Soluble intercellular adhesion molecule-1 (sICAM-1) after kidney transplantation: the origin and role of urinary sICAM-1?
Increased urinary excretion of sICAM-1 was demonstrated in kidney transplanted patients a few days before acute rejection. It seems to originate from activated macrophages and/or from the tubular epithelial cells. The fact that urinary sICAM-1 is not bound to hyaluronan or to leukocytes suggests that it is not able to compete with membrane-bound ICAM-1 for these bindings, but may do so for the binding of activated macrophages.
Our findings suggest that term neonatal encephalopathy resulting from HI induces functional and structural damages to the inner retina, while relatively sparing the photoreceptors. These findings raise the possibility that retinal injuries may contribute to visual impairments with or without the presence of brain injury in term asphyxiated newborns and, thus, warrant further studies with humans and animals to better understand the disease process.