476 PREVENTION OF ALCOHOL-INDUCED DELAYS IN DEVELOPMENTAL MILESTONES ANDLEARNING ABNORMALITIES IN A MODEL OF FETAL ALCOHOL SYNDROMEMELANIE ENDRES1, LAURA TOSO1, ROBIN ROBERSON1, JANE PARK1,VERONICA DUNLAP1, DANIEL ABEBE1, SARAH POGGI2, CATHERINE SPONG1, 1UPDN,NICHD, NIH, Bethesda, Maryland, 2Georgetown University, Obstetrics andGynecology, Washington, District of Columbia

OBJECTIVE: In utero alcohol (ALC) exposure results in developmental delayand learning impairment. Previous work demonstrated that a single novel 12amino acid peptide prevented ALC-induced fetal death (Endres, SMFM 2003).To further evaluate the utility of this novel peptide (ADNF-12) we studiedneonatal behaviors for developmental delay and adult learning using the Morriswatermaze, a model of spatial learning that is specifically impaired withdevelopmental ALC exposure.

STUDY DESIGN: Timed pregnant C57Bl6/J mice on gest day 8 treated withplacebo (CTL), alcohol (ALC) (30% v/v alc 0.03 mL/kg), ADNF-12 (AL-C+ADNF-12) 30 min prior to alcohol, or ADNF-12 alone. Neonatal behaviortests for motor and cognitive developmental milestones were performed onpostnatal days 1-21 (ALC n = 16, CTL n = 46, ALC+ADNF-12 n = 23,ADNF-12 n = 35). Adult males were tested at 8 weeks in the Morris Watermazefor learning assessment. Statistical analysis included Kruskal-Wallis andANOVA with P ! .05 significant.

RESULTS: ALC exposure resulted in significant delay in achieving develop-mental milestones: eye opening and cliff aversion (ability to avoid falling bystepping backwards) with ALC achieving milestones later than all other groups.Eye opening: ALC = 14.8G 1.1d, CTL 13.8G 0.6d, ALC + ADNF-12 13.8G0.6d, ADNF-12 14.1 G 0.4d, P ! .001. Cliff aversion: ALC = 9.8 G 3.3d, CTL8.0 G 3.3d, ALC+ADNF-12 6.8 G 3.4d, ADNF-12 3.0 G 0.9d, P ! .001.Pretreatment with ADNF-12 prevented the alcohol-induced milestone delays.There was no difference between the ALC and CTL for righting, forelimb grasp,audio startle, and air righting. In the Morris watermaze, the CTL learned,decreasing their latency over 70% (46.5+/�20 sec day 1 to 9.1+/�7.1sec day 7,P ! .01). ALC+ADNF-12 also significantly learned, with a learning curve notdifferent than CTL at all timepoints tested (all P O .5) and significantly betterthan ALC on days 4, 6 and 7 (all P ! .05).

CONCLUSION: A single treatment with a novel synthetic peptide preventedALC-induced developmental and learning abnormalities in a model of fetalalcohol syndrome.

477 A COMPARISON OF PLACENTAL PATHOLOGY AND PERINATAL OUTCOME BETWEENMONOCHORIONIC AND DICHORIONIC TWIN SETS SCOTT SULLIVAN1,ROGER NEWMAN1, JANICE LAGE2, SACHIKO MINIMAGUCHI3, MYLA EBELING4,1Medical University of South Carolina, Obstetrics and Gynecology,Charleston, South Carolina, 2Medical University of South Carolina,Department of Pathology & Laboratory Medicine, Charleston, SouthCarolina, 3Medical University of South Carolina, Pathology, Charleston,South Carolina, 4Medical University of South Carolina, Pediatrics,Charleston, South Carolina

OBJECTIVE: To describe the differences in placental pathology betweendiamniotic dichorionic twins (di/di) and diamniotic monochorionic twins(mono/di). Perinatal outcomes by chorionicity will also be determined.

STUDY DESIGN: The placentas of 247 consecutive twin gestations delivered atthe Medical University of South Carolina (1999-2002) were subjected tostandardized examination by a perinatal pathologist who was blinded to theobstetrical outcome. The placentas were graded on 26 separate variablesreflecting major categories of cord/insertional abnormalities, hypoxia/ischemia,hemorrhage, inflammation or abruption. Outcome data was obtained from anestablished, research quality database. Data was analyzed using Student’s t test,c2 and Fisher’s exact test.

RESULTS: There were 100 di/mo twins and 147 di/di twins. Monochorionictwins had significantly increased incidences of villous edema (P ! .01), cordinsertion abnormalities (P ! .025), placental hemorrhage (P ! .01) andmeconium staining (P ! .05). There were no differences seen in placentalweights, acute or chronic chorioamnionitis, placental infarcts or chorangiosisbetween the di/mo and di/di twins. In addition to the differences in placentalpathology, the monochorionic twins had lower birth weights (P ! .03), earlierdelivery (P ! .05), and higher incidences of 5-minute Apgar scores !7 (P !.05). Neonatal outcomes including death, intraventricular hemorrhage, sepsisand necrotizing enterocolitis were not associated with chorionicity.

CONCLUSION: Monochorionic twin placentas demonstrate an increase incord insertion abnormalities and other pathology consistent with villoushypoxia/ischemia but equivalent placental weights compared to dichorionictwins. These findings suggest that the placental injury seen in monochorionictwins occurs late in gestation and may be associated with a greater risk ofprematurity.

SMFM Abstracts S137

478 PLACENTAL PATHOLOGY AND PERINATAL OUTCOME ASSOCIATED WITH SMALL FORGESTATIONAL AGE TWINS SCOTT SULLIVAN1, ROGER NEWMAN1, JANICE LAGE2,SACHIKO MINAMIGUCHI3, MYLA EBELING4, EUGENE CHANG1, 1Medical Universityof South Carolina, Obstetrics and Gynecology, Charleston, South Carolina,2Medical University of South Carolina, Department of Pathology & LaboratoryMedicine, Charleston, South Carolina, 3Medical University of South Carolina,Charleston, South Carolina, 4Medical University of South Carolina, Pediatrics,Charleston, South Carolina

OBJECTIVE: To determine the differences in placental pathology betweensmall for gestational age (SGA) twins and appropriate for gestational age (AGA)twins. The perinatal outcomes of these twins will also be described.

STUDY DESIGN: The placentas of 247 consecutive twin gestations delivered atthe Medical University of South Carolina (1999-2002) were subjected tostandardized examination by a perinatal pathologist who was blinded to theobstetrical outcome. The placentas were graded on 26 variables reflecting majorcategories of cord/insertional abnormalities, hypoxia/ischemia, hemorrhage,inflammation or abruption. SGA was defined as growth !10th percentile basedon gestational age using established twin growth curves. Outcome data wasobtained from a research quality perinatal database. Data was analyzed usingStudent’s t test, c2, and Fisher’s exact test.

RESULTS: There were 57 SGA twins and 190 AGA twins. SGA twins hadsignificantly increased incidences of cord insertion abnormalities, (P ! .025),small placental weights (P ! .001) and placental infarctions (P ! .03). Therewere no differences in chorionicity, chorioamnionitis, villous edema, meconiumstaining or villous stromal hemorrhage. In addition to the differences in placentalpathology, the SGA twins had lower birthweights (P ! .03), higher rates ofneonatal sepsis and higher incidences of 5-minute Apgar scores !7 (P ! .05).There were no differences in rates of death, respitory distress syndrome orintraventricular hemorrhage.

CONCLUSION: SGA twins are associated with a higher incidence of cordinsertion abnormalities and placental infarctions. There was a surprising absenceof differences in the other findings of hypoxic/ischemic placental injury. Sepsiswas the only adverse neonatal outcome increased among SGA twins but therewere no differences in placental findings of chorioamnionitis.

Finding SGA twins AGA twins P value

Placental weight !10% 19/57 19/189 .001Cord insertion abnormality 21/57 33/189 .025Placental infarction 16/57 24/189 .025

479 PROTEOMIC ANALYSIS OF CERVICO-VAGINAL SECRETIONS DURING PREGNANCYIRINA BUHIMSCHI1, CATALIN BUHIMSCHI1, ERROL NORWITZ1, BEN HAMAR1,ANNA SFAKIANAKI1, MERT BAHTIYAR1, CARL P. WEINER2, CHARLES LOCKWOOD1,1Yale University, Ob./Gyn. & Reprod. Sci., New Haven, Connecticut,2University of Maryland, Baltimore, Maryland

OBJECTIVE: Pregnancy is associated with increased susceptibility to ascend-ing infection. The cervico-vaginal mucus plug is ideally positioned between themicrobe-rich vagina and the normally sterile amniotic fluid cavity, suggestinga host defense function.

STUDY DESIGN: The proteomic profile of cervico-vaginal secretions from 20pregnant (P) women (GA: 26.5 G 1.0 wks) with intact membranes and nodetectable uterine activity was compared to that of 7 healthy non-pregnant (NP)ovulating women. Proteomics technology (SELDI-TOF-MS) followed byimmunoassay was undertaken to identify and quantify components of a proteo-mic fingerprint.

RESULTS: The following protein biomarkers were identified in the cervico-vaginal secretions: defensin-2 (3373 Da), defensin-1 (3444 Da), defensin-3 (3488Da), calgranulin C (10,443 Da) and calgranulin A (10,834 Da) (Fig.). A non-discriminatory ELISA for defensins 1-3 confirmed no differences between groups(P: 35.9 [32.4-41.7] vs NP: 39.0 [12.8-41.4 ng/mL, P = .97). Calgranulin C wasthe most abundant biomarker analyzed (P: 309.7 [61.0-1202.0] vs. NP: 110.8[17.5-160.5 ng/mL], P = .12). Similarly, calgranulin A immunoreactivity did notdiffer between P and NP groups (P: 51.7 [15.9-118.6] vs NP: 64.2 [46.3-148.0] ng/mL, P = .530). These relationships were maintained after normalizing for totalprotein.

CONCLUSION: The cervico-vaginal proteomic fingerprint is apparently un-changed by pregnancy. The wide expression of defensins and calgranulins inboth NP and P cervico-vaginal tract suggests these proteins have an importantrole in the innate immune defense against human genital tract infections.