Background: Cell adhesion molecules are proteins expressed on the surface of a variety of cells and mediate the leucocyte response to inflammation. Some of these molecules are released to the plasma as soluble forms, whose presence indicates the degree of vascular endothelial activation or dysfunction. Increased concentrations of soluble adhesion molecules are thought to hamper the immune response and mediate the atherosclerotic inflammatory process. Studies on the effect of exercise on the concentrations of soluble adhesion molecules have almost exclusively used aerobic exercise. Aim: To assess the effect of resistance exercise on the serum concentrations of five cell adhesion molecules during and immediately after 30 min of exercise in lean and obese participants. Methods: Fourteen healthy young men (eight lean and six obese) performed 3 sets of 10 resistance exercises with 10-12 repetitions at 70-75% of one repetition maximum in a circuit training fashion. Venous blood samples were drawn at baseline and at the end of the first, second and third sets. The serum concentrations of vascular cell adhesion molecule-1, intercellular cell adhesion molecule-1, E-selectin, P-selectin and L-selectin were measured in a biochip array analyser. Results: No significant changes were observed in the concentrations of these cell adhesion molecules during exercise, or between lean and obese participants. Conclusion: Our data indicate that resistance exercise of moderate to high intensity does not affect the serum concentrations of cell adhesion molecules in healthy young lean or obese men, suggesting no considerable negative effect on immune function.C ell adhesion molecules are glycoproteins expressed on the surface of a variety of cells (such as vascular endothelial cells, leucocytes and platelets) and mediate the leucocyte response to inflammation. 1 Four main groups of cell adhesion molecules are recognised: the integrin receptor family; the immunoglobulin superfamily, which includes intercellular cell adhesion molecules (ICAM) and vascular cell adhesion molecule-1 (VCAM-l); selectins, including E-selectin, L-selectin and P-selectin; and cadherins. 2 Some of the cell adhesion molecules are released to the plasma as soluble forms, whose presence indicates the degree of vascular endothelial activation or dysfunction. 3 4 Increased concentrations of soluble adhesion molecules are thought to hamper the immune response by occupying the binding sites meant to be used by the corresponding cell-bound adhesion molecules; this may have a temporary negative influence on the ability of leucocytes to adhere to and transmigrate the endothelium. 5 Cell adhesion molecules have also been suggested to be mediators of the atherosclerotic inflammatory process. 6 Their plasma concentrations have been positively correlated with the risk for cardiovascular disease, 7 and are increased in patients with heart failure. 8 Body weight and obesity have been found to affect the plasma concentrations of cell adhesion molecules, as soluble ICAM-1 and E-se...

Calprotectin, also known as the S100A8/A9 or MRP8/14 complex, is a major calcium-binding protein in the cytosol of neutrophils, monocytes, and keratinocytes. It differs from other S100 proteins in its zinc-binding capacity. The authors describe a 4-year-old girl with severe anemia, neutropenia, inflammation, and severe growth failure. Bone marrow examination showed moderate dyserythropoiesis. No hemolysis, iron deficiency, hemoglobinopathies, immunologic diseases, or autoantibodies were detected. Serum levels of copper and ceruloplasmin were within the normal range, although the serum zinc concentration was markedly increased (310 microg/dL). Urinary zinc excretion and erythrocyte zinc concentrations were within the normal range. Family studies showed normal zinc and copper plasma levels. The patient's plasma calprotectin concentration showed a 6,000-fold increase (2,900 mg/L) compared with normal values. The calprotectin concentration is known to be elevated in many inflammatory conditions but is generally below 10 mg/L and thus far below the levels reported in this patient. The authors describe this case as an inborn error of zinc metabolism caused by dysregulation of calprotectin metabolism, which mainly presented with the features of microcytic anemia and inflammation.

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Hyperinsulinemia with or without DM2 is a frequent long-term sequela of BMT, especially following cGvHD. In this report, an extensive evaluation of a patient with cGvHD is described: glucose and insulin during OGTT, markers of inflammation, adiponectin and RBP4, body composition analysis, and the kinetics of GLUT3 and GLUT4 in circulating monocytes were evaluated. Hyperinsulinemia, associated with partial lipodystrophy, elevated RBP4, low adiponectin levels, and decreased expression of GLUT3 and GLUT4 were detected. The defects disclosed in this particular patient possibly explain, at least in part, the mechanisms underlying insulin resistance in patients undergoing BMT. It is not clear whether insulin resistance was caused by the drugs, the process itself, or the residual damage to the muscles and/or adipose tissue.