The Experts below are selected from a list of 69 Experts worldwide ranked by ideXlab platform

Hyoung Doo Shin - One of the best experts on this subject based on the ideXlab platform.

  • association of polymorphisms in thromboxane a2 receptor and thromboxane a Synthase 1 with cerebral infarction in a korean population
    Journal of Biochemistry and Molecular Biology, 2009
    Co-Authors: Sun Ah Park, Byung Lae Park, Jeong Ho Park, Ki Bum Sung, Hun Soo Chang, Choonsik Park, Hyoung Doo Shin
    Abstract:

    Cerebral infarction is one of the most common causes of death and disability (1) with a complex etiology involving both ge-netic and modifiable, pre-disposing determinants (2, 3). Identi-fying the genetic risk for cerebral infarction is important both for risk prediction and for prevention of potential incidents. Although several genes involved in hemostasis, renin angio-tensin system and lipid metabolism have been identified as possible susceptibility genes, their associations with cerebral infarction are still controversial (4). Thromboxane A2 (TBXA2) is a potent vasoconstrictor and stimulator of platelet aggregation with high levels produced in atherosclerosis (5) and during acute stroke (6). The mechanism by which aspirin prevents cerebral infarction is through the po-tent inhibition of cyclooxygenase-1, thereby blocking the pro-duction of TBXA2 (7-9). Thus, TBXA2 is considered an im-portant mediator of cerebral infarction (10). The enzyme that catalyzes its synthesis, thromboxane A2 Synthase 1 (TBXAS1), is a key component for TBXA2 function along with the re-ceptor that mediates its action, thromboxane A2 receptor (TBXA2R). TBXA2R is a member of the family of G pro-tein-coupled receptors and performs an essential role in hemo-stasis by interacting with TBXA2 to induce platelet aggrega-tion. Point mutations in

  • Association of polymorphisms in thromboxane A2 receptor and thromboxane A Synthase 1 with cerebral infarction in a Korean population.
    BMB reports, 2009
    Co-Authors: Sun Ah Park, Byung Lae Park, Jeong Ho Park, Ki Bum Sung, Hun Soo Chang, Choonsik Park, Tae Kyeong Lee, You Kyoung Lee, Hyoung Doo Shin
    Abstract:

    Thromboxane A2 (TBXA2) is a potent vasoconstrictor in cerebral circulation and is a known contributor to the pathogenesis of cerebral infarction. Thromboxane A2 Synthase 1 (TBXAS1) and thromboxane A2 receptors (TBXA2R) are key components in TBXA2 function. We examined whether genetic variants in TBXA2R and TBXAS1 are risk factors for cerebral infarction by genotyping 453 Korean patients with noncardiogenic cerebral infarction and 260 controls. A few, specific polymorphisms in the TBXA2R (-3372G>C, +4710T>C and 4839T>C) and TBXAS1 (+16184G>T, +141931A>T and +177729G>A) genes were chosen and investigated. Logistic regression showed the frequencies of TBXAS1+16184G>T and TBXAS1- ht3 were significantly more frequent in cerebral infarction (P=0.002, OR=2.75 and P=0.01, OR=1.57, respectively), specifically in small-artery occlusion (SAO) type of cerebral infarction (P=0.0003 and 0.005, respectively). These results suggest specific TBXAS1 gene polymorphisms may be a useful marker for development of cerebral infarction, especially SAO type in Korean population.

Sun Ah Park - One of the best experts on this subject based on the ideXlab platform.

  • association of polymorphisms in thromboxane a2 receptor and thromboxane a Synthase 1 with cerebral infarction in a korean population
    Journal of Biochemistry and Molecular Biology, 2009
    Co-Authors: Sun Ah Park, Byung Lae Park, Jeong Ho Park, Ki Bum Sung, Hun Soo Chang, Choonsik Park, Hyoung Doo Shin
    Abstract:

    Cerebral infarction is one of the most common causes of death and disability (1) with a complex etiology involving both ge-netic and modifiable, pre-disposing determinants (2, 3). Identi-fying the genetic risk for cerebral infarction is important both for risk prediction and for prevention of potential incidents. Although several genes involved in hemostasis, renin angio-tensin system and lipid metabolism have been identified as possible susceptibility genes, their associations with cerebral infarction are still controversial (4). Thromboxane A2 (TBXA2) is a potent vasoconstrictor and stimulator of platelet aggregation with high levels produced in atherosclerosis (5) and during acute stroke (6). The mechanism by which aspirin prevents cerebral infarction is through the po-tent inhibition of cyclooxygenase-1, thereby blocking the pro-duction of TBXA2 (7-9). Thus, TBXA2 is considered an im-portant mediator of cerebral infarction (10). The enzyme that catalyzes its synthesis, thromboxane A2 Synthase 1 (TBXAS1), is a key component for TBXA2 function along with the re-ceptor that mediates its action, thromboxane A2 receptor (TBXA2R). TBXA2R is a member of the family of G pro-tein-coupled receptors and performs an essential role in hemo-stasis by interacting with TBXA2 to induce platelet aggrega-tion. Point mutations in

  • Association of polymorphisms in thromboxane A2 receptor and thromboxane A Synthase 1 with cerebral infarction in a Korean population.
    BMB reports, 2009
    Co-Authors: Sun Ah Park, Byung Lae Park, Jeong Ho Park, Ki Bum Sung, Hun Soo Chang, Choonsik Park, Tae Kyeong Lee, You Kyoung Lee, Hyoung Doo Shin
    Abstract:

    Thromboxane A2 (TBXA2) is a potent vasoconstrictor in cerebral circulation and is a known contributor to the pathogenesis of cerebral infarction. Thromboxane A2 Synthase 1 (TBXAS1) and thromboxane A2 receptors (TBXA2R) are key components in TBXA2 function. We examined whether genetic variants in TBXA2R and TBXAS1 are risk factors for cerebral infarction by genotyping 453 Korean patients with noncardiogenic cerebral infarction and 260 controls. A few, specific polymorphisms in the TBXA2R (-3372G>C, +4710T>C and 4839T>C) and TBXAS1 (+16184G>T, +141931A>T and +177729G>A) genes were chosen and investigated. Logistic regression showed the frequencies of TBXAS1+16184G>T and TBXAS1- ht3 were significantly more frequent in cerebral infarction (P=0.002, OR=2.75 and P=0.01, OR=1.57, respectively), specifically in small-artery occlusion (SAO) type of cerebral infarction (P=0.0003 and 0.005, respectively). These results suggest specific TBXAS1 gene polymorphisms may be a useful marker for development of cerebral infarction, especially SAO type in Korean population.

Byung Lae Park - One of the best experts on this subject based on the ideXlab platform.

  • association of polymorphisms in thromboxane a2 receptor and thromboxane a Synthase 1 with cerebral infarction in a korean population
    Journal of Biochemistry and Molecular Biology, 2009
    Co-Authors: Sun Ah Park, Byung Lae Park, Jeong Ho Park, Ki Bum Sung, Hun Soo Chang, Choonsik Park, Hyoung Doo Shin
    Abstract:

    Cerebral infarction is one of the most common causes of death and disability (1) with a complex etiology involving both ge-netic and modifiable, pre-disposing determinants (2, 3). Identi-fying the genetic risk for cerebral infarction is important both for risk prediction and for prevention of potential incidents. Although several genes involved in hemostasis, renin angio-tensin system and lipid metabolism have been identified as possible susceptibility genes, their associations with cerebral infarction are still controversial (4). Thromboxane A2 (TBXA2) is a potent vasoconstrictor and stimulator of platelet aggregation with high levels produced in atherosclerosis (5) and during acute stroke (6). The mechanism by which aspirin prevents cerebral infarction is through the po-tent inhibition of cyclooxygenase-1, thereby blocking the pro-duction of TBXA2 (7-9). Thus, TBXA2 is considered an im-portant mediator of cerebral infarction (10). The enzyme that catalyzes its synthesis, thromboxane A2 Synthase 1 (TBXAS1), is a key component for TBXA2 function along with the re-ceptor that mediates its action, thromboxane A2 receptor (TBXA2R). TBXA2R is a member of the family of G pro-tein-coupled receptors and performs an essential role in hemo-stasis by interacting with TBXA2 to induce platelet aggrega-tion. Point mutations in

  • Association of polymorphisms in thromboxane A2 receptor and thromboxane A Synthase 1 with cerebral infarction in a Korean population.
    BMB reports, 2009
    Co-Authors: Sun Ah Park, Byung Lae Park, Jeong Ho Park, Ki Bum Sung, Hun Soo Chang, Choonsik Park, Tae Kyeong Lee, You Kyoung Lee, Hyoung Doo Shin
    Abstract:

    Thromboxane A2 (TBXA2) is a potent vasoconstrictor in cerebral circulation and is a known contributor to the pathogenesis of cerebral infarction. Thromboxane A2 Synthase 1 (TBXAS1) and thromboxane A2 receptors (TBXA2R) are key components in TBXA2 function. We examined whether genetic variants in TBXA2R and TBXAS1 are risk factors for cerebral infarction by genotyping 453 Korean patients with noncardiogenic cerebral infarction and 260 controls. A few, specific polymorphisms in the TBXA2R (-3372G>C, +4710T>C and 4839T>C) and TBXAS1 (+16184G>T, +141931A>T and +177729G>A) genes were chosen and investigated. Logistic regression showed the frequencies of TBXAS1+16184G>T and TBXAS1- ht3 were significantly more frequent in cerebral infarction (P=0.002, OR=2.75 and P=0.01, OR=1.57, respectively), specifically in small-artery occlusion (SAO) type of cerebral infarction (P=0.0003 and 0.005, respectively). These results suggest specific TBXAS1 gene polymorphisms may be a useful marker for development of cerebral infarction, especially SAO type in Korean population.

Jeong Ho Park - One of the best experts on this subject based on the ideXlab platform.

  • association of polymorphisms in thromboxane a2 receptor and thromboxane a Synthase 1 with cerebral infarction in a korean population
    Journal of Biochemistry and Molecular Biology, 2009
    Co-Authors: Sun Ah Park, Byung Lae Park, Jeong Ho Park, Ki Bum Sung, Hun Soo Chang, Choonsik Park, Hyoung Doo Shin
    Abstract:

    Cerebral infarction is one of the most common causes of death and disability (1) with a complex etiology involving both ge-netic and modifiable, pre-disposing determinants (2, 3). Identi-fying the genetic risk for cerebral infarction is important both for risk prediction and for prevention of potential incidents. Although several genes involved in hemostasis, renin angio-tensin system and lipid metabolism have been identified as possible susceptibility genes, their associations with cerebral infarction are still controversial (4). Thromboxane A2 (TBXA2) is a potent vasoconstrictor and stimulator of platelet aggregation with high levels produced in atherosclerosis (5) and during acute stroke (6). The mechanism by which aspirin prevents cerebral infarction is through the po-tent inhibition of cyclooxygenase-1, thereby blocking the pro-duction of TBXA2 (7-9). Thus, TBXA2 is considered an im-portant mediator of cerebral infarction (10). The enzyme that catalyzes its synthesis, thromboxane A2 Synthase 1 (TBXAS1), is a key component for TBXA2 function along with the re-ceptor that mediates its action, thromboxane A2 receptor (TBXA2R). TBXA2R is a member of the family of G pro-tein-coupled receptors and performs an essential role in hemo-stasis by interacting with TBXA2 to induce platelet aggrega-tion. Point mutations in

  • Association of polymorphisms in thromboxane A2 receptor and thromboxane A Synthase 1 with cerebral infarction in a Korean population.
    BMB reports, 2009
    Co-Authors: Sun Ah Park, Byung Lae Park, Jeong Ho Park, Ki Bum Sung, Hun Soo Chang, Choonsik Park, Tae Kyeong Lee, You Kyoung Lee, Hyoung Doo Shin
    Abstract:

    Thromboxane A2 (TBXA2) is a potent vasoconstrictor in cerebral circulation and is a known contributor to the pathogenesis of cerebral infarction. Thromboxane A2 Synthase 1 (TBXAS1) and thromboxane A2 receptors (TBXA2R) are key components in TBXA2 function. We examined whether genetic variants in TBXA2R and TBXAS1 are risk factors for cerebral infarction by genotyping 453 Korean patients with noncardiogenic cerebral infarction and 260 controls. A few, specific polymorphisms in the TBXA2R (-3372G>C, +4710T>C and 4839T>C) and TBXAS1 (+16184G>T, +141931A>T and +177729G>A) genes were chosen and investigated. Logistic regression showed the frequencies of TBXAS1+16184G>T and TBXAS1- ht3 were significantly more frequent in cerebral infarction (P=0.002, OR=2.75 and P=0.01, OR=1.57, respectively), specifically in small-artery occlusion (SAO) type of cerebral infarction (P=0.0003 and 0.005, respectively). These results suggest specific TBXAS1 gene polymorphisms may be a useful marker for development of cerebral infarction, especially SAO type in Korean population.

Ki Bum Sung - One of the best experts on this subject based on the ideXlab platform.

  • association of polymorphisms in thromboxane a2 receptor and thromboxane a Synthase 1 with cerebral infarction in a korean population
    Journal of Biochemistry and Molecular Biology, 2009
    Co-Authors: Sun Ah Park, Byung Lae Park, Jeong Ho Park, Ki Bum Sung, Hun Soo Chang, Choonsik Park, Hyoung Doo Shin
    Abstract:

    Cerebral infarction is one of the most common causes of death and disability (1) with a complex etiology involving both ge-netic and modifiable, pre-disposing determinants (2, 3). Identi-fying the genetic risk for cerebral infarction is important both for risk prediction and for prevention of potential incidents. Although several genes involved in hemostasis, renin angio-tensin system and lipid metabolism have been identified as possible susceptibility genes, their associations with cerebral infarction are still controversial (4). Thromboxane A2 (TBXA2) is a potent vasoconstrictor and stimulator of platelet aggregation with high levels produced in atherosclerosis (5) and during acute stroke (6). The mechanism by which aspirin prevents cerebral infarction is through the po-tent inhibition of cyclooxygenase-1, thereby blocking the pro-duction of TBXA2 (7-9). Thus, TBXA2 is considered an im-portant mediator of cerebral infarction (10). The enzyme that catalyzes its synthesis, thromboxane A2 Synthase 1 (TBXAS1), is a key component for TBXA2 function along with the re-ceptor that mediates its action, thromboxane A2 receptor (TBXA2R). TBXA2R is a member of the family of G pro-tein-coupled receptors and performs an essential role in hemo-stasis by interacting with TBXA2 to induce platelet aggrega-tion. Point mutations in

  • Association of polymorphisms in thromboxane A2 receptor and thromboxane A Synthase 1 with cerebral infarction in a Korean population.
    BMB reports, 2009
    Co-Authors: Sun Ah Park, Byung Lae Park, Jeong Ho Park, Ki Bum Sung, Hun Soo Chang, Choonsik Park, Tae Kyeong Lee, You Kyoung Lee, Hyoung Doo Shin
    Abstract:

    Thromboxane A2 (TBXA2) is a potent vasoconstrictor in cerebral circulation and is a known contributor to the pathogenesis of cerebral infarction. Thromboxane A2 Synthase 1 (TBXAS1) and thromboxane A2 receptors (TBXA2R) are key components in TBXA2 function. We examined whether genetic variants in TBXA2R and TBXAS1 are risk factors for cerebral infarction by genotyping 453 Korean patients with noncardiogenic cerebral infarction and 260 controls. A few, specific polymorphisms in the TBXA2R (-3372G>C, +4710T>C and 4839T>C) and TBXAS1 (+16184G>T, +141931A>T and +177729G>A) genes were chosen and investigated. Logistic regression showed the frequencies of TBXAS1+16184G>T and TBXAS1- ht3 were significantly more frequent in cerebral infarction (P=0.002, OR=2.75 and P=0.01, OR=1.57, respectively), specifically in small-artery occlusion (SAO) type of cerebral infarction (P=0.0003 and 0.005, respectively). These results suggest specific TBXAS1 gene polymorphisms may be a useful marker for development of cerebral infarction, especially SAO type in Korean population.