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1. |
Reduced Fertility in Female Homozygotes forhgn(Male Hypogonadism) Selected byhgn‐Associated Hypoplastic Kidney |
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Congenital Anomalies,
Volume 32,
Issue 3,
1992,
Page 167-178
Hiroetsu SUZUKI,
Yoji HAKAMATA,
Takayuki KAMEI,
Keiichiro KIKUKAWA,
Katsushi SUZUKI,
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摘要:
AbstractThe male hypogonadism rat (hgn/hgn) shows a characteristic male sterility as a single autosomal recessive trait. Recently, the female homozygotes forhgn, assumed to be fertile, could be detected by a /jgji‐associated hypoplastic kidney (hpk/hpk). The present study was to investigate a possible influence of thehgngene on female reproduction. Thehgn/hgnfemales showed a significant growth retardation as compared with the phenotypically normal ones (+/?;+/hgnor+/+). The litter size at birth and number of implantation traces were significantly less in thehgn/hgnthan in the+/?females. Thehgn/hgnfemales became anestrous and infertile much earlier than the+/?did. Histologically, there were a few corpora lutea, some atretic follicles at different stages of maturation and abundant abnormal interstitial cells with pyknotic or karyorexic nuclei in the ovaries ofhgn/hgnfemales that have been infertile. The birth rate expressed by per cent litter size at birth against number of implantation traces was comparable between thehgn/hgnand the+/?female, suggesting that the small litter size ofhgn/hgnfemale could not be due to the embryonic death in utero. Nevertheless, the number of the tubal ova at estrous was comparable in thehgn/hgnand+/?females. Therefore, it was suggested that the half of ova or embryos may be lost during the period from the fertilization to the implantation. Histological appearances of the neonatal ovary in thehgn/hgnseemed hypoplastic. The number of cells including oocytes and interstitial cells, enzymatically separated from neonatal ovary, was significantly less in thehgn/hgnthan in the+/hgn.These results suggest that the gene product(s) coded by normal allele ofhgngene(s) involves normal gonadal development in both sexes; the defect may lead testicular dysmorphology in the male and reduced fertility in the femal
ISSN:0914-3505
DOI:10.1111/j.1741-4520.1992.tb00248.x
出版商:Blackwell Publishing Ltd
年代:1992
数据来源: WILEY
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2. |
Prenatal Diagnosis of Duchenne Muscular Dystrophy (DMD) by the Polymerase Chain Reaction (PCR) |
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Congenital Anomalies,
Volume 32,
Issue 3,
1992,
Page 179-184
Kazuhiko HAYASHI,
Keisuke NOSAKA,
Seiji TAKAHASHI,
Kyoko YONAMINE,
Hiroshi HAMADA,
Kiyoshi IMAIZUMI,
Yoshikazu KUROKI,
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摘要:
AbstractThe diagnosis of Duchenne muscular dystrophy (DMD) has been drastically improved by recent advances in DNA analysis. The Southern blot hybridization using the cDNA 8 probe and the restriction enzyme Hind III was conducted in a gravida and her family in blood samples. The diagnosis revealed partial gene deletions in both the gravida and the DMD‐affected second child. The prenatal diagnosis was performed by studying the PCR (polymerase chain reaction) for target DNAs of exons 48 and 51 that correspond with cDNA 8 probe. In the affected child, the 506 bp band at exon 48 was detected but 388 bp at exon 51 was missing. On the other hand, both the 506 bp band at exon 48 and the 388 bp band at exon 51 were detected in the cultured amniotic cells. Thus, the fetus was determined to be not affecte
ISSN:0914-3505
DOI:10.1111/j.1741-4520.1992.tb00249.x
出版商:Blackwell Publishing Ltd
年代:1992
数据来源: WILEY
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3. |
Abstract |
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Congenital Anomalies,
Volume 32,
Issue 3,
1992,
Page 214-264
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摘要:
CONTENTS:Lectures by InvitationCONTENTS:SymposiaCONTENTS:WhorkshopsCONTENTS:Papers presented from PlatformCONTENTS:Poster Sessions
ISSN:0914-3505
DOI:10.1111/j.1741-4520.1992.tb00250.x
出版商:Blackwell Publishing Ltd
年代:1992
数据来源: WILEY
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4. |
Announcement |
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Congenital Anomalies,
Volume 32,
Issue 3,
1992,
Page 265-269
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ISSN:0914-3505
DOI:10.1111/j.1741-4520.1992.tb00251.x
出版商:Blackwell Publishing Ltd
年代:1992
数据来源: WILEY
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5. |
INTERNATIONAL FEDERATION OF TERATOLOGY SOCIETIES |
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Congenital Anomalies,
Volume 32,
Issue 3,
1992,
Page 270-270
Niger A. Brown,
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ISSN:0914-3505
DOI:10.1111/j.1741-4520.1992.tb00252.x
出版商:Blackwell Publishing Ltd
年代:1992
数据来源: WILEY
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6. |
Announcement |
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Congenital Anomalies,
Volume 32,
Issue 3,
1992,
Page 271-287
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ISSN:0914-3505
DOI:10.1111/j.1741-4520.1992.tb00253.x
出版商:Blackwell Publishing Ltd
年代:1992
数据来源: WILEY
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