ISSN:0040-3709    

DOI:10.1002/tera.1420150217

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

年代:1977

数据来源: WILEY

摘要:

AbstractThe effects of cytosine arabinoside, 6‐aminonicotinamide, and 6‐mercaptopurine riboside on the incorporation of [14C]glucose moieties and [32P]phosphate into acid‐soluble material and lipids, RNA, DNA, and protein were measured in the dissected mesoderm and ectoderm of mouse limb buds at the 42–45 (day 11) somite stage. Due to the different proliferative capacities of the two tissues the incorporation of the precursors into mesodermal cells was considerably higher than into ectodermal ones. Cytosine arabinoside inhibited the incorporation of the precursor moieties only into DNA, but very early after its application. This effect was more obvious in mesoderm than ectoderm. 6‐Aminonicotinamide interfered only with glucose metabolism, whereas the incorporation of phosphate was not affected.14C radioactivity in the various cell components was similarly reduced in mesoderm and ectoderm. 6‐mercaptopurine riboside caused an increased incorporation of precursor material in all fractions studied in the mesoderm as well as in the ectoderm during the first 12 hours. This was succeeded by a dramatic decrease of incorporated14C and32P radioactivity. Differences of response in the tissues could not be detected with this drug. It is suggested that the malformations of the extremities caused by these antimetabolites may be predominantly attributed to changes in the cell function rather than to gross effects on cell

ISSN:0040-3709    

DOI:10.1002/tera.1420150203

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

年代:1977

数据来源: WILEY

摘要:

AbstractHematological and histological studies of the rabbit brachydactyly mutant were made to clarify the question of the blood abnormality that had previously been implicated in the teratogenic process leading to congenital amputation. The hemoglobin of fetal and adultbr/brrabbits, studied by electrophoresis and cyanmethemoglobin assay, exhibited no differences from that of controls. Thebr/brfetuses were polycythemic and severely macrocytic. Fetal limb vessels showed thrombosis leading to hemorrhages in the extremities. The hepatic tissue was abnormal, being particularly poor in hematopoietic cells; blood cell macrocytosis was attributed to impaired erthropoiesis. Treatment of pregnant rabbits with folic acid plus vitamin B12or with folinic acid was able simultaneously to prevent the fetal blood cell macrocytosis and the congenital abnormalities.

ISSN:0040-3709    

DOI:10.1002/tera.1420150204

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

年代:1977

数据来源: WILEY

摘要:

AbstractD‐Penicillamine was given on the fourth day of culture of limb buds from 11‐day mouse embryos at a dose of 100 μg/ml medium and allowed to react for 24 hours. On day 5 there was found a significant decrease in the [3H] thymidine labeling index of cartilage cells and of cells of the perichondrium, whereas mesenchyme cells showed no decrease in proliferation under these conditions. The toxic effects ofD‐penicillamine on prenatal skeletal development in vivo could therefore result not only from direct action on collagen but also via inhibition of proliferation of cartilage

ISSN:0040-3709    

DOI:10.1002/tera.1420150205

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

年代:1977

数据来源: WILEY

摘要:

AbstractA descriptive system for the nomenclature, notation and classification of congenital limb malformations, suitable for clinical, epidemiological and experimental use is presented. Every developmental limb anomaly is described by stating the type of anomaly and the affected anatomic structure. All anomalies are classified into three basic types: excess, deficiency and fusion. The anatomic structure of the affected limb is defined within a two dimensional order.This system was used to describe 652 cases with isolated developmental limb anomalies obtained from two series of observations. The observed data are presented in a progressively expanded classification ranging from 4 to 497 diagnostic categories. Observed incidence rates for the four main types of anomaly from a sample of 297,299 consecutive livebirths, are: excess: 1.22; deficiency: 0.17; fusion: 0.20; combined: 0.24 per thousand.

ISSN:0040-3709    

DOI:10.1002/tera.1420150206

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

年代:1977

数据来源: WILEY

摘要:

AbstractCraniomyeloschisis (proposed gene symbolcms) was a spontaneous mutation of the rat inherited as an autosomal recessive trait with complete penetrance. Homozygous offspring died at birth with failure of closure of the neural tube caudal to the midbrain. Neural crest derivatives were relatively normal. There were associated severe malformations of the axial skeleton including skull, vertebral column, and ribs. The pattern of malformations was quite uniform. Heterozygotes were anatomically normal. The mutation is extinct.

ISSN:0040-3709    

DOI:10.1002/tera.1420150207

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

年代:1977

数据来源: WILEY

摘要:

AbstractFour to 48 hours after iv and sc administration of teratogenic doses of trypan blue to rats and mice the uterus was removed and rapidly frozen, after having been placed in a horizontal plane, and frozen sections were attached to tape and dried at a low temperature. By this procedure embryos and placental structures were present in the same sections and loss or redistribution of the dye was minimized. The dye was found in the yolk‐sac cavity and to be accumulated in the visceral (proximal) endoderm. It was also accumulated in the embryonic endoderm—forming the embryonic gut. This accumulation occurred after the administration of the trypan blue up to the time of closure of the vitelline duct, which occurs at 11 days postconception in rats and 9.5 days in mice. None was found when injection was made after this closure. No dye was detected in the ecto‐ and mesodermal layers. The period of embryonic uptake of trypan blue largely corresponds with the period of teratogenic sensitivity in these species as reported by o

ISSN:0040-3709    

DOI:10.1002/tera.1420150208

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

年代:1977

数据来源: WILEY

摘要:

AbstractHydralazine (1‐hydrazinophthalazine) produces skeletal defects resembling those observed in experimentally induced manganese deficiencies. Since glycosylation of collagen, a step preceding its secretion, requires Mn2+, the effect of hydralazine on collagen secretion and the formation of hydroxylysine glycosides was examined in explants of embryonic chicken long‐bone rudiments. Auto‐radiographic studies showed that hydralazine blocked collagen secretion. Secretion was restored by Fe2+alone or Fe2++ Mn2+but not by Mn2+alone, suggesting that a Fe2+‐requiring step was involved. Biochemical analyses showed that hydralazine inhibited the formation of hydroxylysine, a step requiring Fe2+, but it did not inhibit the formation of hydroxylysine‐glycosides by Mn2+‐requiring steps, although the reaction was inhibited in vitro. Hydralazine also failed to inhibit intracellular mucopolysaccharide synthesis which involves several Mn2+‐requiring enzymes. These observations suggest that the deleterious effects of hydralazine on bones are caused by its inhibition of hydroxylation steps in colla

ISSN:0040-3709    

DOI:10.1002/tera.1420150209

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

年代:1977

数据来源: WILEY

摘要:

AbstractAttention is drawn to the possibility that neural‐tube defects may sometimes be associated with the so‐called asplenia syndrome (Ivemark syndrome). This hypothesis is based upon a family in which one child had spina bifida and hydrocephaly and another had cardiovascular and other fissural anomalies, similar to Ivemark syndrome. The family history, moreover, revealed several cases of anencephaly and/or spina bifida, both on the paternal and maternal si

ISSN:0040-3709    

DOI:10.1002/tera.1420150210

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

年代:1977

数据来源: WILEY

摘要:

AbstractPregnant New Zealand White rabbits were treated on gestation day 12 with 19.2 mg/kg methotrexate (MTX), 750 mg/kg hydroxyurea (HU), or 1,500 mg/kg acetazolamide. Rabbits were killed either 2–32 hours posttreatment for histological analysis of embryos or at day 29 for gross and skeletal examination of fetuses. MTX produced cleft palate, hydrocephalus, and fore‐ and hindlimb reduction defects. Histological analysis revealed pyknosis and edema in mesenchymal tissues at four to eight hours following treatment. The apical ectodermal ridges (AER) of treated embryos permanently lost their characteristic pseudostratified organization. By 32 hours the limb buds had regained their normal appearance except for the AER. HU affected all fetuses with skull and facial anomalies as well as severe reduction deformities of all limbs. Histologically HU‐treated embryos had numerous, basophilic, intercellular granules (presumably cell debris) which appeared within two to four hours in the limb bud mesenchyme, neural tube, and dorsal root ganglion. The architecture of the AER was unchanged. Acetazolamide produced bilateral retarded ossification or possible aplasia of the first metacarpal and talus in nearly 80% of fetuses. Microscopic examination disclosed no apparent alterations in limb‐bud morphology. Methyl green‐pyronin Y staining called attention to green intracellular droplets within the endoderm of the trachea and bronchi at two hours posttreatment. It was concluded that the three drugs do not produce limb dysplasias by a common teratogenic

ISSN:0040-3709    

DOI:10.1002/tera.1420150211

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

年代:1977

数据来源: WILEY