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Increased thrombin activation was documented in patients with abdominal aortic aneurysm (AAA). Activated protein C-protein C inhibitor (APC-PCI) complex, a new biological marker of thrombin generation, was measured in a population of 232 patients with AAA and a control group, and the association between aneurysm size, growth rate, and APC-PCI was studied. The patients were divided into cohorts according to AAA diameter and compared with a control group. APC-PCI was significantly higher in all AAA cohorts (n = 232; median, 0.36 microg/L; 10th to 90th percentile, 0.18-1.01) compared with the control group (n = 41; median, 0.19 microg/L; 10th to 90th percentile, 0.11-0.31; P

Mevinolin, a competitive inhibitor of 3-hydroxy-3-methylglutaryl-coenzyme A reductase activity, is a potent inhibitor of cholesterol synthesis. We have tested the effects of mevinolin on cell replication (3H-thymidine incorporation), prostacyclin production (6-keto-PGF1α) and cell death (51Cr release) in cell cultures (human umbilical vein endothelial cells, bovine endothelial cells, human fibroblasts and bovine smooth muscle cells). Mevinolin concentrations ranging from 0.05 μmol/l (reported therapeutic concentration) to 20 μmol/l were used. In human endothelial cells the replication was reduced by 11% at a concentration of 2.0 μmol/l (P<0.01). In fibroblasts and smooth muscle cells the reduction was significant already at 0.1 μmol/l (10%, P<0.01). The prostacyclin production was reduced in endothelial cells at 1.0 μmol/l (19%, P<0.01) and in smooth muscle cells at 2.0 μmol/l (15%, P<0.05). At 20 μmol/l both cell replication and prostacyclin production was markedly reduced by about 40% in all cell types. No effects on 51Cr release or trypan blue staining was seen at any concentration. It is concluded that mevinolin has an effect on DNA synthesis and prostacyclin production on the tested cell types in vitro. These effects were, however, observed only at concentrations higher than those recommended for therapeutical use. [ABSTRACT FROM AUTHOR]

In a consecutive series of 53 cases of oral leucoplakia, smoking history, oro-dental status and arylhydrocarbon-hydroxylase (AHH) inducibility were assessed. There was an increased association of leucoplakia with smoking, particularly in the male cases, but no remarkable findings as to dental status. Overall, there was a slightly higher frequency of cases with high AHH inducibility than expected from a normal control population. This difference was confined to the smokers, where there was a statistically highly significant over-representation of high AHH inducibility and under-representation of low AHH inducibility. The figures in the non-smoking patients were close to the expected. [ABSTRACT FROM PUBLISHER]

Release of inflammatory mediators from leukocytes and endothelial release of vasoactive factors are both important in the pathogenesis of atherosclerosis. To evaluate the concentrations of a specific marker for macrophage activation, neopterin, and the potent endothelial derived vasoconstrictive peptide endothelin-1 (ET-1), during the acute and chronic stages of cerebral ischemia, plasma concentrations of neopterin and ET-1 were measured in 59 patients with acute cerebral infarction or transient ischemic attack (median age 73 years, range 43–93, 27 men) and after a 1 year follow-up in 57⁄59 (97%) of patients. Plasma neopterin was higher at follow-up (6.3 nmol/L [3.7–21.6] vs 5.6 nmol/L [3.5–17.2]; p<0.05) than at the acute stage, whereas the plasma ET-1 concentration was unchanged. Plasma concentrations of both neopterin and ET-1 correlated directly with age both in the acute stage (r = 0.42 and r = 0.35, respectively; p < 0.01) and after follow-up (r = 0.34; p<0.05 and r = 0.27; p = 0.05, respectively). In conclusion, plasma neopterin increased after acute cerebral ischemia, indicating chronic inflammatory activity and continuous macrophage activation in ischemic cerebrovascular diseases. [ABSTRACT FROM AUTHOR]

The concentrations of verapamil and norverapamil have been measured in milk and plasma samples from a 32year-old woman treated with verapamil 80 mg tds while breast-feeding her child. The average steady-state concentrations of verapamil and norverapamil in milk were, respectively, 60% and 16% of the concentrations in plasma. The breast-fed child received less than 0.01% of the dose of verapamil given to the mother. No verapamil or norverapamil (<1 ng/ml) could be detected in the plasma from the child. [ABSTRACT FROM AUTHOR]