This feasibility study shows a high accuracy and a good correlation of LE-DECT and LE-MRI to histopathology for the detection of LE in a porcine model of reperfused chronic MI.
The increase of ICAM-3 levels might indicate the anti-inflammatory effect of the MP treatment. It could be interesting to search for similar effects investigating the new immune modulatoring therapy forms of MS.
The present data suggest that IFN beta-1b induces the expression and shedding of TNF-R1 and TNF-R2. The magnitude of an increase of sTNF-Rs may be a marker for the effectiveness of treatment with IFN beta-1b.
Objective ‐ The intercellular adhesion molecule‐1 (ICAM‐1) is a member of the Ig supergene family. ICAM‐1 is expressed on various cells like peripheral blood lymphocytes, endothelial cells or thymic cells and the cell surface form is supposed to be shed into a soluble form. The expression of ICAM‐1 is induced by cytokines like Interleukin‐1, TNF alpha or interferon gamma. The aim of the study was to investigate whether changes of cell surface and soluble ICAM‐1 in the cerebrospinal fluid (CSF) and blood are indicative for disease activity in patients with multiple sclerosis (MS). Material and methods ‐ In all patients with relapsing‐remitting MS (relapse: n=31, remission: n= 11) and controls (n= 13) the expression of cell surface ICAM‐1 (c‐ICAM‐1) was determined by two colour flow cytometry. Soluble ICAM‐1 (s‐ICAM‐1) was measured by ELISA. Follow‐up examinations were done 3 months later. Results ‐ In 31 patients with a current relapse we found significantly decreased expression levels of c‐ICAM‐1 on leukocytes in CSF (P<0.001) and blood (P<0.10), when compared to those 11 individuals experiencing remission. In contrast we observed significantly (P<0.05) increased levels of s‐ICAM‐1 in CSF of patients with relapses. Comparing patients who had been in remission for more than 4 weeks (n= ll) with remission lasting longer than 3 months (n=28) we detected stable c‐ICAM‐1 expression on CD3 + T cells in blood. Conclusion ‐ Our results demonstrate for the first time that c‐ICAM‐1 on CD3 + T‐cells in CSF and blood is an activity marker in MS.
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