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Phenotype Markers (phenotype + marker)

Distribution by Scientific Domains

Medical Sciences	100%

Selected Abstracts

Perspectives on cancer immuno-epidemiology

CANCER SCIENCE, Issue 12 2004
Kei Nakachi
Estimating human cancer risk based on host-environment interaction is one task of epidemiology, and it has provided indispensable knowledge for prevention of cancer. The recent development of gene-engineered mice has also provided solid evidence about the relationship between cancer development and immunity. The aim of this review is to discuss the possible contribution of epidemiology to understanding the role of immunity in host defense against cancer, and also to assess the involvement of inflammation in the occurrence of selected cancers. Here we look at the concepts of cancer immunosurveillance and infection-inflammation-cancer, and include a brief introduction to recent studies in humans and experimental animal models. It has been postulated for many years that the immune system has the ability to recognize and eliminate nascent transformed cells in the body (so-called cancer immunosurveillance hypothesis), and this idea has recently obtained strong support from animal experiments. In humans, follow-up studies among immunosuppressed transplant recipients revealed a remarkably increased risk of not only selected malignancies, but also cancers with no known viral etiology. On the other hand, a prospective cohort study among the general population revealed that individuals with low natural cytotoxic activity of peripheral blood lymphocytes had an increased risk of cancer development. More studies are warranted to allow the construction of a model for the interaction between host immunity, aging, and the environment. The host immune system is also involved in inflammatory responses to pathogen infection: insufficient immune function of the host, or repeated infection, may result in persistent inflammation, where growth/ survival factors continuously act on initiated cells. The combined use of biomarkers will be necessary to define low-grade persistent inflammation in future cohort studies; and, in addition to these phenotype marker-based cohort studies, one plausible future direction will be a genomic approach that can be undertaken within cohort studies, looking at the genetic background underlying individual variations in phenotype markers. [source]

Mesenchymal stem cell function on hybrid organic/inorganic microparticles in vitro

JOURNAL OF TISSUE ENGINEERING AND REGENERATIVE MEDICINE, Issue 5 2010
A. Champa Jayasuriya
Abstract The aim of this study was to investigate mesenchymal stem cell (MSC) function on novel type hybrid organic/inorganic microparticles (MPs) for application to bone regeneration. The MPs were based on chitosan (CS) and consisted of inorganic components, such as dibasic calcium phosphate (CaHPO4) or calcium carbonate (CaCO3). The MPs were crosslinked using tripolyphosphate. Four types of hybrid MPs were fabricated: CS; CS,10% CaHPO4; CS,20% CaHPO4; and CS,10% CaCO3. The MSCs were attached to all the types of MPs at day 1 and started to spread and proliferate further by days 2 and 7, as analysed by fluorescence microcopy. Cell proliferation was measured at days 7, 14, 21 and 28 by counting the cells attached on the MPs. The number of proliferated cells increased significantly for all types of MPs as time increased. MSC differentiation was analysed using osteoblast (OB) phenotype markers, including alkaline phosphatase activity (ALP), collagen I (COLLI) and osteocalcin (OCN) at days 7, 14, 21 and 28, using quantitative real-time PCR. The normalized mRNA expression of ALP for all MPs was observed only at day 7. The normalized mRNA expression of COLLI and OCN was significantly increased for all types of hybrid MPs at each time point compared to the control samples. Collectively, our results proved that hybrid organic/inorganic MPs were non-cytotoxic and supported MSC attachment, spreading, proliferation and differentiation into the OB phenotype. These hybrid MPs have great potential for application as bone-void fillers or bone tissue engineering scaffolds in bone regeneration. Copyright © 2009 John Wiley & Sons, Ltd. [source]

Hypoxia-inducible factor 1, inhibits the fibroblast-like markers type I and type III collagen during hypoxia-induced chondrocyte redifferentiation: Hypoxia not only induces type II collagen and aggrecan, but it also inhibits type I and type III collagen in the hypoxia-inducible factor 1,,dependent redifferentiation of chondrocytes

ARTHRITIS & RHEUMATISM, Issue 10 2009
Elise Duval
Objective Autologous chondrocyte implantation requires expansion of cells ex vivo, leading to dedifferentiation of chondrocytes (loss of aggrecan and type II collagen to the profit of type I and type III collagens). Several approaches have been described for redifferentiation of these cells. Among them, low oxygen tension has been exploited to restore the differentiated chondrocyte phenotype, but molecular mechanisms of this process remain unclear. However, under conditions of hypoxia, one of the major factors involved is hypoxia-inducible factor 1, (HIF-1,). The purpose of this study was to investigate the role of HIF-1, during human chondrocyte redifferentiation. Methods We used complementary approaches to achieving HIF-1, loss (inhibition by cadmium ions and dominant-negative expression) or gain (ectopic expression and cobalt ion treatment) of function. Expression of chondrocyte, as well as fibroblast-like, phenotype markers was determined using real-time reverse transcription,polymerase chain reaction and Western blot analyses. Binding activities of HIF-1, and SOX9, a pivotal transcription factor of chondrogenesis, were evaluated by electrophoretic mobility shift assays and by chromatin immunoprecipitation assay. Results We found that hypoxia and HIF-1, not only induced the expression of SOX9, COL2A1, and aggrecan, but they simultaneously inhibited the expression of COL1A1, COL1A2, and COL3A1. In addition, we identified the binding of HIF-1, to the aggrecan promoter, the first such reported demonstration of this binding. Conclusion This study is the first to show a bimodal role of HIF-1, in cartilage homeostasis, since HIF-1, was shown to favor specific markers and to impair dedifferentiation. This suggests that manipulation of HIF-1, could represent a promising approach to the treatment of osteoarthritis. [source]

Effect of low molecular weight heparin (dalteparin) and fondaparinux (Arixtra®) on human osteoblasts in vitro,

BRITISH JOURNAL OF SURGERY (NOW INCLUDES EUROPEAN JOURNAL OF SURGERY), Issue 2 2005
A. E. Handschin
Background: The prolonged administration of heparin for prevention and treatment of venous thromboembolism has been associated with a risk of heparin-induced osteoporosis. Fondaparinux is a new antithrombotic drug that specifically inhibits factor Xa. Because of the known interactions of other antithrombotic agents with bone remodelling, the effects of fondaparinux on human osteoblasts were analysed in vitro. Methods: Primary human osteoblast cell cultures were incubated with either the low molecular weight heparin dalteparin at concentrations of 30, 300 and 900 µg/ml or with fondaparinux at concentrations of 25, 50, 100, 150, 200 and 250 µg/ml. Cellular proliferation rate and protein synthesis were measured. Expression of genes encoding osteocalcin, collagen type I and alkaline phosphatase was examined by reverse transcriptase,polymerase chain reaction. Results: Incubation with dalteparin led to a significant, dose-dependent inhibition of osteoblast proliferation, inhibition of protein synthesis, and inhibited expression of phenotype markers (osteocalcin and alkaline phosphatase genes) after 3 and 7 days. No inhibitory effects were observed in the fondaparinux-treated cells. Conclusion: Fondaparinux did not inhibit osteoblast proliferation in vitro and may reduce the risk of heparin-induced osteoporosis associated with long-term heparin administration. Copyright © 2004 British Journal of Surgery Society Ltd. Published by John Wiley & Sons, Ltd. [source]