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  • 1
    Electronic Resource
    Electronic Resource
    IGF-I and retinoic acid regulate the distribution pattern of IGFBPs synthesized by the canine mammary tumor cell line CMT-U335 (1999)
    Springer
    Breast cancer research and treatment 54 (1999), S. 11-23 
    Details
    ISSN: 1573-7217
    Keywords: dog ; IGF ; IGFBP ; mammary mesenchymal cell line ; retinoic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Stromal-epithelial interactions modulate growth and development in normal and neoplastic mammary gland. The release of IGF binding proteins (IGFBPs) by the stromal compartment of the mammary gland may play a modulating role in the IGF-mediated proliferation of mammary epithelium. Therefore, the IGFBP-expression pattern of the canine mammary tumor cell line U335 (CMT-U335), which has a mesenchymal phenotype, was determined. In addition, the effects of IGFs and all trans retinoic acid (RA) on DNA synthesis, and IGFBP secretion and distribution were examined. The IGFBPs secreted by CMT-U335 were characterized as IGFBP-2, -4, -5, and -6. Moreover, CMT-U335 appeared to be a suitable mammary mesenchymal cell line for study of the regulatory factors of IGFBP expression and the mechanism(s) involved. IGFs and RA enhanced IGFBP concentrations in cell-conditioned medium with IGF-I and RA having an additive effect. The IGF-I-stimulated DNA synthesis, however, was inhibited by RA. The difference between IGF-I and RA was an enhanced IGFBP-5 binding to the extracellular matrix (ECM) by RA, whereas IGF-I reduced binding to the ECM. Because high doses of insulin had no significant effects on IGFBP concentrations in the medium, it is concluded that IGF-I-induced changes in IGFBP concentrations are not mediated by type-I IGF receptors and may be the consequence of IGFBP redistribution.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1006107703745
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    Effects of a Branched-Chain Amino Acid-Enriched Diet on Chronic Hepatic Encephalopathy in Dogs (1999)
    Springer
    Metabolic brain disease 14 (1999), S. 103-115 
    Details
    ISSN: 1573-7365
    Keywords: hepatic encephalopathy ; portosystemic encephalopathy ; branched-chain amino acids ; dopaminergic neurotransmission ; hypothalamo-pituitary-adrenocortical axis ; diet ; dog ; model
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract A decreased ratio of branched-chain amino acids (BCAA) to aromatic amino acids (AAA) is considered an important pathogenetic factor in hepatic encephalopathy (HE). A relationship between the deranged BCAA/AAA ratio and dopaminergic dysfunction through the formation of “false” neurotransmitters has been postulated. The intermediate lobe of the pituitary is more pronounced in dogs than in humans and because it is primarily under dopaminergic inhibitory influence, it may serve as an indicator of alterations in dopaminergic neurotransmission. We investigated the effects of a diet with a high BCAA/AAA ratio (HR) and an isonitrogenous diet with a low BCAA/AAA ratio (LR) on several physical and biochemical parameters including pituitary function in dogs with portocaval shunts and 40% hepatectomy and in sham-operated pair-fed controls, in a double-blind, randomized cross-over study. Portocaval-shunted dogs had hyperammonemia (33±3 μM (mean ± SEM) before and 214±21 after surgery)) and signs of HE. Their BCAA/AAA ratio in plasma and CSF decreased from 4.3±0.3 and 2.3±0.3 before surgery to 1.3±0.1 and 0.5±0.1 after surgery, respectively. These parameters remained unaltered in the control dogs. The consumption of the LR diet was significantly higher than consumption of the HR diet. In the portocaval-shunted dogs, plasma ammonia concentration was higher on the HR diet than on the LR diet (344±52 v 246±45) and the HE grade was worse. The BCAA /AAA ratio remained abnormal in HE dogs during the feeding of both diets. The basal and haloperidol-stimulated release of α-melanotropin and cortisol in plasma were not significantly different between or within groups during any period. In contrast, urinary cortisol excretion was increased in the HE dogs after surgery (urinary cortisol:creatinine ratio (×10−6) 8.5±1.4 before and 30.4±8.9 after surgery). The basal plasma concentration of adrenocorticotropin in HE dogs was decreased after surgery (68.3±10.2 ng/L before and 40.8±4.4 after surgery). This indicates a non-pituitary-dependent hyperresponsiveness of the adrenals. We conclude from these results that chronic HE in dogs is not associated with an abnormal dopaminergic neurotransmission at least at the level of the pituitary, and that it is not the content of the dietary neutral amino acids but rather the total protein intake that may have a beneficial effect on HE.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1023/A:1020757730386
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Cloning of the canine gene encoding transcription factor Pit-1 and its exclusion as candidate gene in a canine model of pituitary dwarfism (2000)
    Springer
    Mammalian genome 11 (2000), S. 31-36 
    Details
    ISSN: 1432-1777
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract. Combined pituitary hormone deficiency (CPHD) is an autosomal recessive inherited disease of German shepherd dogs characterized primarily by dwarfism. In mice and humans a similar genetic disorder has been described that results from an alteration in the gene encoding the transcription factor Pit-1. In this study we characterized the canine Pit-1 gene, determined the chromosomal localization of the Pit-1 gene, and screened dwarf German shepherd dogs for the presence of mutations in this gene. The full-length canine Pit-1 cDNA contained an open reading frame encoding 291 amino acids, 92 bp of 5′-untranslated region, and 1959 bp of 3′-untranslated region. The deduced amino acid sequence was highly homologous with Pit-1 of other mammalian species. Using a Pit-1 BAC clone as probe, the Pit-1 gene was mapped by FISH to canine Chromosome (Chr) 31. In dwarf German shepherd dogs a C to A transversion was detected, causing a Phe (TTC) to Leu (TTA) substitution at codon 81. This alteration was present neither in other canine breeds analyzed nor in other mammalian species. However, healthy German shepherd dogs were also homozygous for the mutant allele, indicating that it is not the primary disease-causing mutation. In addition, linkage analysis of polymorphic DNA markers flanking the Pit-1 gene, 41K19 and 52L05, revealed no co-segregation between the Pit-1 locus and the CPHD phenotype. These findings suggest that a gene other than Pit-1 is responsible for the pituitary anomaly in dwarf German shepherd dogs.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s003350010006
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    Paper (German National Licenses)
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