Spatial distribution of osteoblast-specific transcription factor Cbfa1 and bone formation in atherosclerotic arteries.

The mechanisms of ectopic bone formation in arteries are poorly understood. Osteoblasts might originate either from stem cells that penetrate atherosclerotic plaques from the blood stream or from pluripotent mesenchymal cells that have remained in the arterial wall from embryonic stages of the development. We have examined the frequency of the expression and spatial distribution of osteoblast-specific factor-2/core binding factor-1 (Osf2/Cbfa1) in carotid and coronary arteries.

In the wake of hospital inquiries: impact on staff and safety.

Mishandled concerns about clinical standards resulted in whistleblowing in four Australian hospitals. Official inquiries followed with recommendations to improve patient safety. In the aftermath of the inquiries, common themes included loss of trust in management and among clinical colleagues, and loss of trust from patients and the community.

Are calcifying matrix vesicles in atherosclerotic lesions of cellular origin?

Over recent years, the role of matrix vesicles in the initial stages of arterial calcification has been recognized. Matrix calcifying vesicles have been isolated from atherosclerotic arteries and the biochemical composition of calcified vesicles has been studied. No studies have yet been carried out to examine the fine structure of matrix vesicles in order to visualize the features of the consequent stages of their calcification in arteries.

Chlamydia pneumoniae in foci of "early" calcification of the tunica media in arteriosclerotic arteries: an incidental presence?

Only a few previous works investigated the involvement of Chlamydia pneumoniae (Chlamydophila pneumoniae) in arterial calcification. The present study investigated a possible association between C. pneumoniae and medial calcification.

S100A8 and S100A9 in human arterial wall. Implications for atherogenesis.

Atherogenesis is a complex process involving inflammation. S100A8 and S100A9, the Ca2+-binding neutrophil cytosolic proteins, are associated with innate immunity and regulate processes leading to leukocyte adhesion and transmigration. In neutrophils and monocytes the S100A8-S100A9 complex regulates phosphorylation, NADPH-oxidase activity, and fatty acid transport.

Expression of GM3 synthase in human atherosclerotic lesions.

We have previously demonstrated that amounts of ganglioside GM3 are markedly higher in human atherosclerotic lesions compared to that in non-diseased arterial tissue. Because the fatty acid composition of GM3 in blood plasma low density lipoproteins (LDL) and the fatty acid composition of GM3 in atherosclerotic lesions differed, we hypothesized that, in addition to GM3 originating from LDL infiltrating the arterial wall from the blood, excessive GM3 may be synthesized locally in atherosclerotic lesions. In the present work, using an anti-GM3 antibody developed by us, we showed that the levels of GM3 synthase in membrane fractions isolated from the atherosclerotic intima were higher compared to those in non-diseased arterial tissue.

Co-accumulation of dendritic cells and natural killer T cells within rupture-prone regions in human atherosclerotic plaques.

We previously reported that CD1d, a molecule responsible for the presentation of lipid antigens, is expressed in atherosclerotic lesions and that its expression is restricted to dendritic cells. Recent studies demonstrating that CD1d-restricted natural killer T (NKT) cells are involved in atherogenesis prompted the present study investigating whether NKT cells are present in human atherosclerotic lesions and, if so, whether there is an association between NKT cells and dendritic cells. We found that NKT cells do accumulate in rupture-prone shoulders of atherosclerotic plaques and observed direct contacts of dendritic cells with NKT cells in rupture-prone regions of plaque.

Graduated compression stockings (20-30 mmHg) do not compress leg veins in the standing position.

Background: Since graduated compression stockings (GCS) reduce the risk of deep venous thrombosis (DVT) in both hospital and ambulant patients, we checked the compressive efficiency of 20-30 mmHg GCS in the standing position.

Methods: In 30 volunteers (17 normal legs, 13 varicose legs), duplex ultrasound was used to measure the internal diameters of the long saphenous vein, posterior tibial veins, peroneal veins, and soleal veins in the lying and standing position and with and without 20-30 mmHg GCS.

Results: Graduated compression stockings effectively compressed both superficial and deep veins in supine individuals but not the superficial or the deep veins when standing.

Detection of Chlamydophila pneumoniae in dendritic cells in atherosclerotic lesions.

Dendritic cells (DCs) populate atherosclerotic lesions and might be involved in the regulation of immune reactions in atherosclerosis. The present work was undertaken to examine a possible association of DCs with Chlamydophila pneumoniae in human atherosclerotic plaques obtained by endarterectomy. C.

Dendritic cells in the arterial wall express C1q: potential significance in atherogenesis.

Objective: Dendritic cells (DCs) accumulate in atherosclerotic lesions but their characteristics and their role in atherogenesis are poorly understood. C1q, an element of the first component of complement, is expressed by interdigitating dendritic cells and follicular dendritic cells in the spleen. It has been suggested that C1q is involved in capturing immune complexes in the lymphoid tissue.

Increased expression of disintegrin-metalloproteinases ADAM-15 and ADAM-9 following upregulation of integrins alpha5beta1 and alphavbeta3 in atherosclerosis.

Regulation of alphavbeta3 and alpha5beta1 integrin function plays a crucial role in atherosclerosis. Possible regulators of integrin-matrix interactions are integrin-binding ADAMs (proteins with a disintegrin- and metalloproteinase-domain), like ADAM-15 and ADAM-9. Molecular interactions between ADAM-15, alpha5beta1, and alphavbeta3 have been demonstrated.

Induction of apoptosis in vascular cells by plasminogen activator inhibitor-1 and high molecular weight kininogen correlates with their anti-adhesive properties.

Plasminogen activator inhibitor-1 (PAI-1) and two-chain high molecular weight kininogen (HKa) exert anti-adhesive properties in vitronectin-dependent cell adhesion. Here, the hypothesis was tested that these anti-adhesive components promote apoptosis in vascular cells. PAI-1 or HKa induced a 2- to 3-fold increase in apoptosis of human umbilical-vein endothelial cells (HUVEC) and vascular smooth muscle cells (VSMC) adherent to vitronectin, as determined by annexin V-FACS assay, similar to alphav-integrin inhibitor cyclo-(Arg-Gly-Asp-D-Phe-Val)-peptide (cRGDfV).

Expression of heat shock protein-70 by dendritic cells in the arterial intima and its potential significance in atherogenesis.

Objective: Overexpression of heat shock proteins (HSPs) is an important means of cell protection during physiologic stress such as occurs during atherogenesis. Immune responses are early events in atherosclerosis, with recent studies indicating that both humoral and cellular autoimmune processes in atherogenesis are directed toward HSPs. Dendritic cells are the key cells in the initiation and regulation of immune responses.