The Experts below are selected from a list of 360 Experts worldwide ranked by ideXlab platform

Celine Demougeot - One of the best experts on this subject based on the ideXlab platform.

  • vascular arginase is a relevant target to improve Cerebrovascular endothelial dysfunction in rheumatoid arthritis evidence from the model of adjuvant induced arthritis
    Translational Stroke Research, 2020
    Co-Authors: Romain Bordy, Aurore Quirie, Christine Marie, Daniel Wendling, Perle Totoson, Celine Demougeot
    Abstract:

    Emerging data revealed that rheumatoid arthritis (RA) is associated with higher risk of Cerebrovascular Diseases. Whereas cerebral endothelial dysfunction is acknowledged as a critical aspect of Cerebrovascular Diseases, its presence in RA and the mechanisms involved are currently unknown. By using the model of rat adjuvant-induced arthritis (AIA), the present study investigated Cerebrovascular reactivity in pressurized middle cerebral arteries (MCA) on day 33 post-immunization. The results revealed that arthritis induced a dramatic decrease in the vasodilatory response to acetylcholine (ACh), ADP, and bradykinin (n = 7–9 arteries, p < 0.0001). By using nor-NOHA, L-NAME, BH4, and Tempol, the results showed that the reduced response to ACh relied on arginase overactivation (n = 8), low NOS activity (n = 8), BH4 deficiency (n = 9), and excessive superoxide production (n = 9). Immunohistological analysis revealed an endothelial upregulation of arginase 2 (p < 0.05, n = 5–6) and NADPH oxidase (p < 0.05, n = 5–7) while eNOS expression was unchanged in AIA (n = 6). To assess whether arginase inhibition may be a relevant therapeutic, AIA rats were treated with an arginase inhibitor (nor-NOHA, 40 mg/kg/day, i.p., n = 20 rats) daily from day 10 to day 33 post-immunization. The treatment alleviated the impaired response of MCA to endothelium-dependent agonists, through an increase in NOS signaling and a suppression of BH4 deficiency and superoxide overproduction. By contrast, it did not change the course of arthritis. In conclusion, arthritis induced a Cerebrovascular endothelial dysfunction involving an imbalance in the arginase/NOS pathway. Arginase inhibition appears as a promising therapy beyond anti-rheumatic drugs for reducing the risk of Cerebrovascular Diseases in RA.

Romain Bordy - One of the best experts on this subject based on the ideXlab platform.

  • vascular arginase is a relevant target to improve Cerebrovascular endothelial dysfunction in rheumatoid arthritis evidence from the model of adjuvant induced arthritis
    Translational Stroke Research, 2020
    Co-Authors: Romain Bordy, Aurore Quirie, Christine Marie, Daniel Wendling, Perle Totoson, Celine Demougeot
    Abstract:

    Emerging data revealed that rheumatoid arthritis (RA) is associated with higher risk of Cerebrovascular Diseases. Whereas cerebral endothelial dysfunction is acknowledged as a critical aspect of Cerebrovascular Diseases, its presence in RA and the mechanisms involved are currently unknown. By using the model of rat adjuvant-induced arthritis (AIA), the present study investigated Cerebrovascular reactivity in pressurized middle cerebral arteries (MCA) on day 33 post-immunization. The results revealed that arthritis induced a dramatic decrease in the vasodilatory response to acetylcholine (ACh), ADP, and bradykinin (n = 7–9 arteries, p < 0.0001). By using nor-NOHA, L-NAME, BH4, and Tempol, the results showed that the reduced response to ACh relied on arginase overactivation (n = 8), low NOS activity (n = 8), BH4 deficiency (n = 9), and excessive superoxide production (n = 9). Immunohistological analysis revealed an endothelial upregulation of arginase 2 (p < 0.05, n = 5–6) and NADPH oxidase (p < 0.05, n = 5–7) while eNOS expression was unchanged in AIA (n = 6). To assess whether arginase inhibition may be a relevant therapeutic, AIA rats were treated with an arginase inhibitor (nor-NOHA, 40 mg/kg/day, i.p., n = 20 rats) daily from day 10 to day 33 post-immunization. The treatment alleviated the impaired response of MCA to endothelium-dependent agonists, through an increase in NOS signaling and a suppression of BH4 deficiency and superoxide overproduction. By contrast, it did not change the course of arthritis. In conclusion, arthritis induced a Cerebrovascular endothelial dysfunction involving an imbalance in the arginase/NOS pathway. Arginase inhibition appears as a promising therapy beyond anti-rheumatic drugs for reducing the risk of Cerebrovascular Diseases in RA.

Min S Park - One of the best experts on this subject based on the ideXlab platform.

  • emerging technologies in flow diverters and stents for Cerebrovascular Diseases
    Current Neurology and Neuroscience Reports, 2017
    Co-Authors: Michael Karsy, Jian Guan, Andrea A Brock, Anubhav G Amin, Min S Park
    Abstract:

    Stents and flow diverters have revolutionized the treatment of Cerebrovascular disease. Guglielmi coils, flexible microcatheters, and first-generation intracranial stents, such as Neuroform (Stryker Neurovascular) and Enterprise stents (Codman/DePuy-Synthes), have paved the way for the development of the Pipeline Embolization Device (PED) (ev3/Covidien/Medtronic) and other endovascular approaches. This review discusses the historical development of flow diverter technologies from the PED to similar devices, such as the Surpass stent (Stryker Neurovascular), the Flow-Redirection Endoluminal Device (FRED; MicroVention, Inc.), the SILK stent (Balt Extrusion), and the p64 Flow Modulation Device (Phenox). In addition, the potential use of drug-eluting stents and various bioresorbable scaffolds (e.g., poly-l-lactic acid, magnesium), new developments in stent material (e.g., thin-film nitinol), design (e.g., biocompatible polymers, embedded microcircuitry, flow models), and potential applications for flow diverters will be considered. Endovascular treatment of Cerebrovascular disease is rapidly advancing via continued development of new technology.

Perle Totoson - One of the best experts on this subject based on the ideXlab platform.

  • vascular arginase is a relevant target to improve Cerebrovascular endothelial dysfunction in rheumatoid arthritis evidence from the model of adjuvant induced arthritis
    Translational Stroke Research, 2020
    Co-Authors: Romain Bordy, Aurore Quirie, Christine Marie, Daniel Wendling, Perle Totoson, Celine Demougeot
    Abstract:

    Emerging data revealed that rheumatoid arthritis (RA) is associated with higher risk of Cerebrovascular Diseases. Whereas cerebral endothelial dysfunction is acknowledged as a critical aspect of Cerebrovascular Diseases, its presence in RA and the mechanisms involved are currently unknown. By using the model of rat adjuvant-induced arthritis (AIA), the present study investigated Cerebrovascular reactivity in pressurized middle cerebral arteries (MCA) on day 33 post-immunization. The results revealed that arthritis induced a dramatic decrease in the vasodilatory response to acetylcholine (ACh), ADP, and bradykinin (n = 7–9 arteries, p < 0.0001). By using nor-NOHA, L-NAME, BH4, and Tempol, the results showed that the reduced response to ACh relied on arginase overactivation (n = 8), low NOS activity (n = 8), BH4 deficiency (n = 9), and excessive superoxide production (n = 9). Immunohistological analysis revealed an endothelial upregulation of arginase 2 (p < 0.05, n = 5–6) and NADPH oxidase (p < 0.05, n = 5–7) while eNOS expression was unchanged in AIA (n = 6). To assess whether arginase inhibition may be a relevant therapeutic, AIA rats were treated with an arginase inhibitor (nor-NOHA, 40 mg/kg/day, i.p., n = 20 rats) daily from day 10 to day 33 post-immunization. The treatment alleviated the impaired response of MCA to endothelium-dependent agonists, through an increase in NOS signaling and a suppression of BH4 deficiency and superoxide overproduction. By contrast, it did not change the course of arthritis. In conclusion, arthritis induced a Cerebrovascular endothelial dysfunction involving an imbalance in the arginase/NOS pathway. Arginase inhibition appears as a promising therapy beyond anti-rheumatic drugs for reducing the risk of Cerebrovascular Diseases in RA.

Daniel Wendling - One of the best experts on this subject based on the ideXlab platform.

  • vascular arginase is a relevant target to improve Cerebrovascular endothelial dysfunction in rheumatoid arthritis evidence from the model of adjuvant induced arthritis
    Translational Stroke Research, 2020
    Co-Authors: Romain Bordy, Aurore Quirie, Christine Marie, Daniel Wendling, Perle Totoson, Celine Demougeot
    Abstract:

    Emerging data revealed that rheumatoid arthritis (RA) is associated with higher risk of Cerebrovascular Diseases. Whereas cerebral endothelial dysfunction is acknowledged as a critical aspect of Cerebrovascular Diseases, its presence in RA and the mechanisms involved are currently unknown. By using the model of rat adjuvant-induced arthritis (AIA), the present study investigated Cerebrovascular reactivity in pressurized middle cerebral arteries (MCA) on day 33 post-immunization. The results revealed that arthritis induced a dramatic decrease in the vasodilatory response to acetylcholine (ACh), ADP, and bradykinin (n = 7–9 arteries, p < 0.0001). By using nor-NOHA, L-NAME, BH4, and Tempol, the results showed that the reduced response to ACh relied on arginase overactivation (n = 8), low NOS activity (n = 8), BH4 deficiency (n = 9), and excessive superoxide production (n = 9). Immunohistological analysis revealed an endothelial upregulation of arginase 2 (p < 0.05, n = 5–6) and NADPH oxidase (p < 0.05, n = 5–7) while eNOS expression was unchanged in AIA (n = 6). To assess whether arginase inhibition may be a relevant therapeutic, AIA rats were treated with an arginase inhibitor (nor-NOHA, 40 mg/kg/day, i.p., n = 20 rats) daily from day 10 to day 33 post-immunization. The treatment alleviated the impaired response of MCA to endothelium-dependent agonists, through an increase in NOS signaling and a suppression of BH4 deficiency and superoxide overproduction. By contrast, it did not change the course of arthritis. In conclusion, arthritis induced a Cerebrovascular endothelial dysfunction involving an imbalance in the arginase/NOS pathway. Arginase inhibition appears as a promising therapy beyond anti-rheumatic drugs for reducing the risk of Cerebrovascular Diseases in RA.