摘要:

AbstractThe objective of this investigation was to find out the histopathological changes of the placenta and to correlate them with fetal malformations and growth retardation in experimental diabetes. Diabetes was induced in Wistar rats at different stages of gestation by intraperitoneal injection of streptozotocin (STZ). The controls were either buffer treated or injected with STZ followed by 2–6 IU insulin until term. All fetuses and placentae were collected on day 20 of gestation. Fetuses of diabetic rats were significantly growth retarded. Maxillary hypoplasia, edema, gastroschisis, exencephaly and septal defects of the heart were the major malformations. Most of the experimental placentae weighed heavier relative to their body mass. Toluidine blue stained sections of the placentae revealed severe histological abnormalities. The unusually large sized placentae had extensive cystic degeneration, often with an increased population of leucocytes. Giant cells were very numerous. Perivascular fibrosis, persistence of fetal mesenchyme, edema, infarcts and vacuolisation were observed in the labyrinths. In the small placentae, the glycogen cells were fewer and the glycogen in them remained unutilized. Reduction of labyrinthine zone, hypovascularity, constriction of vessels, perivascular edema and platelet aggregation characterized these placentae. The placentae of externally malformed fetuses showed cystic degeneration; their labyrinths contained constricted and less extensive vascular network. Phagocytic giant cells, polymorphs and platelet aggregation were also marked. Placentae of externally normal looking fetuses also presented cystic degeneration, reduction in fetal vasculature, dilated maternal sinusoids and giant cell proliferation. Insulin treatment resulted in the preservation of most of the normal histology of the placenta which correlated well with the reduced fetal malformation

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1988.tb00571.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

AbstractA case of 4p trisomy syndrome originated from familial rep (4; 14) is reported. The rearrangement was characterized by a breakpoint at the centromeric region of chromosome 14 and by a reciprocal translocation between chromosomes 4 and 14. The translocation was observed in three generations. As a result of CBG banding analysis in prometaphase cells, the breakpoint of der(14) was considered to be located at 14p11.1, and a part of 14p11.1 was translocated to chromosome 4p. It was unknown whether a part of the centromere was involved in it or not.

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1988.tb00572.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

AbstractDespite the strong activity to induce wavy ribs in rat fetuses, furosemide does not seem to have such activity in the rabbit. Since wavy ribs are known to be repairable in the rat during the early postnatal period, there is a possibility that the anomaly once produced in rabbit fetuses disappeared before the examination at term because of their longer duration of gestation. In order to test this possibility, the authors administered furosemide to pregnant rabbits and examined fetuses shortly after the treatment period for the presence of wavy ribs. Furosemide even at doses which were apparently toxic to maternal animals failed to produce the anomaly. Based on these results and in view of the absence of its occurrence in the literature, it may be concluded that there is species specificity in the induction of wavy ribs and this anomaly does not occur in rabbit fetuses. The temporal difference between the onset of ossification and that of increased myometrial contractions may probably be involved in this species specificity.

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1988.tb00573.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

AbstractSome 137 patients with thalidomide embryopathy have been registered. Of them, 65 were male and 72 female. The age of patients who had a medical examination from 1976 to 1983, ranged from 7 to 22 years. The mean age was 17.0 ± 2.3 (mean ± SD) years. The number of hearing impairments were 35 (25.6%), limb defects were 55 (40.1%) and combined defects were 47 (34.3%). In order to determine the mutual relationships of 34 abnormal symptoms, the correlation coefficient was calculated, and cluster analysis was carried out by utilizing the result. There was a strong inverse correlation between deformities and hearing impairments. The 34 symptoms were divided into three groups. In the first group 11 symptoms were included, but there was little mutual relationship. Fifteen symptoms belonged to the second group, which evidenced strong mutual relationships. The 8 symptoms belonging to the third group were central to all of the symptom

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1988.tb00574.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

AbstractNeurochemical aspect of mental retardation is described, with special reference to phenylketonuria (PKU) as a cause of the inhibition of brain development. Biochemical and behavioral findings are outlined in S few animal models of PKU, including that of “maternal PKU” in which genetically normal offspring of rats with experimental PKU show significantly lowered discrimination learning ability. Possible roles of disordered amino acid metabolism and defective myelination in the inhibited brain development are briefly discus

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1988.tb00575.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

AbstractA prominence on the preaxial border at the proximal end of the forelimb was found to appear in a limited period of limb development in mouse embryos. This prominence is observable around day 11 (vaginal plug = day 0). When compared with the number of tail somites, this prominence first appears in embryos with 10–12 tail somites, becomes prominent in embryos with 14–18 tail somites, and disappears in embryos with 20–22 tail somites. This prominence may be utilized as a simple morphological indicator for staging developing mouse for

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1988.tb00576.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1988.tb00577.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1988.tb00578.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

AbstractSlc:Wistar‐KY rats were administered orally with 62.5, 125, 187.5 or 250 mg/kg aspirin suspended with 0.5 % CMC‐Na on days 9–11 of gestation (plug += day 0). Suppression of maternal weight gain and food consumption during treatment was observed at and over 187.5 mg/kg. At term, the fetal mortality increased at and over 187.5 mg/kg and the fetal weight was lowered at and over 125 mg/kg. Among 15 live fetuses at 250 mg/kg, 4 had external malformations. In the skeletal examination (double staining), skeletal anomalies increased at and over 187.5 mg/kg. The skeletal variations such as vertebral anomalies, fused costal cartilages and increased presacral vertebrae were often encountered and delayed ossification was also found at and over 125 mg/kg. The internal anomalies tended to increase at and over 187.5 mg/kg. The live birth rate was significantly lower at 187.5 mg/kg than that in controls, and all pups, except for 3 from a dam, died before weaning. At 125 mg/kg, the pivoting locomotion on day 7 post partum was poorer as compared with controls. The physical and functional development at 62.5 mg/kg was not changed. There were no significant effects on male offspring in the open‐field, rotarod, under‐water T‐maze and avoidance learning tests. However, in the Biel T‐maze test (9–10 weeks of age), the aspirin‐treated groups showed more errors and the increased elapsed time on the 1st trial day than controls. These results indicate that aspirin may induce a slight learning defect on rat offspring even at the non‐teratogenic dose and the Biel T‐maze test is more sensitive than any other learning test

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1988.tb00588.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY

摘要:

AbstractNation‐wide data in Japan between 1969–1982 on 3,650 cases of fetal death and 2,397 cases of postnatal death caused by congenital hydrocephalus were analyzed. The prevalence rate of congenital hydrocephalus decreased yearly. This reduction is attributed to prenatal detection and selective abortion among fetal deaths, and surgical correction of hydrocephalus postnatally. The prevalence rate per 1,000 births was 0.22 in urban areas and 0.25 in rural areas between 1969–1982, and the difference was significant. The prevalence rate was slightly higher in the southwest part of Japan than in the northeast. Social class variation in the prevalence rate was pr

ISSN:0914-3505    

DOI:10.1111/j.1741-4520.1988.tb00589.x

出版商:Blackwell Publishing Ltd    

年代:1988

数据来源: WILEY