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In order to develop a system of peripheral arterial angioplasty, we carried out an in vitro study to define the quantitative, thermal and morphological characteristics of human-atheroma ablation by excimer laser. A multigas 'Sopra' laser was used. The study was performed by using 248nm, krypton fluoride (KrF), then 308nm, xenon chloride (XeCl) wavelengths. The delivered energy was up to 150 mJ pulse, pulse duration was 25ns, and the repetition rate could be adjusted to up to 20Hz. Irradiated tissue segments of the superficial femoral and external iliac arteries were obtained in man during surgical procedures and were both calcified and non-calcified atherosclerotic lesions. Quantitative measurements showed a linear increase of ablated tissue mass depending on the energy delivered. For the same energy, the loss of mass was greater with the 248nm wavelength than with the 308nm. The maximum temperature rise measured at the site of irradiation was 6°C at 248nm and 25°C at 308nm. Histological analysis of the irradiated segments revealed neat and precise ablation without thermal injury of adjacent tissue. At 248nm, this phenomenon was observed for calcified as well as non-calcified atheromas. It is concluded that quantitative, thermal and morphological characteristics of in vitro ablation of calcified and non-calcified human atheroma by excimer laser are compatible to clinical requirements. The results observed at 248nm were experimentally more satisfactory. [ABSTRACT FROM AUTHOR]

The spectrum of the Guillain-Barre Syndrome (GBS) has recently been widened by the newly identified forms of acute motor axonal neuropathy (AMAN) and acute motor sensory axonal neuropathy (AMSAN). An important question has been raised regarding the possibility for the axon to be a target in immune-mediated damage. Although myelin breakdown is the characteristic feature of classic acute inflammatory demyelinating polyradiculoneuropathy (AIDP), axonal degeneration may occasionally be observed in this form, especially in cases with explosive onset and severe clinical course. Immunohistochemical findings of five frozen sural nerves biopsies of patients with GBS (AIDP variant) tested with a panel of monoclonal antibodies raised against different molecules implicated in immune-mediated processes have principally disclosed an immunoreactivity of tumor necrosis factor-alpha (TNF-alpha) on both Schwann cell membranes and in myelinated and unmyelinated axons. On the other hand, interleukin 1-beta (IL1-beta) labeled Schwann cells, endothelial cells and macrophages; interferon-gamma (IFN-gamma) was observed both in endothelial cells and lymphocytes. Membrane attack complex (C5b-9) deposits were observed on Schwann cell membranes and finally intercellular adhesion molecule-1 (ICAM-1) was localized both on endothelial cells and macrophages. Our findings strongly suggest that TNF-alpha is an important factor in the cascade of events leading to immune-mediated demyelination and axonal damage in GBS. [ABSTRACT FROM AUTHOR]