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Pathological changes of chronic venous insufficiency is characterized by intimal and medial fibrosis of venous wall. Our aim was to link the correlation between Doppler sonography data and the degree of intimal and medial lesions in varicose saphenous veins at different locations.Saphenous veins from ten patients were evaluated by Doppler sonography and inmunohistochemestry. smooth muscular actin, and vimentin were studied from normal to pathological vein lesions. Collagen fibers distribution and extracellular matrix were also studied by Red Sirius Stain. Elastogenesis was studied by confocal microscopy and orcein stain. The evaluation of each molecule was explored using almost two slides per case. Quantification of these molecules and structures were made by Image J software.In initial lesions of varicose vein, intimal layer double their size compared to normal wall vein. Present a progressive increase of extracellular matrix and myofibroblast (vimentin+ and SMA+) proliferation. At severe intimal varicose lesions, lumen of vein decreased, and Doppler sonography blood flow was lower. In this field we observed thickness in intimal wall, corresponding to significatilly increase of SMA+ cells and elastics fibers deposition.The morphometric data showed that SMA+ area at intimal layer is correlated negatively to intimal thickness. In addition, quantification of elastic fibers at intimal varicose veins is significantly high compared to normal vein. Correlation between elastics fibers area and intimal high were negative. In the intima, a deposition of elastic fibers, which were shorter and disorganized was observed. The vascular medial layer shows atrophy of smooth muscular cells and presence of fibrous tissue. The intimal and medial fibrotic changes were not related to mast cell or immunocompetent cells proliferation.These data suggest a progressive transformation from normal to pathological varicose vein. In the eco Doppler sonography area reflux of varicose veins, we found a well established intimal and medial lesions characterized by fibrotic tissue and loss of SMA cells. These lesions are an irreversible fibrotic process in patients with leg chronic venous insufficiency. [ABSTRACT FROM AUTHOR]

Gangliosides (sialylated glycolipids) play an essential role in the CNS by regulating recognition and signaling in neurons. Metabolic blocks in processing and catabolism of gangliosides result in the development of severe neurologic disorders, including gangliosidoses manifesting with neurodegeneration and neuroinflammation. We demonstrate that 2 mammalian enzymes, neuraminidases 3 and 4, play important roles in catabolic processing of brain gangliosides by cleaving terminal sialic acid residues in their glycan chains. In neuraminidase 3 and 4 double-knockout mice, G M3 ganglioside is stored in microglia, vascular pericytes, and neurons, causing micro- and astrogliosis, neuroinflammation, accumulation of lipofuscin bodies, and memory loss, whereas their cortical and hippocampal neurons have lower rate of neuritogenesis in vitro Double-knockout mice also have reduced levels of G M1 ganglioside and myelin in neuronal axons. Furthermore, neuraminidase 3 deficiency drastically increased storage of G M2 in the brain tissues of an asymptomatic mouse model of Tay-Sachs disease, a severe human gangliosidosis, indicating that this enzyme is responsible for the metabolic bypass of β-hexosaminidase A deficiency. Together, our results provide the first in vivo evidence that neuraminidases 3 and 4 have important roles in CNS function by catabolizing gangliosides and preventing their storage in lipofuscin bodies.-Pan, X., De Britto Pará De Aragão, C., Velasco-Martin, J. P., Priestman, D. A., Wu, H. Y., Takahashi, K., Yamaguchi, K., Sturiale, L., Garozzo, D., Platt, F. M., Lamarche-Vane, N., Morales, C. R., Miyagi, T., Pshezhetsky, A. V. Neuraminidases 3 and 4 regulate neuronal function by catabolizing brain gangliosides., (© FASEB.)