Pub Date : 2004-12-01DOI: 10.1111/j.1741-4520.2004.00044.x
E. Hopfinger, R. Verzicco, S. Zaleski
{"title":"Program","authors":"E. Hopfinger, R. Verzicco, S. Zaleski","doi":"10.1111/j.1741-4520.2004.00044.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2004.00044.x","url":null,"abstract":"","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"46 2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2004-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"77483244","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 : 2002-06-01DOI: 10.1111/j.1741-4520.2002.tb00858.x
T. Iguchi, Hajime Watanabe, Y. Katsu, Takeshi Mizutani, S. Miyagawa, A. Suzuki, S. Kohno, K. Sone, Hideo Kato
ABSTRACT Antenatal sex‐hormone exposure induces lesions in mouse reproductive organs, which are similar to those in humans exposed in utero to a synthetic estrogen, diethylstilbestrol. The developing organisms including rodents, fish and amphibians are particularly sensitive to exposure to estrogenic chemicals during a critical window. Exposure to estrogens during the critical period induces long‐term changes in reproductive as well as non‐reproductive organs, including persistent molecular alterations. The antenatal mouse model can be utilized as an indicator of possible long‐term consequences of exposure to exogenous estrogenic compounds including possible environmental endocrine disrupters. Many chemicals released into the environment potentially disrupt the endocrine system in wildlife and humans, some of which exhibit estrogenic activity by binding to the estrogen receptors. Estrogen responsive genes, therefore, need to be identified to understand the molecular basis of estrogenic actions. In order to understand molecular mechanisms of estrogenic chemicals on developing organisms, we are identifying estrogen responsive genes using cDNA microarray, quantitative RT‐PCR, and differential display methods, and genes related to the estrogen‐independent vaginal changes in mice induced by estrogens during the critical window. In this review, discussion of our own findings related to endocrine distuptor issue will be provided.
{"title":"Developmental toxicity of estrogenic chemicals on rodents and other species","authors":"T. Iguchi, Hajime Watanabe, Y. Katsu, Takeshi Mizutani, S. Miyagawa, A. Suzuki, S. Kohno, K. Sone, Hideo Kato","doi":"10.1111/j.1741-4520.2002.tb00858.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2002.tb00858.x","url":null,"abstract":"ABSTRACT Antenatal sex‐hormone exposure induces lesions in mouse reproductive organs, which are similar to those in humans exposed in utero to a synthetic estrogen, diethylstilbestrol. The developing organisms including rodents, fish and amphibians are particularly sensitive to exposure to estrogenic chemicals during a critical window. Exposure to estrogens during the critical period induces long‐term changes in reproductive as well as non‐reproductive organs, including persistent molecular alterations. The antenatal mouse model can be utilized as an indicator of possible long‐term consequences of exposure to exogenous estrogenic compounds including possible environmental endocrine disrupters. Many chemicals released into the environment potentially disrupt the endocrine system in wildlife and humans, some of which exhibit estrogenic activity by binding to the estrogen receptors. Estrogen responsive genes, therefore, need to be identified to understand the molecular basis of estrogenic actions. In order to understand molecular mechanisms of estrogenic chemicals on developing organisms, we are identifying estrogen responsive genes using cDNA microarray, quantitative RT‐PCR, and differential display methods, and genes related to the estrogen‐independent vaginal changes in mice induced by estrogens during the critical window. In this review, discussion of our own findings related to endocrine distuptor issue will be provided.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"239 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2002-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76900847","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 : 2002-06-01DOI: 10.1111/j.1741-4520.2002.tb00865.x
{"title":"THE JAPANESE TERATOLOGY SOCIETY (FOREIGN MEMBERS)","authors":"","doi":"10.1111/j.1741-4520.2002.tb00865.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2002.tb00865.x","url":null,"abstract":"","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"67 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2002-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73880289","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 : 2002-06-01DOI: 10.1111/j.1741-4520.2002.tb00862.x
M. Matsuda
ABSTRACT The time of origin of motor neurons and their distribution in the spinal cord was studied in rat embryos by combining whole‐embryo culture and the Islet‐1 inununostaining technique. Cells immunostained for Islet‐1 appeared in the trunk neural tube by 27 hours (corresponding to E10.625) in culture of E9.5 embryos, at which time the cell number of the neural tube in a transverse section was about 200. When the neural tube retarded developmentally by lithium treatment, the time of appearance of the motor neurons was delayed to 33 hours in culture (corresponding to E10.875), but the cell number of the neural tube was about 200. After the initial appearance of motor neurons in the ventral aspect of the neural tube, they distributed in a group in the periphery of the basal plate by 48 hours (corresponding to E11.5) in culture, although in the retarded neural tube the number of motor neurons was small and they did not form a cluster. The percentage of Islet‐1‐positive cells at the point of the same cell number of the trunk neural tube in the transverse section was higher in the retarded embryos than in controls. These results suggest that motor neurons begin to appear when the cell number of the neural tube in the transverse section becomes about 200 and their initial development is more stable than overall neural tube development.
{"title":"The initial development of motor neurons in the neural tube of rat embryos","authors":"M. Matsuda","doi":"10.1111/j.1741-4520.2002.tb00862.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2002.tb00862.x","url":null,"abstract":"ABSTRACT The time of origin of motor neurons and their distribution in the spinal cord was studied in rat embryos by combining whole‐embryo culture and the Islet‐1 inununostaining technique. Cells immunostained for Islet‐1 appeared in the trunk neural tube by 27 hours (corresponding to E10.625) in culture of E9.5 embryos, at which time the cell number of the neural tube in a transverse section was about 200. When the neural tube retarded developmentally by lithium treatment, the time of appearance of the motor neurons was delayed to 33 hours in culture (corresponding to E10.875), but the cell number of the neural tube was about 200. After the initial appearance of motor neurons in the ventral aspect of the neural tube, they distributed in a group in the periphery of the basal plate by 48 hours (corresponding to E11.5) in culture, although in the retarded neural tube the number of motor neurons was small and they did not form a cluster. The percentage of Islet‐1‐positive cells at the point of the same cell number of the trunk neural tube in the transverse section was higher in the retarded embryos than in controls. These results suggest that motor neurons begin to appear when the cell number of the neural tube in the transverse section becomes about 200 and their initial development is more stable than overall neural tube development.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"31 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2002-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84369434","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 : 2002-06-01DOI: 10.1111/j.1741-4520.2002.tb00860.x
X. Zhao, Y. Ozaki, N. Suzumori, Tsuyoshi Sato, K. Suzumori
ABSTRACT We report here the results of fetal cell enrichment from maternal blood in 58 pregnant women by the use of magnetic activated cell sorting (MACS) with erythroblast‐specific and/or maternal cell specific antibodies. Two approaches were compared; one‐step MACS to enrich CD71+ (a membrane‐bound marker) or GPA+ (another marker, glycophorin A) fetal cells versus two‐step MACS to deplete CD14+ maternal cells and subsequently to enrich fetal (CD71+ or GPA+) cells. The existence of fetal cells was ensured by both FISH with Y‐specific probes and karyotyping of respective anuniotic and/or chorionic vullus cells, the results being applied for comparison of detection rate for XY fetuses between the two MACS procedures.
{"title":"Enrichment of fetal cells from maternal blood by magnetic activated cell sorting (MACS) with fetal cell specific antibodies: One‐step versus two‐step MACS","authors":"X. Zhao, Y. Ozaki, N. Suzumori, Tsuyoshi Sato, K. Suzumori","doi":"10.1111/j.1741-4520.2002.tb00860.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2002.tb00860.x","url":null,"abstract":"ABSTRACT We report here the results of fetal cell enrichment from maternal blood in 58 pregnant women by the use of magnetic activated cell sorting (MACS) with erythroblast‐specific and/or maternal cell specific antibodies. Two approaches were compared; one‐step MACS to enrich CD71+ (a membrane‐bound marker) or GPA+ (another marker, glycophorin A) fetal cells versus two‐step MACS to deplete CD14+ maternal cells and subsequently to enrich fetal (CD71+ or GPA+) cells. The existence of fetal cells was ensured by both FISH with Y‐specific probes and karyotyping of respective anuniotic and/or chorionic vullus cells, the results being applied for comparison of detection rate for XY fetuses between the two MACS procedures.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"64 2 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2002-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73251300","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 : 2002-06-01DOI: 10.1111/j.1741-4520.2002.tb00857.x
E. Todaka, C. Mori
ABSTRACT Our recent study clearly shows that fetuses are exposed to multiple chemicals including endocrine disruptors in Japan. Although the embryo and fetus stages are the most sensitive period to chemicals in humans' life cycle, the health effects of the chemicals such as endocrine disruptors to them are largely unknown. The conventional risk assessment method cannot assess the risk to fetuses precisely. Now we need a new risk assessment, in which the target is fetuses and not the adults, in addition to the conventional risk assessment At the same time, we also need a new strategy to practically eliminate the risk for the future generations. To make the strategy effective, we suggest a new approach to reduce the risk and avoid the possible adverse health effects, using primary, secondary and tertiary preventions as they are used in public health. We also suggest a new concept of “pre‐primary prevention” to reduce the risk for fetuses. Furthermore, to make this method even more practical, we suggest a new risk communication method. In this paper, we present a framework of risk avoidance of multiple chemical exposure to fetuses.
{"title":"Necessity to establish new risk assessment and risk communication for human fetal exposure to multiple endocrine disruptors in Japan","authors":"E. Todaka, C. Mori","doi":"10.1111/j.1741-4520.2002.tb00857.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2002.tb00857.x","url":null,"abstract":"ABSTRACT Our recent study clearly shows that fetuses are exposed to multiple chemicals including endocrine disruptors in Japan. Although the embryo and fetus stages are the most sensitive period to chemicals in humans' life cycle, the health effects of the chemicals such as endocrine disruptors to them are largely unknown. The conventional risk assessment method cannot assess the risk to fetuses precisely. Now we need a new risk assessment, in which the target is fetuses and not the adults, in addition to the conventional risk assessment At the same time, we also need a new strategy to practically eliminate the risk for the future generations. To make the strategy effective, we suggest a new approach to reduce the risk and avoid the possible adverse health effects, using primary, secondary and tertiary preventions as they are used in public health. We also suggest a new concept of “pre‐primary prevention” to reduce the risk for fetuses. Furthermore, to make this method even more practical, we suggest a new risk communication method. In this paper, we present a framework of risk avoidance of multiple chemical exposure to fetuses.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"35 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2002-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75471451","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}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：