"The goals of this study were to characterize the platelet contribution to soluble CD-40 ligand (sCD40L), to correlate its formation with the extent of oxidative stress and platelet activation, and to investigate the effects of improved metabolic control and low-dose aspirin on these processes."

“This study provides several lines of evidence for the dependence of sCD40L release on TXA₂-dependent platelet activation in T2DM and provides novel mechanistic insight into the amplification loops of persistent platelet activation in this setting.”

"Resistance to inhibition of platelet function by aspirin may contribute to future myocardial infarction and stroke.  Adverse cardiovascular outcomes have been associated with aspirin resistance on several different platelet function assays, including the level of urinary 11-dehydro thromboxane B₂ (Tx-M), platelet aggregation to arachidonic acid and adenosine diphosphate, and closure time on the platelet function analyzer-100.  We examined the concordance of these aspirin-resistance assays and their relation to cardiovascular risk factors in a primary prevention population."

“Aspirin resistance by platelet function analyzer-100 was associated only with increased von Willebrand factor levels and not with atherosclerotic risk profile.”

"This study is to investigate the rate of platelet thromboxane (TX) biosynthesis and its determinants in Alzheimer's disease.

“Urinary 11-dehydroTXB2 and 8-iso-PGF2a were significantly higher in Alzheimer patients than in controls”

“No difference was found in CRP, TNF-a and IL-6 levels between the two groups.”

“Platelet activation is persistently enhanced in Alzheimer’s disease.”

"Both environmental and genetic factors, including aspirin pharmacokinetics, inflammation, platelet COX-2, use of non-steroid anti-ainflammatory drugs and dyslipidaemia may determine variable platelet response to acetylsalicylic acid.”’ 

"However, CRP level was significantly associated with the extent of platelet refractoriness to acetylsalicylic acid in these patients, which points out that even subclinical inflammatory states may be considered possible candidates for suboptimal acetylsalicylic acid response."

"Among aspirin-treated patients at high risk of cardiovascular events, persistent thromboxane generation predicts the risk of the composite outcome of myocardial infarction, stroke, or cardiovascular death, independent of other cardiovascular risk factors."

"In aspirin-treated patients, urinary concentrations of 11-dehydro thromboxane B₂ predict the future risk of myocardial infarction or cardiovascular death. These findings raise the possibility that elevated urinary 11-dehydro thromboxane B₂ levels identify patients who are relatively resistant to aspirin and who may benefit from additional antiplatelet therapies or treatments that more effectively block in vivo thromboxane production or activity."

"The aim of this study was to determine the extent of change in platelet and coagulation markers in the acute phase of ischemic stroke and to assess the utility of marker mesurement in stroke subtype classification.  Urinary 11-dehydro-thromboxane B₂ (11-deTXB₂), a marker of in vivo platelet activation, and markers of coagulation activation, including prothrombin fragment 1 +2 (F1 + 2), thrombin-antithrombin complex (TAT) and fibrinogen, were measured in 25 patients with ischemic stoke within 24 h of onset symptoms. Eight patients taking aspirin at the time of the stroke had signficantly lower 11-dTXB2 values than patients not taking aspirin (964 vs. 4,314 pg/mg of creatinine P=0.0007).  Stroke patients not taking aspirin had significantly higher 11-dTXB2 concentration than age-matched controls (4,314 vs. 1,788 pg/mg of creatinine; P= 0.0006)."

"Thromboxane A2 (TXA2) biosynthesis is enhanced in the majority of patients with type lla hypercholesterolemia.  Because simbastatin (a 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor) was previously shown to reduce platelet aggregation and TXB2 production ex vivo, we investigated TXA2 biosynthesis and platelet function in 24 patients with type ll hypercholesterolemia randomized to receive in a double-blind fashion simvastatin (20mg/d) or placebo for 3 months.  The urinary excretion of 11-dehydro-TXb2, largely a reflection of platelet TXA2 production in vivo, was measured by a previously validated radioimmunoassay technique.  Blood lipid levels and urinary 11-dehydo-TXB2 excretion were significantly (p<.001) reduced by simvastatin.  In contrast, placebo-treated patients did not show any statistically signficant changes in either blood lipids or 11-dehydro-TXB2 excretion."

“Tight metabolic control achieved with insulin therapy reduced the levels of 11-dehydro-thromboxane B₂ by approximately 50 percent.”

“Aspirin in low doses (50 mg per day for seven days) reduced urinary excretion of the metabolite by approximately 80 percent in four patients.”