By H. Jellinek (auth.), H. Jellinek (eds.)
This monograph summarizes the result of a fifteen-year vascular pathology study venture subsidized by means of the Hungarian Academy of Sciences. the employees who've participated during this undertaking are indebted to the Academy for financing large investigations and visits to institutes in another country, the goals of that have been to unravel yes difficulties via overseas cooperation. the consequences provided through the collective attempt of study groups, each one learning the following were accomplished a selected challenge, yet operating jointly to an analogous finish. Mutual dialogue of findings and a typical trade of knowledge among the study teams have contributed to the growth of the investigations. typical ebook of info and mutual feedback ensured that the findings have been uniformly interpreted. it's was hoping that the basic target of our long term venture, i. e. the choice of the best method of the advanced challenge of vascular pathology, has been accomplished. the recent strategy effects from the popularity that considering that arteriosclerosis eventually results in several types of vascular harm, recognition can be focussed at the occasions previous the advance of the lesions instead of at the lesions themselves. This declare has been proven through quite a few version experiments within which vascular harm inflicted below varied stipulations uniformly ended in morphologi cally demonstrated arteriosclerotic swap. the new elevate within the prevalence of civi lization illnesses of the vascular process has led to a world-wide growth of arteriosclerosis research.
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Additional info for Arterial Lesions and Arteriosclerosis
The subintimal fibrinoid deposition occasionally extended over one-third of the width of the vessel wall. At this stage, smooth muscle cell necrosis and subendothelial fibrinoid were simultaneously present (Plate LXII/23, 27). A periarterial inflammatory cell reaction might additionally develop, as in the small arteries (Plate LXII/23). Single muscle cells between the elastic fibres might fuse with one another during the development of the subendothelial fibrinoid, but large vessel lesions never assumed the homogeneous appearance found in small vessel changes (see p.
According to Voorhees (1963), the final neo-intima migrates to the vascular prosthesis like a pannus. , 1968). Voorhees et al. , 1963a, b; Simpson et al. 1968) reported that the overwhelming majority of the proliferative cells were modified smooth muscle cells (Plate LXlj20). Probably Voorhees and Wosolowski 45 (1963) mistook the latter for fibroblasts for lack of special muscle stains. Anyhow, Voorhees (1963) reported later that smooth muscle cells were present in the neo-intima of a vascular prosthesis implanted for 8 years.
39 (1952) added elastin to a suspension of elastic fibres and Keech (1960) injected it in vivo into the thoracic aorta prior to embedding for electron-microscopic examination. Yokota (1957) applied elastase to embedded specimens of calf nuchal ligament, after removal of methacrylate from the ultra-thin sections, while Waisman (1968) applied it to the tissue block before embedding. Ross and Bornstein (1969) digested fibres from the nuchal ligament with collagenase and the residues with elastase.