Prenatal growth

The function of DMEs is also thought to include the detoxification of dietary products and the evolution of plant metabolites, including drugs [11]. The selective forces responsible for the maintenance of different alleles in different populations may include the fact that one allele may enable improved rates of implantation, improved prenatal growth and development, improved postnatal health in response to dietary or environmental selective pressures or improved resistance to bacteria, viruses or parasites [11, 14]. Allele frequencies may also reflect ethnic dietary differences that have evolved over thousands of years [15]. 

Furthermore, it has been observed that placental PGP is of great importance in limiting the fetal penetration of various potentially harmful or therapeutic compounds [64]. High PGP levels may have a role in the protection of fetuses from harmful tropical plant metabolites (from which many drugs are derived). An originally balanced polymorphism may have been preferentially selected by improved prenatal growth and development as well as improved postnatal health. This selective pressure may maintain the C allele in populations of African descent. 

Ethanol readily passes across the placenta and into the fetal circulation. The fetal alcohol syndrome has three primary features microcephaly, prenatal growth deficiency, and short palpebral fissures Other characteristics include postnatal growth deficiency, fine motor dysfunction, cardiac defects, and anomalies of the external genitalia and inner ear. A definite risk of producing fetal abnormalities occurs when ethanol consumption by the mother exceeds 3 oz daily, the equivalent of about six drinks. 

Some common developmental effects attributed to 2,3,7,8-TCDD exposure in most laboratory mammals are thymic hypoplasia, subcutaneous edema, decreased prenatal growth, and prenatal mortality (Couture et al. 1990). In addition, there are other species-specific effects, such as cleft palate in mice. Any of... 

Rice, F., Jones, I., Thapar, A. (2007). The impact of gestational stress and prenatal growth on emotional problems in offspring a review. Acta Psychiatr. Scand. 115 171—183. 

Most of what is known about the toxicity of dioxins in the human comes from individuals exposed incidentally or chronically to higher levels (e.g., industrial accidents or presence in areas sprayed with Agent Orange or other herbicides contaminated with dioxins.). The lowest dose effects are probably associated with thymic atrophy and decreased immune response, chloracne and related skin lesions, and neoplasia (cancer). Dioxins can cross into the placenta to cause developmental and reproductive effects, decreased prenatal growth, and prenatal mortality. 

The proportion of esterified cholesterol falls during the prenatal growth of the human brain but shows a transient rise at about the time of birth (Fig. 2)— which suggests that it is associated with rapid myelination. The forebrains of malnourished children contain a higher-than-normal proportion of esterified cholesterol. At present, the explanation for this is not clear. It could be the result of delayed myelination. However, increased amounts of esterified cholesterol are found in the brain in diseases associated with the destruction of myelin. It is tempting to suggest that the higher-than-normal amounts of esterified cholesterol in the forebrains of malnourished children also result from the destruction of myelin. Evidence in... 

Embryotoxicity and Fetotoxicity—Any toxic effect on the conceptus as a result of prenatal exposure to a chemical the distinguishing feature between the two terms is the stage of development during which the insult occurs. The terms, as used here, include malformations and variations, altered growth, and in utero death. 

While the aforementioned studies have described the manifestations of i n ut.ero exposure to PCP by human and animal fetuses as well as behaviors adult monkeys who had received only PCP, the longterm consequences of prenatal abuse have not been described. Therefore, this report will elaborate upon our observations of the effects of PCP upon the growth and development of 12 neonates between 2 and 18 months of age, whom we have followed from August 1983 to March 1985. 

During an 18-month period the growth and development of eight male and four female infants exposed prenatally to phencyclidine was observed. 

Beagles, prenatal and early neonatal stages, given single acute dose of 0.2-1.0 Gy, then observed over 11-year life span Irradiation at all ages was associated with increased risk of decreased fertility inhibited growth and development lower brain weight and increase in fatal neoplasms 5... 

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