrombosis floating to the right atrium. A C-T scan with contrast also showed pulmonary artery emboli to the left upper lobe. With open heart surgery, the right atrial and IVC clot were extracted and the main left and right pulmonary arteries were evaluated for possible clot lodging. The patient had an uneventful postoperative recovery and thrombosis has not reoccurred with periodical follow-up examinations.

  • Supra hepatic inferior vena cava and right atrial thrombosis following a traffic car crash
    Kermanshah University of Medical Sciences, 2016
    Co-Authors: Feridoun Sabzi, Hosein Karim, Marjan Haghi
    Abstract:

    We present a case of nephrotic syndrome associated with right atrial and supra hepatic vein part of inferior vena caval thrombosis. This patient presenting with dyspena, lower extremity edema and back pain after a vehicle accident and blunt trauma to abdomen. Trauma should be considered not only as a thrombophilic pre-disposition, but to be ascertaining as a predisposing factor to IVC Endothelium Injury and thrombosis formation. Echocardiography revealed supra hepatic vein IVC thrombosis floating to right atrium .C-T scan with contrast also showed pulmonary artery emboli to left upper lobe. With open heart surgery right atrial and IVC clot were extracted and main and left and right pulmonary artery was evaluated for possible clot lodging. The patient had a uneventful postoperative recovery and thrombosis was not occurred with periodical follow-up examination

Feridoun Sabzi - One of the best experts on this subject based on the ideXlab platform.

  • Supra hepatic inferior vena cava and right atrial thrombosis following a traffic car crash
    Journal of injury & violence research, 2016
    Co-Authors: Feridoun Sabzi, Hossein Karim, Marjan Haghi
    Abstract:

    We present a case of nephrotic syndrome associated with right atrial and supra hepatic vein part of inferior vena caval thrombosis. This patient presented with dyspena, lower extremity edema and back pain after a vehicle accident and blunt trauma to the abdomen. Trauma should be considered not only as a thrombophilic pre-disposition, but also as a predisposing factor to IVC Endothelium Injury and thrombosis formation. Echocardiography revealed supra hepatic vein IVC thrombosis floating to the right atrium. A C-T scan with contrast also showed pulmonary artery emboli to the left upper lobe. With open heart surgery, the right atrial and IVC clot were extracted and the main left and right pulmonary arteries were evaluated for possible clot lodging. The patient had an uneventful postoperative recovery and thrombosis has not reoccurred with periodical follow-up examinations.

  • Supra hepatic inferior vena cava and right atrial thrombosis following a traffic car crash
    Kermanshah University of Medical Sciences, 2016
    Co-Authors: Feridoun Sabzi, Hosein Karim, Marjan Haghi
    Abstract:

    We present a case of nephrotic syndrome associated with right atrial and supra hepatic vein part of inferior vena caval thrombosis. This patient presenting with dyspena, lower extremity edema and back pain after a vehicle accident and blunt trauma to abdomen. Trauma should be considered not only as a thrombophilic pre-disposition, but to be ascertaining as a predisposing factor to IVC Endothelium Injury and thrombosis formation. Echocardiography revealed supra hepatic vein IVC thrombosis floating to right atrium .C-T scan with contrast also showed pulmonary artery emboli to left upper lobe. With open heart surgery right atrial and IVC clot were extracted and main and left and right pulmonary artery was evaluated for possible clot lodging. The patient had a uneventful postoperative recovery and thrombosis was not occurred with periodical follow-up examination

Hossein Karim - One of the best experts on this subject based on the ideXlab platform.

  • Supra hepatic inferior vena cava and right atrial thrombosis following a traffic car crash
    Journal of injury & violence research, 2016
    Co-Authors: Feridoun Sabzi, Hossein Karim, Marjan Haghi
    Abstract:

    We present a case of nephrotic syndrome associated with right atrial and supra hepatic vein part of inferior vena caval thrombosis. This patient presented with dyspena, lower extremity edema and back pain after a vehicle accident and blunt trauma to the abdomen. Trauma should be considered not only as a thrombophilic pre-disposition, but also as a predisposing factor to IVC Endothelium Injury and thrombosis formation. Echocardiography revealed supra hepatic vein IVC thrombosis floating to the right atrium. A C-T scan with contrast also showed pulmonary artery emboli to the left upper lobe. With open heart surgery, the right atrial and IVC clot were extracted and the main left and right pulmonary arteries were evaluated for possible clot lodging. The patient had an uneventful postoperative recovery and thrombosis has not reoccurred with periodical follow-up examinations.

André Delhon - One of the best experts on this subject based on the ideXlab platform.

  • PPARalpha and PPARdelta activators inhibit cytokine-induced nuclear translocation of NF-kappaB and expression of VCAM-1 in EAhy926 endothelial cells.
    European journal of pharmacology, 2002
    Co-Authors: Yves Rival, Nathalie Benéteau, Thierry Taillandier, Mylène Pezet, Elisabeth Dupont-passelaigue, Jean François Patoiseau, Didier Junquéro, Francis C Colpaert, André Delhon
    Abstract:

    Endothelium Injury is a primary event in atherogenesis, which is followed by monocyte infiltration, macrophage differentiation, and smooth muscle cell migration. Peroxisome proliferator-activated receptors (PPARs) are transcription factors now recognized as important mediators in the inflammatory response. The aim of this study was to develop a human endothelial model to evaluate anti-inflammatory properties of PPAR activators. PPAR proteins (alpha, delta and gamma) are expressed in EAhy926 endothelial cells (ECs). Pirinixic acid (Wy-14643), fenofibrate, fenofibric acid, the Merck ligand PPARdelta activator L-165041, 15-deoxy-Delta(12,14)-prostaglandin J2, but not rosiglitazone (BRL-49653) inhibited the induced expression of vascular cell adhesion molecule-1 (VCAM-1), as measured by enzyme linked immunosorbent assay (ELISA), and monocyte binding to activated-EAhy926 cells. The PPARdelta activator L-165041 had the greatest potency to reduce cytokine-induced monocyte chemotactic protein-1 (MCP-1) secretion. All PPAR activators tested which impaired VCAM-1 expression reduced significantly nuclear p65 amount. These results show that EAhy926 endothelial cells are an adequate tool to substantiate and characterize inflammatory impacts of PPAR activators.

  • PPARα and PPARδ activators inhibit cytokine-induced nuclear translocation of NF-κB and expression of VCAM-1 in EAhy926 endothelial cells
    European Journal of Pharmacology, 2001
    Co-Authors: Yves Rival, Nathalie Benéteau, Thierry Taillandier, Mylène Pezet, Elisabeth Dupont-passelaigue, Jean François Patoiseau, Didier Junquéro, Francis C Colpaert, André Delhon
    Abstract:

    Abstract Endothelium Injury is a primary event in atherogenesis, which is followed by monocyte infiltration, macrophage differentiation, and smooth muscle cell migration. Peroxisome proliferator-activated receptors (PPARs) are transcription factors now recognized as important mediators in the inflammatory response. The aim of this study was to develop a human endothelial model to evaluate anti-inflammatory properties of PPAR activators. PPAR proteins (α, δ and γ) are expressed in EAhy926 endothelial cells (ECs). Pirinixic acid (Wy-14643), fenofibrate, fenofibric acid, the Merck ligand PPARδ activator L-165041, 15-deoxy-Δ 12,14 -prostaglandin J 2 , but not rosiglitazone (BRL-49653) inhibited the induced expression of vascular cell adhesion molecule-1 (VCAM-1), as measured by enzyme linked immunosorbent assay (ELISA), and monocyte binding to activated-EAhy926 cells. The PPARδ activator L-165041 had the greatest potency to reduce cytokine-induced monocyte chemotactic protein-1 (MCP-1) secretion. All PPAR activators tested which impaired VCAM-1 expression reduced significantly nuclear p65 amount. These results show that EAhy926 endothelial cells are an adequate tool to substantiate and characterize inflammatory impacts of PPAR activators.

Vera Luiza Capelozzi - One of the best experts on this subject based on the ideXlab platform.

  • degree of Endothelium Injury promotes fibroelastogenesis in experimental acute lung Injury
    Respiratory Physiology & Neurobiology, 2010
    Co-Authors: Monica C M Chao, Cristiane S N B Garcia, Mariana G Oliveira, Raquel S Santos, Isabela H Lucas, Pedro L Silva, Adriana Vieiraabreu, Hugo C Castrofarianeto, Edwin Roger Parracuentas, Vera Luiza Capelozzi
    Abstract:

    We tested the hypothesis that at the early phase of acute lung Injury (ALI) the degree of Endothelium Injury may predict lung parenchyma remodelling. For this purpose, two models of extrapulmonary ALI induced by Escherichia coli lipopolysaccharide (ALI-LPS) or cecal ligation and puncture (ALI-CLP) were developed in mice. At day 1, these models had similar degrees of lung mechanical compromise, epithelial damage, and intraperitoneal inflammation, but endothelial lesion was greater in ALI-CLP. A time course analysis revealed, at day 7: ALI-CLP had higher degrees of epithelial lesion, denudation of basement membrane, endothelial damage, elastic and collagen fibre content, neutrophils in bronchoalveolar lavage fluid (BALF), peritoneal fluid and blood, levels of interleukin-6, KC (murine analogue of IL-8), and transforming growth factor-β in BALF. Conversely, the number of lung apoptotic cells was similar in both groups. In conclusion, the intensity of fibroelastogenesis was affected by Endothelium Injury in addition to the maintenance of epithelial damage and intraperitoneal inflammation.