Congenital anomalies最新文献_第9页

Sex Differences in the Rat Brain: A Procedure for Estimating Developmental Toxicity 大鼠脑中的性别差异:一种评估发育毒性的方法

Congenital anomalies Pub Date : 1996-03-01 DOI: 10.1111/j.1741-4520.1996.tb00319.x

H. Sumida, T. Moriya, J. Handa, T. Yamashita, Kouta Nakamori, M. Nishizuka, Y. Arai

{"title":"Sex Differences in the Rat Brain: A Procedure for Estimating Developmental Toxicity","authors":"H. Sumida, T. Moriya, J. Handa, T. Yamashita, Kouta Nakamori, M. Nishizuka, Y. Arai","doi":"10.1111/j.1741-4520.1996.tb00319.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.1996.tb00319.x","url":null,"abstract":"The sexually dimorphic nucleus of the preoptic area (SDN‐POA) and the anteroventral periventricular nucleus of the preoptic area (AVPvN‐POA) are sexually dimorphic regions in the rat brain. These regions are sensitive to reproductive function‐related drugs, and thus applied for aromatase inhibitor evaluation in the present study. Effects of NKS01 (an aromatase inhibitor) and tamoxifen on the SDN‐POA and AVPvN‐POA were examined. Five mg of NKS01 or its vehicle was injected to SD male and female rats from days 1 to 14 (the day of birth = day 0). Other 10 males and 10 females received a single injection of 100 μg tamoxifen on day 1. Rats in each group were sacrificed at day 30 or 60. The SDN‐POA was examined at days 30 and 60, and the AVPvN‐POA at day 60. When NKS01 was given to male rats for the first 14 days of life, a significant reduction of SDN‐POA size was observed on day 60. When tamoxifen was given, SDN‐POA reduction in size was also observed at days 30 and 60 in male rats. As for the AVPvN‐POA, tamoxifen markedly reduced volume in female rats, resulting in polycystic ovaries at day 60. This may be due to an estrogenic property of tamoxifen. On the other hand, NKS01 was not significantly effective in the AVPvN‐POA, although the volume of the nucleus in NKS01 males was inclined to increase. From these results, as well as the SDN‐POA, the AVPvN‐POA may be useful to evaluate the side effect of reproductive function‐related drug.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"166 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1996-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81897008","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Personal Remembrances of Dr. Karl‐Heinz Degenhardt (1920–1994) 卡尔-海因茨·德根哈特博士个人回忆(1920-1994)

Congenital anomalies Pub Date : 1994-09-01 DOI: 10.1111/J.1741-4520.1994.TB00598.X

H. Yamamura

引用次数: 0

Molecular Genetic Techniques for Prenatal Diagnosis * 分子遗传学技术用于产前诊断*

Congenital anomalies Pub Date : 1994-09-01 DOI: 10.1111/j.1741-4520.1994.tb00599.x

K. Suzumori, M. Tanemura, R. Adachi

引用次数: 1

Symbrachydactyly of the Foot Associated with Absence of the Contralateral Pectoralis Major Muscle 对侧胸大肌缺失伴足短指联合畸形

Congenital anomalies Pub Date : 1994-09-01 DOI: 10.1111/j.1741-4520.1994.tb00600.x

T. Uchida, T. Kojima, M. Konno

引用次数: 1

Susceptibility of Day‐12.5 and Day‐13.5 Fetal Mouse Palates Cultured in Vitro to 5‐Fluorouracil and Hydroxyurea 体外培养第12.5天和第13.5天胎鼠腭对5 -氟尿嘧啶和羟基脲的敏感性

Congenital anomalies Pub Date : 1994-09-01 DOI: 10.1111/j.1741-4520.1994.tb00601.x

T. Kosazuma, S. Kawauchi, M. Chou, K. Shiota

{"title":"Susceptibility of Day‐12.5 and Day‐13.5 Fetal Mouse Palates Cultured in Vitro to 5‐Fluorouracil and Hydroxyurea","authors":"T. Kosazuma, S. Kawauchi, M. Chou, K. Shiota","doi":"10.1111/j.1741-4520.1994.tb00601.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.1994.tb00601.x","url":null,"abstract":"Abstract The maxillary regions of day‐12.5 and day‐13.5 ICR mouse fetuses were cultivated in a chemically‐defined serumless medium by a suspension culture technique to examine the toxic effects of 5‐fluorouracil (5‐FU) and hydroxyurea (HU) on cultured palates and to compare the sensitivity of fetal mouse palates at different stages of development. The palates of day‐12.5 and day‐13.5 fetal mice were explanted and exposed in vitro for 72 hr to 0.1–50 μg 5‐FU/ml or to 5–76 μg HU/ml. 5‐FU inhibited the growth and fusion of day‐12.5 palatal shelves in vitro dependently on its concentrations. Day‐13.5 palates were significantly less sensitive to 5‐FU than day‐12.5 palates, and the minimal toxic concentrations (MTCs) of 5‐FU were 0.1 and 10 μg/ml for day‐12.5 and day‐13.5 fetal palates, respectively. HU inhibited the in vitro growth and fusion of day‐12.5 fetal palatal shelves in a concentration dependent manner, but only slightly suppressed the growth of day‐13.5 fetal palates. The MTCs of HU were 19 and 76 μg/ml for day‐12.5 and day‐13.5 fetal palates, respectively. Therefore, day‐12.5 fetal mouse palates (at stage‐1 or earlier stages of palatogenesis) seemed significantly more susceptible to these teratogenic chemicals than day‐13.5 fetal palates (at stages 2–3 of palatogenesis). The palates of day‐12.5 ICR fetal mice may be more suitable than day‐13.5 palates for in vitro teratogen screening and for the study of mechanisms of normal and abnormal palatogenesis.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"40 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1994-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90782195","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 8

Program 程序

Congenital anomalies Pub Date : 1994-09-01 DOI: 10.1111/j.1741-4520.1994.tb00602.x

T. Kurashige

引用次数: 0

Neurochemical Correlates of Learning Impairment in Microen‐cephalic Rats Induced by Methylazoxymethanol Acetate * 甲基甲氧甲醇醋酸酯诱导的小头畸形大鼠学习障碍的神经化学相关因素*

Congenital anomalies Pub Date : 1994-03-01 DOI: 10.1111/j.1741-4520.1994.tb00267.x

M. Tamaru

{"title":"Neurochemical Correlates of Learning Impairment in Microen‐cephalic Rats Induced by Methylazoxymethanol Acetate *","authors":"M. Tamaru","doi":"10.1111/j.1741-4520.1994.tb00267.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.1994.tb00267.x","url":null,"abstract":"ABSTRACTNewborn infants with histogenetic brain malformations can be long‐lived with mental retardation, which is considered a major problem in social medicine. Among these infants with mental retardation, many cases are accompanied by microencephaly. Experimentally induced microencephaly in rats presents a useful model for understanding human cerebral disorders. We have studied how neurochemical changes in the brains of microencephalic rats induced by prenatal treatment with methylazoxymethanol acetate (MAM) can affect their learning abilities. We reported that densities of monoaminergic transmitters in the atrophic cerebral hemisphere (CH; consisting of cerebral cortex and hippocampus) of MAM rats was markedly elevated, but that their total quantity per CH unchanged. As for the ability of operant discrimination learning, MAM rats could discriminate tasks. However, excitatory amino acid receptors, in which N‐methyl‐D‐aspartate (NMDA) is well known to be involved in spatial memory, showed decreased total binding in the CH of MAM‐treated rats. Spatial recognition ability evaluated using an 8‐armed radial maze task was impaired. These results suggest that the condensation of monoaminergic terminals in the atrophic CH of MAM rats may compensate for disability in discrimination learning, but the significant reduction of NMDA receptors may impair spatial memory in MAM rats.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"10 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1994-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75496488","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Developmental Abnormalities Due to Exposure of Mouse Paternal Germ Cells, Preimplantation Embryos, and Organogenic Embryos to Acrylamide 丙烯酰胺暴露于小鼠父系生殖细胞、着床前胚胎和器官胚胎的发育异常

Congenital anomalies Pub Date : 1994-03-01 DOI: 10.1111/j.1741-4520.1994.tb00269.x

T. Nagao

{"title":"Developmental Abnormalities Due to Exposure of Mouse Paternal Germ Cells, Preimplantation Embryos, and Organogenic Embryos to Acrylamide","authors":"T. Nagao","doi":"10.1111/j.1741-4520.1994.tb00269.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.1994.tb00269.x","url":null,"abstract":"ABSTRACT The developmental toxicity of acrylamide was investigated after paternal germ cells and preimplantation and organogenic embryos were exposed to the agent. In the first experiment, ICR male mice were injected intraperitoneally with single doses of 62.5 or 125 mg/kg acrylamide or daily doses of 50 mg/kg for 5 days. They were mated with untreated virgin ICR female mice on days 1–21 and 64–80 after the last injection. The sperms involved in fertilization during these two periods were postmeiotic germ cells and spermatogonial stem cells, respectively, at the time of acrylamide treatment. The uterine contents were examined on day 18 of gestation for dominant lethal effects, and the fetuses were examined for external malformation. Acrylamide exposure during the postmeiotic cell or spermatogonial stem cell stage caused no significant increases in the incidence of abnormal fetuses. Dominant lethals, however, were clearly induced when the germ cells had been postmeiotic at the time of acrylamide exposure. In the second experiment, ICR mice were injected intraperitoneally with a single dose of 125 mg/kg acrylamide on day 0, 1, 2, or 3 of gestation. The uterine contents were examined on day 18 of gestation. Acrylamide treatment on day 0 of gestation caused a significant increase in the incidence of malformed fetuses, while treatment on day 1, 2, or 3 of gestation failed to cause an increase in malformation. Polydactyly was the most common type of abnormality. In the third experiment, pregnant mice were treated with three daily doses of 50 or 100 mg/kg acrylamide on days 6–8 or 9–11 of gestation, respectively. There was no significant difference between the incidence of malformed fetuses in the control and acrylamide‐treated groups. These experiments demonstrate the vulnerability of preimplantation embryos to the toxic effects of acrylamide, while paternal germ cells and the organogenic embryos are resistant to the induction of fetal malformations.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"43 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1994-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91356213","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 5

Transplacentally‐Administered Enalapril Inhibits the Spontaneous Constriction of the Ductus Arteriosus in the Newborn Rat 经胎盘给药依那普利抑制新生大鼠动脉导管自发收缩

Congenital anomalies Pub Date : 1994-03-01 DOI: 10.1111/j.1741-4520.1994.tb00270.x

T. Takizawa, K. Arishima, Masako Yamamoto, H. Somiya, K. Shiota

引用次数: 4

Induction of Congenital Malformations in Mice by Paternal Methylnitrosourea Treatment 父代甲基亚硝基脲诱导小鼠先天性畸形

Congenital anomalies Pub Date : 1994-03-01 DOI: 10.1111/j.1741-4520.1994.tb00272.x

Azusa Wada, T. Nagao

{"title":"Induction of Congenital Malformations in Mice by Paternal Methylnitrosourea Treatment","authors":"Azusa Wada, T. Nagao","doi":"10.1111/j.1741-4520.1994.tb00272.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.1994.tb00272.x","url":null,"abstract":"ABSTRACTA single dose of methylnitrosourea (MNU, 25–100 mg/kg) was injected intraperitoneally into ICR strain male mice. The males were mated to untreated females of the same strain on days 1–21 and 64–80 after the treatment. On day 18 of pregnancy, the fetuses were examined for external and skeletal abnormalities. MNU treatment of paternal germ cells caused significant increases in the incidence of abnormal fetuses over the control level. The induction rate per live fetus per unit dose in mg/kg by treating spermatogonial stem cells was estimated to be 3.0 × 10−4, which is quite similar to the rate previously estimated for the same endpoint at the same germ cell stage with the fractionated doses of MNU (daily doses at 5–25 mg/kg for 5 days). Cleft palate and dwarfism were the most frequent external abnormalities in the MNU‐treated and the control series. Malformed ribs was the most frequent skeletal abnormality in the treated series. It was concluded that congenital malformations induced after treating male mice with a single dose of MNU were quantitatively and qualitatively similar to those induced after treating male mice with the fractionated doses of MNU.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"39 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1994-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88798346","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 4