The Experts below are selected from a list of 72 Experts worldwide ranked by ideXlab platform

Chang Hee Lee - One of the best experts on this subject based on the ideXlab platform.

  • Effects of cadmium on the expression of placental lactogens and Pit-1 genes in the rat placental trophoblast cells.
    Molecular and cellular endocrinology, 2008
    Co-Authors: Chae Kwan Lee, Jong Tae Lee, Sung Goo Kang, Chan Seok Moon, Young Ha Choi, Jeong Ho Kim, Dae Hwan Kim, Byung Chul Son, Chang Hee Lee
    Abstract:

    Cadmium is an endocrine disrupter (ED) with detrimental effects on mammalian reproduction. The placenta is a primary target for cadmium Toxicity During Pregnancy. Very little of this metal crosses the placenta to the fetus, and consequently it accumulates in high concentrations in the placenta. Cadmium affects on steroid synthesis and has estrogen- and androgen-like activities. In this study, we investigated the toxic effects of cadmium on placental trophoblast cells as well as the mRNA levels of placental lactogens (PLs), which are under the control of estrogen and play a pivotal role During Pregnancy. Pregnant F344 Fisher rats were injected subcutaneously with 0, 0.2, and 2.0mg/kg BW/day of cadmium (CdCl(2)) dissolved in saline from days 11 to 19 of Pregnancy and were sacrificed on day 20. The mRNA levels of the PL-Iv and -II genes and Pit-1alpha and beta isotype genes, the trans-acting factor of PLs, were analyzed by Northern blot hybridization and reverse transcription-polymerase chain reaction, respectively. The frequency of the placental trophoblast cells was observed histochemically. Developmental data and apoptotic chromosomal DNA fragmentation of placental cells were also observed. The mRNA levels of PL-Iv and -II were reduced in a dose-dependent manner by cadmium. The mRNA levels of the Pit-1alpha and beta isotype genes were also reduced by cadmium. In the uterus-conjugated region of the placental junctional zone, the frequency rates of trophoblast cells were lower in the cadmium-treated groups than in the control group. High-dose cadmium exposure (2.0mg) induced not only the reduction of trophoblast cell frequency but also apoptotic chromosomal DNA fragmentation in the junctional zone of the placenta. Developmental metrics such as placental and fetal weights and a number of live fetuses, decreased, while a numbers of resorptions, dead fetuses, and post-implantation losses increased significantly (p

  • Effects of cadmium on the expression of placental lactogens and Pit-1 genes in the rat placental trophoblast cells
    Molecular and Cellular Endocrinology, 2008
    Co-Authors: Chae Kwan Lee, Jong Tae Lee, Sung Goo Kang, Chan Seok Moon, Young Ha Choi, Jeong Ho Kim, Dae Hwan Kim, Byung Chul Son, Chang Hee Lee
    Abstract:

    Abstract Cadmium is an endocrine disrupter (ED) with detrimental effects on mammalian reproduction. The placenta is a primary target for cadmium Toxicity During Pregnancy. Very little of this metal crosses the placenta to the fetus, and consequently it accumulates in high concentrations in the placenta. Cadmium affects on steroid synthesis and has estrogen- and androgen-like activities. In this study, we investigated the toxic effects of cadmium on placental trophoblast cells as well as the mRNA levels of placental lactogens (PLs), which are under the control of estrogen and play a pivotal role During Pregnancy. Pregnant F344 Fisher rats were injected subcutaneously with 0, 0.2, and 2.0 mg/kg BW/day of cadmium (CdCl2) dissolved in saline from days 11 to 19 of Pregnancy and were sacrificed on day 20. The mRNA levels of the PL-Iv and -II genes and Pit-1α and β isotype genes, the trans-acting factor of PLs, were analyzed by Northern blot hybridization and reverse transcription-polymerase chain reaction, respectively. The frequency of the placental trophoblast cells was observed histochemically. Developmental data and apoptotic chromosomal DNA fragmentation of placental cells were also observed. The mRNA levels of PL-Iv and -II were reduced in a dose-dependent manner by cadmium. The mRNA levels of the Pit-1α and β isotype genes were also reduced by cadmium. In the uterus-conjugated region of the placental junctional zone, the frequency rates of trophoblast cells were lower in the cadmium-treated groups than in the control group. High-dose cadmium exposure (2.0 mg) induced not only the reduction of trophoblast cell frequency but also apoptotic chromosomal DNA fragmentation in the junctional zone of the placenta. Developmental metrics such as placental and fetal weights and a number of live fetuses, decreased, while a numbers of resorptions, dead fetuses, and post-implantation losses increased significantly (p

Luis D Pacheco - One of the best experts on this subject based on the ideXlab platform.

  • Digoxin Therapy of Fetal Superior Ventricular Tachycardia: Are Digoxin Serum Levels Reliable?
    AJP reports, 2016
    Co-Authors: Antonio F Saad, Luis Monsivais, Luis D Pacheco
    Abstract:

    Despite its seldom occurrence, fetal tachycardia can lead to poor fetal outcomes including hydrops and fetal death. Management can be challenging and result in maternal adverse effects secondary to high serum drug levels required to achieve effective transplacental antiarrhythmic drug therapy. A 33-year-old woman at 33 weeks of gestation with a diagnosis of a fetal sustained superior ventricular tachycardia developed chest pain, shortness of breath, and bigeminy on electrocardiogram secondary to digoxin Toxicity despite subtherapeutic serum drug levels. She required supportive care with repletion of corresponding electrolyte abnormalities. After resolution of cardiac manifestations of digoxin Toxicity, the patient was discharged home. The newborn was discharged at day 9 of life on maintenance amiodarone. We describe an interesting case of digoxin Toxicity with cardiac manifestations of digoxin Toxicity despite subtherapeutic serum drug levels. This case report emphasizes the significance of instituting an early diagnosis of digoxin Toxicity During Pregnancy, based not only on serum drug levels but also on clinical presentation. In cases of refractory supportive care, digoxin Fab fragment antibody administration should be considered. With timely diagnosis and treatment, excellent maternal and perinatal outcomes can be achieved.

  • Digoxin Therapy of Fetal Superior Ventricular Tachycardia: Are Digoxin Serum Levels Reliable?
    American Journal of Perinatology Reports, 2016
    Co-Authors: Antonio F Saad, Luis Monsivais, Luis D Pacheco
    Abstract:

    Background  Despite its seldom occurrence, fetal tachycardia can lead to poor fetal outcomes including hydrops and fetal death. Management can be challenging and result in maternal adverse effects secondary to high serum drug levels required to achieve effective transplacental antiarrhythmic drug therapy. Case  A 33-year-old woman at 33 weeks of gestation with a diagnosis of a fetal sustained superior ventricular tachycardia developed chest pain, shortness of breath, and bigeminy on electrocardiogram secondary to digoxin Toxicity despite subtherapeutic serum drug levels. She required supportive care with repletion of corresponding electrolyte abnormalities. After resolution of cardiac manifestations of digoxin Toxicity, the patient was discharged home. The newborn was discharged at day 9 of life on maintenance amiodarone. Conclusion  We describe an interesting case of digoxin Toxicity with cardiac manifestations of digoxin Toxicity despite subtherapeutic serum drug levels. This case report emphasizes the significance of instituting an early diagnosis of digoxin Toxicity During Pregnancy, based not only on serum drug levels but also on clinical presentation. In cases of refractory supportive care, digoxin Fab fragment antibody administration should be considered. With timely diagnosis and treatment, excellent maternal and perinatal outcomes can be achieved.

Chae Kwan Lee - One of the best experts on this subject based on the ideXlab platform.

  • Effects of cadmium on the expression of placental lactogens and Pit-1 genes in the rat placental trophoblast cells.
    Molecular and cellular endocrinology, 2008
    Co-Authors: Chae Kwan Lee, Jong Tae Lee, Sung Goo Kang, Chan Seok Moon, Young Ha Choi, Jeong Ho Kim, Dae Hwan Kim, Byung Chul Son, Chang Hee Lee
    Abstract:

    Cadmium is an endocrine disrupter (ED) with detrimental effects on mammalian reproduction. The placenta is a primary target for cadmium Toxicity During Pregnancy. Very little of this metal crosses the placenta to the fetus, and consequently it accumulates in high concentrations in the placenta. Cadmium affects on steroid synthesis and has estrogen- and androgen-like activities. In this study, we investigated the toxic effects of cadmium on placental trophoblast cells as well as the mRNA levels of placental lactogens (PLs), which are under the control of estrogen and play a pivotal role During Pregnancy. Pregnant F344 Fisher rats were injected subcutaneously with 0, 0.2, and 2.0mg/kg BW/day of cadmium (CdCl(2)) dissolved in saline from days 11 to 19 of Pregnancy and were sacrificed on day 20. The mRNA levels of the PL-Iv and -II genes and Pit-1alpha and beta isotype genes, the trans-acting factor of PLs, were analyzed by Northern blot hybridization and reverse transcription-polymerase chain reaction, respectively. The frequency of the placental trophoblast cells was observed histochemically. Developmental data and apoptotic chromosomal DNA fragmentation of placental cells were also observed. The mRNA levels of PL-Iv and -II were reduced in a dose-dependent manner by cadmium. The mRNA levels of the Pit-1alpha and beta isotype genes were also reduced by cadmium. In the uterus-conjugated region of the placental junctional zone, the frequency rates of trophoblast cells were lower in the cadmium-treated groups than in the control group. High-dose cadmium exposure (2.0mg) induced not only the reduction of trophoblast cell frequency but also apoptotic chromosomal DNA fragmentation in the junctional zone of the placenta. Developmental metrics such as placental and fetal weights and a number of live fetuses, decreased, while a numbers of resorptions, dead fetuses, and post-implantation losses increased significantly (p

  • Effects of cadmium on the expression of placental lactogens and Pit-1 genes in the rat placental trophoblast cells
    Molecular and Cellular Endocrinology, 2008
    Co-Authors: Chae Kwan Lee, Jong Tae Lee, Sung Goo Kang, Chan Seok Moon, Young Ha Choi, Jeong Ho Kim, Dae Hwan Kim, Byung Chul Son, Chang Hee Lee
    Abstract:

    Abstract Cadmium is an endocrine disrupter (ED) with detrimental effects on mammalian reproduction. The placenta is a primary target for cadmium Toxicity During Pregnancy. Very little of this metal crosses the placenta to the fetus, and consequently it accumulates in high concentrations in the placenta. Cadmium affects on steroid synthesis and has estrogen- and androgen-like activities. In this study, we investigated the toxic effects of cadmium on placental trophoblast cells as well as the mRNA levels of placental lactogens (PLs), which are under the control of estrogen and play a pivotal role During Pregnancy. Pregnant F344 Fisher rats were injected subcutaneously with 0, 0.2, and 2.0 mg/kg BW/day of cadmium (CdCl2) dissolved in saline from days 11 to 19 of Pregnancy and were sacrificed on day 20. The mRNA levels of the PL-Iv and -II genes and Pit-1α and β isotype genes, the trans-acting factor of PLs, were analyzed by Northern blot hybridization and reverse transcription-polymerase chain reaction, respectively. The frequency of the placental trophoblast cells was observed histochemically. Developmental data and apoptotic chromosomal DNA fragmentation of placental cells were also observed. The mRNA levels of PL-Iv and -II were reduced in a dose-dependent manner by cadmium. The mRNA levels of the Pit-1α and β isotype genes were also reduced by cadmium. In the uterus-conjugated region of the placental junctional zone, the frequency rates of trophoblast cells were lower in the cadmium-treated groups than in the control group. High-dose cadmium exposure (2.0 mg) induced not only the reduction of trophoblast cell frequency but also apoptotic chromosomal DNA fragmentation in the junctional zone of the placenta. Developmental metrics such as placental and fetal weights and a number of live fetuses, decreased, while a numbers of resorptions, dead fetuses, and post-implantation losses increased significantly (p

Antonio F Saad - One of the best experts on this subject based on the ideXlab platform.

  • Digoxin Therapy of Fetal Superior Ventricular Tachycardia: Are Digoxin Serum Levels Reliable?
    AJP reports, 2016
    Co-Authors: Antonio F Saad, Luis Monsivais, Luis D Pacheco
    Abstract:

    Despite its seldom occurrence, fetal tachycardia can lead to poor fetal outcomes including hydrops and fetal death. Management can be challenging and result in maternal adverse effects secondary to high serum drug levels required to achieve effective transplacental antiarrhythmic drug therapy. A 33-year-old woman at 33 weeks of gestation with a diagnosis of a fetal sustained superior ventricular tachycardia developed chest pain, shortness of breath, and bigeminy on electrocardiogram secondary to digoxin Toxicity despite subtherapeutic serum drug levels. She required supportive care with repletion of corresponding electrolyte abnormalities. After resolution of cardiac manifestations of digoxin Toxicity, the patient was discharged home. The newborn was discharged at day 9 of life on maintenance amiodarone. We describe an interesting case of digoxin Toxicity with cardiac manifestations of digoxin Toxicity despite subtherapeutic serum drug levels. This case report emphasizes the significance of instituting an early diagnosis of digoxin Toxicity During Pregnancy, based not only on serum drug levels but also on clinical presentation. In cases of refractory supportive care, digoxin Fab fragment antibody administration should be considered. With timely diagnosis and treatment, excellent maternal and perinatal outcomes can be achieved.

  • Digoxin Therapy of Fetal Superior Ventricular Tachycardia: Are Digoxin Serum Levels Reliable?
    American Journal of Perinatology Reports, 2016
    Co-Authors: Antonio F Saad, Luis Monsivais, Luis D Pacheco
    Abstract:

    Background  Despite its seldom occurrence, fetal tachycardia can lead to poor fetal outcomes including hydrops and fetal death. Management can be challenging and result in maternal adverse effects secondary to high serum drug levels required to achieve effective transplacental antiarrhythmic drug therapy. Case  A 33-year-old woman at 33 weeks of gestation with a diagnosis of a fetal sustained superior ventricular tachycardia developed chest pain, shortness of breath, and bigeminy on electrocardiogram secondary to digoxin Toxicity despite subtherapeutic serum drug levels. She required supportive care with repletion of corresponding electrolyte abnormalities. After resolution of cardiac manifestations of digoxin Toxicity, the patient was discharged home. The newborn was discharged at day 9 of life on maintenance amiodarone. Conclusion  We describe an interesting case of digoxin Toxicity with cardiac manifestations of digoxin Toxicity despite subtherapeutic serum drug levels. This case report emphasizes the significance of instituting an early diagnosis of digoxin Toxicity During Pregnancy, based not only on serum drug levels but also on clinical presentation. In cases of refractory supportive care, digoxin Fab fragment antibody administration should be considered. With timely diagnosis and treatment, excellent maternal and perinatal outcomes can be achieved.

Byung Chul Son - One of the best experts on this subject based on the ideXlab platform.

  • Effects of cadmium on the expression of placental lactogens and Pit-1 genes in the rat placental trophoblast cells.
    Molecular and cellular endocrinology, 2008
    Co-Authors: Chae Kwan Lee, Jong Tae Lee, Sung Goo Kang, Chan Seok Moon, Young Ha Choi, Jeong Ho Kim, Dae Hwan Kim, Byung Chul Son, Chang Hee Lee
    Abstract:

    Cadmium is an endocrine disrupter (ED) with detrimental effects on mammalian reproduction. The placenta is a primary target for cadmium Toxicity During Pregnancy. Very little of this metal crosses the placenta to the fetus, and consequently it accumulates in high concentrations in the placenta. Cadmium affects on steroid synthesis and has estrogen- and androgen-like activities. In this study, we investigated the toxic effects of cadmium on placental trophoblast cells as well as the mRNA levels of placental lactogens (PLs), which are under the control of estrogen and play a pivotal role During Pregnancy. Pregnant F344 Fisher rats were injected subcutaneously with 0, 0.2, and 2.0mg/kg BW/day of cadmium (CdCl(2)) dissolved in saline from days 11 to 19 of Pregnancy and were sacrificed on day 20. The mRNA levels of the PL-Iv and -II genes and Pit-1alpha and beta isotype genes, the trans-acting factor of PLs, were analyzed by Northern blot hybridization and reverse transcription-polymerase chain reaction, respectively. The frequency of the placental trophoblast cells was observed histochemically. Developmental data and apoptotic chromosomal DNA fragmentation of placental cells were also observed. The mRNA levels of PL-Iv and -II were reduced in a dose-dependent manner by cadmium. The mRNA levels of the Pit-1alpha and beta isotype genes were also reduced by cadmium. In the uterus-conjugated region of the placental junctional zone, the frequency rates of trophoblast cells were lower in the cadmium-treated groups than in the control group. High-dose cadmium exposure (2.0mg) induced not only the reduction of trophoblast cell frequency but also apoptotic chromosomal DNA fragmentation in the junctional zone of the placenta. Developmental metrics such as placental and fetal weights and a number of live fetuses, decreased, while a numbers of resorptions, dead fetuses, and post-implantation losses increased significantly (p

  • Effects of cadmium on the expression of placental lactogens and Pit-1 genes in the rat placental trophoblast cells
    Molecular and Cellular Endocrinology, 2008
    Co-Authors: Chae Kwan Lee, Jong Tae Lee, Sung Goo Kang, Chan Seok Moon, Young Ha Choi, Jeong Ho Kim, Dae Hwan Kim, Byung Chul Son, Chang Hee Lee
    Abstract:

    Abstract Cadmium is an endocrine disrupter (ED) with detrimental effects on mammalian reproduction. The placenta is a primary target for cadmium Toxicity During Pregnancy. Very little of this metal crosses the placenta to the fetus, and consequently it accumulates in high concentrations in the placenta. Cadmium affects on steroid synthesis and has estrogen- and androgen-like activities. In this study, we investigated the toxic effects of cadmium on placental trophoblast cells as well as the mRNA levels of placental lactogens (PLs), which are under the control of estrogen and play a pivotal role During Pregnancy. Pregnant F344 Fisher rats were injected subcutaneously with 0, 0.2, and 2.0 mg/kg BW/day of cadmium (CdCl2) dissolved in saline from days 11 to 19 of Pregnancy and were sacrificed on day 20. The mRNA levels of the PL-Iv and -II genes and Pit-1α and β isotype genes, the trans-acting factor of PLs, were analyzed by Northern blot hybridization and reverse transcription-polymerase chain reaction, respectively. The frequency of the placental trophoblast cells was observed histochemically. Developmental data and apoptotic chromosomal DNA fragmentation of placental cells were also observed. The mRNA levels of PL-Iv and -II were reduced in a dose-dependent manner by cadmium. The mRNA levels of the Pit-1α and β isotype genes were also reduced by cadmium. In the uterus-conjugated region of the placental junctional zone, the frequency rates of trophoblast cells were lower in the cadmium-treated groups than in the control group. High-dose cadmium exposure (2.0 mg) induced not only the reduction of trophoblast cell frequency but also apoptotic chromosomal DNA fragmentation in the junctional zone of the placenta. Developmental metrics such as placental and fetal weights and a number of live fetuses, decreased, while a numbers of resorptions, dead fetuses, and post-implantation losses increased significantly (p