Congenital anomalies最新文献_第10页

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

Variations in Palatal Rugae in Near Term Fetuses from Untreated Jcl:ICR Mice 未经治疗的Jcl:ICR小鼠早期胎儿腭纹的变化

Congenital anomalies Pub Date : 1994-03-01 DOI: 10.1111/j.1741-4520.1994.tb00273.x

M. Yasuda, R. Ohya, Toshio J. Sato

引用次数: 6

Analysis of Palatogenesis in the Mouse with Exencephaly Induced by Cadmium Chloride 氯化镉致畸形小鼠胚胎发育分析

Congenital anomalies Pub Date : 1994-03-01 DOI: 10.1111/j.1741-4520.1994.tb00271.x

Toshio J. Sato

{"title":"Analysis of Palatogenesis in the Mouse with Exencephaly Induced by Cadmium Chloride","authors":"Toshio J. Sato","doi":"10.1111/j.1741-4520.1994.tb00271.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.1994.tb00271.x","url":null,"abstract":"ABSTRACT It has been revealed that exencephalic mouse embryos were resistant to cleft palate induction when they were exposed to several teratogens known as cleft palate inducing agents. In the present study, palatogenesis in exencephalic mouse embryos, which were not exposed to cleft palate inducing teratogens, was observed. A single dose of 6 mg CdCl2/kg body weight was intraperitoneally injected into pregnant Jcl:ICR mice at day 7.5 of gestation (plug day = day 0). Embryos were dissected from uterus at day 13.5 to 15.5, and the secondary palate was observed with a dissecting microscope or a scanning electron microscope (SEM). Of live embryos, 71.5% had exencephaly. Palatal shelves of exencephalic embryos were elevated earlier than non‐exencephalic embryos, and there seem to be two modes of palatal fusion in exencephalic embryos. (1) “Parallel‐shape.” The anterior part of shelves were elevated at day 13.5. Distance between the opposite medial edges of both shelves decreased at the posterior part, and this closing proceeded to the anterior part, where the shelves began to fuse. (2) “V‐shape.” The posterior part of palatal shelves became closer at day 14.0 or day 14.25. The medial edge of both shelves began to fuse at this part, and this fusion proceeded anteriorly. The anterior parts of the shelves were elevated, and the medial edge of the anterior shelves was fused independently. It is suggested that these alterations of palatogenesis in exencephalic embryos are related to inhibitive mechanism(s) against cleft palate induction. Key words: palate, neural tube defects, skull, mice, cadmium","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"59 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1994-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78794378","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: 2

Lethal Multiple Pterygium Syndrome with Complete Intestinal Duplication 致死性多发性翼状胬肉综合征伴完全肠道复制

Congenital anomalies Pub Date : 1994-03-01 DOI: 10.1111/j.1741-4520.1994.tb00268.x

Eun Kyung Kim, J. Chi

引用次数: 1

Clinical Features and Operative Findings of Congenital Flexion Deformity of Multiple Digits 先天性多指屈曲畸形的临床特点及手术表现

Congenital anomalies Pub Date : 1993-12-01 DOI: 10.1111/j.1741-4520.1993.tb00539.x

T. Ogino, S. Ishii, H. Kato

引用次数: 1

A Thoracic Expansion Technique as a Life‐Saving Procedure for Jeune Syndrome (Asphyxiating Thoracic Dysplasia) 胸腔扩张术作为Jeune综合征(窒息性胸腔发育不良)的救命手术

Congenital anomalies Pub Date : 1993-12-01 DOI: 10.1111/j.1741-4520.1993.tb00540.x

R. Hashimoto, M. Esaki, T. Umeda, Tetsuyuki Sugitou, T. Hattori

引用次数: 1

Bronchial Branching Abnormalities and Emphysema‐like Changes in Mutant Rats Having Congenital Lobation Anomalies in the Lung 先天性肺叶异常突变大鼠的支气管分支异常和肺气肿样变化

Congenital anomalies Pub Date : 1993-12-01 DOI: 10.1111/j.1741-4520.1993.tb00538.x

H. Aoyama, S. Fujii, S. Teramoto

{"title":"Bronchial Branching Abnormalities and Emphysema‐like Changes in Mutant Rats Having Congenital Lobation Anomalies in the Lung","authors":"H. Aoyama, S. Fujii, S. Teramoto","doi":"10.1111/j.1741-4520.1993.tb00538.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.1993.tb00538.x","url":null,"abstract":"ABSTRACT The present study aimed at investigating in fpl/fpl mutant rats survived to adulthood 1) whether bronchial branching abnormalities were the primary defects of pulmonary lobation anomalies, and if this was the case, 2) whether these anomalies could lead to respiratory dysfunction. Examination of corrosion casts made from the malformed lungs of adult fpl/fpl rats revealed a variety of branching abnormalities in the right bronchial tree, such as ventral ramification of the middle lobar bronchus, abnormal curvature of the intermediate lobar bronchus, and positional abnormalities of the middle lobar bronchus and first segmental bronchus of the intermediate lobar bronchus, while reduction in the number of segmental bronchi was the only minor abnormality found in the left lung. These results conformed to our previous observations in which the main manifestation of the fpl mutation was restricted to the right lung lobes, and indicated that the primary defect of this malformation was bronchial branching abnormalities. In these rats, stenosis of the trachea, right and left principal bronchi, and some lobar and segmental bronchi also became evident by calipering their circumference. Histopathological examination of the lungs revealed abnormally expanded airspaces accompanied by destruction of alveolar walls and macrophage infiltration in aged fpl/fpl rats. These observations suggest that fpl/fpl rats suffer emphysema‐like respiratory dysfunction with advancing age from pulmonary lobation anomalies conforming to tracheal and bronchial malformations.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1993-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80234782","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: 2