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Stillborn fetuse

Lethal form of osteogenesis imperfecta in which the fractures appear in utero. as revealed by this radiograph of a stillborn fetus. [Pg.49]

I had never been allowed to show distaste during a dissection in the laboratory or to recoil from putrefaction, so I brought my face closer, closer, and remembered the weight of my own stillborn fetus, hot like a stewed plum, and the few moments I had spent examining its petal-thin ears. When I looked again, I distinctly saw the infant s mouth gape. [Pg.124]

Increased perinatal mortality (stillbirths and newborn deaths) occurred in mice as a consequence of maternal treatment with 0.02 mg NDMA/kg/day in the drinking water (Anderson et al. 1978). The mice were treated for 75 days prior to mating and throughout pregnancy and lactation. Histological examinations of the stillborn fetuses and dead neonates showed no abnormalities. The 0.02 mg/kg/day dose represents a LOAEL for developmental effects due to intermediate duration exposure (Table 2-2 and Figure 2-2). [Pg.47]

Stillborn fetuses from the Netherlands in 1993 and found that median (range) concentration of PCBs in adipose tissue was 235 (97-768) ng/g lipid weight (Lanting et al. 1998b). [Pg.641]

Beck (1990) studied the induction of skeletal malformations in maneb-exposed CD-I mice. Administration of 960 mg/kg/day maneb in 1% carboxymethylcellulose by gavage to pregnant dams on gestation days 6-15 resulted in a highly significant (p<0.001) increase in fetal mortality (51 stillborn fetuses in treated... [Pg.163]

Stillborn Fetuses (16-20wk gestation) Liveborn Neonates (27-36 wk gestation) Children (6-12y)... [Pg.235]

There have been a number of criticisms of body composition analysis studies. Firstly, intrauterine accretion estimates have assumed that stillborn fetuses were of normal size for gestational age and, therefore, that the accretion of each specific nutrient was normal for that gestational age. Based on the argument that infants who die in utero are probably not of normal size for gestational age, the estimated fetal content of each nutrient is likely an underestimate of true fetal composition. Secondly, when estimating oral requirements for the pre-term infant, the values used for absorption and excretion of nutrients were based on metabolic studies on full-term infants (Fomon and May, 1958). These values have been extra-... [Pg.258]

However, it had not been discovered that the thalidomide drug molecule could cross the placental barrier and affect fetal development. As a result, thousands of babies were born with crippled extremities, disfigurement, and disabilities. Numerous fetuses were stillborn or died soon after birth. [Pg.209]

Heptachlor epoxide was measured in a strip of skin, fat, and subcutaneous tissue from 68 children who died in the perinatal period and ranged from not detected (nondetectable) to 0.563 ppm (mean 0.173) (Zavon et al. 1969). In 10 other stillborn infants, heptachlor epoxide levels measured in various tissues were as follows brain (nondetectable), lung (0.17 0.07 ppm), adipose (0.32 0.10 ppm), spleen (0.35 0.08 ppm), liver (0.68 0.50 ppm), kidney (0.70 0.28 ppm), adrenal (0.73 0.27 ppm), and heart (0.80 0.30 ppm) (Curley et al. 1969). In another study, the following heptachlor epoxide levels were measured in extracted lipids from mothers and newborn infants maternal adipose tissue (0.28 0.31 ppm), maternal blood (0.28 0.46 ppm), uterine muscle (0.49 0.51 ppm), fetal blood (1.00 0.95 ppm), placenta (0.50 0.40 ppm), and amniotic fluid (0.67 1.16 ppm) (Polishuk et al. 1977a). These data provide evidence of transplacental transfer to the fetus. [Pg.48]

In two three-generation studies with rats administered heptachlor, heptachlor epoxide, or a mixture of the two in the diet, the number of resorbed fetuses increased and the fertility decreased with succeeding generations. No adverse effects on reproductive capacity were reported in male mice receiving single oral doses of 7.5 or 15mg/kg heptachlor heptachlor epoxide (25% 75%) in a dominant lethal assay. Heptachlor epoxide has been found in tissues of stillborn infants, indicating transplacental transfer. ... [Pg.368]

There is nothing to suggest that the human BBB is not at least equally well formed at birth than it is in the rat. Occludin and claudin-5 expression is detected in the capillary endothelium of the brain of the 14 week human fetus, and it has the same pericellular distribution as seen in the adult [72]. Pioneering studies by Grontoft [73] in stillborn human fetuses from approximately 12 week gestation and perinatal deaths have demonstrated a postmortem BBB to trypan blue present from at least the start of the second trimester, which is comparable to that of the adult human. [Pg.589]

Schecter A, P pke O, Ball M. 1990a. Evidence for transplacental transfer of dioxins from mother to fetus Chlorinated dioxinal dibenzofuran levels in the livers of stillborn infants. Chemosphere 21 1017-1022. [Pg.684]

Symptoms included ataxia, numbness in the hands and feet, general muscle weakness, narrowing of the field of vision and damage to hearing and speech. In extreme cases, insanity, paralysis, coma and death followed within weeks of the onset of symptoms. A congenital form of the disease also affected fetuses in the womb. Some were given birth with the congenital disease and many were stillborn. [Pg.88]

The homozygous state of a-thalassemia type-1 (a-Thi) leads to a form of erythroblastosis fetalis and intrauterine death [ (K2, L18, L20, L21, L22, L23, L24, L26, P4, T6, T7, T8) and others]. This form of hydrops fetalis is found in Chinese from various countries, in Filippinos, and in Thais. All children are either stillborn or die within hours after birth. The hematological observations usually include anemia with reticulo-cytosis, hypochromia with macrocytosis, aniso- and poikilocytosis, and many erythroblasts. The red cells sickle rather easily. Most fetuses are hydropic (but not all). [Pg.196]

Hemoglobin Bart s hydrops fetails This occurs due to inheritance of two a-thalassemia-1 allels and the offspring does not have any functional a genes. This condition is incompatible with life and results in stillborn or critically ill fetus with hydrops fetalis. Hemoglobin... [Pg.960]

Pregnant squirrel monkeys (N= 31), fetuses, 19 mothers PbB maternal mean =37 (ig/dl, range 22—87 trg/ dl, oral exposure Lead encephalopathic effects One abortion, eight stillborns, three neonatal deaths, reduced cerebral weights, white matter hemorrhages Logdberg et al. (1988)... [Pg.555]

Lipid deposition in the large blood vessels in the very young, even in stillborn babies (Aschoff 1925), might have its origin in faulty metabolism of the mother, such as deficient intake of food factors and thus inadequate supply of these factors to the fetus. Intoxication also, as for instance with excessive single or daily doses of vitamin D, should be mentioned. [Pg.289]


See other pages where Stillborn fetuse is mentioned: [Pg.18]    [Pg.102]    [Pg.2169]    [Pg.654]    [Pg.149]    [Pg.448]    [Pg.18]    [Pg.102]    [Pg.2169]    [Pg.654]    [Pg.149]    [Pg.448]    [Pg.71]    [Pg.58]    [Pg.21]    [Pg.101]    [Pg.164]    [Pg.513]    [Pg.1453]    [Pg.259]    [Pg.118]    [Pg.120]    [Pg.128]    [Pg.238]    [Pg.238]    [Pg.65]    [Pg.198]    [Pg.74]    [Pg.75]   
See also in sourсe #XX -- [ Pg.448 ]




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