Pub Date : 2000-06-01DOI: 10.1111/j.1741-4520.2000.tb00912.x
T. Nakatsu, K. Shiota
ABSTRACT It used to be widely accepted that neural tube closure in the human initiates at the level of the future neck and proceeds both cranially and caudally like zip fastener closing. This continuous closure model was recently challenged, and observation of human embryos at the neurulation stage revealed that the closure of the human neural tube initiates at multiple sites. Multi‐site closure of the neural tube has been observed in many other animal species, but the initiation sites and the process of neural tube closure are variable among species. Therefore we should be careful when extrapolating the data of normal and abnormal neurulation in laboratory animals to the human. Recent studies in mouse genetics and developmental biology have shown that neural tube defects are quite heterogeneous both etiologically and pathogenetically. Gene mutations responsible for human neural tube defects are largely unknown, but molecular studies of human cases of neural tube defects and their comparison with the mouse genome data should provide a molecular basis for human neural tube defects.
{"title":"Neurulation in the human embryo revisited","authors":"T. Nakatsu, K. Shiota","doi":"10.1111/j.1741-4520.2000.tb00912.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2000.tb00912.x","url":null,"abstract":"ABSTRACT It used to be widely accepted that neural tube closure in the human initiates at the level of the future neck and proceeds both cranially and caudally like zip fastener closing. This continuous closure model was recently challenged, and observation of human embryos at the neurulation stage revealed that the closure of the human neural tube initiates at multiple sites. Multi‐site closure of the neural tube has been observed in many other animal species, but the initiation sites and the process of neural tube closure are variable among species. Therefore we should be careful when extrapolating the data of normal and abnormal neurulation in laboratory animals to the human. Recent studies in mouse genetics and developmental biology have shown that neural tube defects are quite heterogeneous both etiologically and pathogenetically. Gene mutations responsible for human neural tube defects are largely unknown, but molecular studies of human cases of neural tube defects and their comparison with the mouse genome data should provide a molecular basis for human neural tube defects.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"213 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2000-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79003817","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}
Pub Date : 2000-03-01DOI: 10.1111/j.1741-4520.2000.tb00906.x
H. Schmitt, C. Sergi
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.
{"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}
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
{"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}
Pub Date : 2000-03-01DOI: 10.1111/j.1741-4520.2000.tb00908.x
Y. Fukushima
Multi-disciplinary Clinical Evaluation of Disabilities in Hunter Syndrome Patients Byung-Eul Lee, Yang Sun Cho, Hyo-Yeol Kim, Sung-Hwa Hong, Soo-Jin Hwang, Hye-Kyung Yoon, Son-A Chang, Hyeon-Sook Kim, Jung-Sim Kim, Kye-Won Jun, Seng-Mi Song, and Dong-Kyu Jin Departments of Otorhinolaryngology-Head and Neck Surgery, Radiology and Physical Medicine and Rehabilitation, and Pediatrics, Sungkyunkwan University School of Medicine, Samsung Medical Center, Seoul, Korea
Hunter综合征患者残疾的多学科临床评价:Byung-Eul Lee, Yang Sun Cho, Hyo-Yeol Kim, Sung-Hwa Hong, Soo-Jin Hwang, Hye-Kyung Yoon, Son-A Chang, Hyeon-Sook Kim, Jung-Sim Kim, Kye-Won Jun, sung - mi Song, Dong-Kyu Jin，韩国首尔成均馆大学医学院，三星医疗中心，耳鼻喉头颈外科，放射和物理医学与康复，儿科
{"title":"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","authors":"Y. Fukushima","doi":"10.1111/j.1741-4520.2000.tb00908.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2000.tb00908.x","url":null,"abstract":"Multi-disciplinary Clinical Evaluation of Disabilities in Hunter Syndrome Patients Byung-Eul Lee, Yang Sun Cho, Hyo-Yeol Kim, Sung-Hwa Hong, Soo-Jin Hwang, Hye-Kyung Yoon, Son-A Chang, Hyeon-Sook Kim, Jung-Sim Kim, Kye-Won Jun, Seng-Mi Song, and Dong-Kyu Jin Departments of Otorhinolaryngology-Head and Neck Surgery, Radiology and Physical Medicine and Rehabilitation, and Pediatrics, Sungkyunkwan University School of Medicine, Samsung Medical Center, Seoul, Korea","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2000-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84209894","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}
Pub Date : 2000-03-01DOI: 10.1111/j.1741-4520.2000.tb00902.x
Y. Fukui, K. Bedi
ABSTRACT Two unbiased stereological techniques, the disector and the fractionator have been introduced. Synapse‐to‐neuron ratios were calculated from estimates of the numerical densities of neurons and synapses in the rat cerebral cortex. These estimates were made using the disector method at the light and electron microscopical levels. Neuronal nuclei were as the counting unit for neurons and paramembranous densities for synapses. The fractionator method was employed to estimate the total number of cerebellar Purkinje cells in rats. We employed a five‐stage scheme to count the nucleoli of Purkinje cells. The cerebellum was first divided into uniform random slices, which were cut, in turn, into strips. The chosen strips were cut into pieces. A systematic selection of tissues was taken, and embedded together in the same mold. Subsequently the sections sampled were examined with a light microscope. All Purkinje cell nucleoli visible in these sections were counted.
{"title":"Application of stereology to the central nervous system: estimation of numerical densities of neurons and synapses or neuron number","authors":"Y. Fukui, K. Bedi","doi":"10.1111/j.1741-4520.2000.tb00902.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2000.tb00902.x","url":null,"abstract":"ABSTRACT Two unbiased stereological techniques, the disector and the fractionator have been introduced. Synapse‐to‐neuron ratios were calculated from estimates of the numerical densities of neurons and synapses in the rat cerebral cortex. These estimates were made using the disector method at the light and electron microscopical levels. Neuronal nuclei were as the counting unit for neurons and paramembranous densities for synapses. The fractionator method was employed to estimate the total number of cerebellar Purkinje cells in rats. We employed a five‐stage scheme to count the nucleoli of Purkinje cells. The cerebellum was first divided into uniform random slices, which were cut, in turn, into strips. The chosen strips were cut into pieces. A systematic selection of tissues was taken, and embedded together in the same mold. Subsequently the sections sampled were examined with a light microscope. All Purkinje cell nucleoli visible in these sections were counted.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"13 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2000-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79174706","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}
Pub Date : 2000-03-01DOI: 10.1111/j.1741-4520.2000.tb00907.x
Y. Shinmura, Y. Tsutsui, T. Nishiguchi, Takao Kobayashi
ABSTRACT We report an autopsy case of acrania with a review of the literature. A 31‐year‐old woman was admitted in poor genaral condition and diagnosed as pregnant at the 26th week of gestation. The fetus was suspected to be anencephalic or hydrocephalic by ultrasonography. She delivered a stillbirth male baby at the 28th week of gestation. Autopsy showed the cranium lacked the cranial vault The scalp directly covered the hydrocephalic brain without calvaria. No cerebellum was found macroscopically. On histological examination, the thinned cerebral layer was composed of white matter‐like brain tissue with glial and ependymal cells. In the cerebral layer near the base of the skull, a few NSE‐positive neurons among many GFAP‐positive glial cells and oligodendrocyte‐like cells were observed. The choroid plexuses were observed inside the ependymal layers. The brain stem and the spinal cord were normally preserved with clusters of NSE‐positive neurons. Agnethia and horseshoe kidney were combined as malformations other than the brain. We reviewed 42 cases of acrania from the literature.
{"title":"Acrania: an autopsy case and review of the literature","authors":"Y. Shinmura, Y. Tsutsui, T. Nishiguchi, Takao Kobayashi","doi":"10.1111/j.1741-4520.2000.tb00907.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2000.tb00907.x","url":null,"abstract":"ABSTRACT We report an autopsy case of acrania with a review of the literature. A 31‐year‐old woman was admitted in poor genaral condition and diagnosed as pregnant at the 26th week of gestation. The fetus was suspected to be anencephalic or hydrocephalic by ultrasonography. She delivered a stillbirth male baby at the 28th week of gestation. Autopsy showed the cranium lacked the cranial vault The scalp directly covered the hydrocephalic brain without calvaria. No cerebellum was found macroscopically. On histological examination, the thinned cerebral layer was composed of white matter‐like brain tissue with glial and ependymal cells. In the cerebral layer near the base of the skull, a few NSE‐positive neurons among many GFAP‐positive glial cells and oligodendrocyte‐like cells were observed. The choroid plexuses were observed inside the ependymal layers. The brain stem and the spinal cord were normally preserved with clusters of NSE‐positive neurons. Agnethia and horseshoe kidney were combined as malformations other than the brain. We reviewed 42 cases of acrania from the literature.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"60 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2000-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"78140834","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}
Pub Date : 2000-03-01DOI: 10.1111/j.1741-4520.2000.tb00903.x
M. Ema
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.
{"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}
Pub Date : 2000-03-01DOI: 10.1111/j.1741-4520.2000.tb00905.x
H. Naitoh, C. Mori, N. Ohyama, Hidekazu Irie, N. Nakamura, Y. Nishimura, K. Shiota
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.
{"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}
Pub Date : 2000-03-01DOI: 10.1111/j.1741-4520.2000.tb00904.x
M. Matsuda
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.
采用免疫染色和反义实验研究了巢素在大鼠胚胎神经管发育中的作用。在妊娠10.5天的胚胎(E10.5)的神经管中检测到Nestin，而在妊娠9.5天的胚胎(神经板由3 ~ 4层神经上皮细胞组成)中未观察到Nestin染色。随着胚胎的发育，神经管由多层细胞组成，在从脑室表面到脑脊液表面的丝状结构中可见染色。巢蛋白反义寡脱氧核苷酸(Nestin anti - sense oligodeoxynucleotide, ODN)可抑制胚胎神经管内巢蛋白的积累。处理后的胚胎出现两种类型的神经管变形。一种是神经上皮细胞分布在3 ~ 4层的薄神经管，另一种是神经上皮细胞局部分布在基底膜附近。虽然在巢蛋白反义ODN处理的胚胎中，神经管中的神经上皮细胞比对照组少，但相对于神经上皮细胞，胰岛1阳性神经元的百分比在处理胚胎和对照胚胎之间没有差异。这些结果表明，巢素在神经管细胞的增殖以及神经管中多细胞层的形成和维持中发挥作用，但不抑制胰岛1阳性神经元的发育。
{"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}
Pub Date : 1999-09-30DOI: 10.1016/s0021-5198(19)48580-6
M. Akita, A. Yokoyama, S. Shimizu, H. Shikuma, Y. Kuroda
{"title":"P-06 Effects of Bisphenol A on Cultured Rat Embryos.","authors":"M. Akita, A. Yokoyama, S. Shimizu, H. Shikuma, Y. Kuroda","doi":"10.1016/s0021-5198(19)48580-6","DOIUrl":"https://doi.org/10.1016/s0021-5198(19)48580-6","url":null,"abstract":"","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"51 1","pages":"163"},"PeriodicalIF":0.0,"publicationDate":"1999-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75277826","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}
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