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  • 1
    ISSN: 1432-041X
    Keywords: Collagen ; Fibronectin ; Laminin ; Skin ; Scale morphogenesis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology
    Notes: Summary Collagen types I and III were purified from the skin of 3-or 7-week-old chickens, collagen type IV from bovine skin or EHS mouse tumour, fibronectin from human serum, and laminin from EHS mouse tumour. Antibodies were produced in rabbits or sheep, and used in indirect immunofluorescence on frozen sections of 9-to 16-day-old normal or mutant (scaleless) chick-embryo foot skin. In normal scale-forming skin and inscaleless skin, the distribution of anti-laminin and anti-type IV collagen label was uniform along the dermal-epidermal junction and showed no stage-related variations, except for fluorescent granules located in the dermis of early scale rudiments. By contrast, in normal scale-forming skin, the density of anti-types I and III label decreased in the dermis within scale rudiments, whereas it gradually increased in interscale skin. Conversely, anti-fibronectin label accumulated at a higher density within scale rudiments than in interscale skin. In the dermis of thescaleless mutant, anti-types I and III label and antifibronectin label were distributed evenly: the density of anti-collagen label increased with age, while that of antifibronectin decreased and almost completely vanished in 16-day-old skin, except around blood vessels. The microheterogeneous distribution of some extracellular matrix components, namely interstitial collagen types I and III and fibronectin, is interpreted as part of the morphogenetic message that the dermis is known to transmit to the epidermis during the formation of scales. The even distribution of these components in mutantscaleless skin is in agreement with this view. Basement membrane constituents laminin and type-IV collagen do not appear to be part of the dermal morphogenetic message.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1471-0528
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Objective To compare the effects on endometrium, climacteric symptoms and the menstrual cycle, and the clinical and biological tolerance of two percutaneous oestradiol gels used as hormone replacement therapy.Design A large open randomised multicentre study.Setting France and Belgium.Participants Two-hundred and fifty-four women with an intact uterus and who had experienced a natural menopause received either Oestrogel® (n= 126) or Estreva®, a new formulation of oestradiol gel (n= 128), (1.5 mg of oestradiol/day) for the 24 first days of each calendar month during six consecutive months. Nomegestrol acetate (Lutenyl®), a norprogesterone derivative, was administered (5 mg/day) from day 11 to day 24 of each oestradiol cycle.Main outcome measures Examination of endometrial biopsies taken before treatment and between days 18 and 24 of the last treatment cycle, climacteric symptoms assessed using a modified Kupperman index, control of menstrual cycle evaluated by diary cards, and clinical and biological tolerance.Results Both treatments lowered the frequency and intensity of hot flushes and the global Kupperman index. 96% of the cycles were followed by withdrawal bleeding. Breakthrough bleeding or spotting resulted in premature discontinuation of treatment in one volunteer. Mastodynia occurred in 20 women and contributed to the premature termination of treatment in three of them. Endometrial biopsies taken at the end of treatment showed identical histologies in both groups, with a secretory pattern in the majority of women, and absence of hyperplasia.Conclusions This trial confirmed that, when the two oestradiol gels tested were administered cyclically with nomegestrol acetate to postmenopausal women, they were well tolerated, effective and suitable for the treatment of oestrogen deficiency syndrome.
    Type of Medium: Electronic Resource
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  • 3
    ISSN: 1399-3054
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Habituated calli have long been classified as neoplasms together with tumors from different origins. The general opinion is that habituation is a reversible process with an epigenetic basis. This is probably true in most cases examined. However, we show here that there might be several degrees of habituation, which can be considered as steps of a neoplastic progression leading to cancerisation in the absence of an introduced oncogenic pathogen. Cell rejuvenation, loss of the capacity to organize meristematic centers, and loss of totipotency are proposed to define plant cancer through this neoplastic progression of a callus.Habituated tissues share many morphological and biochemical similarities with so-called vitreous shoots from micropropagation. Vitrification and hyperhydric malformations of shoots raised in vitro may be considered as steps of another neoplastic progression, which leads to cancerisation also in the absence of introduced oncogenic pathogens. In this case death of the whole organism occurs either through direct apex necrosis or indirectly, from the loss of the capacity for the primary meristems to function normally, which gives rise to completely anarchic structures. As in the animal kingdom, carcinogenesis in plants is the final result of a multistep process involving the irreversible conversion of a stem cell to a terminal-differentiation-resistant cell.
    Type of Medium: Electronic Resource
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  • 4
    ISSN: 1365-2133
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Basement membrane components and collagen biosynthesis were studied in suction blisters in human skin. The basement membrane components were characterized by immunofluorescence using specific antibodies to type IV collagen, laminin and fibronectin, and collagen biosynthesis was studied by assaying galactosylhydroxylysyl glucosyltransferase.In suction blisters, the separation of epidermis and dermis occurred above the lamina lucida, indicating that the basement membrane, composed of lamina lucida and lamina dcnsa, forms a mechanically strong entity. During the regeneration phase of blisters, type IV collagen and laminin were not observed in the old epidermal blister roof. This indicates that keratinocytes when separated from the underlying basement membrane or connective tissue do not synthesize laminin or type IV collagen.GalactosylhydroxylysyJ glucosyltransferase activity could be demonstrated in blister fluid and was about the same as in serum when expressed on the basis of protein in fresh blisters. It increased by 2–3 fold during the repair of blisters, indicating that there was local production of this enzyme. Further studies revealed that pure epidermis contained galactosylhydroxylysyl glucosyltransferase and hydroxyproline and this suggests that epidermis may synthesize some collagen type which, according to these studies, is not type IV (basement membrane) collagen.
    Type of Medium: Electronic Resource
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  • 5
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 438 (1984), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 6
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 349 (1980), S. 0 
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
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  • 7
    Electronic Resource
    Electronic Resource
    Springer
    Journal of mammary gland biology and neoplasia 3 (1998), S. 215-225 
    ISSN: 1573-7039
    Keywords: BREAST CARCINOMA ; EXTRACELLULAR MATRIX ; LAMININ ; FIBROBLASTS ; MATRIX METALLOPROTEINASES ; IN VIVO TUMORIGENICITY
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The malignant progression of tumors is thoughtto be related to the expression of oncogenes and loss ofexpression of tumor suppressor gene. These factors areintrinsic to the cancer cells themselves. However, carcinomas are also infiltrated by host cells(fibroblasts, endothelial cells, inflammatory cells) andsurrounded by an extracellular matrix which isextensively remodeled. The extracellular matrixcomponents and infiltrating host cells provide amicroenvironment that conditions both tumor progressionand the metastatic process. Transplantation of humantumors into athymic nude mice has become an importantexperimental approach to study the biology of human cancers.The different models developed so far are beginning toelucidate the role of matrix molecules, growth factorsand enzymes as well as fibroblasts in tumor progression. These animal models are likely toprovide a useful tool to evaluate new antitumortreatments.
    Type of Medium: Electronic Resource
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  • 8
    ISSN: 1573-7276
    Keywords: breast adenocarcinoma ; calcium ; endothelial cell ; extravasation ; signaling
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Tumor cell extravasation is a determinant step in the process of hematogenous metastasis. The signal transduction pathways involved in the interactions between tumor cells and the vascular endothelium during transendothelial migration are still undefined. In the present study, we have investigated the influence of human breast adenocarcinoma cells (MCF7) on human umbilical vein endothelial cell (HUVEC) intracellular Ca2+ concentration ([Ca2+]i). We show that the contact between MCF7 cells and a confluent HUVEC monolayer induces an immediate and transient increase in HUVEC [Ca2+]i. This [Ca2+]i rise could not be elicited by tumor cell-conditioned medium, isolated tumor cell membranes, inert beads or normal breast epithelial cells, demonstrating the involvement of specific recognition mechanisms between MCF7 cells and HUVEC. Depletion of HUVEC intracellular Ca2+ stores by the endoplasmic reticulum Ca2+-ATPase inhibitor thapsigargin as well as the selective depletion of inositol 1,4,5-tri phosphate (IP3)-sensitive Ca2+ stores by prior activation of HUVEC using histamine resulted in a complete inhibition of tumor cell-induced [Ca2+]i elevation. Similar results were obtained when HUVEC monolayers were treated with the tyrosine kinase inhibitor herbimycin A, suggesting a role for tyrosine kinase-associated cell surface receptors in tumor cell-endothelial cell interactions. The depletion of HUVEC intracellular Ca2+ stores by thapsigargin was also shown to delay MCF7-induced endothelial cell disjunction, to prevent their spreading on the subendothelial extracellular matrix and transendothelial migration in vitro. These results suggest that transient changes in endothelial [Ca2+]i may govern multiple steps of tumor cell extravasation. © Rapid Science 1998
    Type of Medium: Electronic Resource
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  • 9
    ISSN: 1546-170X
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Medicine
    Notes: [Auszug] Vascular endothelial growth factor (VEGF) stimulates angiogenesis by activating VEGF receptor-2 (VEGFR-2). The role of its homolog, placental growth factor (PlGF), remains unknown. Both VEGF and PlGF bind to VEGF receptor-1 (VEGFR-1), but it is unknown whether VEGFR-1, which exists as a soluble or ...
    Type of Medium: Electronic Resource
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  • 10
    ISSN: 1573-7217
    Keywords: FGF-3 ; FGF-4 ; MCF-7 breast cancer cells ; tumorigenicity ; VEGF
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The transforming properties of fibroblast growth factor 3 (FGF-3) were investigated in MCF7 breast cancer cells and compared to those of FGF-4, a known oncogenic product. The short form of fgf-3 and the fgf-4 sequences were each introduced with retroviral vectors and the proteins were only detected in the cytoplasm of the infected cells, as expected. In vitro, cells producing FGF-3 (MCF7.fgf-3) and FGF-4 (MCF7.fgf-4) displayed an amount of estrogen receptors decreased to around 45% of the control value. However, MCF7.fgf-3 cell proliferation remained responsive to estradiol supply. The sensitivity of the MCF7.fgf-4 cells, if existant, was masked by the important mitogenic action exerted by FGF-4. In vivo, the MCF7.fgf-3 and MCF7.fgf-4 cells gave rise to tumors under conditions in which the control cells were not tumorigenic. Supplementing the mice with estrogen had the paradoxical effect of totally suppressing the start of the FGF-3 as well as the FGF-4 tumors. Tumorigenicity in the presence of matrigel was similar for MCF7.fgf-3 and control cells and was increased by estrogen supplementation. Once started, the MCF7.fgf-4 tumors grew with a characteristic high rate. Remarkably, FGF-4 but not FGF-3, stimulated the secretion of vascular endothelial growth factor (VEGF65) without altering the steady-state level of its mRNA, suggesting a possible regulation of VEGF synthesis at the translational level in MCF7 cells. The increased VEGF secretion is probably involved in the more aggressive phenotype of the MCF7.fgf-4 cells while a decreased dependence upon micro-environmental factors might be part of the increased tumorigenic potential of the MCF7.fgf-3 cells.
    Type of Medium: Electronic Resource
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