Congenital anomalies最新文献_第6页

Neurulation in the human embryo revisited 重新审视人类胚胎的神经发育

Congenital anomalies Pub Date : 2000-06-01 DOI: 10.1111/j.1741-4520.2000.tb00912.x

T. Nakatsu, K. Shiota

引用次数: 2

The central nervous system in microcephalic primordial dwarfism: Is there a characteristic developmental brain pathology in Seckel or Seckel‐like syndrome? 小头型原始侏儒症的中枢神经系统:Seckel或Seckel样综合征是否存在特征性的发育性脑病理?

Congenital anomalies Pub Date : 2000-03-01 DOI: 10.1111/j.1741-4520.2000.tb00906.x

H. Schmitt, C. Sergi

{"title":"The central nervous system in microcephalic primordial dwarfism: Is there a characteristic developmental brain pathology in Seckel or Seckel‐like syndrome?","authors":"H. Schmitt, C. Sergi","doi":"10.1111/j.1741-4520.2000.tb00906.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2000.tb00906.x","url":null,"abstract":"ABSTRACT In spite of the description of more than 70 cases of Seckel syndrome (SS) or Seckel‐like primordial microcephalic dwarfism, reports about investigations into the central nervous system pathology in SS remaind infrequent Here we comment on the thorough neuropathological examination of the brain in a familial case of Seckel‐like microcephalic dwarfism. The male fetus of a 6 gravida, 3 para was aborted at 19 weeks of gestation after prenatal ultrasound examination with the demonstration of severe microcephaly and retarded intrauterine development The propositus had two healthy sisters. Of two aborted fetuses and one deceased sibling, the deceased had also exhibited a Seckel‐like phenotype as well as, in MRI scans, micrencephaly, callosal agenesis and pachygyria. Neuropathological examination of the brain in the propositus resulted in the demonstration of two main categories of changes: (1) defective telencephalic midline structures (arhinencephaly as well as callosal, septal, fornical, and hippocampal agenesis), and (2) impairment of migration (micrencephaly with lack of cortical neuroblasts in both the telencephalon and the rhombencephalon as well as heterotopias in the former). These findings corresponded with those described in the few neuropathological and neuroradiological literature reports, indicating that there appears to be in SS‐like primordial microcephalic dwarfism and a characteristic, although not specific brain pathology which might be adequately summarized by the designation mediodysgenetic micrencephaly. The genetic background of SS as a basis for the CNS maldevelopment is discussed.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"58 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2000-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82900751","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: 3

2000 JAPANESE TERATOLOGY SOCIETY MEMBERS 2000名日本畸形学会会员

Congenital anomalies Pub Date : 2000-03-01 DOI: 10.1111/j.1741-4520.2000.tb00909.x

Masataka, Baba, Kazuo, Brent, L., Fujimoto, Toyoaki, Fukuyama, Yukio, Furuya, Hiroshi, Ito, Tetsuo, Kameyama, Yoshiro, Kitagawa, Teruo, Marumo, Eiji, Miller, W. Robert, Murachi, Shunji, Okamoto, Naomasa, Toshiaki, Shepard, H. Thomas, Masakuni, Watanabe

{"title":"2000 JAPANESE TERATOLOGY SOCIETY MEMBERS","authors":"Masataka, Baba, Kazuo, Brent, L., Fujimoto, Toyoaki, Fukuyama, Yukio, Furuya, Hiroshi, Ito, Tetsuo, Kameyama, Yoshiro, Kitagawa, Teruo, Marumo, Eiji, Miller, W. Robert, Murachi, Shunji, Okamoto, Naomasa, Toshiaki, Shepard, H. Thomas, Masakuni, Watanabe","doi":"10.1111/j.1741-4520.2000.tb00909.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2000.tb00909.x","url":null,"abstract":"Arima, Masataka Baba, Kazuo Brent, Robert, L. Fujimoto, Toyoaki Fukuyama, Yukio Furuya, Hiroshi Ito, Tetsuo Kameyama, Yoshiro Kitagawa, Teruo Marumo, Eiji Miller, Robert W. Murachi, Shunji Okamoto, Naomasa Om, Toshiaki Shepard, Thomas H. Suzuki, Masakuni Watanabe, Gen-ichi Higashiyamato Ryoiku Center, 3-4410 Sakuragaoka, Higashiyamato, Tokyo 207-0022 Dept. of Pediatrics, Nihon University, Itabashi, Tokyo 173-0032 Alfred I. DuPont Insitute, 1600 Rock Road, PO Box 269, Wilmington, DE 19899, USA Kawasaki College of Allied Health Professions, 316 Matsushima, Kurashiki, Okayama 701-0194 Saitama Medical College, Moroyama, Iruma-gun, Saitama 354-045 1 Mishuku Hospital, Kamimeguro, Meguro, Tokyo 153-005 1 Kyoto City Rehabilitation Center for the Handicapped, Mibu, Kyoto 604-8854 Sugiyama Women's College, Chikusa, Nagoya 464-0802 Metropolitan Association of Preventive Medicine, Shinjuku, Tokyo 162-0842 Kitashinagawa Clinic, Kitashinagawa, Shinagawa, Tokyo 140-0001 Clinical Epidemiology Branch, National Cancer Institute, Suite 400, Bethesda, MD 20892, USA Japan Red Cross Aichi College, Nakamura-ku, Nagoya 453-0046 3-28-9 Kohinaka, Nishi-ku, Hiroshima 733-0813 Osaka City Rehabilitation Center, Hirano-ku, Osaka 547-0026 Dept of Pediatrcs, University of Washington, Seattle, WA 98195, USA Suzuki Hospital, Iwanuma 989-2481 Niigata Association of Labor Hygiene Medicine, Niigata 95 1-8133","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"40 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2000-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73606098","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

Joint International Symposium of Congenital Anomalies for The Korea‐Japan Basic Scientific Promotion 1–3 October 1999, Doosan Resort Hotel, Chum Chon, Kangwon‐do, Korea 1999年10月1日至3日，韩国江原道春村斗山度假酒店举行的“韩日基础科学促进先天性异常国际联合研讨会”

Congenital anomalies Pub Date : 2000-03-01 DOI: 10.1111/j.1741-4520.2000.tb00908.x

Y. Fukushima

引用次数: 0

Application of stereology to the central nervous system: estimation of numerical densities of neurons and synapses or neuron number 立体学在中枢神经系统中的应用:估计神经元和突触的数值密度或神经元数目

Congenital anomalies Pub Date : 2000-03-01 DOI: 10.1111/j.1741-4520.2000.tb00902.x

Y. Fukui, K. Bedi

引用次数: 2

Acrania: an autopsy case and review of the literature 阿克兰尼亚:一例尸检病例及文献回顾

Congenital anomalies Pub Date : 2000-03-01 DOI: 10.1111/j.1741-4520.2000.tb00907.x

Y. Shinmura, Y. Tsutsui, T. Nishiguchi, Takao Kobayashi

引用次数: 0

Reproductive and developmental toxicity of triphenyltin chloride in rats. 三苯基氯化锡对大鼠的生殖和发育毒性。

Congenital anomalies Pub Date : 2000-03-01 DOI: 10.1111/j.1741-4520.2000.tb00903.x

M. Ema

{"title":"Reproductive and developmental toxicity of triphenyltin chloride in rats.","authors":"M. Ema","doi":"10.1111/j.1741-4520.2000.tb00903.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2000.tb00903.x","url":null,"abstract":"ABSTRACT Reproductive and developmental toxicity of triphenyltin chloride (TPTCI) was evaluated in rats. Although no significant increase in the incidence of fetuses with malformations was observed following administration of TPTCI during organogenesis, a significant increase in the incidence of postimplantation embryonic loss was found. TPTCI during early pregnancy, especially on days 0–3 of pregnancy, caused implantation failure, i. e., preimplantation embryonic loss. The effects of TPTCI on the uterine function, as a cause of implantation failure, were determined using pseudopregnant rats. TPTCI was given on days 0–3 of pseudopregnancy and the decidual cell response was induced on day 4 of pseudopregnancy. Rats was sacrificed on day 9 of pseudopregnancy and the uterine weight served as an index of the uterine decidualization. A significantly lower weight of the uterus, which indicates the suppression of uterine decidualization, was found at the doses which induced implantation failure. These doses of TPTCI also caused a significant decrease in the progesterone levels, which indicates reduced ovarian function. These findings suggest that TPTCI exerts adverse effects on uterine decidualization correlated with the reduction in serum progesterone levels and these effects are responsible, at least in part, for the implantation failure induced by TPTCI.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"11 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2000-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"85868609","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: 13

Tissue uptake of EGF receptor antisense oligonucleotides in organ culture of fetal mouse palates and their effects on in vitro palatogenesis 胚胎小鼠腭器官培养中EGF受体反义寡核苷酸的组织摄取及其对体外腭发育的影响

Congenital anomalies Pub Date : 2000-03-01 DOI: 10.1111/j.1741-4520.2000.tb00905.x

H. Naitoh, C. Mori, N. Ohyama, Hidekazu Irie, N. Nakamura, Y. Nishimura, K. Shiota

{"title":"Tissue uptake of EGF receptor antisense oligonucleotides in organ culture of fetal mouse palates and their effects on in vitro palatogenesis","authors":"H. Naitoh, C. Mori, N. Ohyama, Hidekazu Irie, N. Nakamura, Y. Nishimura, K. Shiota","doi":"10.1111/j.1741-4520.2000.tb00905.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2000.tb00905.x","url":null,"abstract":"ABSTRACT To investigate the incorporation of oligonucleotides (ODNs) into the tissues of cultured fetal mouse palates and their effects on in vitro palatogenesis, we cultured day‐12.5 fetal mouse palates in a chemically defined serumless medium supplemented with either antisense or sense ODNs to epidermal growth factor receptor (EGF‐r). The EGF‐r ODNs were found to be incorporated into the palatal tissue and remained detectable for at least 72 hr. Immunohistochemical and immunoblot analyses revealed that the treatment with 5μM EGF‐r antisense ODN suppressed the production of EGF‐r protein. No pathological change was observed in the explanted palates when they were treated with 5 μM EGF‐r antisense or sense ODNs, but the treatment with 10 or 20 μM ODN caused pyknotic changes in the palatal epithelium, probably due to the ODN toxicity. The present results indicate that under optimal conditions, antisense ODNs to EGF‐r can be incorporated into fetal organs cultured in vitro and specifically inhibit the production of EGF‐r protein. Since the suppression of the production of EGF‐r protein did not prevent the palate fusion, EGF and/or EGF‐r alone may not play a critical role in palatogenesis, as suggested by previous studies. The antisense ODN technique could be of potential use for analyzing the roles of specific molecules in normal and abnormal morphogenesis.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"195 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2000-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79819548","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

Antisense attenuation of nestin accumulation causes neural tube deformation in rat embryo cultures 巢蛋白积累的反义衰减引起大鼠胚胎培养神经管变形

Congenital anomalies Pub Date : 2000-03-01 DOI: 10.1111/j.1741-4520.2000.tb00904.x

M. Matsuda

{"title":"Antisense attenuation of nestin accumulation causes neural tube deformation in rat embryo cultures","authors":"M. Matsuda","doi":"10.1111/j.1741-4520.2000.tb00904.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2000.tb00904.x","url":null,"abstract":"ABSTRACT The roles of nestin in neural tube development were studied using immunostaining and antisense experiments in rat embryos. Nestin was detected in the neural tube of embryos of day 10.5 of gestation (E10.5), while no nestin staining was observed in E9.5 embryos in which the neural plate comprised 3 to 4 layers of neuroepithelial cells. As embryos developed, the neural tube became comprised of multiple cell layers and staining was observed in filamentous structures spanning from the ventricular surface to the pial surface of the neural tube. Nestin accumulation was suppressed in the neural tube of embryos treated with nestin antisense oligodeoxynucleotide (ODN). The treated embryos showed two types of neural tube deformation. One type was a thin neural tube which had 3 to 4 layers of neuroepithelial cells and the other was a local distribution of neuroepithelial cells near the basement membrane. While neuroepithelial cells in the neural tube were fewer in embryos treated with nestin antisense ODN than in controls, the percentage of Islet‐1‐positive neurons relative to the neuroepithelial cells was not different between the treated and control embryos. These results suggested that nestin plays roles in the proliferation of neural tube cells and in the formation and the maintenance of multiple cell layers in the neural tube but not in suppression of development of Islet‐1‐positive neurons.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"25 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2000-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82502841","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

P-06 Effects of Bisphenol A on Cultured Rat Embryos. 双酚A对培养大鼠胚胎的影响。

Congenital anomalies Pub Date : 1999-09-30 DOI: 10.1016/s0021-5198(19)48580-6

M. Akita, A. Yokoyama, S. Shimizu, H. Shikuma, Y. Kuroda

引用次数: 0