Controlling the work function of indium tin oxide: differentiating dipolar from local surface effects.

Indium tin oxide (ITO) reacts with tetra(tert-butoxy)tin to give surface bound alkoxytin species. Ligand exchange occurs in these surface bound species by reaction with substituted phenols. The speciation of surface phenoxides was measured in ultrahigh vacuum by X-ray photoelectron spectroscopy, as was the work function for the surface modified ITO.

CMV induced vascular injury: an electron-microscopic study in the rat.

There is evidence in support of a viral etiology for atherosclerosis. In our study, we demonstrated that cytomegalovirus (CMV) infection in rats caused morphological alterations of the endothelium and subendothelial space of the large vessels and that these alterations are similar to those which are induced by hypercholesterolemia. These alterations consisted of swollen endothelial cells with a surface showing bleb and microvilli formation.

Cytomegalovirus infection induces vascular injury in the rat.

The role of cytomegalovirus (CMV) in the early development of atherosclerosis was studied in a rat model. Arterial samples derived from virus-infected normo- and hypercholesterolaemic animals were investigated by light microscopy at 1, 4, 8 and 16 weeks post infection. Early atherogenic lesions comparable to those seen in non-infected hypercholesterolaemic rats were found in CMV-infected normocholesterolaemic and hypercholesterolaemic animals, starting at 1 week post infection.

The effect of virus infection on the adherence of leukocytes or platelets to endothelial cells.

It has been reported that atherosclerotic lesions contain genomic material belonging to members of the herpes family. This suggests that latent viral infection may be one of the atherogenic triggers. In this study we show that early infection of endothelial cell monolayers with Herpes Simplex virus type 1 (HSV-1) or Cytomegalovirus (CMV) results in an increased monocyte (MC) and polymorphonuclear leukocyte (PMN) adherence, but not in an increased platelet adhesion.

Cytomegalovirus induced PMN adherence in relation to an ELAM-1 antigen present on infected endothelial cell monolayers.

In human umbilical vein endothelial cells infected with cytomegalovirus (CMV), an activation antigen recognized by monoclonal antibody (mAb) ENA1 appeared. mAb ENA1 reacts with an inducible endothelial surface antigen which has characteristics similar to those of ELAM-1. Incubation with anti-IL-1 partly inhibited this appearance and, parallel to this, the virus-induced polymorphonuclear cell (PMN) adhesion was decreased.

The effect of cytomegalovirus infection on the adherence of polymorphonuclear leucocytes to endothelial cells.

Adherence of polymorphonuclear leucocytes (PMN) to the endothelial lining of blood vessels is an essential component of the inflammatory response. In this study the effect of cytomegalovirus (CMV) infection on the adherence of PMNs has been examined using an in vitro model system. Human umbilical venous endothelial cells (HUVEC) were grown on fibronectin-coated plastics.

Virus induced adherence of monocytes to endothelial cells.

In this study we have demonstrated that infection of human umbilical vein endothelial cells (HUVEC) with Herpes simplex virus type 1 (HSV-1) resulted in an increased adherence of monocytes (MC). This enhanced adherence occurred at 3 h post infection (p.i.