			Home About us Contact

Postnatal Mortality (postnatal + mortality)

Distribution by Scientific Domains

Life Sciences	60%

Selected Abstracts

Systemic inactivation of Hs6st1 in mice is associated with late postnatal mortality without major defects in organogenesis

GENESIS: THE JOURNAL OF GENETICS AND DEVELOPMENT, Issue 10 2008
Konstantin I. Izvolsky
No abstract is available for this article. [source]

Dietary Zinc Supplementation Throughout Pregnancy Protects Against Fetal Dysmorphology and Improves Postnatal Survival After Prenatal Ethanol Exposure in Mice

ALCOHOLISM, Issue 4 2009
Brooke L. Summers
Background:, We have previously demonstrated that ethanol teratogenicity is associated with metallothionein-induced fetal zinc (Zn) deficiency, and that maternal subcutaneous Zn treatment given with ethanol in early pregnancy prevents fetal abnormalities and spatial memory impairments in mice. Here we investigated whether dietary Zn supplementation throughout pregnancy can also prevent ethanol-related dysmorphology. Methods:, Pregnant mice were injected with saline or 25% ethanol (0.015 ml/g intraperitoneally at 0 and 4 hours) on gestational day (GD) 8 and fed either a control (35 mg Zn/kg) or a Zn-supplemented diet (200 mg Zn/kg) from GD 0 to 18. Fetuses from the saline, saline + Zn, ethanol and ethanol + Zn groups were assessed for external birth abnormalities on GD 18. In a separate cohort of mice, postnatal growth and survival of offspring from these treatment groups were examined from birth until postnatal day 60. Results:, Fetuses from dams treated with ethanol alone in early pregnancy had a significantly greater incidence of physical abnormalities (26%) compared to those from the saline (10%), saline + Zn (9%), or ethanol + Zn (12%) groups. The incidence of abnormalities in ethanol + Zn-supplemented fetuses was not different from saline-treated fetuses. While ethanol exposure did not affect the number of fetal resorptions or pre- or postnatal weight, there were more stillbirths with ethanol alone, and cumulative postnatal mortality was significantly higher in offspring exposed to ethanol alone (35% deaths) compared to all other treatment groups (13.5 to 20.5% deaths). Mice supplemented with Zn throughout pregnancy had higher plasma Zn concentrations than those in un-supplemented groups. Conclusions:, These findings demonstrate that dietary Zn supplementation throughout pregnancy ameliorates dysmorphology and postnatal mortality caused by ethanol exposure in early pregnancy. [source]

Three Common Intronic Variants in the Maternal and Fetal Thiamine Pyrophosphokinase Gene (TPK1) are Associated with Birth Weight

ANNALS OF HUMAN GENETICS, Issue 5 2007
D. Fradin
Summary Extreme variations in birth weight increase immediate postnatal mortality and morbidity, and are also associated with the predisposition to metabolic diseases in late adulthood. Birth weight in humans is influenced by yet unknown genetic factors. Since the 7q34-q35 region showed linkage with birth weight in a recent human genome scan (p = 8.10,5), this study investigated the TPK1 (thiamine pyrophosphokinase) gene locus, located in 7q34-36. Having found no coding variants in the TPK1 gene, we genotyped 43 non coding SNPs spanning a region of 420kb, and used the QTDT method to test their association with birth weight in 964 individuals from 220 families of European ancestry. Family-based tests detected association of 8 SNPs with birth weight (p<0.008), but after correction for multiple tests only rs228581 C/T (p = 0.03), rs228582 A/G (p = 0.04) and rs228584 C/T (p = 0.03) were still associated with birth weight, as well as their T-A-T haplotype (p = 0.03). In addition, we found an association between maternal rs228584 genotype and offspring birth weight (p = 0.027). These observations suggest that genomic variations in the fetal and maternal TPK1 gene could contribute to the variability of birth weight in normal humans. [source]

Gestational stage sensitivity to ultrasound effect on postnatal growth and development of mice

BIRTH DEFECTS RESEARCH, Issue 8 2006
Suresh Rao
Abstract BACKGROUND: An experiment was conducted to find out whether ultrasound exposure leads to changes in postnatal growth and development in the mouse. METHODS: A total of 15 pregnant Swiss albino mice were exposed to diagnostic levels of ultrasound (3.5 MHz, 65 mW/cm2, ISPTP = 1 mW/cm2 Intensity(Spatial Peak-Temporal Peak), ISATA = 240 mW/cm2 Intensity(Spatial Average-Temporal Average)) for 30 min for a single day between days 10 and 18 of gestation (GD 10,18). Virgin female mice were placed with same age group males for mating in the ratio 2 females : 1 male and examined the next morning for the presence of vaginal plug, a sign of successful copulation. The females with vaginal plugs were separated and labeled as 0-day pregnant. Maternal vaginal temperature was also measured. A sham exposed control group of 15 pregnant mice was maintained for comparison. All exposed as well as control animals were left to complete gestation and parturition. Their offspring were used in our further studies. They were monitored during early postnatal life for standard developmental markers, postnatal mortality, body weight, body length, head length, and head width, and growth restriction was recorded up to 6 weeks of age. RESULTS: An exposure to ultrasound induced nonsignificant deviations in the maternal vaginal temperature or developmental markers. Significant low birth weight was observed in the present study, after exposure at GD 11, 12, 14, and 16. However, 14 and 16 days postcoitus during the fetal period appears to be the most sensitive to the ultrasound effect, in view of the number of different effects as well as severity of most of the observed effects when exposed on these gestation days. CONCLUSIONS: The results indicate that diagnostic ultrasound can induce harmful effects on mouse growth and development when given at certain critical periods of gestation. Birth Defects Research (Part A) 76:602,608, 2006. © 2006 Wiley-Liss, Inc. [source]