Pub Date : 2002-06-01DOI: 10.1111/j.1741-4520.2002.tb00859.x
T. Iguchi, M. Sumi, S. Tanabe
ABSTRACT Monitoring of environmental chemicals in Japan has revealed that several endocrine active chemicals are in river water, sediments, and wildlife as well as in the human umbilical cord. In 2001, risk assessments of tributyltin and nonylphenol have been conducted by the Ministry of the Environment, Japan. Risk assessments of di(2‐ethylhexyl)phthalate and di‐isononyl phthalate have also been performed by the Ministry of Health, Labour and Welfare using a toxicological point of view in 2001. In this review, an overview of recent progress in endocrine disruptor research in Japan will be provided.
{"title":"Endocrine disruptor issues in Japan","authors":"T. Iguchi, M. Sumi, S. Tanabe","doi":"10.1111/j.1741-4520.2002.tb00859.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2002.tb00859.x","url":null,"abstract":"ABSTRACT Monitoring of environmental chemicals in Japan has revealed that several endocrine active chemicals are in river water, sediments, and wildlife as well as in the human umbilical cord. In 2001, risk assessments of tributyltin and nonylphenol have been conducted by the Ministry of the Environment, Japan. Risk assessments of di(2‐ethylhexyl)phthalate and di‐isononyl phthalate have also been performed by the Ministry of Health, Labour and Welfare using a toxicological point of view in 2001. In this review, an overview of recent progress in endocrine disruptor research in Japan will be provided.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"21 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2002-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74530987","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.tb00861.x
K. Sawada, H. Sakata-Haga, S. Komatsu, Kyoko Ohta, Y. Jeong, Y. Fukui
ABSTRACT Pregnant rats were fed an ethanol‐containing liquid diet between gestational days 10 and 21. The optic nerves of their litters at 49 days of age were examined using quantitative stereological procedures. Cross‐sectional areas of the optic nerve in ethanol‐exposed rats were significantly smaller than those in controls. This was reflected in the reduced number of myelinated fibers, but not of non‐myelinated fibers. The size distribution histogram indicated a decreased number of small axonal‐diameter myelinated fibers in ethanol‐exposed rats. The results suggested optic nerve hypoplasia hi ethanol‐exposed rats characterized by a selective loss of small‐diameter myelinated fibers.
{"title":"A selective loss of small‐diameter myelinated optic nerve axons in rats prenatally exposed to ethanol","authors":"K. Sawada, H. Sakata-Haga, S. Komatsu, Kyoko Ohta, Y. Jeong, Y. Fukui","doi":"10.1111/j.1741-4520.2002.tb00861.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2002.tb00861.x","url":null,"abstract":"ABSTRACT Pregnant rats were fed an ethanol‐containing liquid diet between gestational days 10 and 21. The optic nerves of their litters at 49 days of age were examined using quantitative stereological procedures. Cross‐sectional areas of the optic nerve in ethanol‐exposed rats were significantly smaller than those in controls. This was reflected in the reduced number of myelinated fibers, but not of non‐myelinated fibers. The size distribution histogram indicated a decreased number of small axonal‐diameter myelinated fibers in ethanol‐exposed rats. The results suggested optic nerve hypoplasia hi ethanol‐exposed rats characterized by a selective loss of small‐diameter myelinated fibers.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"49 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2002-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81318798","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.tb00863.x
Ryuju Hashimoto, I. Kihara, H. Otani
ABSTRACT We compared the structures of the femoral head (FH) of neonates between normal and operated legs with restrained fetal movement using an exo utero technique. At embryonic day (E) 16.5, one hind limb was sutured onto the embryonic membrane and the fetuses were allowed to develop exo utero until the term (E22.5). There was no significant difference in the largest diameter of the FH between the non‐operated and operated side FH in the operated neonates and the FH of the non‐operated neonates. By scanning electron microscopy, roughness and collagen fiber bundles, which were detected on the surface of the operated side FH at E18.5, disappeared at E22.5. However, the operated side FH was deformed and the surface cell arrangement was more irregular than that of the controls at E22.5 by light microscopy. These results suggest that the abnormality of cell arrangement caused by the restraint of fetal movement may induce the deformity and irregularity of the FH surface, although this operation may not disturb the basic cellular activities such as cell proliferation as well as the secretion of cartilage matrix and collagen fibers. To further investigate the recovery process in the operated newborns after releasing the restraint, we bred them artificially for a considerable period after birth. The operated side FH surface of the neonate bred for 45 hours was smoother than that at E22.5 and similar to that of the non‐operated side FH. This result suggests that the proper movement of the extremities after birth may recover the deformity caused by restrained fetal joint movement
{"title":"Perinatal development of the rat hip joint with restrained fetal movement","authors":"Ryuju Hashimoto, I. Kihara, H. Otani","doi":"10.1111/j.1741-4520.2002.tb00863.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2002.tb00863.x","url":null,"abstract":"ABSTRACT We compared the structures of the femoral head (FH) of neonates between normal and operated legs with restrained fetal movement using an exo utero technique. At embryonic day (E) 16.5, one hind limb was sutured onto the embryonic membrane and the fetuses were allowed to develop exo utero until the term (E22.5). There was no significant difference in the largest diameter of the FH between the non‐operated and operated side FH in the operated neonates and the FH of the non‐operated neonates. By scanning electron microscopy, roughness and collagen fiber bundles, which were detected on the surface of the operated side FH at E18.5, disappeared at E22.5. However, the operated side FH was deformed and the surface cell arrangement was more irregular than that of the controls at E22.5 by light microscopy. These results suggest that the abnormality of cell arrangement caused by the restraint of fetal movement may induce the deformity and irregularity of the FH surface, although this operation may not disturb the basic cellular activities such as cell proliferation as well as the secretion of cartilage matrix and collagen fibers. To further investigate the recovery process in the operated newborns after releasing the restraint, we bred them artificially for a considerable period after birth. The operated side FH surface of the neonate bred for 45 hours was smoother than that at E22.5 and similar to that of the non‐operated side FH. This result suggests that the proper movement of the extremities after birth may recover the deformity caused by restrained fetal joint movement","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"13 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2002-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82099220","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.tb00864.x
M. Tsukuno, Yoko Kite, K. Kurihara
ABSTRACT Midline cervical cleft is a rare congenital developmental anomaly of the ventral neck. Less than 100 cases have been reported in published journals to date (Ayache et al., 1997). It is usually found as congenital scar‐like skin defect or cord‐like contractive abnormality of the skin at the ventral neck. Unlike “median cervical cyst” or “lateral cervical cyst”, midline cervical cleft usually has no anatomical association with the hyoid bone. We will present a case of midline cervical cleft without fistula but with very small protuberant tissue. The subject was operated at the age of 5 months. We will discuss the clinical aspect and surgical management of this infrequent anomaly.
中线颈裂是一种罕见的先天性腹侧颈部发育异常。迄今为止，在已发表的期刊上报道的病例不到100例(Ayache et al.， 1997)。它通常被发现为先天性疤痕样皮肤缺损或脊髓样皮肤收缩异常在腹颈部。与“宫颈正中囊肿”或“宫颈外侧囊肿”不同，颈椎中线裂通常与舌骨没有解剖关联。我们将提出一个病例的中线宫颈裂没有瘘，但有非常小的突起组织。受试者于5个月大时手术。我们将讨论这种罕见异常的临床表现和手术治疗。
{"title":"A case of midline cervical cleft","authors":"M. Tsukuno, Yoko Kite, K. Kurihara","doi":"10.1111/j.1741-4520.2002.tb00864.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2002.tb00864.x","url":null,"abstract":"ABSTRACT Midline cervical cleft is a rare congenital developmental anomaly of the ventral neck. Less than 100 cases have been reported in published journals to date (Ayache et al., 1997). It is usually found as congenital scar‐like skin defect or cord‐like contractive abnormality of the skin at the ventral neck. Unlike “median cervical cyst” or “lateral cervical cyst”, midline cervical cleft usually has no anatomical association with the hyoid bone. We will present a case of midline cervical cleft without fistula but with very small protuberant tissue. The subject was operated at the age of 5 months. We will discuss the clinical aspect and surgical management of this infrequent anomaly.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"161 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2002-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80203872","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 : 2001-06-01DOI: 10.1111/j.1741-4520.2001.tb00820.x
Y. Yasuda, Y. Fujita, Koichi Ueda, T. Matsuo, M. Onozaki, M. Sakamoto, H. Konishi
ABSTRACT Vascular endothelial growth factor (VEGF) is induced by hypoxic environment and contributes to vascular formation in both developing embryos and adults. Exogenous retinoic acid (RA) induces avascular yolk sacs with anemic stunted embryos of day 9 and 10 of gestation when RA is given to pregnant mice on day 6, 6.5 or 7 of pregnancy (Yasuda et al., 1996). We undertook the present studies to find out whether VEGF is activated and plays any role in those RA‐exposed embryos. Embryos were obtained from dams given 60 mg/kg of RA on day 6 or 7 of pregnancy and sacrificed three days later. Most RA‐exposed embryos showed edematous swelling without prominent vascular nets, but had beating heart tubes on day 9 and day 10 of gestation. Microscopic examination of developing tissue components showed various degrees of degeneration, and distension of the dorsal aorta when the body cavity was dosed. Northern blot analysis revealed expression of VEGF mRNA in the RA‐exposed and control embryos. The highest expression of VEGF mRNA was seen in the embryos of day 10 exposed to RA on day 7, and these embryos had a significantly lower ATP content than did the controls (p < 0.01). Immunoreactive VEGF was detectable in both experimental and control embryos; in the former it was especially visible in the distended neuroepithelium, endothelium and membranes. These VEGF‐immunoreactive regions also expressed another permeability factor, bradykinin. These findings suggest that VEGF upregulated by hypoxic conditions in edematous embryos induced by RA exposure in utero acts as hyperpermeability.
{"title":"Vascular endothelial growth factor in edematous mouse embryos induced by retinoic acid in utero","authors":"Y. Yasuda, Y. Fujita, Koichi Ueda, T. Matsuo, M. Onozaki, M. Sakamoto, H. Konishi","doi":"10.1111/j.1741-4520.2001.tb00820.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2001.tb00820.x","url":null,"abstract":"ABSTRACT Vascular endothelial growth factor (VEGF) is induced by hypoxic environment and contributes to vascular formation in both developing embryos and adults. Exogenous retinoic acid (RA) induces avascular yolk sacs with anemic stunted embryos of day 9 and 10 of gestation when RA is given to pregnant mice on day 6, 6.5 or 7 of pregnancy (Yasuda et al., 1996). We undertook the present studies to find out whether VEGF is activated and plays any role in those RA‐exposed embryos. Embryos were obtained from dams given 60 mg/kg of RA on day 6 or 7 of pregnancy and sacrificed three days later. Most RA‐exposed embryos showed edematous swelling without prominent vascular nets, but had beating heart tubes on day 9 and day 10 of gestation. Microscopic examination of developing tissue components showed various degrees of degeneration, and distension of the dorsal aorta when the body cavity was dosed. Northern blot analysis revealed expression of VEGF mRNA in the RA‐exposed and control embryos. The highest expression of VEGF mRNA was seen in the embryos of day 10 exposed to RA on day 7, and these embryos had a significantly lower ATP content than did the controls (p < 0.01). Immunoreactive VEGF was detectable in both experimental and control embryos; in the former it was especially visible in the distended neuroepithelium, endothelium and membranes. These VEGF‐immunoreactive regions also expressed another permeability factor, bradykinin. These findings suggest that VEGF upregulated by hypoxic conditions in edematous embryos induced by RA exposure in utero acts as hyperpermeability.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"68 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2001-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81499648","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 : 2001-06-01DOI: 10.1111/j.1741-4520.2001.tb00822.x
Kiyoshi Matsumoto, N. Seki, K. Fukuta, Y. Ooshima
ABSTRACT Aniline hydrochloride (AH), a methemoglobin formation‐stimulating substance, at a dosage level of 520 mg/kg which does not induce apparent fetal death, was injected subcutaneously into pregnant rats once on day 14, 15 or 16 of gestation in order to assess the stage specificity of cleft palate induction. Also, doses of 260, 390, 520 and 650 mg/kg were administered to pregnant rats on day 15 of gestation, and the dose‐response relationships with respect to fetal cleft palate and maternal methemo‐globinemia induction were studied. In the stage‐specificity study, paleness, decreased body weight gain and elevated methemoglobin concentration were noted in the dams treated with AH. Upon fetal examinations, although reduced body weight was noted in all AH‐treated groups, cleft palate was observed only in fetuses from those dams treated on day 15 of gestation. In the dose‐dependency study, AH induced maternal methemoglobinemia, decreased fetal body weight and increased the incidence of cleft palate dose dependently when administered at dosage levels of 260, 390, 520 and 650 mg/kg on day 15 of gestation. Additionally, administration of methylene blue, a methemoglobinemia‐preventing substance, to the AH‐treated dams ameliorated maternal methemoglobinemia and reduced the incidence of fetal cleft palate. In summation, it is considered that AH stage‐specifically induces cleft palate in rats and that cleft palate is caused not by a direct teratogenic effect of AH but by maternal hypoxia due to methemoglobinemia.
{"title":"Induction of cleft palate in aniline hydrochloride‐treated rats: Possible effect of maternal methemoglobinemic hypoxia","authors":"Kiyoshi Matsumoto, N. Seki, K. Fukuta, Y. Ooshima","doi":"10.1111/j.1741-4520.2001.tb00822.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2001.tb00822.x","url":null,"abstract":"ABSTRACT Aniline hydrochloride (AH), a methemoglobin formation‐stimulating substance, at a dosage level of 520 mg/kg which does not induce apparent fetal death, was injected subcutaneously into pregnant rats once on day 14, 15 or 16 of gestation in order to assess the stage specificity of cleft palate induction. Also, doses of 260, 390, 520 and 650 mg/kg were administered to pregnant rats on day 15 of gestation, and the dose‐response relationships with respect to fetal cleft palate and maternal methemo‐globinemia induction were studied. In the stage‐specificity study, paleness, decreased body weight gain and elevated methemoglobin concentration were noted in the dams treated with AH. Upon fetal examinations, although reduced body weight was noted in all AH‐treated groups, cleft palate was observed only in fetuses from those dams treated on day 15 of gestation. In the dose‐dependency study, AH induced maternal methemoglobinemia, decreased fetal body weight and increased the incidence of cleft palate dose dependently when administered at dosage levels of 260, 390, 520 and 650 mg/kg on day 15 of gestation. Additionally, administration of methylene blue, a methemoglobinemia‐preventing substance, to the AH‐treated dams ameliorated maternal methemoglobinemia and reduced the incidence of fetal cleft palate. In summation, it is considered that AH stage‐specifically induces cleft palate in rats and that cleft palate is caused not by a direct teratogenic effect of AH but by maternal hypoxia due to methemoglobinemia.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"131 1 Suppl 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2001-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81142997","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 : 2001-06-01DOI: 10.1111/j.1741-4520.2001.tb00823.x
Kiyoshi Matsumoto, S. Matsumoto, K. Fukuta, Y. Ooshima
ABSTRACT Aniline hydrochloride (AH), a methemoglobin‐formation stimulating substance, at a dosage level that does not induce apparent fetal death was injected subcutaneously into pregnant rats once a day on days 6–8, 9–11, 12–14 or 15–17 of gestation in order to assess its ability to stage‐specifically produce cardiovascular malformations. In addition, AH at dosage levels of 195, 260, 325 and 395 rag/kg was injected into pregnant rats subcutaneously once a day on days 12–14 of gestation, and the dose‐dependent induction of ventricular septal defect (VSD) in relation to maternal methemoglobinemia was studied. In the stage‐specificity study, paleness, decreased body weight gain and elevated methemoglobin concentration were noted in the dams. Upon fetal examination, reduced body weight was noted in all AH‐treated groups. AH induced cardiovascular malformations, mainly VSD, which was most frequently observed in the day 12–14 group and also observed in the day 15–17 group. Abnormal branching of subclavian, pulmonary and vertebral arteries were most frequently observed in the day 9–11 group. In the dose‐dependency study, AH induced maternal methemoglobinemia, decreased fetal body weight and increased the incidence of VSD dose dependency. Additionally, administration of methylene blue, a methemoglobinemia‐preventing substance, to the AH‐treated dams ameliorated maternal methemoglobinemia and reduced the incidence of fetal VSD. From these results, it is considered that AH stage‐specifically induces cardiovascular defects, mainly VSD, in rats and that VSD is induced not by a direct teratogenic effect of AH but by maternal hypoxia due to methemoglobinemia.
{"title":"Cardiovascular malformations associated with maternal hypoxia due to methemoglobinemia in aniline hydrochloride‐treated rats","authors":"Kiyoshi Matsumoto, S. Matsumoto, K. Fukuta, Y. Ooshima","doi":"10.1111/j.1741-4520.2001.tb00823.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2001.tb00823.x","url":null,"abstract":"ABSTRACT Aniline hydrochloride (AH), a methemoglobin‐formation stimulating substance, at a dosage level that does not induce apparent fetal death was injected subcutaneously into pregnant rats once a day on days 6–8, 9–11, 12–14 or 15–17 of gestation in order to assess its ability to stage‐specifically produce cardiovascular malformations. In addition, AH at dosage levels of 195, 260, 325 and 395 rag/kg was injected into pregnant rats subcutaneously once a day on days 12–14 of gestation, and the dose‐dependent induction of ventricular septal defect (VSD) in relation to maternal methemoglobinemia was studied. In the stage‐specificity study, paleness, decreased body weight gain and elevated methemoglobin concentration were noted in the dams. Upon fetal examination, reduced body weight was noted in all AH‐treated groups. AH induced cardiovascular malformations, mainly VSD, which was most frequently observed in the day 12–14 group and also observed in the day 15–17 group. Abnormal branching of subclavian, pulmonary and vertebral arteries were most frequently observed in the day 9–11 group. In the dose‐dependency study, AH induced maternal methemoglobinemia, decreased fetal body weight and increased the incidence of VSD dose dependency. Additionally, administration of methylene blue, a methemoglobinemia‐preventing substance, to the AH‐treated dams ameliorated maternal methemoglobinemia and reduced the incidence of fetal VSD. From these results, it is considered that AH stage‐specifically induces cardiovascular defects, mainly VSD, in rats and that VSD is induced not by a direct teratogenic effect of AH but by maternal hypoxia due to methemoglobinemia.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"109 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2001-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"79746864","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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