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  • 1
    Electronic Resource
    Electronic Resource
    Killing of preimplantation mouse embryos by main ingredients of cleansers AS and LAS
    Amsterdam : Elsevier
    Mutation Research Letters 190 (1987), S. 25-29 
    Details
    ISSN: 0165-7992
    Keywords: (Mouse embryos) ; Alcohol sulphate ; Cleansers ; Preimplantation ; alkylbenzene sulphonate ; killing
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Biology , Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1016/0165-7992(87)90077-7
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    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    The RET proto-oncogene: a challenge to our understanding of disease pathogenesis (1996)
    Springer
    Pediatric surgery international 12 (1996), S. 11-18 
    Details
    ISSN: 1437-9813
    Keywords: Key words RET ; RET proto-oncogene ; Hirschsprung’s disease ; Multiple endocrine neoplasia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  RET gene alterations as disease-causative mutations have been demonstrated in five different disease entities: Hirschsprung’s disease (HD); papillary thyroid carcinoma; and three types of inherited cancer syndromes: multiple endocrine neoplasia (MEN) 2A, MEN 2B, and familial medullary thyroid carcinoma. RET is expressed during embryogenesis in a temporally and spatially regulated manner, and plays an important role in the normal development of a variety of cell lineages, particularly in the establishment of the enteric nervous system. RET mutations observed in patients with HD are scattered along the gene without any hot spots, and possess a loss-of-function effect. RET mutations are detected with a higher incidence among familial cases (50%) than sporadic cases (15% – 20%), and are more closely associated with long-segment HD than short-segment disease. In contrast to HD mutations, missense mutations observed in MEN 2 syndromes occur at specific codons, and gene rearrangements are characteristic in papillary thyroid carcinoma. Both missense mutations and gene rearrangements act in a dominant fashion, and cause constitutive phosphorylation on the tyrosine of RET and highly enhance RET kinase activity, leading to transforming or oncogenic activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01194794
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    TheRET proto-oncogene: A challenge to our understanding of disease pathogenesis (1996)
    Springer
    Pediatric surgery international 12 (1996), S. 11-18 
    Details
    ISSN: 1437-9813
    Keywords: RET ; RET proto-oncogene ; Hirschsprung's disease ; Multiple endocrine neoplasia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract RET gene alterations as disease-causative mutations have been demonstrated in five different disease entities: Hirschsprung's disease (HD); papillary thyroid carcinoma; and three types of inherited cancer syndromes: multiple endocrine neoplasia (MEN) 2A, MEN 213, and familial medullary thyroid carcinoma. RET is expressed during embryogenesis in a temporally and spatially regulated manner, and plays an important role in the normal development of a variety of cell lineages, particularly in the establishment of the enteric nervous system.RET mutations observed in patients with HD are scattered along the gene without any hot spots, and possess a loss-of-function effect.RET mutations are detected with a higher incidence among familial cases (50%) than sporadic cases (15%–20%), and are more closely associated with long-segment HD than short-segment disease. In contrast to HD mutations, missense mutations observed in MEN 2 syndromes occur at specific codons, and gene rearrangements are characteristic in papillary thyroid carcinoma. Both missense mutations and gene rearrangements act in a dominant fashion, and cause constitutive phosphorylation on the tyrosine of RET and highly enhance RET kinase activity, leading to transforming or oncogenic activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01194794
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Mutations of the endothelin-B receptor and endothelin-3 genes in Hirschsprung’s disease (1996)
    Springer
    Pediatric surgery international 12 (1996), S. 19-23 
    Details
    ISSN: 1437-9813
    Keywords: Key words Hirschsprung’s disease ; Endothelin-B receptor gene ; Endothelin-3 gene ; Mutation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  The endothelin-B receptor gene (EDNRB) and the endothelin-3 gene (EDN3) have recently been recognized as susceptibility genes for Hirschsprung’s disease (HD). Novel EDNRB mutations have been detected in non-syndromic HD patients with heterozygous forms, and homozygous mutations of the EDNRB or the EDN3 genes have been reported in HD patients associated with type 2 Waardenburg syndrome. These observations confirm that impaired function of the endothelin-B receptor or endothelin-3 is involved in the aetiology of some human HD cases. EDNRB mutations appear to be associated with short-segment HD, in contrast to RET mutations, which are found mainly in long-segment aganglionosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01194795
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Mutations of the endothelin-B receptor and endothelin-3 genes in Hirschsprung's disease (1996)
    Springer
    Pediatric surgery international 12 (1996), S. 19-23 
    Details
    ISSN: 1437-9813
    Keywords: Hirschsprung's disease ; Endothelin-B receptor gene ; Endothelin-3 gene ; Mutation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The endothelin-B receptor gene (EDNRB) and the endothelin-3 gene (EDN3) have recently been recognized as susceptibility genes for Hirschsprung's disease (HD). Novel EDNRB mutations have been detected in non-syndrommc HD patients with heterozygous forms, and homozygous mutations of the EDNRB or the EDN3 genes have been reported in HD patients associated with type 2 Waardenburg syndrome. These observations confirm that impaired function of the endothelin-B receptor or endothelin-3 is involved in the aetiology of some human HD cases. EDNRB mutations appear to be associated with shortsegment HD, in contrast to RET mutations, which are found mainly in long-segment aganglionosis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01194795
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 6
    Electronic Resource
    Electronic Resource
    Altered messenger RNA expression of the neuronal nitric oxide synthase gene in infantile hypertrophic pyloric stenosis (1997)
    Springer
    Pediatric surgery international 12 (1997), S. 576-579 
    Details
    ISSN: 1437-9813
    Keywords: Key words Infantile hypertrophic pyloric stenosis ; Neuronal nitric oxide synthase ; messenger RNA ; Reverse transcription-polymerase chain reaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Nitric oxide (NO) has been described as a mediator of smooth muscle relaxation in the mammalian gastrointestinal tract. The enzyme neuronal nitric oxide synthase (NOS) catalyzes the formation of NO. We examined the expression of the neuronal NOS gene at the messenger RNA (mRNA) level in pyloric smooth-muscle biopsy specimens from six patients with infantile hypertrophic pyloric stenosis (IHPS) using a reverse transcription-polymerase chain reaction (RT-PCR) technique. For controls, smooth-muscle layer specimens of pylorus (n=3), ileum (n=2), and colon (n=2) were used. With 31 cycles of PCR reaction, control specimens revealed detectable signals for neuronal NOS mRNA. In contrast, signals of IHPS specimens were undetectable in five cases and very weak in one. By increasing the PCR to 37 cycles, detectable signals for neuronal NOS mRNA were observed in all IHPS specimens, but they were significantly weaker than those of controls. Since a low level of neuronal NOS mRNA may lead to impaired production of NO, our observations indicate that the excessively contracted, hypertrophied pyloric muscle in IHPS is a result of reduced expression of the neuronal NOS gene at the mRNA level.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01371902
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 7
    Electronic Resource
    Electronic Resource
    Altered messenger RNA expression of the neuronal nitric oxide synthase gene in infantile hypertrophic pyloric stenosis (1997)
    Springer
    Pediatric surgery international 12 (1997), S. 576-579 
    Details
    ISSN: 1437-9813
    Keywords: Infantile hypertrophic pyloric stenosis ; Neuronal nitric oxide synthase ; messenger RNA ; Reverse transcription-polymerase chain reaction
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Nitric oxide (NO) has been described as a mediator of smooth muscle relaxation in the mammalian gastrointestinal tract. The enzyme neuronal nitric oxide synthase (NOS) catalyzes the formation of NO. We examined the expression of the neuronal NOS gene at the messenger RNA (mRNA) level in pyloric smooth-muscle biopsy specimens from six patients with infantile hypertrophic pyloric stenosis (IHPS) using a reverse transcription-polymerase chain reaction (RT-PCR) technique. For controls, smooth-muscle layer specimens of pylorus (n = 3), ileum (n = 2), and colon (n = 2) were used. With 31 cycles of PCR reaction, control specimens revealed detectable signals for neuronal NOS mRNA. In contrast, signals of IHPS specimens were undetectable in five cases and very weak in one. By increasing the PCR to 37 cycles, detectable signals for neuronal NOS mRNA were observed in all IHPS specimens, but they were significantly weaker than those of controls. Since a low level of neuronal NOS mRNA may lead to impaired production of NO, our observations indicate that the excessively contracted, hypertrophied pyloric muscle in IHPS is a result of reduced expression of the neuronal NOS gene at the mRNA level.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01371902
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
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