Foetal development

Vitamin A is essential throughout life, including foetal development, but perhaps its most well researched role is that in vision where 11 -cis retinaldehyde is the initial part of the photoreceptor complex in rods and cones. Retinoic acid induces differentiation in epithelial cells and deficiency leads to... 

Foetal development promotes growth and differentiation of foetal cells and organogenesis Promotes longitudinal body growth and increased body weight Promotes enhanced functioning of the male and female reproductive tissue Promotes growth and differentiation of neuronal tissue... 

Provided that blood supply and innervation remain intact, skeletal muscle heals well after injury or disease. Damage to fibres causes endothelial cells to secrete general growth factors (e.g. fibroblast growth factor, insulin-like growth factors) and growth factors specific to muscle development which stimulate proliferation of satellite cells. These then migrate to the site of injury to form myotubes, as in foetal development. If, however, the number of satellite cells is... 

Reproductive toxicology, usually embryo/ foetal development studies in two species, is required in Europe and Japan if women of childbearing potential are included. Not required in the United States for some early trials... 

Embryo-foetal development (rat and rabbit). This is a standard Segment II, teratogenicity study. 

The FDA allows women to enter carefully controlled and monitored trials in which adequate contraceptive measures and pregnancy testing are performed without requiring results from animal reproductive toxicity tests. In Japan and Europe, because of the high level of concern regarding imintentional exposure of the developing embryo or foetus, an assessment of fertility in a rodent, and embryo/foetal development in a rodent or non-rodent are required if women of childbearing potential are to be included in a Phase I trial. The FDA would expect such results to support Phase II and Phase III studies. 

Teratogenesis Defects in embryonic and foetal development caused by a substance. Teratogenic capable of producing birth defects. 

Frieling WJAM, Heijink E, Tesh SA, et al. Embryo-foetal development toxicity of propylene glycol in NZW rabbits. Repro Tox 2000 14 562. 

Tetrahydrocannabinol is metabolized in the liver to form active metabolites which are further metabolized to inactive polar compounds these are excreted in the urine. Some metabolites are excreted into the bile and then recycled via the enterohepatic circulation. Because of their high lipophilicity, most active metabolites are widely distributed in fat deposits and the brain, from which sources they are only slowly eliminated. The half-life of elimination for many of the active metabolites has been calculated to be approximately 30 hours. Accordingly, accumulation occurs with regular, chronic dosing. Traces of the cannabinoids can be detected in the blood and urine of users for many days after the last administration. There is some evidence of metabolic tolerance occurring after chronic use of the drug. THC and related cannabinoids readily penetrate the placental barrier and may possibly detrimentally affect foetal development. 

The adverse human impacts of PCBs have been investigated in occupationally exposed workers as well as individuals poisoned with PCB-contaminated rice oil in Japan and Taiwan (Yusho and Yu-Cheng poisonings).91,107-109 In addition, recent studies have shown a correlation with in utero exposure to PCBs and subtle neurodevelopmental and neurobehavioural deficits in children.110 These effects were observed in children with relatively low-level environmental exposure to PCBs and thus have raised concerns regarding the potential adverse effects of low level in utero exposure to organochlorine compounds during critical periods of foetal development. 

Segment II the embryo-foetal development (embryo during major organ development i.e. organogenesis, the foetus in the post-embryonic period) and... 

It is only the ability of modern chemistry to detect very small quantities of materials that made the following discovery possible. In some recent research it was reported that one subtle way in which cancer tumours cells differ from normal cells is how they metabolize carbohydrates present on their surfaces. Cancer cells have far more of the carbohydrate sialic acid, which can be detected with MRI (magnetic resonance imaging) analytical techniques. It was found that the sialic acid normally appears on the surface of the cells only in foetal development, but it appears abnormally in patients with gastric, colon, pancreatic, liver, lung, prostate and breast cancers, as well as in leukaemia. Research is continuing.1... 

Some genetic defects can cause disturbed restructuring of the ductal plates in foetal development, so-called ductal plate malformations, (s. p. 660) In contrast, in genetically determined metabolic disorders, secondary ductopenia (or paucity of bile ducts) may arise during the subsequent course of disease. 

Domosedan) on the maintenance of equine pregnancy and foetal development ten cases. Equine Veterinary Journal 20 323-326... 

Reproductive toxicity Fertility studies are not generally required during early clinical development unless there is good reason. Embryotoxicity/foetal development studies in two species are normally expected if women of childbearing potential are to be included in clinical trials interaction potential with oral contraceptives should be considered in this case. 

Saillenfait AM, Bonnet P, deCeaurriz J. 1989. The effects of maternally inhaled formaldehyde on embryonal and foetal development in rats. Food Chem Toxicol 27 545-548. 

The sensitive period for induction of malformations is the 5-14 day period in the rat and mouse and the 3rd week to the 3rd month in humans. This is illustrated in figure 6,13 for the teratogen actinomycin D. The later period of foetal development, like the initial proliferative stage, is less susceptible to specific effects and an all or none type of response is usually seen, such as either death or no gross effect. 

Singh, S. C., Ectopic neurones in the hippocampus of the postnatal rat exposed to methylazoxymethanol during foetal development. Acta Neuropath. (Berl.), 1977, 40 111-116. 

I) The total exposure to a drug during the lifetime of the patient or an important period of life (i. e., the quantity of the drug administered). This factor may be of influence on reproduction, foetal development, teratogenicity, oncogenicity, etc. and also on a disease such as analgesic-interstitial nephritis. 

Osorio, C. and N.B. Myrant. The passage of thyroid hormones from mother to foetus and its relation to foetal development. Brit. Med. Bui. 16 159-164, 1980. 

Ekins, R. P. Hypothesis The roles of serum thyroxine binding proteins and maternal thyroid hormones in foetal development. Lancet (i) 1129-1132, 1985... 

An increase in body water accounts for a large percentage of weight gain exhibited during a natural pregnancy. This occurs as a result of placental and foetal development, the formation of amniotic fluid and an increased maternal plasma... 

Reprotoxic may produce or increase the incidence of non-heritable adverse effects in the offspring and/or causes either a decrease in fertility or problems with foetal development... 

In pregnant animals, two opposing effects influence food intake. The increased need for nutrients for foetal development causes intake to rise. In the later stages of pregnancy, the effective volume of the abdominal cavity is reduced as the foetus... 

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