ISSN:0040-3709    

DOI:10.1002/tera.1420380302

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

ISSN:0040-3709    

DOI:10.1002/tera.1420380303

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

ISSN:0040-3709    

DOI:10.1002/tera.1420380304

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

ISSN:0040-3709    

DOI:10.1002/tera.1420380305

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

ISSN:0040-3709    

DOI:10.1002/tera.1420380306

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

ISSN:0040-3709    

DOI:10.1002/tera.1420380307

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

ISSN:0040-3709    

DOI:10.1002/tera.1420380308

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

摘要:

AbstractIn order to determine the embryotoxic and teratogenic potential of aluminum, pregnant Sprague‐Dawley rats were treated by gavage with a daily dose of 180, 360, or 720 mg/kg of aluminum nitrate from the sixth through to the fourteenth day of gestation. Fetal examinations were performed on day 20. The number of corpora lutea, total implants, and resorptions as well as the number of live and dead fetuses in the treated animals were not significantly different from the control group. Therefore, embryolethality of aluminum cannot be induced (as a measure of percent dead and resorbed fetuses). However, exposure of rats to aluminum nitrate resulted in decreased fetal body weight and increased the incidence and types of external, visceral, and skeletal malformations and variations in all the treated groups. Consequently, teratogenic effects of aluminum‐nitrate administration may result in rats given high oral doses that induce concomitant maternal toxic

ISSN:0040-3709    

DOI:10.1002/tera.1420380309

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

摘要:

AbstractThe pathogenetic sequence for TAC‐induced encephalocele is in agreement with hypotheses proposing that neural tube closure is followed by protrusion of the mesencephalon, with subsequent growth and development resulting in herniation of the cerebrum and cerebellum. This model could serve to clarify the pathogenesis of encephalocele and to stimulate further study in comparing this defect to other dysraphic states. Triamcinolone acetonide (TAC) was administered intramuscularly (10 mg/kg) to 16 pregnant rhesus monkeys (Macaca mulatta) for 5 alternate days of pregnancy, beginning on gestational day (GD) 23. Conceptuses were removed by hysterotomy at GD 35, 42, 50, or 70 and examined grossly and histologically. Length, area, and perimeter of the tectum and aqueduct area and perimeter were measured with an image analyzer. Changes in treated specimens were suggestive of forces within or ventral to the tectum resulting in dorsal protrusion, rostral‐posterior stretching, and attenuation. The angle of the cephalic, pontine, and cervical flexures was also measured. The more acute angle of the cephalic flexure and less acute cervical flexure of treated specimens could represent altered orientation secondary to a mesenchymal deficiency. However, the less acute angle of the pontine flexure in treated specimens suggests an intrinsic alteration in the neural tube. This suggests that encephalocele may result from a combination of mesenchymal and neural tube abnormalit

ISSN:0040-3709    

DOI:10.1002/tera.1420380310

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY

摘要:

AbstractExposure of rats to either estrogens or antiestrogens during early postnatal development reduces subsequent uterine growth as measured by uterine weight. However, individual uterine cell types respond differently to these agents and uterine weight alone cannot discern subtle or even large alterations in individual cell populations. Using a computerized planimetric technique, we estimated the prepubertal growth of the uterine luminal epithelium, endometrial stroma, glands, and circular and longitudinal muscle after exposure of neonatal rats (postnatal days 1–5) to the estrogens 17β‐estradiol (E2), diethylstilbestrol (DES), or ethynylestradiol (EE), and the antiestrogens tamoxifen or clomiphene citrate. On postnatal day 26, the cross‐sectional areas of the luminal epithelium, endometrial stroma, and circular muscle were reduced after estrogen exposure, compared to untreated controls, while longitudinal muscle cross‐sectional area was not affected. Since cell densities (cell number/unit area) were increased, these estrogen‐induced area reductions demonstrate a decrease in cell size. Total cell numbers, estimated as the product of cell type areas and their respective cell densities, were also reduced by neonatal estrogen exposure. The synthetic estrogens DES and EE were more potent than E2with respect to reduction of uterine growth. Neonatal antiestrogen exposure caused large area reductions only in the uterine glands and luminal epithelium. Little change in cell density occurred in any cell population exposed to antiestrogen. These data demonstrate that the decreased uterine growth resulting from estrogen exposure during early postnatal development is a consequence of combined hypotrophy and hypoplasia in all cell types except longitudinal muscle while antiestrogen‐induced morphological alterations were limited to hypoplasia having epithelial cell

ISSN:0040-3709    

DOI:10.1002/tera.1420380311

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1988

数据来源: WILEY