If decisive anatomic structures are clearly depicted and the measuring points are set correctly, there is a good correlation between HRUS and MRI measurements of the optic nerve and the ONSD even on transbulbar sonography. As most of the standard and cut-off values that have been published for ultrasound are significantly lower than the results obtained with MRI, a reevaluation of sonographic ONSD measurement with correlation to MRI is necessary.

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Adhesion of tumor cells to endothelium via cell-adhesion molecules constitutes a crucial step in metastasis, which is largely responsible for the poor prognosis of small-cell lung carcinoma (SCLC). Patients with SCLC were reported to have elevated levels of intercellular adhesion molecule-1 (ICAM-1). The present study therefore focusses on endothelial ICAM-1 in tumor-cell adhesion. We found that the adherence of SCLC cells (cell lines H24, H69, H82) to cultured vascular endothelium in stasis and flow depends on the expression of ICAM-1. After blocking endothelial ICAM-1 with monoclonal antibodies, adhesion was significantly reduced. These results pinpoint ICAM-1 for the first time as a molecule crucially involved in SCLC cell-endothelial adhesion.

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SummaryDeposition of blood components in branching flow has been investigated primarily with regard to platelets. We instead examined thrombin-induced fibrin clot formation in separated laminar as well as turbulent branching flow. The most rapid clot growth and largest clot mass was obtained at the lowest inflow rate. Increased inflow reduced the clot size and turbulence completely prevented clot formation. Examination of corresponding flow conditions revealed the recirculation zone in laminar flow to be characterized by two stationary, counterrotating vortices. Niches of stagnant flow, exhibiting long residence times, low wall shear rates and characterized by convergent flow, were spared between the bulk flow and these vortices. Here, fibrin clot growth continued even when shear rates were increased more than 100-fold. Our results indicate that, in branching flow, the long residence times and convergent flow characteristic of flow niches rather than shear rate are critical for fibrin clot formation.

SummaryAs we demonstrated earlier, platelets adhere to intact endothelium provided they are activated and convectively transported against the endothelial surface. To identify the platelet receptors involved we superfused cultured endothelium with activated platelet rich plasma (PRP) by means of the Stagnation Point Flow Adhesio- Aggregometer while blocking various platelet receptors. Inhibition was performed with the tetrapeptide RGDS, the non-peptide Ro-43-8857, or a monoclonal antibody directed against integrin αIIbβ3. Platelet deposition was video-recorded and quantified by image analysis. Infusion of RGDS or Ro-43-8857 into ADP-stimulated PRP completely prevented adhesion as well as subsequent aggregation. Interrupting the inhibitor infusion while ADP stimulation persisted, prompted adhesion and aggregation, demonstrating the reversibility of the inhibition. Platelet adhesion was irreversibly blocked by preincubation of the PRP with the moab against αIIbβ3. Its specific binding was confirmed by immuno-electron microscopy. Our results suggest that platelet adhesion to intact endothelium is mediated via platelet integrin αIIbβ3.

SummaryFibrinogen substitution can correct bleeding in afibrinogenemia. We assessed the effect of fibrinogen substitution in a patient lacking immunoreactive fibrinogen. Fibrinogen and thrombin time were not measurable before, but became detectable within 30 min after substitution, parallelled by an increase in ADP-induced platelet aggregation from <10% to 32%. Platelet adhesion, measured by Stagnation Point Flow Adhesio- Aggregometry, was notdetectable prior to substitution but attained normal values thereafter. Scanning electron microscopy of adhering platelets revealed pseudopodia protrusion and spreading. Morphometry revealed two populations of spread platelets one of which demonstrated inhibited spreading as compared to healthy controls. Immunoelectron microscopy revealed normal GPIIb/IIIa receptor expression, both before and after substitution. Dynamic and kinematic viscosity of plasma and whole blood remained below the 99.9% confidence border of a healthy control group. In afibrinogenemia fibrinogen levels as low as 10% of normal concentration sufficed to normalize coagulation, platelet adhesion, and, partially, spreading.