Non-glandular leaf trichomes positively inXuence the abundance of many phytoseiid mites. We characterized the inXuence of grape leaf trichomes (domatia, hairs, and bristles) on Typhlodromus pyri Scheuten abundance over two years in a common garden planting of many grape varieties and 2 years of sampling in a commercial vineyard. In general, a lack of trichomes was associated with much lower predator numbers and in the case of Dechaunac, a cultivar with almost no trichomes, very few T. pyri were found. Phytoseiid abundance was best predicted by a model where domatia and hair had an additive eVect (r 2 = 0.815). Over two years of sampling at a commercial vineyard there were T. pyri present on all of the 5 cultivars except Dechaunac. At the same time, European red mite prey were present on Dechaunac alone. These results suggest that on grape cultivars lacking leaf trichomes, T. pyri likely will not attain suYcient densities to provide biological control of European red mite, despite presence of the mite food source. The relationship between leaf trichomes and phytoseiid abundance that is observed at the scale of single vines in a garden planting appears to also be manifest at the scale of a commercial vineyard. Because persistence of predatory mites in or nearby the habitats of prey mites is important for eVective mite biological control, leaf trichomes, through their inXuence on phytoseiid persistence, may be critical for successful mite biological control in some systems.

The influence of hyperlipidemic sera on prostacyclin (PGI 2 ) production by cultured endothelial cells was assessed by comparing sera from three types of hyperlipidemias with sera from normal subjects. Sera prepared from normal whole blood (WBS), platelet-rich plasma (PRPS), and platelet-poor plasma (PPPS) were also compared. Bovine aortic endothelial cells (BAEC) incubated with 25% WBS increased PGI 2 synthesis significantly within 1 hour, with little further increase by 16 hours; human umbilical vein endothelial cells (HUEC) incubated with 25% WBS for 1 hour showed no elevation in PGI 2 , whereas PGI 2 levels increased substantially after 16 hours. PPPS and PRPS stimulated PGI 2 synthesis by BAEC equally at 1 hour. However, there was no rise in PGI 2 after PPPS in HUEC; PGI 2 rose after 16 hours with PRPS and rose further with WBS after 16 hours.Since WBS best enhanced PGI 2 production in human endothelial cells, it was chosen for comparison of the effects of hyperlipidemic and normolipidemic sera. PGI 2 synthesis by HUEC significantly increased upon incubation with WBS from Types Mb and IV patients in comparison to WBS from Type lla hypercholesterolemic patients or normal controls. In contrast, WBS from all these hyperlipidemic subjects stimulated PGI 2 synthesis by BAEC similarly to WBS from controls. We conclude that incubation of human endothelial cells with WBS containing high levels of atherogenic lipoproteins does not reduce PGI 2 formation by the cells. Moreover, the time course and the contribution of lipid, plasma, or cellular factors to PGI 2 formation vary according to the cell type tested. Caution should be exercised in extrapolating results achieved with serum and cells from the same species to other settings. shown that high density lipoproteins (HDL) can provide arachidonic acid for PGI 2 synthesis by porcine and human endothelial cells, while low density lipoproteins (LDL) apparently have a negligible effect under the same experimental conditions. 45 In other studies, incubation of human umbilical cord endothelial cells (HUEC) with low density lipoproteins diminished PGI 2 production, 6 but this effect may have reflected oxidation of LDL during isolation.7 Since endothelial cells in vivo are not exposed to isolated lipoprotein fractions, and little information is available on the effect of hyperlipidemic sera on PGI 2 production by endothelial cells, the influence of different serum lipoprotein patterns on PGI 2 formation by cells requires further examination. Clarification of such effects takes on clinical relevance in view of recent evidence that vascular PGI 2 may have an antiatherogenic effect both through regulation of cholesteryl ester deposition in vascular smooth muscle and through regulation of smooth muscle cell proliferation.