venous insufficiency/protease

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Modulation of urokinase-type and tissue-type plasminogen activator occurs at an early stage of progressing stages of chronic venous insufficiency.

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Chronic venous insufficiency (CVI) progresses through a series of clinical stages, from healthy skin to poorly healing leg ulcers. The aim of this study was to analyse the distribution pattern and activity level of urokinase-type (uPA) and tissue-type plasminogen activators (tPA) in normal skin and

Anti-elastase and anti-hyaluronidase activities of saponins and sapogenins from Hedera helix, Aesculus hippocastanum, and Ruscus aculeatus: factors contributing to their efficacy in the treatment of venous insufficiency.

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Triterpene and steroid saponins and sapogenins of medicinal plants (Aesculus hippocastanum L., Hedera helix L., Ruscus aculeatus L.) are claimed to be effective for the treatment/prevention of venous insufficiency. In this work we evaluated the inhibitory effects of these plant constituents on the

Multiplexed analysis of matrix metalloproteinases in leg ulcer tissue of patients with chronic venous insufficiency before and after compression therapy.

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Elevated matrix metalloproteinases (MMP) levels have been implicated in the pathogenesis of chronic venous insufficiency ulcers. Quantitative measurements of a broad range of MMP proteins in human tissue treated with compression bandaging have not been reported. The goal of this study was to

Effect of oxidised regenerated cellulose/collagen matrix on proteases in wound exudate of patients with chronic venous ulceration.

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Oxidised regenerated cellulose/collagen matrix (ORC/collagen matrix) modifies wound microenvironments by binding and inactivating excess levels of proteases such as elastase, plasmin and gelatinases in wound exudates. To compare levels of the gelatinases matrix metalloproteinase 2 (MMP-2), elastase

[New trends in the treatment of venous leg ulcer. Personal experience].

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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

Lipodermatosclerosis and the significance of proteolytic remodeling in the pathogenesis of venous ulceration (Review).

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The preceding stage of venous ulceration represents a scleroderma-like hardening of the skin called lipodermatosclerosis. Clinical stages such as lipodermatosclerosis and venous ulceration, which succeed one another are highly associated to chronic venous insufficiency. Lipodermatosclerosis is

Ligation of the jugular veins does not result in brain inflammation or demyelination in mice.

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An alternative hypothesis has been proposed implicating chronic cerebrospinal venous insufficiency (CCSVI) as a potential cause of multiple sclerosis (MS). We aimed to evaluate the validity of this hypothesis in a controlled animal model. Animal experiments were approved by the institutional animal

Varicose veins possess greater quantities of MMP-1 than normal veins and demonstrate regional variation in MMP-1 and MMP-13.

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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,

Elevated fasting cholecystokinin levels in pancreatic exocrine impairment: evidence to support feedback regulation.

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Previous studies have suggested that intraduodenal protease suppression of pancreatic exocrine secretion may be mediated through cholecystokinin (CCK) release. Our study compares basal plasma immunoreactive CCK concentrations in normal human subjects with those obtained in patients with chronic

Matrix metalloproteinases and venous leg ulceration.

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Metalloproteinase-mediated proteolysis plays an important role during the phase of venous ulcer formation and wound repair. Venous ulcers manifest as a breakdown of the collagenous stromal tissue and are highly associated to chronic venous insufficiency. A major change in our understanding of the

Role of the leucocyte in the pathogenesis of vascular disease.

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The leucocyte plays a key role in the local and systemic tissue injury that results from peripheral arterial disease and chronic venous insufficiency. Despite the apparent dissimilarities between limb ischaemia and chronic venous ulceration, in both diseases macrovascular abnormalities lead to

Effect of aescine on hypoxia-induced neutrophil adherence to umbilical vein endothelium.

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Although venous stasis due to blood stagnation in lower limbs has been recognised as an important etiological factor for the development of varicose veins, the mechanism linking this ischemic situation to the modifications of the venous wall in varicose veins is still unclear. There is evidence that

Proteolytic enzymes in wound healing: the role of enzymatic debridement.

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Proteolytic enzymes are a family of proteins that serve to degrade necrotic debris derived from cell breakdown. They are produced endogenously often as precursor proteins whose activation is precisely regulated. These activated enzymes serve many functions in normal as well as pathological

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