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  • Title: Trisomy 13 in the mouse.
    Author: Hongell K, Gropp A.
    Journal: Teratology; 1982 Aug; 26(1):95-104. PubMed ID: 7135263.
    Abstract:
    The fetal development of mice trisomic for chromosome 13 (Ts 13) was investigated. Trisomic fetuses were obtained from the progeny of male mice heterozygous for the two Robertsonian translocation chromosomes Rb (11.13)4Bnr and Rb (6.13)3Rma mated to "all acrocentric" NMRI females. Trisomic fetuses were found at all stages between days 12 and 19 of gestation (vaginal plug day counted as day 1). The frequency of trisomy was 24.8% of all surviving implants. The frequency of Ts decreased slightly but not significantly with progressing pregnancy. In eight newborn litters, two dead and four living trisomic newborns (13.6%) were found. The latter died within a few hours after birth. The most conspicuous features of Ts 13 fetuses were their small size and a marked hypoplasia as compared with their normal euploid in utero mates. The weight of the the trisomic fetuses and that of their placentas was significantly lower than of the normal controls at all stages studied. The general developmental delay and the delay of the ossification of Ts 13 fetuses were about 1 to 11/2 days. Cleft palate was observed in 86% of the Ts 13 fetuses. Edema developed in the neck and back of the trisomic fetuses from day 14 on; this disappeared after day 17. It is suggested that the hypoplasia and general retardation of growth found in trisomy 13 and in other autosomal trisomies, as well as the more or less specific palatal and cardiovascular malformations in this disorder, may be caused by impaired proliferation of trisomic cells. This postulated impairment of cell growth may also affect the fetal part of the placenta.
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