Acta Universitatis Carolinae. Medica. Monographia最新文献

The study presents the author's experience of 15 years of electron microscopic study of 339 resected respiratory tract tumours, an unusually large group. A dual purpose was pursued: a) to present a systematic analysis of carcinomas which prevailed in the material, and b) to interpret some of the unusual or poorly studied phenomena found in some tumours. The author has been using electron microscopy to study carcinomas since 1973 as a corrective factor giving more precision to routine classification (according to WHO, 1981), on which modern diversified therapy depends. He presents more evidence of the phenotypic heterogeneity of carcinomas, puts aside the histogenetic approach and supports the idea of a common genotypical source of all the programmes of tumour cell differentiation. As regards individual tumours studied by electron microscopy, the author introduced the first ever observation of extrapulmonary neuroendocrine laryngeal carcinoma verified at post mortem examination, a third observation of filamentous bodies in four bronchial carcinoids, and the first observation of a flat epitheloid hemangioma of the larynx. Another case, one of intravascular bronchioloalveolar tumour, is unique for the presence of cytoplasmic crystalline inclusions and leptomeric fibrils which used to be associated with contractile proteins. In a case of bronchioloalveolar carcinoma resembling jaagsiekte, unusual paracrystalline inclusions are demonstrated in a second ever observation, and diagnosed as viral metabolites. Radial cisternae, a peculiar variety of annulate lamellae, found in a lung adenocarcinoma receive closer scruitny because altogether five such cases are on record (two more tumours in the author's archives and another two taken from illustrations to other authors' reports).(ABSTRACT TRUNCATED AT 250 WORDS)

Lipid peroxidation is a free radical initiated chain oxidation of unsaturated lipids. With respect to the ubiquity of unsaturated fatty acids in the cellular membranes, the peroxidative damage has the potential to affect many cellular functions. Some of the products of lipid peroxidation are diffusible and can spread the damage far beyond the site of the original free radical attack. There is an interdependency between reactive oxygen species and lipid peroxidation - reactive oxygen species initiate the reactions of lipid peroxidation and are also produced in these reactions as intermediates. The generation of reactive oxygen species can be triggered either by nonenzymatic mechanisms, in which iron ions play the major role, or by a wide range of enzymatic systems. The primary damaging effect of lipid peroxidation is exerted by the interactions with proteins and DNA. These interactions are then revealed at the subcellular (cellular organelles), cellular, and organ levels. The production of lipid peroxides interferes with the regulation of several metabolic pathways. In this review, particular attention is focused on the interaction of non-specifically formed lipid peroxides with the regulatory factors produced by the controlled oxidation of arachidonic acid (prostaglandins and leukotrienes), the effects on ionic pumps and intracellular calcium metabolism, the participation of lipid peroxidation in the ageing process, and the modulation of hormonal regulations by lipid peroxidation. Lipid peroxidation is induced at the level of the whole organism by various extrinsic factors such as ionizing irradiation, physical activity, diet and fasting, and various drugs. There is increasing awareness of the association between pathologic states and lipid peroxidation. Among the most studied are inflammation, ischaemia-reperfusion injury, and atherogenesis. Lipid peroxidation also plays a dual and complex role in cancer. Organisms have developed an efficient multilevel protective system against lipid peroxidation, but this can be overwhelmed by certain pathologies.

Basing on the results of radiological, clinical and laboratory examinations of 200 children with juvenile rheumatoid arthritis, we tried to obtain a comprehensive picture of radiological changes in the joints, the spine and the remaining skeleton caused by JRA. The bulk of data was obtained in the period between 1954 and 1972, but for some of the patients, our follow-up continued until 1987. Our main interest were differences in morphological changes caused by JRA and adult RA. We described initial changes and their progress in childhood, adolescence and adulthood, drawing attention to fundamental differences in radiological changes and their progress in patients with an onset of disease in the first half of childhood (up to the age of 8) and in those with an onset in the second half of childhood, where these changes were similar already to those caused by adult RA. Juvenile rheumatoid arthritis affects mainly skeletal growth by either retarding or accelerating various ossification processes. The skeleton of children has a great regenerative capacity, but this, on the other hand, supports various disturbances of growth brought forth by disease. This, apparently, account for differences of changes in the skeleton of the joints observed in JRA patients during childhood and adulthood. Whenever a case is suspected of JRA, a radiological examination of the joints involved ought to be complemented by a radiological examination of the hands because most of our radiographs showed structural changes in the hands. Particular attention should also be given to the knees and hips of children with active disease over a period of 3-6 years. Synostosis of arches and joints of the cervical spine, a typical feature of JRA, was observed in 20-25% of former JRA patients. Synostoses occurred either in the individual segments or in the whole cervical spine, but were never absent at the level of vertebral bodies C2-C3. There were neither objective nor subjective complaints.