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  • Amplification  (2)
  • Blood gas analysis  (1)
  • Membrane metalloendopeptidase  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Mammalian tachykinins stimulate rat uterus by activating NK-2 receptors
    Amsterdam : Elsevier
    Peptides 14 (1993), S. 169-174 
    Details
    ISSN: 0196-9781
    Keywords: Atropine ; Estradiol cypionate ; Membrane metalloendopeptidase ; NK-2 receptor ; Neurokinin A ; Neurokinin B ; Peptidase inhibitors ; Radioligand binding ; Substance P ; Uterine contractions ; [^1^2^5I]-Iodohistidyl-neurokinin A
    Source: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Topics: Chemistry and Pharmacology
    Type of Medium: Electronic Resource
    URL: http://linkinghub.elsevier.com/retrieve/pii/0196-9781(93)90025-C
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Genetics of bladder cancer (1996)
    Springer
    Journal of molecular medicine 74 (1996), S. 441-445 
    Details
    ISSN: 1432-1440
    Keywords: Bladder carcinoma ; Proto-oncogenes ; Tumor suppressor genes ; Chromosomes ; Loss of heterozygosity ; p53 ; Point mutation ; Amplification
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Bladder cancer manifests many different forms, ranging from superficial to aggressive muscle invasion, which suggests that various genetic alterations are responsible. Several attempts have been made to establish correlations between specific genetic alterations and various grades of the disease. Numerous types of chromosomal abnormalities have been observed, involving [1p, 1q, 2q, 3p, 4p, 5q, i(5p), +7, +8, 8p, 9p, 9q, 10q23–25, 11p, 11q, +11, 13q, 14q, 17p, 18q, 21q, and Y]. In addition, p53 mutations and loss of heterozygosity on various chromosomes have recently begun to shed light on the molecular pathways of transitional cell carcinomas of the bladder. We have begun to focus on specific genomic sites (especially 9q), although the heterogeneity of the disease and the variable presentation suggests divergent progression pathways. When the genetic basis of bladder cancer is fully understood, new diagnostic and therapeutic strategies will be developed, which in turn may promote better clinical management by pathologists and urologists.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00217519
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    Genetics of bladder cancer (1996)
    Springer
    Journal of molecular medicine 74 (1996), S. 441-445 
    Details
    ISSN: 1432-1440
    Keywords: Key words Bladder carcinoma ; Proto-oncogenes ; Tumor suppressor genes ; Chromosomes ; Loss of heterozygosity ; p53 ; Point mutation ; Amplification
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Bladder cancer manifests many different forms, ranging from superficial to aggressive muscle invasion, which suggests that various genetic alterations are responsible. Several attempts have been made to establish correlations between specific genetic alterations and various grades of the disease. Numerous types of chromosomal abnormalities have been observed, involving [1p, 1q, 2q, 3p, 4p, 5q, i(5p), +7, +8, 8p, 9p, 9q, 10q23-25, 11p, 11q, +11, 13q, 14q, 17p, 18q, 21q, and Y]. In addition, p53 mutations and loss of heterozygosity on various chromosomes have recently begun to shed light on the molecular pathways of transitional cell carcinomas of the bladder. We have begun to focus on specific genomic sites (especially 9q), although the heterogeneity of the disease and the variable presentation suggests divergent progression pathways. When the genetic basis of bladder cancer is fully understood, new diagnostic and therapeutic strategies will be developed, which in turn may promote better clinical management by pathologists and urologists.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001090050045
    Library Location Call Number Volume/Issue/Year Availability
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    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Correlation of morphologic brain lesions with physiologic alterations and blood-brain barrier impairment in 3-intropropionic acid toxicity in rats (1987)
    Springer
    Acta neuropathologica 74 (1987), S. 67-74 
    Details
    ISSN: 1432-0533
    Keywords: 3-Nitropropionic acid ; Cerebral hypoxia ; Blood pressure determination ; Blood gas analysis ; Blood-brain barrier
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 3-Nitropropionic acid (NPA), a toxin which irreversibly inhibits the Krebs cycle enzyme succinate dehydrogenase, causes severe neurologic disease and a specific pattern of morphologic brain damage when given subcutaneously to rats. To determine whether hypotension or hypoxemia were necessary for development of morphologic brain lesions in NPA neurotoxicity, systemic blood pressure and arterial blood gases were measured in NPA-intoxicated rats. The extent and distribution of albumin extravasation was examined by immunohistochemistry, and was compared to the extent and severity of morphological injury in the caudate-putamen. Neither hypotension nor hypoxemia were necessary for the development of morphologic injury in the brains of NPA-intoxicated rats. In fact, intoxicated rats had significantly higher systolic blood pressure and arterial blood oxygen than did controls. Arterial bicarbonate and pH were significantly lower in intoxicated rats than controls, however, suggesting that acidosis may be involved in the pathogenesis of NPA toxicity. When morphologic injury was severe, albumin extravasation was extensive occupying approximately 30%–80% of the lesion area in the caudate-putamen of NPA-intoxicated rats. When morphologic injury was mild, albumin extravasation was absent, or limited to small cuffs around individual capillaries (〈1% of the lesion area). There was no leakage of albumin in the cerebral cortex, which was resistant to morphologic injury. It was concluded that leakage of protein-rich fluid into cerebral parenchyma from blood-brain barrier impairment is not responsible for the initiation of morphologic injury in NPA toxicity, but may contribute to the severity of injury later in the evolution of brain lesions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00688340
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    Paper (German National Licenses)
    Fulltext
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