Proteinase-activated receptor-1-triggered activation of tumor progression locus-2 promotes actin cytoskeleton reorganization and cell migration.

Tumor progression locus 2 (Tpl2), a mitogen-activated protein kinase kinase kinase (MAP3K) that is activated by provirus insertion in retrovirus-induced rodent lymphomas and mammary adenocarcinomas, is known to transduce Toll-like receptor, interleukin 1, tumor necrosis factor alpha, and CD40 signals and to play an important role in inflammation. Here we show that Tpl2 is also required for the transduction of cell migration and gene expression signals originating in the G-protein-coupled receptor proteinase-activated receptor 1 (PAR1). PAR1 signals transduced by Tpl2 activate Rac1 and focal adhesion kinase, and they are required for reorganization of the actin cytoskeleton and cell migration.

The monarch and the master: Peter the Great and Frederik Ruysch.

The extraordinary European journey of Tsar Peter the Great and his passage to Amsterdam, The Netherlands, allowed him to meet a great figure of medical history who offered insight into the mysteries surrounding the structure of the human body. The famous Dutch anatomist Frederik Ruysch, preeminent in dissection and anatomical preservation, impressed the emperor and inspired his love for anatomy and surgery. Peter the Great was fascinated by the study of the structure of the human body and spent many hours in the anatomical cabinet of Ruysch.

Effects of polymorphisms in chemokine ligands and receptors on susceptibility to coronary artery disease.

Introduction: Atherosclerosis, the underlying disorder of coronary artery disease (CAD), is an inflammatory process involving multiple molecular pathways. Chemokine-mediated mechanisms are potent regulators of atherosclerosis. Genetic variations that alter such signaling pathways could affect susceptibility to CAD.

Expression of heregulin in human coronary atherosclerotic lesions.

Background: Endothelial cells, monocytes/macrophages, and vascular smooth muscle cells contribute to the establishment and progression of atherosclerotic lesions by expressing growth and inflammatory factors. The aim of the present study was to determine whether heregulin (HRG) is associated with human coronary artery disease.

Methods: Twenty-six fresh human coronary artery segments were collected at autopsy.

"Most brilliant in judgment": Alexander the Great and Aristotle.

From historical sources, it is evident that Alexander the Great was indebted to one of his teachers, Aristotle of Stagira. It was the teaching of Aristotle that evoked all the nascent talents of young Alexander and turned him into a great man. Alexander was extremely interested in the secrets of medicine and considered it an art.

Protein and mRNA expression levels of VEGF-A and TGF-beta1 in different types of human coronary atherosclerotic lesions.

It is well documented that inflammation plays a major role in the establishment and progression of atherosclerosis. Endothelial cells, vascular smooth muscle cells and monocytes/macrophages are involved in this process by expressing inflammatory factors. The aim of the present study was to evaluate potential association and risk of VEGF-A and TGF-beta1 in human coronary atherosclerotic lesions.

Peripheral monocytes from diabetic patients with coronary artery disease display increased bFGF and VEGF mRNA expression.

BACKGROUND: Macrophages can produce vascular endothelial growth factor (VEGF) in response to hypoxia, transforming growth factor beta1 (TGF-beta1), angiotensin II, basic fibroblast growth factor (bFGF), and interleukin-1. These factors have been found in the serum of coronary artery disease (CAD) patients as well as in atherosclerotic lesions. The aim of the present study was to test the hypothesis that the expression of VEGF, TGF-beta1 and bFGF in peripheral monocytes and lymphocytes is related to CAD.