SummaryA group of 100 patients with intermittent claudication (70 male, 30 female), treated with 100 mg ASA per day, were followed over 18 months after elective percutaneous balloon angioplasty. Platelet function was monitored over a period of 12 months by corrected whole blood aggregometry (CWBA). Upon stimulation by arachidonic acid (AA), adenosine diphosphate (ADP) and collagen, CWBA-results were obtained by an electronic acquisition and evaluation system correcting for hematocrit and platelet count of the blood sample.All patients showed a completely inhibited platelet response to AA stimulation. Comparison of the CWB A-results with clinical parameters revealed that reocclusions at the site of angioplasty occurred exclusively in male patients for which CWBA failed to prove an inhibition of aggregation upon both agonists, ADP and collagen, and for these patients the risk of complication is at least 87% higher (p = 0.0093).Only 40% of male patients show the expected effect of ASA on in vitro platelet aggregation at any given point in time and CWBA is capable of predicting those male patients which are at an elevated risk of reocclusion following peripheral angioplasty.

Arterial branchings closely fulfill several "bifurcation rules" which are deemed to optimize blood flow. The question is whether these local criteria in conjunction with a general optimization principle can explain the overall structure of an arterial tree. We present a model of an arterial vascular tree which is grown on the computer by successively adding terminal vessel segments. Each new terminal segment is connected to the optimum site within the preexisting tree, and the new bifurcation is optimized geometrically. After each step of adding and optimizing, the whole tree is rescaled to meet invariant boundary conditions of pressure and flow at each terminal site. Thus, local geometric optimization is used to induce simultaneously an optimized global structure. The comparison between the model and real coronary arterial trees shows good agreement regarding structural appearance, morphometric parameters, and pressure profiles.

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The synergy of TGF-β and Axl induces CXCL5 secretion causing the infiltration of neutrophils into HCC tissue. Intervention with TGF-β/Axl/CXCL5 signaling may be an effective therapeutic strategy to combat HCC progression in TGF-β-positive patients. This article is protected by copyright. All rights reserved.