The Experts below are selected from a list of 1665 Experts worldwide ranked by ideXlab platform

Ping Wang - One of the best experts on this subject based on the ideXlab platform.

  • amaurosis fugax caused by heritable thrombophilia hypofibrinolysis in cases without carotid atherosclerosis thromboprophylaxis prevents subsequent transient monocular Partial Blindness
    Clinical and Applied Thrombosis-Hemostasis, 2007
    Co-Authors: Charles J Glueck, Karl C. Golnik, Ping Wang
    Abstract:

    Nineteen patients (age 60 ± 14) with amaurosis fugax associated with heritable thrombophilia-hypofibrinolysis without ipsilateral atherosclerotic carotid plaque or other causes of amaurosis fugax were studied. Our hypothesis was that case-specific thromboprophylaxis would prevent subsequent amaurosis fugax episodes. Prospective treatment data were available for 13 cases. Thrombophilic disorders included high Factors VIII and XI, G20210A prothrombin heterozygosity, low proteins C and S, MTHFR mutations, and the PL A1/A2 mutation. Hypofibrinolytic disorders included plasminogen activator inhibitor-1 4G4G, and high lipoprotein (a). Treatments included Coumadin; Lovenox, folic acid-vitamin B6-vitamin B12, discontinuation of estrogens-selective estrogen receptor modulators, Glucophage, and aspirin, as appropriate. Usually within 1 month on therapy, patients became asymptomatic and have remained asymptomatic for ≥ 1 year on therapy, without adverse treatment side effects. When amaurosis fugax occurs without car...

  • 18 amaurosis fugax caused by thrombophilia hypofibrinolysis in cases without carotid atherosclerosis therapy with coumadin lovenox or folic acid b6 b12 prevents subsequent transient monocular Partial Blindness
    Journal of Investigative Medicine, 2006
    Co-Authors: Charles J Glueck, Karl C. Golnik, Ping Wang
    Abstract:

    In 8 men and 9 women (age 60 ± 14, all white) without ipsilateral atherosclerotic carotid plaque and with no other known causes of amaurosis fugax (AF), whose AF was associated with thrombophilia-hypofibrinolysis, we hypothesized that case-specific thromboprophylaxis (Coumadin-Lovenox, folic acid [5 mg]-B 6 [100 mg]-B 12 [2,000 μg], aspirin, cessation of exogenous estrogens, glucophage [2.5 g]) would prevent subsequent episodes of transient monocular Partial or total Blindness. All 17 cases had $ 1 thrombophilic-hypofibrinolytic disorder thought to be etiologic for AF. Seven cases had MTHFR C677T homozygosity or C677T-A1298C compound heterozygosity, 5 4G4G PAI-1 homozygosity, 4 high factor VIII, 4 lupus anticoagulant, 4 the platelet glycoprotein PL A1/A2 mutation, 2 low free protein S, 2 high plasminogen activator inhibitor activity (PAI-Fx), 1 V Leiden heterozygosity, 1 prothrombin gene (PTG) heterozygosity, and 1 protein C deficiency. In 4 cases on Coumadin for 16,16, 21, and 98 months (1 PTG heterozygote, 1 protein C deficient [41%], 1 free protein S deficient [53%] with high factor VIII [157%], and 1 with high factor VIII [207%]), AF resolved, usually within 1 month of starting Coumadin, and the patients remained asymptomatic provided that the INR remained 2.5 or higher. In 1 case with low free protein S (28%), treated for 8 months of pregnancy and 1 month postpartum on Lovenox 80 mg/day, AF disappeared within 1 week, and she remained asymptomatic. In 3 cases with MTHFR C677T homozygosity treated with folic acid-B 6 -B 12 for 10, 15, and 29 months, AF resolved, usually within 1 month of starting therapy, and has not recurred. AF stopped within 1 month in 2 cases (1 high factor VIII 157%, 1 PAI-1 4G4G, PL A1/A2) when exogenous estrogens-SERMS were discontinued and has not recurred. The frequency of AF events was reduced in 2 cases on aspirin alone (1 PL A1/A2, I high VIII 157%) and AF events have remained less frequent over 5 and 11 months on aspirin. In 1 case with hypofibrinolysis (4G4G PAI-1 polymorphism, high PAI Fx, 31.7 IU/mL) treated with Glucophage (2.55 g/day), symptoms resolved within 1 month and have not recurred in 9 months on Glucophage. When AF occurs in the absence of carotid artery atherosclerosis or other known causes of AF, thrombophilia and/or hypofibrinolysis are nearly universal, reversible pathoetiologies.

  • 61 amaurosis fugax caused by thrombophilia hypofibrinolysis in cases without carotid atherosclerosis therapy with coumadin lovenox or folic acid b6 b12 prevents subsequent transient monocular Partial Blindness
    Journal of Investigative Medicine, 2005
    Co-Authors: Charles J Glueck, L Sieve, Dawit Aregawi, Ping Wang
    Abstract:

    In 8 men and 9 women, age 60 ± 14, all white) without carotid atherosclerosis, whose amaurosis fugax was caused by thrombophilia-hypofibrinolysis, we hypothesized that case-specific intervention for coagulation disorders (Coumadin-Lovenox or folic acid [5 mg]-B6 [100 mg]-B12 [2000 μg]) would prevent subsequent episodes of transient monocular Partial or total Blindness. PCR measures of thrombophilia (V Leiden, prothrombin, MTHFR, platelet glycoprotein PL A1/A2 mutations) and hypofibrinolysis (plasminogen activator inhibitor-1 4G4G mutation) were compared in 17 cases vs 276 healthy controls, 145 male, 131 female, 240 white, 32 black, 4 other. MTHFR C677T homozygosity or C677T-A1298C compound heterozygosity was more common in cases (7/16 [44%]) than controls (35/276 [13%]), Fisher9s p = .003. Serologic measures of thrombophilia (proteins C, antithrombin III, free S, homocysteine, anticardiolipin antibody IgG and IgM, lupus anticoagulant, Factor VIII, Factor XI) and hypofibrinolysis (plasminogen activator inhibitor-1 [PAI-Fx], Lp[a]) were compared in the 17 cases vs 78 healthy adults. High (> 150%) Factor VIII was more common in cases (4/16 [25%]) than controls (5/72 [7%]), Fisher9s p = .053. All 17 cases had ≥ 1 thrombophilic-hypofibrinolytic disorder, with the most common being MTHFR C677T homozygosity or C677T-A1298C compound heterozygosity (7 cases), 4G4G homozygosity (5 cases), high Factor VIII (4 cases), lupus anticoagulant (4 cases), the platelet PL A1/A2 mutation (4 cases), low free protein S (2 cases), high PAI-Fx (2 cases), V Leiden heterozygosity (1 case), prothrombin gene mutation (1 case), and protein C deficiency (1 case). In 4 cases on Coumadin for 3, 5, 11, and 84 months, in 1 case for 8 months of pregnancy on Lovenox, and in 4 cases on folic acid-B6-B12 for 2, 3, 10, and 13 months, amaurosis fugax disappeared, usually within 1 month of starting therapy. Amaurosis fugax stopped in 2 cases when exogenous estrogens-SERMS were discontinued, stopped in 1 case on aspirin alone, and stopped spontaneously in 1 case. When amaurosis fugax occurs in the absence of carotid artery atherosclerosis, thrombophilia and/or hypofibrinolysis are nearly universal, reversible pathoetiologies.

Charles J Glueck - One of the best experts on this subject based on the ideXlab platform.

  • amaurosis fugax caused by heritable thrombophilia hypofibrinolysis in cases without carotid atherosclerosis thromboprophylaxis prevents subsequent transient monocular Partial Blindness
    Clinical and Applied Thrombosis-Hemostasis, 2007
    Co-Authors: Charles J Glueck, Karl C. Golnik, Ping Wang
    Abstract:

    Nineteen patients (age 60 ± 14) with amaurosis fugax associated with heritable thrombophilia-hypofibrinolysis without ipsilateral atherosclerotic carotid plaque or other causes of amaurosis fugax were studied. Our hypothesis was that case-specific thromboprophylaxis would prevent subsequent amaurosis fugax episodes. Prospective treatment data were available for 13 cases. Thrombophilic disorders included high Factors VIII and XI, G20210A prothrombin heterozygosity, low proteins C and S, MTHFR mutations, and the PL A1/A2 mutation. Hypofibrinolytic disorders included plasminogen activator inhibitor-1 4G4G, and high lipoprotein (a). Treatments included Coumadin; Lovenox, folic acid-vitamin B6-vitamin B12, discontinuation of estrogens-selective estrogen receptor modulators, Glucophage, and aspirin, as appropriate. Usually within 1 month on therapy, patients became asymptomatic and have remained asymptomatic for ≥ 1 year on therapy, without adverse treatment side effects. When amaurosis fugax occurs without car...

  • 18 amaurosis fugax caused by thrombophilia hypofibrinolysis in cases without carotid atherosclerosis therapy with coumadin lovenox or folic acid b6 b12 prevents subsequent transient monocular Partial Blindness
    Journal of Investigative Medicine, 2006
    Co-Authors: Charles J Glueck, Karl C. Golnik, Ping Wang
    Abstract:

    In 8 men and 9 women (age 60 ± 14, all white) without ipsilateral atherosclerotic carotid plaque and with no other known causes of amaurosis fugax (AF), whose AF was associated with thrombophilia-hypofibrinolysis, we hypothesized that case-specific thromboprophylaxis (Coumadin-Lovenox, folic acid [5 mg]-B 6 [100 mg]-B 12 [2,000 μg], aspirin, cessation of exogenous estrogens, glucophage [2.5 g]) would prevent subsequent episodes of transient monocular Partial or total Blindness. All 17 cases had $ 1 thrombophilic-hypofibrinolytic disorder thought to be etiologic for AF. Seven cases had MTHFR C677T homozygosity or C677T-A1298C compound heterozygosity, 5 4G4G PAI-1 homozygosity, 4 high factor VIII, 4 lupus anticoagulant, 4 the platelet glycoprotein PL A1/A2 mutation, 2 low free protein S, 2 high plasminogen activator inhibitor activity (PAI-Fx), 1 V Leiden heterozygosity, 1 prothrombin gene (PTG) heterozygosity, and 1 protein C deficiency. In 4 cases on Coumadin for 16,16, 21, and 98 months (1 PTG heterozygote, 1 protein C deficient [41%], 1 free protein S deficient [53%] with high factor VIII [157%], and 1 with high factor VIII [207%]), AF resolved, usually within 1 month of starting Coumadin, and the patients remained asymptomatic provided that the INR remained 2.5 or higher. In 1 case with low free protein S (28%), treated for 8 months of pregnancy and 1 month postpartum on Lovenox 80 mg/day, AF disappeared within 1 week, and she remained asymptomatic. In 3 cases with MTHFR C677T homozygosity treated with folic acid-B 6 -B 12 for 10, 15, and 29 months, AF resolved, usually within 1 month of starting therapy, and has not recurred. AF stopped within 1 month in 2 cases (1 high factor VIII 157%, 1 PAI-1 4G4G, PL A1/A2) when exogenous estrogens-SERMS were discontinued and has not recurred. The frequency of AF events was reduced in 2 cases on aspirin alone (1 PL A1/A2, I high VIII 157%) and AF events have remained less frequent over 5 and 11 months on aspirin. In 1 case with hypofibrinolysis (4G4G PAI-1 polymorphism, high PAI Fx, 31.7 IU/mL) treated with Glucophage (2.55 g/day), symptoms resolved within 1 month and have not recurred in 9 months on Glucophage. When AF occurs in the absence of carotid artery atherosclerosis or other known causes of AF, thrombophilia and/or hypofibrinolysis are nearly universal, reversible pathoetiologies.

  • 61 amaurosis fugax caused by thrombophilia hypofibrinolysis in cases without carotid atherosclerosis therapy with coumadin lovenox or folic acid b6 b12 prevents subsequent transient monocular Partial Blindness
    Journal of Investigative Medicine, 2005
    Co-Authors: Charles J Glueck, L Sieve, Dawit Aregawi, Ping Wang
    Abstract:

    In 8 men and 9 women, age 60 ± 14, all white) without carotid atherosclerosis, whose amaurosis fugax was caused by thrombophilia-hypofibrinolysis, we hypothesized that case-specific intervention for coagulation disorders (Coumadin-Lovenox or folic acid [5 mg]-B6 [100 mg]-B12 [2000 μg]) would prevent subsequent episodes of transient monocular Partial or total Blindness. PCR measures of thrombophilia (V Leiden, prothrombin, MTHFR, platelet glycoprotein PL A1/A2 mutations) and hypofibrinolysis (plasminogen activator inhibitor-1 4G4G mutation) were compared in 17 cases vs 276 healthy controls, 145 male, 131 female, 240 white, 32 black, 4 other. MTHFR C677T homozygosity or C677T-A1298C compound heterozygosity was more common in cases (7/16 [44%]) than controls (35/276 [13%]), Fisher9s p = .003. Serologic measures of thrombophilia (proteins C, antithrombin III, free S, homocysteine, anticardiolipin antibody IgG and IgM, lupus anticoagulant, Factor VIII, Factor XI) and hypofibrinolysis (plasminogen activator inhibitor-1 [PAI-Fx], Lp[a]) were compared in the 17 cases vs 78 healthy adults. High (> 150%) Factor VIII was more common in cases (4/16 [25%]) than controls (5/72 [7%]), Fisher9s p = .053. All 17 cases had ≥ 1 thrombophilic-hypofibrinolytic disorder, with the most common being MTHFR C677T homozygosity or C677T-A1298C compound heterozygosity (7 cases), 4G4G homozygosity (5 cases), high Factor VIII (4 cases), lupus anticoagulant (4 cases), the platelet PL A1/A2 mutation (4 cases), low free protein S (2 cases), high PAI-Fx (2 cases), V Leiden heterozygosity (1 case), prothrombin gene mutation (1 case), and protein C deficiency (1 case). In 4 cases on Coumadin for 3, 5, 11, and 84 months, in 1 case for 8 months of pregnancy on Lovenox, and in 4 cases on folic acid-B6-B12 for 2, 3, 10, and 13 months, amaurosis fugax disappeared, usually within 1 month of starting therapy. Amaurosis fugax stopped in 2 cases when exogenous estrogens-SERMS were discontinued, stopped in 1 case on aspirin alone, and stopped spontaneously in 1 case. When amaurosis fugax occurs in the absence of carotid artery atherosclerosis, thrombophilia and/or hypofibrinolysis are nearly universal, reversible pathoetiologies.

Karl C. Golnik - One of the best experts on this subject based on the ideXlab platform.

  • amaurosis fugax caused by heritable thrombophilia hypofibrinolysis in cases without carotid atherosclerosis thromboprophylaxis prevents subsequent transient monocular Partial Blindness
    Clinical and Applied Thrombosis-Hemostasis, 2007
    Co-Authors: Charles J Glueck, Karl C. Golnik, Ping Wang
    Abstract:

    Nineteen patients (age 60 ± 14) with amaurosis fugax associated with heritable thrombophilia-hypofibrinolysis without ipsilateral atherosclerotic carotid plaque or other causes of amaurosis fugax were studied. Our hypothesis was that case-specific thromboprophylaxis would prevent subsequent amaurosis fugax episodes. Prospective treatment data were available for 13 cases. Thrombophilic disorders included high Factors VIII and XI, G20210A prothrombin heterozygosity, low proteins C and S, MTHFR mutations, and the PL A1/A2 mutation. Hypofibrinolytic disorders included plasminogen activator inhibitor-1 4G4G, and high lipoprotein (a). Treatments included Coumadin; Lovenox, folic acid-vitamin B6-vitamin B12, discontinuation of estrogens-selective estrogen receptor modulators, Glucophage, and aspirin, as appropriate. Usually within 1 month on therapy, patients became asymptomatic and have remained asymptomatic for ≥ 1 year on therapy, without adverse treatment side effects. When amaurosis fugax occurs without car...

  • 18 amaurosis fugax caused by thrombophilia hypofibrinolysis in cases without carotid atherosclerosis therapy with coumadin lovenox or folic acid b6 b12 prevents subsequent transient monocular Partial Blindness
    Journal of Investigative Medicine, 2006
    Co-Authors: Charles J Glueck, Karl C. Golnik, Ping Wang
    Abstract:

    In 8 men and 9 women (age 60 ± 14, all white) without ipsilateral atherosclerotic carotid plaque and with no other known causes of amaurosis fugax (AF), whose AF was associated with thrombophilia-hypofibrinolysis, we hypothesized that case-specific thromboprophylaxis (Coumadin-Lovenox, folic acid [5 mg]-B 6 [100 mg]-B 12 [2,000 μg], aspirin, cessation of exogenous estrogens, glucophage [2.5 g]) would prevent subsequent episodes of transient monocular Partial or total Blindness. All 17 cases had $ 1 thrombophilic-hypofibrinolytic disorder thought to be etiologic for AF. Seven cases had MTHFR C677T homozygosity or C677T-A1298C compound heterozygosity, 5 4G4G PAI-1 homozygosity, 4 high factor VIII, 4 lupus anticoagulant, 4 the platelet glycoprotein PL A1/A2 mutation, 2 low free protein S, 2 high plasminogen activator inhibitor activity (PAI-Fx), 1 V Leiden heterozygosity, 1 prothrombin gene (PTG) heterozygosity, and 1 protein C deficiency. In 4 cases on Coumadin for 16,16, 21, and 98 months (1 PTG heterozygote, 1 protein C deficient [41%], 1 free protein S deficient [53%] with high factor VIII [157%], and 1 with high factor VIII [207%]), AF resolved, usually within 1 month of starting Coumadin, and the patients remained asymptomatic provided that the INR remained 2.5 or higher. In 1 case with low free protein S (28%), treated for 8 months of pregnancy and 1 month postpartum on Lovenox 80 mg/day, AF disappeared within 1 week, and she remained asymptomatic. In 3 cases with MTHFR C677T homozygosity treated with folic acid-B 6 -B 12 for 10, 15, and 29 months, AF resolved, usually within 1 month of starting therapy, and has not recurred. AF stopped within 1 month in 2 cases (1 high factor VIII 157%, 1 PAI-1 4G4G, PL A1/A2) when exogenous estrogens-SERMS were discontinued and has not recurred. The frequency of AF events was reduced in 2 cases on aspirin alone (1 PL A1/A2, I high VIII 157%) and AF events have remained less frequent over 5 and 11 months on aspirin. In 1 case with hypofibrinolysis (4G4G PAI-1 polymorphism, high PAI Fx, 31.7 IU/mL) treated with Glucophage (2.55 g/day), symptoms resolved within 1 month and have not recurred in 9 months on Glucophage. When AF occurs in the absence of carotid artery atherosclerosis or other known causes of AF, thrombophilia and/or hypofibrinolysis are nearly universal, reversible pathoetiologies.

Zaaijer, Michiel B. - One of the best experts on this subject based on the ideXlab platform.

  • Wind farm layout optimization using pseudo-gradients
    'Copernicus GmbH', 2021
    Co-Authors: Quaeghebeur Erik, Bos René, Zaaijer, Michiel B.
    Abstract:

    This paper presents a heuristic building block for wind farm layout optimization algorithms. For each pair of wake-interacting turbines, a vector is defined. Its magnitude is proportional to the wind speed deficit of the waked turbine due to the waking turbine. Its direction is chosen from the inter-turbine, downwind, or crosswind directions. These vectors can be combined for all waking or waked turbines and averaged over the wind resource to obtain a vector, a “pseudo-gradient”, that can take the role of gradient in classical gradient-following optimization algorithms. A proof-of-concept optimization algorithm demonstrates how such vectors can be used for computationally efficient wind farm layout optimization. Results for various sites, both idealized and realistic, illustrate the types of layout generated by the proof-of-concept algorithm. These results provide a basis for a discussion of the heuristic's strong points – speed, competitive reduction in wake losses, and flexibility – and weak points – Partial Blindness to the objective and dependence on the starting layout. The computational speed of pseudo-gradient-based optimization is an enabler for analyses that would otherwise be computationally impractical. Pseudo-gradient-based optimization has already been used by industry in the design of large-scale (offshore) wind farms

  • Wind farm layout optimization using pseudo-gradients
    'Copernicus GmbH', 2021
    Co-Authors: Quaeghebeur Erik, Bos R., Zaaijer, Michiel B.
    Abstract:

    This paper presents a heuristic building block for wind farm layout optimization algorithms. For each pair of wake-interacting turbines, a vector is defined. Its magnitude is proportional to the wind speed deficit of the waked turbine due to the waking turbine. Its direction is chosen from the inter-turbine, downwind, or crosswind directions. These vectors can be combined for all waking or waked turbines and averaged over the wind resource to obtain a vector, a "pseudo-gradient", that can take the role of gradient in classical gradient-following optimization algorithms. A proof-of-concept optimization algorithm demonstrates how such vectors can be used for computationally efficient wind farm layout optimization. Results for various sites, both idealized and realistic, illustrate the types of layout generated by the proof-of-concept algorithm. These results provide a basis for a discussion of the heuristic's strong points-speed, competitive reduction in wake losses, and flexibility-and weak points-Partial Blindness to the objective and dependence on the starting layout. The computational speed of pseudo-gradient-based optimization is an enabler for analyses that would otherwise be computationally impractical. Pseudo-gradient-based optimization has already been used by industry in the design of large-scale (offshore) wind farms. Wind Energ

Quaeghebeur Erik - One of the best experts on this subject based on the ideXlab platform.

  • Wind farm layout optimization using pseudo-gradients
    'Copernicus GmbH', 2021
    Co-Authors: Quaeghebeur Erik, Bos René, Zaaijer, Michiel B.
    Abstract:

    This paper presents a heuristic building block for wind farm layout optimization algorithms. For each pair of wake-interacting turbines, a vector is defined. Its magnitude is proportional to the wind speed deficit of the waked turbine due to the waking turbine. Its direction is chosen from the inter-turbine, downwind, or crosswind directions. These vectors can be combined for all waking or waked turbines and averaged over the wind resource to obtain a vector, a “pseudo-gradient”, that can take the role of gradient in classical gradient-following optimization algorithms. A proof-of-concept optimization algorithm demonstrates how such vectors can be used for computationally efficient wind farm layout optimization. Results for various sites, both idealized and realistic, illustrate the types of layout generated by the proof-of-concept algorithm. These results provide a basis for a discussion of the heuristic's strong points – speed, competitive reduction in wake losses, and flexibility – and weak points – Partial Blindness to the objective and dependence on the starting layout. The computational speed of pseudo-gradient-based optimization is an enabler for analyses that would otherwise be computationally impractical. Pseudo-gradient-based optimization has already been used by industry in the design of large-scale (offshore) wind farms

  • Wind farm layout optimization using pseudo-gradients
    'Copernicus GmbH', 2021
    Co-Authors: Quaeghebeur Erik, Bos R., Zaaijer, Michiel B.
    Abstract:

    This paper presents a heuristic building block for wind farm layout optimization algorithms. For each pair of wake-interacting turbines, a vector is defined. Its magnitude is proportional to the wind speed deficit of the waked turbine due to the waking turbine. Its direction is chosen from the inter-turbine, downwind, or crosswind directions. These vectors can be combined for all waking or waked turbines and averaged over the wind resource to obtain a vector, a "pseudo-gradient", that can take the role of gradient in classical gradient-following optimization algorithms. A proof-of-concept optimization algorithm demonstrates how such vectors can be used for computationally efficient wind farm layout optimization. Results for various sites, both idealized and realistic, illustrate the types of layout generated by the proof-of-concept algorithm. These results provide a basis for a discussion of the heuristic's strong points-speed, competitive reduction in wake losses, and flexibility-and weak points-Partial Blindness to the objective and dependence on the starting layout. The computational speed of pseudo-gradient-based optimization is an enabler for analyses that would otherwise be computationally impractical. Pseudo-gradient-based optimization has already been used by industry in the design of large-scale (offshore) wind farms. Wind Energ