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Fetal development

Antibodies have been generated which produce immunoassays that discriminate between GH-V and GH-N. These assay systems have shown that the secretion of GH-V becomes elevated at about three weeks of pregnancy and increases to approximately 15 ng/mL near term (8). The physiological role of GH-V is uncertain. Genetic deficiency of GH-V does not adversely affect pregnancy or fetal development (9). GH-V is a potent growth-stimulator but possesses considerably less lactogenic activity than GH-N (10). There are no clinical appHcations (ca 1993) for GH-V. [Pg.181]

Rabbit DOT stabilizer mix (DOT(IOMA) MOT(IOMA) 80 20) Gestation days 6-18 atO, 1, 10, and 100 mg/kg body weight Marginal retardation of fetal development marginal maternal toxicity at 100 mg/kg body weight per day LOAEL = 10 NOAEL =1 Sobering AG (1992)... [Pg.31]

Developmental Effects. Adverse effects of methyl parathion on hirman fetal development have not been reported. Based on studies in animals, such effects appear to be possible if pregnant women were exposed during the first trimester to high concentrations of methyl parathion that resulted in significant depression of cholinesterase levels, particularly if concomitant signs and symptoms of organophosphate intoxication occur. Such an exposure scenario may occur with occupational exposure, exposure in homes or offices illegally sprayed with methyl parathion, or accidental exposure to methyl parathion, but is less likely as a result of low-level exposure. [Pg.36]

Fish SA. 1966. Organophosphorus cholinesterase inhibition and fetal development. Am J Obstet Gynecol 96 1148-1154. [Pg.207]

Epstein, C. J. "Genetic Counseling - Past, Present and Future" In "Birth Defects and Fetal Development, Endocrine and Mietabollc Factors", ed. K. S. Moghlssl, Charles C. Thomas Publisher, Springfield, Illinois, 1974. [Pg.88]

Cosby NC, Dukelow WR. 1992. Toxicology of maternally ingested trichloroethylene (TCE) on embryonal and fetal development in mice and of TCE metabolites on in vitro fertilization. Fundam Appl Toxicol 19 268-274. [Pg.258]

Healy TEJ, Poole TR, Hooper A. 1982. Rat fetal development and maternal exposure to trichloroethylene 100 ppm. Br J Anaesth 54 337-341. [Pg.270]

Schwetz BA, Leong KJ, Gehring PJ. 1975. The effect of maternally inhaled trichloroethylene, perchloroethylene, methylchloroform, and methylene chloride on embryonal and fetal development in mice and rats. Toxicol Appl Pharmacol 32 84-96. [Pg.289]

Ronnekliev O. and Resko J.A. (1990). Ontogeny of GnRH-containing neurons in early fetal development of rhesus macaques. Endocrinology 126, 498-511. [Pg.242]

Identify the stages of fetal development when birth defects are most likely to occur. [Pg.721]

Male patients with RA must receive counseling about the effects of certain medications on their fertility and potential harm to the fetus. It is difficult to establish causality between use of a medication by a male and the effect on fertility or fetal development therefore, a conservative approach must be taken. Patients of childbearing potential and their partners must be counseled to (1) use proper birth control while undergoing treatment for RA and (2) discontinue medications at least 3 months before conception.37... [Pg.876]

Carcinoembryonic antigen A protein normally seen during fetal development. When carcinoembryonic antigen is elevated in adults it suggests the presence of colorectal and other cancers. The normal level in nonsmokers is about less than 2.5 ng/mL, but it can be elevated in smokers and other nonmalignant conditions such as pancreatitis. [Pg.1561]

HCH also penetrates the placenta barrier [A96, A101]. Complications during pregnancy occurred 1.5 times more frequently in the 213 women whose blood contained HCH than in the 89 women with no signs of this insecticide (78.3% and 58.4% respectively). It is especially significant that twice as many women with HCH in their blood spontaneously miscarried during the first trimester as those without HCH (7.5% and 3.4% respectively). Causal factors included disruptions in prenatal fetal development, and disruptions in women s hormonal systems under the effect of HCH [A96]. Postpartum complications in women who had HCH in their blood were 2.5... [Pg.69]

Saillenfait AM, Bonnet P, de Ceaurriz J. 1989. Effects of inhalation exposure to carbon disulfide and its combination with hydrogen sulfide on embryonal and fetal development in rats. Toxicol Lett 48 57-66. [Pg.199]

McMahon I have a more general question about how the IGF system works. Your explanation for the absence of a tissue-specific effect of modulating IGF levels presupposes that there would be some data that suggest that IGF2 is acting locally. It is certainly expressed broadly throughout the whole embryo. An alternative hypothesis is that there are key places where it has been expressed during embryonic fetal development that are important and some places that are unimportant. What has been done in terms of tissue-specific removal or activation of this pathway ... [Pg.35]

McClain RM, Becker BA. 1972. Effects of organolead compounds on rat embryonic and fetal development. Toxicol Appl Pharmacol 21 265-274. [Pg.548]

Ward Ni, Watson R, Brvce-Smith D. 1987. Placental element levels in relation to fetal development for obstetrically normal births A study of 37 elements Evidence for the effects of cadmium, lead, and zinc on fetal growth and for smoking as a source of cadmium. Int J Biosoc Res 9 63-81. [Pg.584]

Zajac CS, Abel EL. 1990. Lack of lead effects on fetal development and offspring learning when combined with alcohol in the Long-Evans rat. Teratology 41 33-41. [Pg.588]

Muscle fibers are incapable of mitosis. In fact, the number of muscle fibers per muscle is likely determined by the second trimester of fetal development. Therefore, enlargement of a whole muscle is not due to an increase in the number of fibers in the muscle, but rather to the hypertrophy of existing fibers. Because muscle fibers have no gap junctions between them, electrical activity cannot spread from one cell to the next. Therefore, each muscle fiber is innervated by a branch of an alpha motor neuron. A motor unit is defined as an alpha motor neuron and all of the muscle fibers that it innervates. [Pg.141]

Wu G, Bazer FW, Cudd TA, Meininger CJ, Spencer TE Maternal nutrition and fetal development. J Nutr 2004 134 2169-2172. [Pg.66]

This material is hazardous through inhalation, skin absorption, penetration through broken skin, ingestion, and produces local skin/eye impacts. It is known to mimic estrogen in the body (hyperestrogenism). In animals, it has caused feminization of male animals and interfered with conception, ovulation, and fetal development in female animals. Specific signs and symptoms of acute high-dose exposure to zearalenone have not been established or have not been published. [Pg.488]

Marks, T.A., G.L. Kimmel, and R.E. Staples. 1981. Influence of symmetrical polychlorinated biphenyl isomers on embryo and fetal development in mice. I. Teratogenicity of 3,3, 4,4, 5,5 -hexachlorobiphenyl. Toxicol. Appl. Pharmacol. 61 269-276. [Pg.1332]


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And fetal development

Blood fetal development

Embryo-fetal development

Embryo-fetal development study

Embryonic and fetal development

Embryonic/fetal development

Female reproductive system fetal development

Fetal

Fetal brain development

Fetal development causes

Fetal development developmental programming

Fetal development disruptions/disruptive effects

Fetal development environmental impact

Fetal development immunity

Fetal development influences

Fetal nervous system brain-development

Fetal sexual development

Human body fetal development

Male reproductive system fetal development

Neuroscience fetal brain development

Reproductive toxicity embryonic /fetal development

Thyroid hormones, maternal fetal brain development

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