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ABSTRACT: The mechanical integrity of the uterine cervix is critical for a pregnancy to successfully reach full term. It must be strong to retain the fetus throughout gestation and then undergo a remodeling and softening process before labor for delivery of the fetus. It is believed that cervical insufficiency (CI), a condition in pregnancy resulting in preterm birth (PTB), is related to a cervix with compromised mechanical strength which cannot resist deformation caused by external forces generated by the growing fetus. Such PTBs are responsible for infant developmental problems and in severe cases infant mortality. To understand the etiologies of CI, our overall research goal is to investigate the mechanical behavior of the cervix. Permeability is a mechanical property of hydrated collagenous tissues that dictates the time-dependent response of the tissue to mechanical loading. The goal of this study was to design a novel soft tissue permeability testing device and to present direct hydraulic permeability measurements of excised nonpregnant (NP) and pregnant (PG) human cervical tissue from women with different obstetric histories. Results of hydraulic permeability testing indicate repeatability for specimens from single patients, with an order of magnitude separating the NP and PG group means (2.1 ± 1.4×10 and 3.2 ± 4.8×10m/N[middle dot]s, respectively), and large variability within the NP and PG sample groups. Differences were found between samples with similar obstetric histories, supporting the view that medical history may not be a good predictor of permeability (and therefore mechanical behavior) and highlighting the need for patient-specific measurements of cervical mechanical properties. The permeability measurements from this study will be used in future work to model the constitutive material behavior of cervical tissue and to develop in vivo diagnostic tools to stage the progression of labor.
Journal of Biomechanical Engineering 02/2013; 135(2):021024. · 1.90 Impact Factor
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ABSTRACT: Twin gestations face an increased risk of structural abnormalities compared with singleton gestations, as well as an increased risk of aneuploidy. Accordingly, there is a need for accurate prenatal diagnosis of fetal genetic disorders and structural anomalies in twin gestations. Given the increased risk of congenital anomalies, a detailed sonographic survey of fetal anatomy is recommended in the early second trimester of twin gestations. In addition, fetal echocardiography should be considered in monochorionic twin gestations and in dichorionic twin pregnancies conceived using assisted reproductive technologies given the increased risk of congenital heart disease in these populations. Although first- and second-trimester aneuploidy screening in twin gestations is available, screening is less accurate than in singleton gestations. Invasive prenatal diagnosis in twin pregnancies is associated with a risk of pregnancy loss that is higher than the baseline risk of loss among twin gestations. Precise procedure-related loss rates in twin gestations undergoing chorionic villus sampling or amniocentesis, however, remain unclear because of methodological differences between published studies investigating diagnostic procedures in twins.
Seminars in perinatology 06/2012; 36(3):169-74. · 2.33 Impact Factor
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ABSTRACT: Using published data, we sought to determine the amniocentesis-related loss rate in twin gestations.
We searched the PUBMED database using keywords "amniocentesis", "twin" and "twins" to identify articles evaluating genetic amniocentesis in twin gestations published from January 1970 to December 2010. Random effects models were used to pool procedure-related loss rates from included studies.
The definition of "loss" varied across the 17 studies identified (Table 1). The pooled procedure-related loss rate at < 24 weeks was 3.5% (95% confidence interval [CI] 2.6-4.7) (Figure 2). Pooled loss rates at < 28 weeks (Figure 4) and to term (Figure 5) could not be calculated due to unacceptable heterogeneity of available data. Seven studies included a control (no amniocentesis) group and reported a pooled odds ratio for total pregnancy loss among cases of 1.8 (95% CI 1.2-2.7) (Figure 3). Only 1 study reported procedure-related loss rates by chorionicity (7.7% among monochorionics vs 1.4% among controls; p 0.02).
Analysis of published data demonstrated a pooled amniocentesis-related loss rate of 3.5% in twin gestations < 24 weeks. Pooled loss rates within other post-amniocentesis intervals or other gestational age windows and the impact of chorionicity on procedure-related loss rates cannot be determined from published data.
Prenatal Diagnosis 10/2011; 32(5):409-16. · 2.11 Impact Factor
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The Journal of heart and lung transplantation: the official publication of the International Society for Heart Transplantation 09/2011; 30(9):1065-7. · 3.54 Impact Factor
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ABSTRACT: To evaluate whether peptides given to adult mice with Down syndrome prevent learning deficits, and to delineate the mechanisms behind the protective effect.
Ts65Dn mice were treated for 9 days with peptides D-NAPVSIPQ (NAP)+D-SALLRSIPA (SAL) or placebo, and wild-type animals were treated with placebo. Beginning on treatment day 4, the mice were tested for learning using the Morris watermaze. Probe tests for long-term memory were performed on treatment day 9 and 10 days after treatment stopped. Open-field testing was performed before and after the treatment. Calibrator-normalized relative real-time polymerase chain reaction (PCR) with glyceraldehyde-3-phosphate dehydrogenase (GAPD) standardization was performed on the whole brain and hippocampus for activity-dependent neuroprotective protein, vasoactive intestinal peptide (VIP), glial fibrillary acidic protein (GFAP), NR2B, NR2A, and γ-aminobutyric acid type A (GABAA)-α5. Statistics included analysis of variance and the Fisher protected least significant difference, with P<.05 significant.
The Ts65Dn plus placebo animals did not learn over the 5-day period compared with the controls (P<.001). The Ts65Dn +(D-NAP+D-SAL) learned significantly better than the Ts65Dn plus placebo (P<.05), and they retained learning similar to controls on treatment day 9, but not after 10 days of no treatment. Treatment with D-NAP+D-SAL prevented the Ts65Dn hyperactivity. Adult administration of D-NAP+D-SAL prevented changes in activity-dependent neuroprotective protein, intestinal peptide, and NR2B with levels similar to controls (all P<.05).
Adult treatment with D-NAP+D-SAL prevented learning deficit in Ts65Dn, a model of Down syndrome. Possible mechanisms of action include reversal of vasoactive intestinal peptide and activity-dependent neuroprotective protein dysregulation, as well as increasing expression of NR2B, thus facilitating learning.
Obstetrics and Gynecology 02/2011; 117(2 Pt 1):354-61. · 4.73 Impact Factor
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ABSTRACT: Fetal alcohol syndrome (FAS) is the most common nongenetic cause of mental retardation and is characterized by neurodevelopmental anomalies. C-FOS is a cellular marker of transcriptional activity in the stress-signal pathway. Previously, we showed the treatment with NAP (NAPVSIPQ) + SAL (SALLRSIPA) reversed the learning deficit after prenatal alcohol exposure in FAS. Our objective was to evaluate if the mechanism of actions of NAP + SAL involves the stress-signal pathway differentiating C-FOS expression in mouse brains after prenatal alcohol exposure. C57Bl6/J mice were treated with alcohol (0.03 mL/g) or placebo on gestational day 8. On postnatal day 40, in utero alcohol-exposed males were treated via gavage with 40 μg D-NAP and 40 μg D-SAL ( N = 6) or placebo ( N = 4); controls were gavaged with placebo daily ( N = 12). After learning evaluation, hippocampus, cerebellum, and cortex were isolated. Calibrator-normalized relative real-time polymerase chain reaction and Western blot analysis were performed. Statistics included analysis of variance and post hoc Fisher analysis. Adult treatment with NAP + SAL restored the down-regulation of C-FOS in the hippocampus after prenatal alcohol exposure ( P < 0.05), but not in the cerebellum. There was no difference in C-FOS expression in the cortex. Adult treatment with NAP + SAL restored the down-regulation of C-FOS expression in hippocampus attenuating the alcohol-induced alteration of the stress-signal pathway.
American Journal of Perinatology 05/2010; 27(9):743-8. · 1.32 Impact Factor
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ABSTRACT: Our objective was to evaluate whether brain-derived neurotrophic factor (BDNF) expression is affected by prenatal alcohol exposure and whether the neuroprotective effects of the vasoactive intestinal peptide (VIP)-related peptides, NAPVSIPQ (NAP) and SALLRSIPA (SAL), are mediated through BDNF.
Using a well-characterized fetal alcohol syndrome (FAS) model, timed pregnant C57BL6/J mice were treated on gestational day (E) 8 with alcohol (0.03 mL/g), placebo, or alcohol plus (NAP plus SAL). Embryos were harvested at 6 hours (E8), 24 hours (E9), and 10 days (E18) and pups at postnatal day 40. Calibrator-normalized relative real time polymerase chain reaction was performed to quantify BDNF with hypoxanthine phosphoribosyl transferase-1 standardization.
BDNF expression was lower in the alcohol-exposed embryos than in controls at 6 hours and higher at 24 hours and 10 days (all P<.05). Pretreatment with NAP plus SAL prevented the alcohol-induced rise in BDNF expression (P<.05) at 24 hours and 10 days after alcohol exposure. We found no difference between alcohol and control in young-adults' brain (P>.05).
NAP plus SAL treatment prevented alcohol-induced changes in BDNF expression 24 hours and 10 days after alcohol exposure in mouse embryos. This may explain, at least in part, the peptides' prevention of neurodevelopmental anomalies in FAS.
American journal of obstetrics and gynecology 05/2010; 202(5):457.e1-4. · 3.28 Impact Factor
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ABSTRACT: To evaluate whether treatment with neuroprotective peptides to young adult mice prenatally exposed to alcohol reverses alcohol-induced learning deficits in a mouse model of fetal alcohol syndrome, whether the mechanism involves the N-methyl-d-aspartate (NMDA) and gamma-aminobutyric acid type A (GABAA) receptors, and whether it is related to glial cells.
C57Bl6/J mice were treated with alcohol (0.03 ml/g) or placebo on gestational day 8. On day 40, male mice exposed to alcohol in utero were treated daily for 10 days with D-NAPVSIPQ and D-SALLRSIPA (n=20) or placebo (n=13); and control offspring were treated with placebo (n=46), with the treatment blinded. Learning evaluation began after 3 days using the Morris watermaze and the T-maze. The hippocampus, cortex, and cerebellum were isolated. Expression of NR2A, NR2B, GABAAbeta3, GABAAalpha5, vasoactive intestinal peptide (VIP), activity-dependent neuroprotective protein, and glial fibrillary acidic protein was measured using calibrator-normalized relative real-time polymerase chain reaction. Statistical analysis included analysis of variance and Fisher's protected least significant difference.
Treatment with D-NAPVSIPQ and D-SALLRSIPA reversed the alcohol-induced learning deficit in both learning tests as well as the NR2A and NR2B down-regulation in the hippocampus and the up-regulation of NR2A in the cortex and NR2B in the cortex and cerebellum (all P<.05). No significant differences were found in GABAA expression. Moreover, the peptides changed activity-dependent neuroprotective protein expression in the cortex (P=.016) but not the down-regulation of VIP (P=.883), probably because the peptides are downstream from VIP.
Alcohol-induced learning deficit was reversed and expression of NR2A and NR2B was restored in the hippocampus and cortex of young adult mice treated with D-NAPVSIPQ and D-SALLRSIPA. Given the role of NMDA receptors in learning, this may explain in part the mechanism of prevention of alcohol-induced learning deficits by D-NAPVSIPQ and D-SALLRSIPA.
Obstetrics and Gynecology 02/2010; 115(2 Pt 1):350-6. · 4.73 Impact Factor
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ABSTRACT: Down syndrome (DS) affects 1/800 infants. Prenatal NAPVSIPQ (NAP) and SALLRSIPA (SAL) (NAP+SAL) prevent developmental delay in Ts65Dn mice, a mouse model of DS. We investigated whether this finding involves N-methyl-D-aspartic acid and gamma-aminobutyric acid (GABA) receptor subunits.
Pregnant Ts65Dn mice were treated with placebo or NAP+SAL on gestational days 8-12. After developmental delay prevention was shown, 4 trisomic (Ts), 4 control, and 3 Ts+NAP+SAL adult offspring brains (from 3 litters) were collected. Calibrator-normalized real-time polymerase chain reaction was performed using primers for N-methyl-D-aspartic acid subunits NR2A and NR2B, and for GABA subunits GABA(A)alpha5 and GABA(A)beta3 with glyceraldehyde-3-phosphate dehydrogenase standardization. Statistics included analysis of variance and Fisher PLSD with P < .05 as significant.
NR2A, NR2B, and GABA(A)beta3 levels were decreased in Ts vs control (all P < .05). Prenatal NAP+SAL increased NR2A, NR2B, and GABA(A)beta3 to levels similar to control (all P < .05). A significant difference in GABA(A)alpha5 levels was not found.
Prenatal NAP+SAL increases NR2A, NR2B, and GABA(A)beta3 expression in adult DS mice to levels similar to controls. This may explain how NAP+SAL improve developmental milestone achievement.
American journal of obstetrics and gynecology 04/2009; 200(5):524.e1-4. · 3.28 Impact Factor
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ABSTRACT: Oligohydramnios is related to adverse perinatal outcomes particularly when associated with fetal growth restriction. The purpose of this study was to delineate predictors of adverse perinatal outcomes in cases of preterm idiopathic oligohydramnios associated with appropriate-for-gestational-age (AGA) fetal biometry. A database of preterm AGA fetuses (< 37 weeks) presenting for evaluation of idiopathic oligohydramnios (defined as an amniotic fluid index [AFI] < 10th percentile) in the third trimester with delivery information and uterine artery Doppler indices (average resistance index [RI] and bilateral notching) available was prospectively collected ( N = 90). AFI and birth weight (BW) percentiles were calculated using standard tables. Chi-square and Student T test were used to evaluate for predictors of adverse perinatal outcomes including BW < or = 10th percentile, stillbirth, neonatal intensive care unit admission, 5-minute Apgar score < 7, preterm delivery < 35 weeks, and preeclampsia. Patients destined to experience poor perinatal outcomes (22%) were demographically similar to those experiencing normal outcomes in terms of maternal age ( P = 0.5), ethnicity ( P = 0.9), body mass index ( P = 0.3), and parity ( P = 0.9). However, at-risk patients were more likely to present with oligohydramnios at an earlier gestational age (GA) than those not at risk (33.0 +/- 3.0 versus 34.4 +/- 2.0 weeks; P = 0.02). There were no differences in perinatal outcomes associated with AFI percentile ( P = 0.9), increased average uterine artery RI ( P = 0.5), bilateral notching ( P = 0.4) or a combination of increased uterine artery RI and bilateral notching ( P = 0.2). Patients with preterm AGA fetuses who present with idiopathic oligohydramnios at an earlier GA are at risk for adverse perinatal outcomes compared with those presenting later in gestation. Sonographic indices, particularly uterine artery Doppler findings, were not found to be useful predictors of adverse outcomes.
American Journal of Perinatology 10/2008; 26(1):21-5. · 1.32 Impact Factor
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ABSTRACT: Previous work has demonstrated that two synthetic peptides can prevent prenatal alcohol-induced damage as assessed by prevention of learning abnormalities in adult offspring as well as improve outcome from traumatic brain damage. The current studies were undertaken to evaluate whether these peptides could enhance performance in a learning and memory paradigm when administered either prenatally or to aged mice.
For prenatal treatment, C57Bl6/J mice were treated on gestational day 8 with 1 oral administration of D-NAP or D-SAL alone or D-NAP+D-SAL or a double dose of D-SAL. Control groups were same-regimen treated with vehicle alone. Learning was assessed in adult male offspring (35-50 days) by using the Morris water maze. To evaluate aged animals, 12-month-old mice were treated with D-NAP and D-SAL or vehicle alone daily and tested on the Morris water maze.
Offspring exposed prenatally to D-NAP+D-SAL learned significantly faster than controls, with an earlier onset of learning and an overall decreased latency to find the hidden platform (P < .05). Animals exposed prenatally to either D-NAP or D-SAL alone learned similar to control, with a trend toward faster latencies. Aged animals who received D-NAP+D-SAL learned significantly faster than age-matched controls, with an earlier onset of learning (P < .05).
Combined D-NAP+D-SAL enhanced learning in healthy young mice and aged mice. These findings suggest potential therapeutic interventions not only during a critical developmental period, but also in aged animals.
American journal of obstetrics and gynecology 05/2006; 194(4):1153-8; discussion 1158-9. · 3.28 Impact Factor
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ABSTRACT: Previously, the novel peptides NAPVSIPQ and SALLRSIPA were shown to prevent alcohol-induced fetal death and growth abnormalities in a mouse model of fetal alcohol syndrome. This study evaluated whether these peptides could prevent long-term alcohol-induced learning abnormalities. In addition, because specific cytokines are known to effect long-term potentiation, a model of learning at the molecular level, we studied the effect of these novel peptides on tumor necrosis factor-alpha, interleukin-6, and interferon-gamma levels.
We used a well-characterized mouse model of fetal alcohol syndrome. Pregnant mice were injected on day 8 with alcohol (0.03 mL/kg) or placebo. Pretreatment with NAPVSIPQ+SALLRSIPA (20 mug) or placebo was given 30 minutes before alcohol. Embryos were removed after 6 hours, at which time cytokine, tumor necrosis factor-alpha, interleukin-6, and interferon-gamma levels were measured with enzyme-linked immunoassays. To test spatial learning, adult offspring from litters that were treated with alcohol, control, NAPVSIPQ+SALLRSIPA then alcohol, or NAPVSIPQ+SALLRSIPA alone were evaluated for latency to find a hidden platform in the Morris water maze.
Alcohol treatment increased tumor necrosis factor-alpha levels versus control levels (50.0 +/- 3.5 pg/mL vs 32.7 +/- 2.4 pg/mL; P < .001). NAPVSIPQ+SALLRSIPA pretreatment prevented this increase (39.9 9 +/- 2.8 pg/mL; P </= .01), with levels similar to control (P=.1). Similarly, alcohol increased interleukin-6 levels versus control levels (22.6 +/- 1.4 pg/mL vs 17.3 +/- 0.6 pg/mL; P < .001), and NAPVSIPQ+SALLRSIPA prevented this increase (19.1 +/- 1.0 pg/mL; P </= .02), with levels similar to control levels (P=.2). Interferon-gamma levels were not different among the 3 groups (alcohol, 14.6 +/- 4.9 pg/mL; control, 17.9 +/- 6.6 pg/mL; alcohol+NAPVSIPQ+SALLRSIPA, 13.6 +/- 4.9 pg/mL; P=.2). In the Morris water maze, alcohol-treated groups did not learn over the 7-day trial compared with the control group (P=.001). Groups that were pretreated with NAPVSIPQ+SALLRSIPA then alcohol learned significantly, which was similar to the control group. Groups that were treated with only NAPVSIPQ+SALLRSIPA learned significantly earlier, with the shortest latency once learning commenced.
The peptides, NAPVSIPQ+SALLRSIPA, prevented the alcohol-induced spatial learning deficits and attenuated alcohol-induced proinflammatory cytokine increase in a model of fetal alcohol syndrome. This study demonstrates the peptides' significant in vivo efficacy with long-lasting effects obtained after prenatal administration.
American Journal of Obstetrics and Gynecology 10/2005; 193(3 Pt 1):825-9. · 3.47 Impact Factor
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ABSTRACT: Lamellar body count is a new and fast technique to establish the presence of fetal lung maturity. We have assessed the predictive ability of lamellar body count for neonatal respiratory distress syndrome (RDS) in a non-diabetic population.
We accessed a cohort of amniocenteses in non-diabetic women from 1998 to 2002 (n=102). Neonatal RDS was defined as need for surfactant, intubation, or continuous positive airway pressure (CPAP) in the setting of chest X-ray findings consistent with RDS. The predictive ability of lamellar body count was compared with those of lecithin/sphingomyelin (L/S) ratio and presence of phosphatidylglycerol (PG) using logistic regression analysis. The optimal threshold value of lamellar body count for prediction of neonatal RDS was established with receiver operating characteristic (ROC) curve analysis.
Lamellar body count ROC curve analysis identified a lamellar body count >37,000 microl(-1) as optimal diagnostic threshold for diagnosis of lung maturity, having a negative predictive value of 98%. Lamellar body count and PG, but not L/S ratio, added significantly to the prediction of RDS.
Lamellar body count is a reliable predictor of fetal lung maturity in non-diabetic women and it can replace the L/S ratio.
Archives of Gynecology and Obstetrics 04/2005; 271(4):325-8. · 1.28 Impact Factor
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ABSTRACT: To assess which values of the lecithin/sphingomyelin (L/S) ratio and lamellar body count (LBC) optimally correspond to the presence of phosphatidylglycerol (PG).
A database of clear amniotic fluid specimens obtained by amniocentesis was accessed. Receiver operating characteristic curve analysis was performed for both L/S ratio and LBC to identify the optimal thresholds for predicting the presence of PG.
One hundred eighty-eight patients were included in the analysis. "Trace" PG was more like "absent" PG in relation to both L/S ratio and LBC. There were significant relationships between L/S ratios and presence of PG (area under the curve = .909, P < .0001) and between LBC and presence of PG (area under the curve = .94, P < .0001). The positive predictive value of L/S ratio > 2 was 76%, and that of LBC > 30,000 was 82% in predicting the presence of PG. Optimal threshold values for the prediction of PG presence were > 3.0 for L/S ratio, which had a positive predictive value of 95% and false positive rate of 5%, and > 50,000 for LBC, with a 96% positive predictive value and 5% false positive rate.
"Mature" results for PG in amniotic fluid are equivalent to an L/S ratio of > 3.0 and LBC > 50,000 and help explain the later gestational age at the appearance of lung maturity by PG than by L/S > 2 or LBC > 30,000.
The Journal of reproductive medicine 05/2003; 48(5):330-4. · 0.87 Impact Factor
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ABSTRACT: Activity-dependent neuroprotective protein (ADNP) potently enhances the survival of neurons and is regulated by vasoactive intestinal peptide, which also mediates postimplantation mouse embryonic growth. The objective of this study was to characterize ADNP in mouse embryonic tissues throughout development.
Developmental tissues (embryo, decidua, placenta) from timed pregnant C57B16/J mice were harvested on days 6 though 18. To evaluate ADNP expression, RNA was extracted from at least three samples from three different mice per day. Five micrograms of total RNA from each sample was used per reverse transcriptase-polymerase chain reaction. Immunocytochemistry with anti-ADNP-derived peptide immunoglobulin and anti-gammadelta T-cell receptor was performed on 20 microm thick fixed sections of day 9.5 uteri.
Embryonic ADNP messenger RNA (mRNA) has a temporal pattern with greater amounts present from gestational days 9 to 16. Placental ADNP mRNA was uniformly expressed on gestational days 11 to 18. Levels of decidual ADNP mRNA were greatest early in gestation and declined until delivery. Within the decidua, ADNP and gammadelta T-cell receptor immunoreactivity was present in the same cells.
The expression of ADNP during pregnancy supports a developmental role for this protein. These data indicate both embryonic and maternal sources of ADNP during the critical period of organogenesis.
American Journal of Obstetrics and Gynecology 11/2002; 187(4):973-6. · 3.47 Impact Factor
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ABSTRACT: Vasoactive intestinal peptide (VIP) regulates growth in the early post-implantation embryo. Previous work has demonstrated that peptide agonists (SALLRSIPA and NAPVSIPQ) from downstream mediators that are regulated by VIP were able to prevent the alcohol-induced fetal death, growth restriction and microcephaly associated with fetal alcohol syndrome. Here we evaluated the role of VIP in this mouse model of fetal alcohol syndrome, to determine if fetal or maternal levels of VIP are altered. In addition, we evaluated whether peptide treatment would alter the effects of alcohol on VIP levels. Treatment groups included control, alcohol, and alcohol+peptides. VIP levels were measured with enzyme immunoassay [EIA] (Peninsula Laboratories, Belmont, CA). Quantitation of VIP expression was measured with rt-PCR using mimic cDNA primers. Embryo/decidual VIP levels were similar in control and alcohol-treated groups 6 h after treatment. However, in the embryo/deciduas at 12 and 24 h, VIP levels were below the EIA's detection limit in the alcohol-treated groups, and significantly lower than the control or peptide-pretreated groups (p<0.05). Maternal cortex VIP levels were undetectable and significantly lower in the alcohol-treated group than control or peptide+alcohol group at 6 and 12 h (p<0.001). VIP mRNA expression was quantitated in the embryo and deciduas, with a significant decline noted at 6 h to 58% of control levels (p=0.02). Pretreatment with the peptides attenuated the alcohol-induced decrease in VIP mRNA. These studies demonstrate that treatment with alcohol can decrease the expression and immunoreactivity of VIP in both maternal and fetal tissues. This alcohol-induced loss of a recognized regulator of embryonic growth and differentiation may contribute to the sequelae of toxicity observed in fetal alcohol syndrome.
Regulatory Peptides 11/2002; 108(2-3):143-7. · 2.11 Impact Factor
