Disease relevance of Maternal Exposure

• Birth defects following maternal exposure to ergotamine, beta blockers, and caffeine [1].
• However, because tamoxifen may act as an estrogen in the fetus and high fetal estrogenic activity, in turn, may increase subsequent breast cancer risk, we wanted to determine the effects of a maternal exposure to tamoxifen during pregnancy on offspring's susceptibility to mammary tumorigenesis [2].
• We analyzed the spectrum of neural-tube defects associated with maternal exposure to antiepileptic drugs (AEDs) and the possible contribution of familial and genetic factors to epilepsy or neural-tube defects [3].
• We studied the effects of maternal exposure to endotoxin on pregnancy outcome, stimulation of the hypothalamo-hypophyseal-adrenal axes (HHAA) of ewes and their fetuses, and maternal production of tumor necrosis factor alpha (TNF alpha), a central mediator in the pathogenesis of bacterial endotoxemia [4].
• Behavioral toxicity in the offspring of rats following maternal exposure to dichloromethane [5].

Psychiatry related information on Maternal Exposure

• Maternal exposure is assessed relative to specific tobacco-related chemicals and the feto-placental impact of mutagenic products, in addition to nicotine replacement as a pharmacological intervention for smoking cessation [6].

High impact information on Maternal Exposure

• We report a case of maternal exposure to the antihypertensive drug losartan during weeks 20-31 of pregnancy [7].
• Letter: Cardiovascular maldevelopment associated with maternal exposure to amantadine [8].
• MLL rearrangement status was derived by Southern blot analysis, and maternal exposure data were obtained by interviews using a structured questionnaire [9].
• The active triphosphate has not been detected in placental perfusion studies or in the fetal rhesus monkey 3 h after maternal exposure to ddI or ddC [10].
• Through the Acyclovir in Pregnancy Registry, all cases of reported prenatal exposures to acyclovir are tracked to ascertain maternal exposure, risk factor, and pregnancy outcome information [11].

Chemical compound and disease context of Maternal Exposure

• The effect of increasing gestational age and maternal exposure to cannabinoids on body weight, ano-genital distance and androgen concentration in fetal mice was examined [12].
• The written obstetric records of maternal exposure to diethylstilbestrol (DES) were used as a criterion standard and compared with the DES exposure history recalled by mothers of women with vaginal, cervical, or indeterminable vaginal/exocervical clear cell adenocarcinoma [13].
• We tested the hypothesis that maternal exposure to synthetic estrogen can cause hypospadias in male offspring and defined the morphological changes in the disrupted urethral seam [14].
• The present investigation examines the outcomes of rats' pregnancy following pre- and post-implantation maternal exposure (orally) to benzyl isothiocyanate (BITC; 12.5, 25 and 50 mg/kg body weight) [15].
• These results indicate that propiconazole interferes with the later stages of daphnid embryonic development, and that this toxicity is manifested largely via maternal exposure to the fungicide [16].

Biological context of Maternal Exposure

• We conclude that maternal exposure to octylphenol inhibits the secretion of FSH in the fetus with a concomitant decrease in testis size and Sertoli cell number at birth [17].
• To determine how maternal exposure to environmental tobacco smoke affects birthweight, maternal sera obtained from 3529 pregnant women around 27 weeks gestation were analyzed for cotinine, a metabolite of nicotine [18].
• In two patients that closely resembled the phenotype of the syndrome produced by aminopterin in early pregnancy, no evidence of maternal exposure could be elicited [19].
• CONCLUSION: The duration of fetal and maternal exposure to betamethasone can be minimized by direct fetal intramuscular administration that, in sheep, affords lung maturation without adverse effects on fetal growth [20].
• Based on AUC comparisons for cocaine, fetal exposures are thus approximately one-third of maternal exposures, demonstrating that substantial exposure to cocaine does occur in utero [21].

Anatomical context of Maternal Exposure

• Although naproxen is excreted into breast milk the amount of drug transferred comprises only a small fraction of the maternal exposure [22].
• Thus, in the present study, we examined the effect of two APs, OP and NP, on the expression of Calbindin-D(9k) (CaBP-9k) following maternal exposure during late pregnancy in maternal and fetal uteri [23].
• Ultrastructural observations on rabbit blastocysts after maternal exposure to cadmium chloride [24].
• These results suggest that while this model may not capture all of the critical events involved in the induction of hindlimb defects following maternal exposure to 5-FU, it does reflect a central mechanism of its developmental toxicity.(ABSTRACT TRUNCATED AT 400 WORDS)[25]
• GGT is present in embryonic yolk sac and its activity increases with gestational age, suggesting that the developing embryo might be at risk from maternal exposure to glutathione conjugates or compounds which are shown to form glutathione conjugates [26].

Associations of Maternal Exposure with chemical compounds

• In mice, maternal exposures to a small dosage of nicotine throughout both gestational and lactating periods appear to induce more baby lung changes than when the exposure to nicotine is limited to either period alone [27].
• Several chemical and/or cellular components of milk are potentially useful as biomarkers, and may be developed as convenient, biologically relevant indicators of maternal exposure to dioxin-like compounds [28].
• There was a differential developmental response in the induction of neonatal hepatic ethanol metabolizing enzyme by maternal exposure to Cs+ [29].
• Maternal exposure to tamoxifen during pregnancy increases carcinogen-induced mammary tumorigenesis among female rat offspring [2].
• This study revealed that steroidogenic acute-regulatory protein (StAR), a key transporter of cholesterol for steroidogenesis, in the testes of fetal rats are down-regulated by maternal exposure to TCDD [30].

Gene context of Maternal Exposure

• Effects of the GSTM1 and GSTT1 polymorphisms on the relationship between maternal exposure to environmental tobacco smoke and neonatal birth weight [31].
• These results suggest that maternal exposure to real-life levels of nicotine and/or chlorpyrifos causes differential regulation of brainstem AChE activity [32].
• Changes in TNFalpha, BDNF, and NGF after maternal exposure to poly I:C represent a potential mechanism through which maternal infection increases risk for neurodevelopmental disorders [33].
• Maternal exposure to solvents (OR 3.1, 95% CI 1.0-9.7) and plastic materials (OR 6.9, 95% CI 1.2-39.7) during pregnancy and plastic materials after pregnancy (OR 8.3, 95% CI 1.4-48.8) were related to K-ras mutation [34].
• This finding indicates that the perinatal opiate syndrome associated with maternal exposure to methadone is caused by the inhibition in MAO-A development in monoaminergic neurons in the brain [35].

Analytical, diagnostic and therapeutic context of Maternal Exposure

• OBJECTIVE: The purpose of this study was to establish whether nimesulide causes fewer fetal side effects than indomethacin or sulindac after short-term maternal exposure for tocolysis [36].
• Constriction of the ductus arteriosus in the fetus is well studied, but mostly secondary to maternal exposure to indomethacin or other non-steroidal anti-inflammatory medications, or structural cardiac lesions [37].
• The etiology of these tumors remains obscure, although may be linked to therapeutic radiotherapy, previous history of hematopoietic malignancy and maternal exposure to nitrosamine-laden foods [38].
• Abnormalities of the secondary palate were studied in an animal model in which features of Treacher Collins syndrome (TCS) and Nager or Miller syndromes (both of which are facially similar to Treacher Collins, but include limb malformations) were induced by acute maternal exposure to 13-cis-retinoic acid (13-cis-RA, isotretinoin, Accutane) [39].
• Decreased sex ratio following maternal exposure to polychlorinated biphenyls from contaminated Great Lakes sport-caught fish: a retrospective cohort study [40].

References