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Background Since 1990 our group has been using extracorporeal circulation to ozonate blood by an original method, known as extracorporeal blood oxygenation and ozonation (EBOO), with the aim of amplifying the results observed with ozone autohemotherapy. Objective To verify the hypothesis that EBOO improves the skin lesions typical of peripheral artery disease (PAD) patients. Methods Twenty-eight patients with PAD were randomized to receive EBOO or intravenous prostacyclin in a controlled clinical trial. The primary efficacy parameters were regression of skin lesions and pain, and improvement in quality of life and vascularisation. Results Patients treated with EBOO showed highly significant regression of skin lesions with respect to patients treated with prostacyclin. Other parameters that were significantly different in the two groups of patients were pain, pruritus, heavy legs and well-being. No significant differences in vascularisation of the lower limbs before and after treatment were found in either group. No side effects or complications were recorded during the 210 EBOO treatments. Conclusion EBOO was much more effective than prostacyclin for treating skin lesions in PAD patients and also had a positive effect on patient general condition without any apparent change in arterial circulation. This suggests other mechanisms of action of EBOO.

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This study was carried out on carotid artery plaque and plasma of 50 patients. We analyzed uric acid, hypoxanthine, xanthine, and allantoin levels to verify if enzymatic purine degradation occurs in advanced carotid plaque; we also determined free radicals and sulphydryl groups to check if there is a correlation between oxidant status and purine catabolism. Comparing plaque and plasma we found higher levels of free radicals, hypoxanthine, xanthine, and a decrease of some oxidant protectors, such as sulphydryl groups and uric acid, in plaque. We also observed a very important phenomenon in plaque, the presence of allantoin due to chemical oxidation of uric acid, since humans do not have the enzyme uricase. The hypothetical elevated activity of xanthine oxidase in atherosclerosis could be reduced by specific therapies using its inhibitors, such as oxypurinol or allopurinol.

Atherosclerosis is a complex disease that affects medium and large arteries, leading to the formation and progression of plaque. In this process the proteins play an essential role and as a consequence, proteomic-based strategies examining the protein content of cells or tissues could offer a useful approach for the study of plaque proteins. Due to the heterogeneous cell composition of plaque, proteome analysis of whole lesions is difficult, besides being also complicated by the presence of plasma proteins that cannot be completely eliminated. A good way to study variations in protein expression among series of gels is to construct a synthetic gel. This type of gel is obtained by averaging the positions, shapes and optical densities of spots in a given set of gels. To be included in the synthetic gel, spots must be found in at least three gels. To obtain a profile representative of the proteome of atherosclerotic plaque, canceling its high variability, we constructed a synthetic gel using an average of ten carotid plaque samples. We then compared it with an equivalent synthetic gel constructed using ten plasma samples from the same carotid surgery patients. For the comparison of two synthetic gels (plasma/plaque) we could discriminate plasma proteins from plaque proteins. Besides analysis of spots common to plasma, the synthetic gel is useful to detect spots exclusive to plaque, thus simplifying a very complex mixture.Atherosclerosis is a chronic disease that affects medium and large arteries. The process originates from the interaction between cells of the arterial wall, lipoproteins and inflammatory cells (1), leading to the development of complex lesions or plaque that protrude into the arterial lumen. Mediators of inflammation are not only instrumental in the formation of plaque, but may also be involved in the rapid progression of atheromatous lesions, leading to plaque fissuring and intraluminal thrombosis. Several gene products including lipoprotein receptors, adhesion molecules, growth factors, cytokines, matrix metalloproteinases and proteins associated with cell death are also involved (2-3). This suggests that proteins play an essential role in the formation and progression of plaque.The use ofproteomic-based strategies, examining the protein content of cells or tissues, offers a useful approach for the study of plaque proteins (4). Proteins obtained from fragments of tissue with atherosclerotic lesions were recently studied in vitro (5-6), revealing an increase in transport proteins (Apo AIV, haptoglobin, transferrin, actin), signal transduction proteins (serum amyloid protein P) and a decrease in shock protein 27. The only proteins detected directly in coronary and carotid