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Figures will be available only online Underline represents presenting author; Asterisk represents senior author; Dagger represents an in-training author. 58A Reproductive Sciences Vol. 27, Supplement 1, March 2020 Scientifi c Abstracts O-001 Premenstrual Dysphoric Disorder (PMDD) is Associated with Estradiol-dependent Aberrations in Cellular Ca2+ Homeostasis and the Endoplasmic Reticulum Stress Response. Howard Li†,1,2 Neelima Dubey†,2 Jessica F Hoff man†,2 David R Rubinow,3 Peter J Schmidt∗,2 David Goldman∗.4 1Yale School of Medicine, New Haven, CT, United States; 2National Institute of Mental Health (NIMH), Bethesda, MD, United States; 3UNC Chapel Hill, Chapel Hill, NC, United States; 4National Institute of Alcohol Abuse and Alcoholism (NIAAA), Bethesda, MD, United States. Introduction: Premenstrual Dysphoric Disorder (PMDD) is characterized by debilitating mood symptoms during the luteal phase of the menstrual cycle. Evidence suggests an etiology involving an abnormal response to ovarian steroids, but the molecular basis of a diff erential response to hormone remains poorly understood. Methods: RNAseq analysis of lymphoblastoid cell lines (LCLs) derived from women with PMDD (n=10) and asymptomatic controls (n=9) cultured under untreated (steroid-free), estradiol-treated (E2), and progesterone-treated (P4) conditions. Results: In a module-level analysis, weighted gene correlation network analysis (WGCNA) identifi ed 4 gene modules with signifi cant diagnosis x hormone interactions, including 1 enriched for neuronal functions. Ontologic analysis of hub genes underlying neuronal enrichment signals revealed multiple pathways related to cellular Ca2+ dynamics. In a genelevel analysis comparing transcriptional response to hormone, 1522 genes were diff erentially responsive to E2 (E2-DRGs) and 480 diff erentially responsive to P4 (P4-DRGs). Among top 10 E2-DRGs was a gene network (NUCB1, DST, GCC2, GOLGB1) involved in endoplasmic reticulum (ER)-Golgi function. qPCR validated a diagnosis x E2 interaction (F(1, 24)=7.01, p=0.014) in NUCB1, which regulates cellular Ca2+ and the ER stress response. Finally, we used a thapsigargin (Tg) challenge assay to test whether E2 induces diff erences in Ca2+ homeostasis and the ER stress response. PMDD LCLs had a 27% decrease in Tg-induced XBP1 splicing compared to controls, and E2 resulted in a signifi cant 38% decreased response (p=0.005), with a signifi cant diagnosis x treatment interaction (F(3,33)=3.51, p=0.026). Conclusion: E2-dependent aberrations in cellular Ca2+ handling and ER stress may contribute to the pathophysiology of PMDD. O-002 Fetal Heart Rate Decelerations in Women with Sleep-Disordered Breathing. D’Angela S Pitts†, Marjorie C Treadwell, Louise O’Brien∗. University of Michigan, Ann Arbor, MI, United States. Introduction: Women with sleep-disordered breathing (SDB) are at increased risk for gestational hypertension, preeclampsia, gestational diabetes, and fetal growth restriction. While case reports suggest an association between maternal apnea and fetal heart rate decelerations, data are lacking on how maternal sleep impacts fetal wellbeing. Late and/or prolonged decelerations can be associated with adverse fetal outcomes. We sought to determine whether late and/or prolonged fetal heart rate decelerations were associated with maternal SDB. Methods: A cohort study of third trimester women with a single fetus was conducted. Snoring and non-snoring women underwent an overnight home sleep test using an ambulatory device (Watch-PAT) with continuous portable electronic fetal monitoring (Monica DK). SDB was considered present with a respiratory disturbance index (RDI)>=10 events per hour. The temporality between a respiratory event and fetal decelerations was determined to be present if a deceleration occurred within 30 seconds after a respiratory event. Fetal tracings were analyzed by a maternal fetal medicine physician blinded to the sleep data. Results: 41 women have been recruited (76% Caucasian). Mean (SD) maternal age, BMI and gestational age at time of study was 32.0+/-5.5 years, 37.1+/-7.9kg/m2 and 34.6+/-2.4 weeks respectively (see Table 1). Overall, n=23 (56%) women had SDB. A total of 37 late decelerations were observed in 18 women; 9/18 women (50%) had SDB. Of the 37 late decelerations, 76% were temporally associated with a respiratory event. Ten prolonged decelerations were observed in 6 women; all women (100%) had an RDI>5 and 5/6 women (83%) had an RDI>10. Nine of ten (90%) prolonged decelerations were temporally associated with a respiratory event. Duration of the prolonged decelerations ranged from 3-6 minutes, mean 4.7 minutes. Figure 1 provides details of women with prolonged decelerations. Conclusion: These initial data suggest that the majority of both late and prolonged fetal heart rate decelerations occur with a maternal respiratory event. Since respiratory events are characteristic of maternal SDB, this raises the possibility that SDB may play a role in fetal wellbeing. Thrsday O als Scientific Abstracts Reproductive Sciences Vol. 27, Supplement 1, March 2020 59A Table 1: Demographics of women with SDB and non-SDB SDB n=23 No SDB n=18 p-value Mean age (years 32.2±5.3 31.8±6.0 0.81 Mean BMI (kg/m2) 37.3±8.9 36.8±6.9 0.85 Mean GA (week 34.8±2.5 34.2±2.4 0.51