varicose veins/protease

OBJECTIVE Imbalance of matrix metalloproteinase enzymes (MMP) and their inhibitors (TIMPs) may contribute to the development of varicose veins. We hypothesised that, histological changes in varicose vein wall correlate with alterations in expression of MMP/TIMP. METHODS Varicose veins (n=26) were

Varicose veins are a major chronic venous disease characterised by extensive remodelling of the extracellular matrix architecture in the vascular wall. Although matrix metalloproteinases have been implicated in these pathologic events, little is known about the functional relevance of other protease

Varicose veins of lower extremities, varicocele and varicose dilation of pelvic veins including ovaricovaricocele are the most common non-inflammatory diseases of venous system. The same mechanisms determined varicose dilatation regardless localization of the vein. First of all, these are wall

BACKGROUND Studies have reported that structural proteins such as elastin and collagen are decreased in varicose veins compared to normal controls. We hypothesized that the changes observed in varicose vein wall composition may be related to alterations in extracellular matrix remodeling proteins,

An alteration of extracellular matrix is involved in varicose veins. We have previously shown that collagen III production, but not its mRNA expression, is decreased in cultured smooth muscle cells (SMC) from varicose veins, involving an over-production of collagen I. In this study, the mechanisms

If venous stasis due to blood stagnation has been recognized to be involved in the development of varicose veins, the mechanism linking this situation to the modifications of the venous wall observed in varicoses is still unclear. In order to study this mechanism, human saphenous veins were

Extracellular matrix remodelling has been implicated in a number of vascular conditions, including venous hypertension and varicose veins. However, to date, no systematic analysis of matrix remodelling in human veins has been performed. To understand the consequences of venous hypertension, normal

We report a case of an HIV seropositive female patient treated with a protease inhibitor-containing regimen who developed recurrent severe life-threathening episodes of haematemesis over time, caused by ruptured oesophageal varices as a consequence of a portal vein thrombosis. Coagulation tests

Varicose veins (VVs) classically result from venous hypertension owing to incompetence of the major communications between the superficial and deep veins of the lower extremity. In a significant number of patients, there is no demonstrable truncal saphenous reflux and varicosities are the result of

Quantitative changes in plasma wound healing factors in cirrhotic patients after esophageal transection were evaluated and compared with those of non-cirrhotic esophageal cancer patients (controls) after esophageal resection. Serum total protein, albumin and fibronectin were maintained at the same

Chronic venous disease (CVD) and its most frightening complication, chronic venous ulceration (CVU), represent an important socioeconomic burden in the western world. Metalloproteinases have been identified in the pathogenesis of several vascular diseases such as venous problems. The aim of this

Venous leg ulcer is the most frequent cause of trophic lesions of the limbs in patients with chronic venous insufficiency. Appropriate management of cutaneous vascular lesions is based on systemic, vascular and local assessment. The Authors used a protease-modulating matrix in 126 patients suffering

IVR has attracted much attention in Japan over the past decade, and it is expected to be rapidly developed and widely used. Not surprisingly, IVR has already become essential in emergency medicine. This paper addresses IVR of the thoracic and abdominal areas and the pelvis in emergency medicine, in

Venous stasis is a situation encountered commonly in varicose disorders. The potential implications of this decrease in oxygen levels in terms of the status of the cells of the vein were assessed. When endothelial cells are subjected to hypoxia, there is stimulation of the cells which shows itself