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Theresa L. Powell

Priyadarshini Pantham, Fredrick J Rosario, Susan T Weintraub, Peter W Nathanielsz, Theresa L Powell, Cun Li, Thomas Jansson
Intrauterine growth restriction (IUGR) is an important risk factor for perinatal complications and adult disease. IUGR is associated with down-regulation of placental amino acid (AA) transporter expression and activity at birth. It is unknown whether these changes are a cause or a consequence of human IUGR. We hypothesized that placental AA transport capacity is reduced prior to onset of reduced fetal growth in baboons with maternal nutrient restriction (MNR). Pregnant baboons were fed either a control (n=8) or MNR diet (70% of control diet, n=9) from Gestational Day (GD) 30...
September 7, 2016: Biology of Reproduction
Robert J Morgan, Deborah K Armstrong, Ronald D Alvarez, Jamie N Bakkum-Gamez, Kian Behbakht, Lee-May Chen, Larry Copeland, Marta Ann Crispens, Maria DeRosa, Oliver Dorigo, David M Gershenson, Heidi J Gray, Ardeshir Hakam, Laura J Havrilesky, Carolyn Johnston, Shashikant Lele, Lainie Martin, Ursula A Matulonis, David M O'Malley, Richard T Penson, Sanja Percac-Lima, Mario Pineda, Steven C Plaxe, Matthew A Powell, Elena Ratner, Steven W Remmenga, Peter G Rose, Paul Sabbatini, Joseph T Santoso, Theresa L Werner, Jennifer Burns, Miranda Hughes
This selection from the NCCN Guidelines for Ovarian Cancer focuses on the less common ovarian histopathologies (LCOHs), because new algorithms were added for LCOHs and current algorithms were revised for the 2016 update. The new LCOHs algorithms include clear cell carcinomas, mucinous carcinomas, and grade 1 (low-grade) serous carcinomas/endometrioid epithelial carcinomas. The LCOHs also include carcinosarcomas (malignant mixed Müllerian tumors of the ovary), borderline epithelial tumors (also known as low malignant potential tumors), malignant sex cord-stromal tumors, and malignant germ cell tumors...
September 2016: Journal of the National Comprehensive Cancer Network: JNCCN
Fredrick J Rosario, Theresa L Powell, Thomas Jansson
Folate deficiency in fetal life is strongly associated with structural malformations and linked to intrauterine growth restriction. In addition, limited availability of methyl donors, such as folate, during pregnancy may result in abnormal gene methylation patterns and contribute to developmental programming. The fetus is dependent on placental transfer of folate, however the molecular mechanisms regulating placental folate transport are unknown. We used cultured primary human trophoblast cells to test the hypothesis that mechanistic target of rapamycin complex 1 (mTORC1) and 2 (mTORC2) regulate folate transport by post-translational mechanisms...
2016: Scientific Reports
Ian Christie, Jessica L Reiner, John A Bowden, Hannes Botha, Theresa M Cantu, Danny Govender, Matthew P Guillette, Russell H Lowers, Wilmien J Luus-Powell, Danie Pienaar, Willem J Smit, Louis J Guillette
Perfluorinated alkyl acids (PFAAs) are environmental contaminants that have been used in many products for over 50 years. Interest and concern has grown since 2000 on the widespread presence of PFAAs, when it was discovered that PFAAs were present in wildlife samples around the northern hemisphere. Since then, several studies have reported PFAAs in wildlife from many locations, including the remote regions of Antarctica and the Arctic. Although there are a multitude of studies, few have reported PFAA concentrations in reptiles and wildlife in the Southern Hemisphere...
July 2016: Chemosphere
Susanne Lager, Vanessa I Ramirez, Francesca Gaccioli, Brian Jang, Thomas Jansson, Theresa L Powell
BACKGROUND: Obese and overweight women are more likely to deliver a large infant or an infant with increased adiposity, however the underlying mechanisms are not well established. We tested the hypothesis that placental capacity to transport fatty acid is increased in overweight/obese women. METHODS: Pregnant women with body mass index (BMI) ranging from 18.4 to 54.3 kg/m(2) and with uncomplicated term pregnancies were recruited for collection of blood samples and placental tissue...
April 2016: Placenta
Kris Genelyn Dimasuay, Philippe Boeuf, Theresa L Powell, Thomas Jansson
Placental responses to maternal perturbations are complex and remain poorly understood. Altered maternal environment during pregnancy such as hypoxia, stress, obesity, diabetes, toxins, altered nutrition, inflammation, and reduced utero-placental blood flow may influence fetal development, which can predispose to diseases later in life. The placenta being a metabolically active tissue responds to these perturbations by regulating the fetal supply of nutrients and oxygen and secretion of hormones into the maternal and fetal circulation...
2016: Frontiers in Physiology
Evangelina Capobianco, Daiana Fornes, Ivana Linenberg, Theresa L Powell, Thomas Jansson, Alicia Jawerbaum
A family history of diabetes predisposes to gestational diabetes mellitus (GDM). We hypothesized that female offspring of rats with pre-gestational diabetes will develop GDM, a pathology associated with fetal overgrowth and altered placental signaling. We found normal glycemia and insulinemia in the offspring from pre-gestational diabetic rats at three months of age. However, consistent with GDM, maternal hyperglycemia and hyperinsulinemia and increased fetal weight were evident when compared to controls. In this intrauterine programmed GDM model, the placentas showed alterations in mTOR pathway: unchanged phosphorylation of 4EBP-1 and PKCα despite reduced total expression of 4EBP-1 and PKCα, and increased phosphorylation of SGK1...
February 15, 2016: Molecular and Cellular Endocrinology
Fredrick J Rosario, Kris Genelyn Dimasuay, Yoshikatsu Kanai, Theresa L Powell, Thomas Jansson
Changes in placental amino acid transfer directly contribute to altered fetal growth, which increases the risk for perinatal complications and predisposes for the development of obesity, diabetes and cardiovascular disease later in life. Placental amino acid transfer is critically dependent on the expression of specific transporters in the plasma membrane of the trophoblast, the transporting epithelium of the human placenta. However, the molecular mechanisms regulating this process are largely unknown. Nedd4-2 is an ubiquitin ligase that catalyses the ubiquitination of proteins, resulting in proteasomal degradation...
April 1, 2016: Clinical Science (1979-)
Irving L M H Aye, Thomas Jansson, Theresa L Powell
Maternal obesity and gestational diabetes mellitus (GDM) increase the risk of delivering infants that are large for gestational age with greater adiposity, who are prone to the development of metabolic disease in childhood and beyond. These maternal conditions are also associated with increased levels of the proinflammatory cytokine TNF-α in maternal tissues and the placenta. Recent evidence suggests that changes in placental amino acid transport contribute to altered fetal growth. TNF-α was previously shown to stimulate System A amino acid transport in primary human trophoblasts (PHTs), however the molecular mechanisms remain unknown...
October 2015: Physiological Reports
Paula Díaz, Jessica Harris, Fredrick J Rosario, Theresa L Powell, Thomas Jansson
Obesity in pregnancy is associated with increased fetal growth and adiposity, which, in part, is determined by transplacental nutrient supply. Trophoblast uptake and intracellular trafficking of lipids are dependent on placental fatty acid transport proteins (FATP), translocase (FAT/CD36), and fatty acid binding proteins (FABP). We hypothesized that maternal obesity in mice leads to increased placental expression of FAT/CD36, FATPs, and FABPs, and lipid accumulation in the fetal liver. C57/BL6J female mice were fed either a control (C; n = 10) or an obesogenic (OB; n = 10) high-fat, high-sugar diet before mating and throughout pregnancy...
December 15, 2015: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
Fredrick J Rosario, Theresa L Powell, Thomas Jansson
Fetal overgrowth is common in obese women and is associated with perinatal complications and increased risk for the child to develop metabolic syndrome later in life. Placental nutrient transport capacity has been reported to be increased in obese women giving birth to large infants; however, the underlying mechanisms are not well established. Obesity in pregnancy is characterized by elevated maternal serum insulin and leptin, hormones that stimulate placental amino acid transporters in vitro. We hypothesized that maternal obesity activates placental insulin/IGF-I/mTOR and leptin signaling pathways...
January 1, 2016: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
Irving L M H Aye, Fredrick J Rosario, Theresa L Powell, Thomas Jansson
Mothers with obesity or gestational diabetes mellitus have low circulating levels of adiponectin (ADN) and frequently deliver large babies with increased fat mass, who are susceptible to perinatal complications and to development of metabolic syndrome later in life. It is currently unknown if the inverse correlation between maternal ADN and fetal growth reflects a cause-and-effect relationship. We tested the hypothesis that ADN supplementation in obese pregnant dams improves maternal insulin sensitivity, restores normal placental insulin/mechanistic target of rapamycin complex 1 (mTORC1) signaling and nutrient transport, and prevents fetal overgrowth...
October 13, 2015: Proceedings of the National Academy of Sciences of the United States of America
Yi-Yung Chen, Fredrick J Rosario, Majida Abu Shehab, Theresa L Powell, Madhulika B Gupta, Thomas Jansson
Placental amino acid transport is decreased in intrauterine growth restriction (IUGR); however, the underlying mechanisms remain largely unknown. We have shown that mechanistic target of rapamycin (mTOR) signalling regulates system A amino acid transport by modulating the ubiquitination and plasma membrane trafficking of sodium-coupled neutral amino acid transporter 2 (SNAT-2) in cultured primary human trophoblast cells. We hypothesize that IUGR is associated with (1) inhibition of placental mTORC1 and mTORC2 signalling pathways, (2) increased amino acid transporter ubiquitination in placental homogenates and (3) decreased protein expression of SNAT-2 in the syncytiotrophoblast microvillous plasma membrane (MVM)...
December 2015: Clinical Science (1979-)
Priyadarshini Pantham, Fredrick J Rosario, Mark Nijland, Alex Cheung, Peter W Nathanielsz, Theresa L Powell, Henry L Galan, Cun Li, Thomas Jansson
Intrauterine growth restriction increases the risk of perinatal complications and predisposes the infant to diabetes and cardiovascular disease in later life. Mechanisms by which maternal nutrient restriction (MNR) reduces fetal growth are poorly understood. We hypothesized that MNR decreases placental amino acid (AA) transporter activity, leading to reduced transplacental transfer of AAs. Pregnant baboons were fed either a control (ad libitum, n = 7), or MNR diet (70% of control diet, n = 7) from gestational day (GD) 30...
October 2015: American Journal of Physiology. Regulatory, Integrative and Comparative Physiology
Fredrick J Rosario, Yoshikatsu Kanai, Theresa L Powell, Thomas Jansson
OBJECTIVE: To identify possible mechanisms linking obesity in pregnancy to increased fetal adiposity and growth, a unique mouse model of maternal obesity associated with fetal overgrowth was developed, and the hypothesis that maternal obesity causes up-regulation of placental nutrient transporter expression and activity was tested. METHODS: C57BL/6J female mice were fed a control (C) or a high-fat/high-sugar (HF/HS) pelleted diet supplemented by ad libitum access to sucrose (20%) solution, mated, and studied at embryonic day 18...
August 2015: Obesity
Francesca Gaccioli, Irving L M H Aye, Sara Roos, Susanne Lager, Vanessa I Ramirez, Yoshikatsu Kanai, Theresa L Powell, Thomas Jansson
BACKGROUND: System L transporters LAT1 (SLC7A5) and LAT2 (SLC7A8) mediate the uptake of large, neutral amino acids in the human placenta. Many System L substrates are essential amino acids, thus representing crucial nutrients for the growing fetus. Both LAT isoforms are expressed in the human placenta, but the relative contribution of LAT1 and LAT2 to placental System L transport and their subcellular localisation are not well established. Moreover, the influence of maternal body mass index (BMI) on placental System L amino acid transport is poorly understood...
2015: Reproductive Biology and Endocrinology: RB&E
Vanessa I Ramirez, Evelyn Miller, Christiane L Meireles, Jonathan Gelfond, Debra A Krummel, Theresa L Powell
OBJECTIVE: Gestational diabetes mellitus (GDM) is more common in pregnancies complicated by obesity and both diseases increase the risk for fetal overgrowth and long-term adverse health consequences for the mother and child. Previous studies have linked low maternal serum adiponectin to GDM in normal and overweight women. We hypothesized that lower adiponectin, in particular the high-molecular-weight form, and insulin-like growth factor I (IGF-I) and its binding protein (IGFBP-1) are associated with GDM in pregnant obese Hispanic women...
2014: BMJ Open Diabetes Research & Care
Susanne Lager, Thomas Jansson, Theresa L Powell
No abstract text is available yet for this article.
December 1, 2014: American Journal of Physiology. Cell Physiology
Susanne Lager, Thomas Jansson, Theresa L Powell
Fatty acids are critical for normal fetal development but may also influence placental function. We have previously reported that oleic acid (OA) stimulates amino acid transport in primary human trophoblasts (PHTs). In other tissues, saturated and unsaturated fatty acids have distinct effects on cellular signaling, for instance, palmitic acid (PA) but not OA reduces IκBα expression. We hypothesized that saturated and unsaturated fatty acids differentially affect trophoblast amino acid transport and cellular signaling...
October 15, 2014: American Journal of Physiology. Cell Physiology
Ometeotl Acosta, Vanessa I Ramirez, Susanne Lager, Francesca Gaccioli, Donald J Dudley, Theresa L Powell, Thomas Jansson
OBJECTIVE: Obese women are at increased risk to deliver a large infant, however, the underlying mechanisms are poorly understood. Fetal glucose availability is critically dependent on placental transfer and is linked to fetal growth by regulating the release of fetal growth hormones such as insulin. We hypothesized that (1) umbilical vein glucose and insulin levels and (2) placental glucose transporter (GLUT) expression and activity are positively correlated with early pregnancy maternal body mass index and infant birthweight...
February 2015: American Journal of Obstetrics and Gynecology
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