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34 ABSTRACT #O9 ABDOMINAL VISCERAL ADIPOSITY IN THE FIRST TRIMESTER PREDICTS GLUCOSE INTOLERANCE IN LATER PREGNANCY Aisling Martin [F](1), Howard Berger (1), Andrea Lausman (1), Joel G Ray (1,2,3). (1)Department of Obstetrics and Gynaecology, St. Michael’s Hospital, (2)Department of Medicine, Divisions of Endocrinology and Metabolism and General Internal Medicine, St. Michael’s Hospital, (3)Department of Health Policy Management and Evaluation, St. Michael’s Hospital, University of Toronto. Objectives: To assess the reliability of ultrasound measurement of maternal subcutaneous and visceral adiposity at 11-14 weeks gestation and to elucidate whether greater visceral adiposity is associated with a higher risk of glucose intolerance later in pregnancy. Study Design: This is a prospective cohort study at a single outpatient clinic in Toronto, Ontario. Women with a singleton pregnancy and no history of diabetes were enrolled between 11 and 14 weeks gestation. Subcutaneous and visceral fat depths were independently measured three times by two sonographers. Intra- and inter-observer reliability were calculated for each. A 50-g glucose challenge test (GCT) was subsequently performed between 24 and 28 weeks' gestation, with a positive test at a cut off point ≥ 7.8 mmol/L. Results: There were 62 women enrolled in the study, of whom 58 also underwent a GCT. Intraobserver agreement was ≥ 0.94 for all sonographic measurements. Inter-observer reliability was 0.79 (95% confidence interval [CI] 0.69 to 0.88) for subcutaneous adiposity and 0.87 (95% CI 0.82 to 0.93) for visceral adiposity. A visceral adipose tissue depth above the upper quartile was significantly associated with a positive GCT in later pregnancy (adjusted OR 16.9, 95% CI 1.5 to 194.6). No association was seen for subcutaneous adipose tissue, however (adjusted 1.7, 95% CI 0.18 to 16.5). Conclusions: Measurement of subcutaneous and visceral adipose tissue depth in early pregnancy is both feasible and reliable. Visceral adiposity may be associated with glucose intolerance in pregnancy, but it remains to be determined whether it predicts the overt development of gestational DM, fetal macrosomia or birth-related trauma.
35 ABSTRACT #O10 GCM1 REGULATION OF SFLT-1 EXPRESSION IN FIRST TRIMESTER PLACENTAL VILLI: THE MISSING LINK BETWEEN DISORDERED TROPHOBLAST DIFFERENTIATION AND THE DEVELOPMENT OF SEVERE EARLY-ONSET PREECLAMPSIA Sascha Drewlo [PD] (1), Dora Baczyk (1), John Kingdom (1,2,3) (1) Research Centre for Women’s and Infants’ Health (RCWIH) at the Samuel Lunenfeld Research Institute of Mount Sinai Hospital, University of Toronto, (2) Department of Obstetrics and Gynaecology, Mount Sinai Hospital, University of Toronto, (3) Department of Pathology, Mount Sinai Hospital, University of Toronto. Introduction/Objective Women with severe early-onset preeclampsia have a reversible vasculopathy and renal injury mediated by anti-angiogenic proteins released from placental villi; these include the soluble receptors of vascular endothelial growth factor (sflt-1) and endoglin (sEng). By contrast women whose pregnancies have the related but distinct placental pathology causing severe intrauterine growth restriction (IUGR) remain normotensive, and have relatively low circulating levels of these proteins. We previously reported the key physiologic role of Glial Cell Missing-1 (GCM1) in mediating the proper differentiation of villous syncytiotrophoblast. In loss-of-function studies, where GCM1 is repressed, placental villi have increased cytotrophoblast proliferation yet shed necrotic syncytiotrophoblast, analagous to the villous pathology of severe pre-eclampsia. We recently reported the divergent anatomical and molecular pathology of placental villi of severe early preeclamptic vs. IUGR placentas to IFPA 2008; in severe pre-eclampsia GCM1 is reduced, whereas in severe IUGR it is increased. We therefore tested the hypothesis that GCM1 regulates the secretion of sflt- 1 into maternal blood using our first trimester floating villous explants model. Methods and Results: We silenced (by siRNAor antisense oligo's) or induced (using forskolin) GCM1 expression in a floating villous explant model in first trimester tissue and assessed a.) syncytiotrophoblast differentiation and GCM1 protein expression b.) Cytotrophoblast proliferation (by BrdU incorporation and Ki67 staining) and c.) soluble flt-1 secretion by ELISA assessment of the culture supernatants. In conditions that repress GCM1 translation by 95 ±2.8% at 72 hours the secretion of sflt-1 was significantly increased up to 7.2-fold (mean 5.2 ±2 fold; mean values 456.38 ±142pg/ml vs. 92.48 ±35.7pg/ml n=6) compared to control conditions that maintain physiologic turnover of syncytiotrophoblast. Conclusions: Our data indicate that GCM1, the key regulator of syncytiotrophoblast differentiation that is expressed divergently in these serious pathologies, acts in a downstream manner to explain the development of pre-eclampsia via a sflt1-dependent manner. Funded by: CIHR
Page 1: Department of Obstetrics and Gynaec
Page 4 and 5: 2 PROGRAMME-AT-A-GLANCE (A.M.) 7:30
Page 7 and 8: 5 PROGRAMME 26TH ANNUAL RESEARCH DA
Page 9 and 10: 7 P-A4 PHENOTYPE OF EARLY ONSET INT
Page 11 and 12: 9 P-C2 ESTROGEN EXTRACTION FROM MIC
Page 13 and 14: 11 P-E4 LAPAROSCOPIC PERITONEAL ENT
Page 15 and 16: 13 12:05 - 1:05 p.m. LUNCH [Dining
Page 17 and 18: 15 P-G2 P16 ONCOPROTEIN AS A TRIAGE
Page 19 and 20: 17 GROUP I: Chairs/Judges: Drs. Jon
Page 21 and 22: 19 GROUP K: Chairs/Judges: Drs. Gra
Page 23 and 24: 21 4:15 - 5:15 p.m. Henderson Lectu
Page 25: 23 AWARDS The Papsin Award The Dr.
Page 28 and 29: 26 ABSTRACT #O1* CO-ENZYME Q10 SUPP
Page 30 and 31: 28 ABSTRACT #O3* VEPH1 IS A NOVEL R
Page 32 and 33: 30 ABSTRACT #O5* TISSUE SPECIFIC TR
Page 34 and 35: 32 ABSTRACT #O7 JOB SATISFACTION AM
Page 38 and 39: 36 ABSTRACT #O11 REGULATORY EFFECTS
Page 40 and 41: 38 ABSTRACT #O13 THE EFFECT OF CHRO
Page 42 and 43: POSTER ABSTRACTS 40
Page 44 and 45: 42 ABSTRACT #P-A2 INCREASED MATERNA
Page 46 and 47: 44 ABSTRACT #P-A4 PHENOTYPE OF EARL
Page 48 and 49: 46 ABSTRACT #P-B1* ANGIOGENIC CD56
Page 50 and 51: 48 ABSTRACT #P-B3 UNDERSTANDING THE
Page 52 and 53: 50 ABSTRACT #P-B5 LOW VITAMIN D LEV
Page 54 and 55: 52 ABSTRACT #P-C2* ESTROGEN EXTRACT
Page 56 and 57: 54 ABSTRACT #P-C4 PRETERM PERMATURE
Page 58 and 59: 56 ABSTRACT #P-D2 CRYOPRESERVATION
Page 60 and 61: 58 ABSTRACT #P-D4 DIFFERENTIAL EXPR
Page 62 and 63: 60 ABSTRACT #P-E1 THE ROLE OF ANDRO
Page 64 and 65: 62 ABSTRACT #P-E3 CELL CYCLE INHIBI
Page 66 and 67: 64 ABSTRACT #P-F1 DEXAMETHASONE STI
Page 68 and 69: 66 ABSTRACT #P-F3 EDUCATING SURGICA
Page 70 and 71: 68 ABSTRACT #P-F5 OUTCOMES IN ROBOT
Page 72 and 73: 70 ABSTRACT #P-G2 P16 ONCOPROTEIN A
Page 74 and 75: 72 ABSTRACT #P-G4 ALTERED ADRENOCOR
Page 76 and 77: 74 ABSTRACT #P-H1 RETINAL HEMORRHAG
Page 78 and 79: 76 ABSTRACT #P-H3 A ROLE FOR MCL-1
Page 80 and 81: 78 ABSTRACT #P-H5 A NOVEL ROLE FOR
Page 82 and 83: 80 ABSTRACT #P-I2 THE TIMING OF DEL
Page 84 and 85: 82 ABSTRACT #P-I4 OMEGA-3 FATTY ACI
Page 86 and 87:
84 ABSTRACT #P-J1* WHAT IS KEEPING
Page 88 and 89:
86 ABSTRACT #P-J3 HUMAN EMBRYONIC F
Page 90 and 91:
88 ABSTRACT #P-J5 BARRIERS TO COMPL
Page 92 and 93:
90 ABSTRACT #P-K2 THE “DUC” TRI
Page 94 and 95:
92 ABSTRACT #P-K4 IS THERE A ROLE F
Page 96 and 97:
94 ABSTRACT #P-L1 EXPRESSION AND RE
Page 98 and 99:
96 ABSTRACT #P-L3 IS ZONA PELLUCIDA
Page 100 and 101:
98 ABSTRACT #P-L5 SPECTRUM OF VASCU
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100 Presenters by Last Name cont’
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102 Presenters by Abstract # and Se
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104 Presenters by Abstract # and Se
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