Pub Date : 1997-06-01DOI: 10.1111/j.1741-4520.1997.tb00973.x
B. Bay, S. Tay, Y. Ng
Congenital anomalies of the inferior vena cava (IVC) may have clinical implications. The present case study describes a male cadaver with a duplicated IVC and a hypoplastic right kidney. The IVC is derived embryologically from the development and remodeling of the posterior cardinal, subcardinal and supracardinal veins. The definitive kidneys develop from the metanephros. Transforming growth factor‐β (TGF‐β), a positive regulator of angiogenesis and a known inhibitor of tubulogenesis of metanephric tissue in vitro, may provide the link for the concomitant occurrence of the congenital anomalies seen in this case study.
{"title":"Duplication of Inferior Vena Cava with Right Renal Hypoplasia","authors":"B. Bay, S. Tay, Y. Ng","doi":"10.1111/j.1741-4520.1997.tb00973.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.1997.tb00973.x","url":null,"abstract":"Congenital anomalies of the inferior vena cava (IVC) may have clinical implications. The present case study describes a male cadaver with a duplicated IVC and a hypoplastic right kidney. The IVC is derived embryologically from the development and remodeling of the posterior cardinal, subcardinal and supracardinal veins. The definitive kidneys develop from the metanephros. Transforming growth factor‐β (TGF‐β), a positive regulator of angiogenesis and a known inhibitor of tubulogenesis of metanephric tissue in vitro, may provide the link for the concomitant occurrence of the congenital anomalies seen in this case study.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"41 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1997-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"90167248","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 : 1997-06-01DOI: 10.1111/j.1741-4520.1997.tb00974.x
M. Uno, T. Takano, T. Yamano, M. Shimada
Tight junctions in the central nervous system (CNS) are a major component of brain barriers including the blood‐brain barrier (BBB) and blood‐CSF barrier, which regulate solute entry and protect against invasion by microorganisms. In this study, we examined the breach of tight junctions in mumps virus‐induced hydrocephalic brain in hamsters using antibodies to Laminin B1 chain and zonula occludentes (ZO‐1) immuno‐histochemistry, and evaluated the role of tight junctions in the pathogenesis of hydrocephalus after mumps virus infection.
{"title":"Tight Junctional Damage in Experimental Mumps‐Associated Hydrocephalus","authors":"M. Uno, T. Takano, T. Yamano, M. Shimada","doi":"10.1111/j.1741-4520.1997.tb00974.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.1997.tb00974.x","url":null,"abstract":"Tight junctions in the central nervous system (CNS) are a major component of brain barriers including the blood‐brain barrier (BBB) and blood‐CSF barrier, which regulate solute entry and protect against invasion by microorganisms. In this study, we examined the breach of tight junctions in mumps virus‐induced hydrocephalic brain in hamsters using antibodies to Laminin B1 chain and zonula occludentes (ZO‐1) immuno‐histochemistry, and evaluated the role of tight junctions in the pathogenesis of hydrocephalus after mumps virus infection.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"136 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1997-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76400799","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 : 1996-09-30DOI: 10.1111/j.1741-4520.2001.tb00819.x
I. Naruse, H. Keino, Yasukazu Yamada, S. Masaki, C. Hui
ABSTRACT The genetic polydactyly/arhinencephaly mouse, Pdn/Pdn, exhibits severe polydactyly both in the fore‐and hindlimbs, agenesis of the olfactory bulbs, corpus callosum, anterior commissure, and hydrocephalus. A candidate gene for the Pdn mouse has been speculated to be Gli3, because Pdn has been considered to be an allele of Xt whose responsible gene has been clarified to be Gli3. Recently, it has been cleared that retro‐transposons are inserted into nitron 3, upstream of zinc finger domain, of the Gli3 gene in the Pdn mouse, resulting to the severe suppression of Gli3 gene expression in Pdn/Pdn embryos. Meanwhile, XtJ/XtJ mice exhibit more severe polydactyly than that of Pdn/Pdn. Arhinencephaly and microholoprosencephaly including agenesis of the olfactory bulbs, corpus callosum, anterior commissure, hippocampal commissure, habenular commissure, and posterior commissure, and moreover, the cerebral cortical plates and hippocampus are not formed in the XtJ/XtJ mice. The XtJ/XtJ mouse has a large deletion in Gli3 structural gene and shows null expression. From these corroborations, we speculated that the differences in the Gli3 gene expression levels resulted in the phenotypic differences between the Pdn/Pdn and XtJ/XtJ mice.
{"title":"Phenotypic differences in the brains and limbs of mutant mice caused by differences of Gli3 gene expression levels","authors":"I. Naruse, H. Keino, Yasukazu Yamada, S. Masaki, C. Hui","doi":"10.1111/j.1741-4520.2001.tb00819.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.2001.tb00819.x","url":null,"abstract":"ABSTRACT The genetic polydactyly/arhinencephaly mouse, Pdn/Pdn, exhibits severe polydactyly both in the fore‐and hindlimbs, agenesis of the olfactory bulbs, corpus callosum, anterior commissure, and hydrocephalus. A candidate gene for the Pdn mouse has been speculated to be Gli3, because Pdn has been considered to be an allele of Xt whose responsible gene has been clarified to be Gli3. Recently, it has been cleared that retro‐transposons are inserted into nitron 3, upstream of zinc finger domain, of the Gli3 gene in the Pdn mouse, resulting to the severe suppression of Gli3 gene expression in Pdn/Pdn embryos. Meanwhile, XtJ/XtJ mice exhibit more severe polydactyly than that of Pdn/Pdn. Arhinencephaly and microholoprosencephaly including agenesis of the olfactory bulbs, corpus callosum, anterior commissure, hippocampal commissure, habenular commissure, and posterior commissure, and moreover, the cerebral cortical plates and hippocampus are not formed in the XtJ/XtJ mice. The XtJ/XtJ mouse has a large deletion in Gli3 structural gene and shows null expression. From these corroborations, we speculated that the differences in the Gli3 gene expression levels resulted in the phenotypic differences between the Pdn/Pdn and XtJ/XtJ mice.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"47 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1996-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86013009","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 : 1996-06-01DOI: 10.1111/j.1741-4520.1996.tb00628.x
{"title":"Notice for Contributors to “Diagnostic Problems” Section","authors":"","doi":"10.1111/j.1741-4520.1996.tb00628.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.1996.tb00628.x","url":null,"abstract":"","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"11 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1996-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84535658","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 : 1996-03-01DOI: 10.1111/j.1741-4520.1996.tb00316.x
Murray Smith, M. Edwards, P. Waugh
The effects of maternal hyperthermia on the prenatal development of the guinea pig lens is described with particular reference to cataract formation. Cataracts were observed at birth most commonly following maternal hyperthermia in early pregnancy (E11‐25) but also at mid‐pregnancy (E39‐46) and in late pregnancy (E56‐60). Cell death was observed in the lens and neural retina up to 8 hours following heating at E21 and vacuoles were frequently found in the lens fibres immediately beneath the anterior lens epithelium. After heating at E18 and observation at E26 the vesicles in the anterior part of the lens fibres were of varying sizes with the smaller appearing to coalesce into larger vesicles. These vacuoles may be an example of compromised lens fibres whose cellular changes may remain latent and form cataracts in later life following any event which alters fluid balance of the lens.
{"title":"Maternal Hyperthermia and the Formation of Cataracts in the Lens of the Embryonic and Fetal Guinea Pig.","authors":"Murray Smith, M. Edwards, P. Waugh","doi":"10.1111/j.1741-4520.1996.tb00316.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.1996.tb00316.x","url":null,"abstract":"The effects of maternal hyperthermia on the prenatal development of the guinea pig lens is described with particular reference to cataract formation. Cataracts were observed at birth most commonly following maternal hyperthermia in early pregnancy (E11‐25) but also at mid‐pregnancy (E39‐46) and in late pregnancy (E56‐60). Cell death was observed in the lens and neural retina up to 8 hours following heating at E21 and vacuoles were frequently found in the lens fibres immediately beneath the anterior lens epithelium. After heating at E18 and observation at E26 the vesicles in the anterior part of the lens fibres were of varying sizes with the smaller appearing to coalesce into larger vesicles. These vacuoles may be an example of compromised lens fibres whose cellular changes may remain latent and form cataracts in later life following any event which alters fluid balance of the lens.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"42 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1996-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88245362","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 : 1996-03-01DOI: 10.1111/j.1741-4520.1996.tb00318.x
T. Nagao, K. Fujikawa
Male mice of inbred strain C57BL/6 were intraperitoneally treated with ethylnitrosourea (ENU). On days 64–80 after the treatment, the males were mated with untreated virgin females of the same strain and allowed to utilize sperm that were spermatogonial stem cells at the time of treatment. On day 18 of gestation, viable fetuses were inspected for external malformations. The frequency of externally malformed fetuses in the ENU‐treated series increased significantly over the control level. Malformations occurred spontaneously in the control series were microphthalmia and micrognathia. In the ENU‐treated series as well, they occurred and no other malformations were encountered. The frequencies among total malformations of microphthalmia were 95% and 92% in the control and the ENU‐treated series, respectively. Based on these results and other data, we propose that the male‐mediated teratogenesis represents spontaneous teratogenesis that is enhanced over the normal level by paternally transmitted germ‐line mutation(s).
{"title":"Frequency and Type of Malformations in the Offspring of C57BL/6 Male Mice Treated with Ethylnitrosourea","authors":"T. Nagao, K. Fujikawa","doi":"10.1111/j.1741-4520.1996.tb00318.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.1996.tb00318.x","url":null,"abstract":"Male mice of inbred strain C57BL/6 were intraperitoneally treated with ethylnitrosourea (ENU). On days 64–80 after the treatment, the males were mated with untreated virgin females of the same strain and allowed to utilize sperm that were spermatogonial stem cells at the time of treatment. On day 18 of gestation, viable fetuses were inspected for external malformations. The frequency of externally malformed fetuses in the ENU‐treated series increased significantly over the control level. Malformations occurred spontaneously in the control series were microphthalmia and micrognathia. In the ENU‐treated series as well, they occurred and no other malformations were encountered. The frequencies among total malformations of microphthalmia were 95% and 92% in the control and the ENU‐treated series, respectively. Based on these results and other data, we propose that the male‐mediated teratogenesis represents spontaneous teratogenesis that is enhanced over the normal level by paternally transmitted germ‐line mutation(s).","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"1 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1996-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82315812","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 : 1996-03-01DOI: 10.1111/j.1741-4520.1996.tb00317.x
Noriyuki HATAKENAKA, H. Aoyama, M. Kaneda, S. Teramoto
The effects of the Ay gene on the normal development were investigated by using a inbred strain of C57BL/6 (a/a) and its congenic strain of C57BL/6‐Ay (Ay/a) mice. Three mating groups (female× male), i. e., group I, a/a × a/a; group II, a/a × Ay/a; and group III, Ay/a × a/a, were set, and the rating of normal development was compared among the groups on gestation days 13, 14, 15 or 16 with special attention to the secondary palate. On day 13, the palates were wide‐open and the palatal shelves were vertical in all embryos in all groups. In group I, both shelves became horizontal in 63.3% of the embryos on day 14. The incidences of embryos having completely closed palates were 95.8% and 100% on days 15 and 16, respectively. In group II, in which half of the embryos were expected to carry the Ay gene, the frequencies of shelf horizontalization on day 14 (31.1%) and of the complete closure on day 15 (74.3%) were significantly lowered as compared with those in group I, although the external morphological rating was comparable. On day 16, however, the palatal closure was completed in almost all embryos. In group III, in which maternal mice as well as half of their embryos carried the Ay gene, the external morphological rating was delayed as compared with that in either group I or II, and the frequencies of shelf horizontalization on day 14 and of the complete closure on day 15 were as low as 10.9% and 39.6%, respectively. The palatal closure was not yet completed in 15.3% of the embryos on day 16. These results indicate that the Ay gene causes a delay in shelf horizontalization and closure of the secondary palate of mouse embryos as compared with the a gene.
{"title":"Delay in the Development of the Secondary Palate in Ay/a Mouse Embryos","authors":"Noriyuki HATAKENAKA, H. Aoyama, M. Kaneda, S. Teramoto","doi":"10.1111/j.1741-4520.1996.tb00317.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.1996.tb00317.x","url":null,"abstract":"The effects of the Ay gene on the normal development were investigated by using a inbred strain of C57BL/6 (a/a) and its congenic strain of C57BL/6‐Ay (Ay/a) mice. Three mating groups (female× male), i. e., group I, a/a × a/a; group II, a/a × Ay/a; and group III, Ay/a × a/a, were set, and the rating of normal development was compared among the groups on gestation days 13, 14, 15 or 16 with special attention to the secondary palate. On day 13, the palates were wide‐open and the palatal shelves were vertical in all embryos in all groups. In group I, both shelves became horizontal in 63.3% of the embryos on day 14. The incidences of embryos having completely closed palates were 95.8% and 100% on days 15 and 16, respectively. In group II, in which half of the embryos were expected to carry the Ay gene, the frequencies of shelf horizontalization on day 14 (31.1%) and of the complete closure on day 15 (74.3%) were significantly lowered as compared with those in group I, although the external morphological rating was comparable. On day 16, however, the palatal closure was completed in almost all embryos. In group III, in which maternal mice as well as half of their embryos carried the Ay gene, the external morphological rating was delayed as compared with that in either group I or II, and the frequencies of shelf horizontalization on day 14 and of the complete closure on day 15 were as low as 10.9% and 39.6%, respectively. The palatal closure was not yet completed in 15.3% of the embryos on day 16. These results indicate that the Ay gene causes a delay in shelf horizontalization and closure of the secondary palate of mouse embryos as compared with the a gene.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"36 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1996-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"74954688","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 : 1996-03-01DOI: 10.1111/j.1741-4520.1996.tb00319.x
H. Sumida, T. Moriya, J. Handa, T. Yamashita, Kouta Nakamori, M. Nishizuka, Y. Arai
The sexually dimorphic nucleus of the preoptic area (SDN‐POA) and the anteroventral periventricular nucleus of the preoptic area (AVPvN‐POA) are sexually dimorphic regions in the rat brain. These regions are sensitive to reproductive function‐related drugs, and thus applied for aromatase inhibitor evaluation in the present study. Effects of NKS01 (an aromatase inhibitor) and tamoxifen on the SDN‐POA and AVPvN‐POA were examined. Five mg of NKS01 or its vehicle was injected to SD male and female rats from days 1 to 14 (the day of birth = day 0). Other 10 males and 10 females received a single injection of 100 μg tamoxifen on day 1. Rats in each group were sacrificed at day 30 or 60. The SDN‐POA was examined at days 30 and 60, and the AVPvN‐POA at day 60. When NKS01 was given to male rats for the first 14 days of life, a significant reduction of SDN‐POA size was observed on day 60. When tamoxifen was given, SDN‐POA reduction in size was also observed at days 30 and 60 in male rats. As for the AVPvN‐POA, tamoxifen markedly reduced volume in female rats, resulting in polycystic ovaries at day 60. This may be due to an estrogenic property of tamoxifen. On the other hand, NKS01 was not significantly effective in the AVPvN‐POA, although the volume of the nucleus in NKS01 males was inclined to increase. From these results, as well as the SDN‐POA, the AVPvN‐POA may be useful to evaluate the side effect of reproductive function‐related drug.
{"title":"Sex Differences in the Rat Brain: A Procedure for Estimating Developmental Toxicity","authors":"H. Sumida, T. Moriya, J. Handa, T. Yamashita, Kouta Nakamori, M. Nishizuka, Y. Arai","doi":"10.1111/j.1741-4520.1996.tb00319.x","DOIUrl":"https://doi.org/10.1111/j.1741-4520.1996.tb00319.x","url":null,"abstract":"The sexually dimorphic nucleus of the preoptic area (SDN‐POA) and the anteroventral periventricular nucleus of the preoptic area (AVPvN‐POA) are sexually dimorphic regions in the rat brain. These regions are sensitive to reproductive function‐related drugs, and thus applied for aromatase inhibitor evaluation in the present study. Effects of NKS01 (an aromatase inhibitor) and tamoxifen on the SDN‐POA and AVPvN‐POA were examined. Five mg of NKS01 or its vehicle was injected to SD male and female rats from days 1 to 14 (the day of birth = day 0). Other 10 males and 10 females received a single injection of 100 μg tamoxifen on day 1. Rats in each group were sacrificed at day 30 or 60. The SDN‐POA was examined at days 30 and 60, and the AVPvN‐POA at day 60. When NKS01 was given to male rats for the first 14 days of life, a significant reduction of SDN‐POA size was observed on day 60. When tamoxifen was given, SDN‐POA reduction in size was also observed at days 30 and 60 in male rats. As for the AVPvN‐POA, tamoxifen markedly reduced volume in female rats, resulting in polycystic ovaries at day 60. This may be due to an estrogenic property of tamoxifen. On the other hand, NKS01 was not significantly effective in the AVPvN‐POA, although the volume of the nucleus in NKS01 males was inclined to increase. From these results, as well as the SDN‐POA, the AVPvN‐POA may be useful to evaluate the side effect of reproductive function‐related drug.","PeriodicalId":93953,"journal":{"name":"Congenital anomalies","volume":"166 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"1996-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"81897008","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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