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Multiple sclerosis markers

S.2.2.9. Markers of immune activation and process. Acting with TNF-a-mRNA, sICAM-1, IL-lO-mRNA, and sTNF-R, these proteins and nucleic acids can be used as markers of the immunologically mediated inflammatory process seen in multiple sclerosis (M4). This disorder is associated with deregulation of cytokine expression, especially in regard to TNF-a. [Pg.21]

Tetranectin (TN). Tetranectin is a plasma protein of about 80 kDa. A reduction in the serum TN level has been described in malignant disease and in other conditions with tissue remodeling, whereas it does not seem to exhibit acute-phase reactant behavior. Using a polyclonal ELISA to determine the TN concentrations in pair of CSF/serum quotient in pair of CSE and serum, it was found that the CSE/serum quotient compared to the QAib was compatible with intrathecal TN synthesis. In clinically definite multiple sclerosis a reduced CSF/serum quotient was found, suggesting that the hypothesis of a reduced TN level as a marker of tissue remodeling may be extended to the CNS (C5). [Pg.25]

Inflammation is associated with various diseases such as rheumatoid arthritis, cancer, myocarditis, arteriosclerosis, bowel diseases, multiple sclerosis, asthma, and many others. While several inflammatory markers are commonly expressed during any inflammatory disorder, some are symptom specific. Therefore, the gene array data will be particularly helpful in indicating the appropriate disease model for subsequent preclinical and clinical tests. Only functional, active extracts with potentially safe and novel modes of actions may then be subjected to labor-intensive large-scale extraction, fractionation, characterization, and isolation of novel bioactive components. We believe that the strategy as described schematically in Figure 4.1 will allow efficient use of plant extracts and other natural resources toward identification of novel drug leads for human health care. [Pg.81]

Because of the instability of peroxynitrite under physiological conditions, the detection of 3-nitrotyrosine (NC>2-Tyr) has become a biochemical marker for the presence of peroxynitrite in pathophysiological processes. The biological significance of tyrosine nitration is a subject of great interest, because extensive evidence supports the formation of nitrotyrosine in vivo in diverse pathological conditions such as heart diseases, chronic inflammation and autoimmune diseases, cancer, Parkinson s disease, Alzheimer s disease, multiple sclerosis, amyotrophic lateral sclerosis, and ischemia-reperfusion injury [11]. [Pg.192]

Lennon VA, Kryzer TJ, Pittock SJ, Verkman AS, Hinson SR (2005) IgG marker of optic-spinal multiple sclerosis binds to the aquapo-rin-4 water channel. J Exp Med 202 473 77. [Pg.253]

Patient was treated with Copaxone for multiple sclerosis and has developed breast cancer. Doctors analyzed the blood samples and found an increase in regulatory T cell numbers based on CD25 and Foxp3 markers. The suggestion made by doctors was that Copaxone induces regulatory T cells and this may lead to cancer development. Which of the comments bellow is FALSE. [Pg.671]

The targeting of molecular markers associated with inflammation could, in principle, be useful for the imaging and therapy of several other inflammatory diseases. Besides rheumatoid arthritis, these include inflammatory bowel diseases (Crohn s disease and ulcerative cohtis), psoriasis, atherosclerosis, and diseases of the central nervous system (Alzheimeris disease, multiple sclerosis, etc.). [Pg.1285]

Qin, J., Goswami, R., Balabanov, R. and Dawson, G. Oxidized phosphatidylcholine is a marker for neuroinflammation in multiple sclerosis brain. J Neurosci Res 85 (2007) 977-984. [Pg.267]

Jonasdottir, A., Thorlacius, T., Fossdal, R., et al. (2003) A whole genome association study in Icelandic multiple sclerosis patients with 4804 markers. J. [Pg.70]

Gl. Galboiz, Y., Shapiro, S., Lahat, N., Rawashdeh, H., and Miller, A., Matrix metalloproteinases and their tissue inhibitors as markers of disease subtype and response to interferon-beta therapy in relapsing and secondary-progressive multiple sclerosis patients. Ann. Neurol. 50, 443-451 (2001). [Pg.77]

Dermatomyositis occurred in a 57-year-old patient who took interferon beta for multiple sclerosis [56 ]. Immunohistochemical staining of skin biopsies for myxovirus-resistance protein A (a surrogate marker of cutaneous type I interferon signalling) showed increased staining that correlated temporally with interferon beta treatment and subsequent disease activity. In vitro treatment with interferon beta of peripheral blood mononuclear cells isolated from this patient showed enhanced type I interferon signaling, assessed by interferon-induced gene expression profiles. [Pg.776]


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