Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “PRENATAL INFLUENCES”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMedDate not supplied

Fluctuating dermatoglyphic asymmetry: genetic and prenatal influences.

Genetic and environmental prenatal factors influencing the fluctuating asymmetry of the a-b interdigital ridge count are examined. From the results obtained we can conclude that fluctuating asymmetry of the a-b interdigital ridge count is poorly influenced by genetic factors. We suggest that fluctuating asymmetry of dermatoglyphics provides a good measure of developmental stability in humans, especially for males. The results also indicate that random environmental factors, acting before the 19th week of embryonic development, could be related to the differential timing of maturation of the sexes.

Dermatoglyphics↗
PubMed2005

Cord blood lipoproteins and prenatal influences.

PURPOSE OF REVIEW: Blood lipoprotein profiles in early life are known to be related to and predictive of those in adulthood, but little is known about their determinants. Genetic and environmental influences affect cord blood lipoproteins, but how this occurs and the relative contribution of these influences to the overall profile in healthy newborns remains uncertain. RECENT FINDINGS: This review discusses findings from a range of earlier and more recent studies, and summarizes the key influences on cord blood lipoproteins. In particular, we review the potential contribution of maternal blood total cholesterol levels during pregnancy and the increased maternal transmission in newborns of mothers with diabetes. SUMMARY: In cord blood, cholesterol levels are lower than in adults and the relative proportion present in HDL as opposed to LDL is much higher. The currently available evidence suggests that several factors influence the composition of cord blood lipoproteins. Although inheritance of major monogenic disorders can affect cord lipids in general, the genetic contribution appears to be minimal, although effects of the proprotein convertase subtilisin/kexine type 9 gene (PCSK9) need fuller exploration in this regard in certain ethnic groups. Evidence is summarized that maternal lipoprotein levels, particularly those due to diet or induced by pregnancy, influence cord lipid levels. Placental insufficiency and other conditions affecting fetal growth and the mode of delivery may also influence cord lipoprotein concentrations. How maternal glucose tolerance during pregnancy affects cord blood lipoproteins remains unclear. In view of increasing evidence that cardiovascular risk may have prenatal antecedents, this would seem to be an important area for further investigation.

Cholesterol↗
PubMed2001

Prenatal influence of ischemia-hypoxia-induced intrauterine growth retardation on brain development and behavioral activity in rats.

The effects of intrauterine growth retardation (IUGR) on brain histological or functional development were examined in rats. IUGR was induced by ligating the bilateral uterine arteries at day 17 of pregnancy. On day 22 of pregnancy, cesarean section was performed, and pups with a birth weight of <2 SD of the mean birth weight of control pups were regarded as IUGR rats. Morphological changes of the brain were studied by Nissl's staining at different timepoints during prenatal and postnatal periods. For behavioral study, an open-field test was performed at 5, 7 and 10 weeks after birth. Histological studies showed the migration disorder of the neurons in the cerebral cortex from embryonic day 17 to postnatal day (PD) 49. The open-field test revealed locomotor disturbance at PD49 in male IUGR rats, but not in female IUGR rats or control rats. It is concluded that IUGR due to antenatal ischemia-hypoxia causes morphological changes in the central nervous system, and induces behavioral impairment, particularly in male rats.

Animals↗
PubMed2003

Prenatal influences on stroke mortality in England and Wales.

BACKGROUND AND PURPOSE: Within Britain and the United States there are geographic variations in mortality from stroke that are not explained by differences in adult lifestyle. We report on the geographic distribution of stroke mortality in England and Wales and compare it with that in the United States. METHODS: Data from 4 studies are presented. The geographic distribution of stroke deaths in England and Wales during 1968-1978 is compared with the distribution of (1) other causes of death during the same years, (2) neonatal and maternal mortality during 1911-1925, (3) average adult height, and (4) place of birth. RESULTS: Areas of England and Wales with high stroke mortality were characterized in the past by poor living standards, demonstrated by high infant and maternal mortality rates and short stature in the adult population. People who were born in areas of high stroke mortality rather than migrating into them are at high risk. Stroke mortality is not geographically correlated with past postneonatal mortality independently of neonatal or maternal mortality. The geographic distribution of stroke mortality in the United States and England and Wales has features in common. CONCLUSIONS: Stroke may originate through maternal influences associated with poverty. This conclusion is supported by recent findings that rates of stroke in adult life are higher among people who had low birth weight.

Aged↗
PubMed2000

Prenatal influences on neuroimmune set points in infancy.

Many factors during fetal life and early infancy have been found to affect the development of immune responses in animals. This study investigated whether acute exposure of the fetal monkey to high levels of corticosteroids would also have a lingering effect on the expression of immune responses still manifest postpartum in yearling juveniles. One month prior to parturition, pregnant rhesus monkeys were administered dexamethasone for two days. Lymphocyte proliferative responses to mitogen were then examined in their offspring when they were between 1.0-1.5 years of age. In addition, cell sensitivity to corticosteroid feedback was assessed by testing the ability of a gradation of cortisol doses to inhibit proliferation. Monkeys generated from dexamethasone-treated pregnancies tended to have lower responses to concanavalin A. Further, their cells were less sensitive to in vitro incubation with cortisol, suggesting that elevated adrenal activity in vivo had downregulated hormone receptors on their cells. These findings concur with the view that steroidal hormones in utero can influence the fetal immune system, resulting in prolonged effects on immune responses after birth. The similarity of the dexamethasone condition to the clinical treatment used in obstetrical practice raises a potential concern about the widespread antenatal exposure of premature infants to steroidal drugs.

Animals↗
PubMed1992

Evidence of prenatal influences on breast cancer risk.

Intrauterine exposure to high concentrations of endogenous pregnancy oestrogens may be important in the aetiology of breast cancer. In a nested case-control study we have assessed the relation between breast cancer risk and indicators of pregnancy oestrogen concentrations; pre-eclampsia/eclampsia is negatively related and measures of fetal size are positively related to oestrogen concentrations. Standard records for women born at Uppsala University Hospital between 1874 and 1954 were linked with records of invasive breast cancer cases, identified through their unique national registration numbers in the Swedish Cancer Registry during 1958-90. For each breast cancer case, we selected as potential controls female offspring of the first three mothers admitted to the hospital after the case's mother; only controls still living in Sweden and free from breast cancer when it was diagnosed in the case were finally included. Conditional logistic regression analysis was done for 458 breast cancer cases and 1197 matched controls. Pre-eclampsia/eclampsia was associated with a breast cancer rate ratio of 0.24 (95% confidence interval 0.09-0.70, p = 0.01). Linear trends for breast cancer incidence with increasing birth weight, birth length, and placental weight were positive but not significant. Thus, prenatal factors are important in breast carcinogenesis. Concentrations of pregnancy oestrogens may be one such factor, but other prenatal or perinatal factors cannot be excluded.

Adult↗