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An example of a benign haemorrhagic spindle cell tumour of the lymph node (synonym: intranodal myofibroblastoma) is presented, which was first described 5 years ago and has not as yet been documented in the German literature. This rare benign mesenchymal neoplasm of the lymph node occurs almost exclusively in the inguinal region. Diagnostic criteria include its composition of myofibroblastic cells (with immunoreactivity for vimentin and actin), which may show nuclear palisading, the presence of peripheral haemorrhage zones and the occurrence of characteristic amianthoid structures, which have the ultrastructural appearance of dense meshworks of collagen fibers. Knowledge of this tumour entity is important for differential diagnosis of primary and secondary malignant mesenchymal neoplasias of the lymph node.

A 75-year-old patient presented with bullae, poilokilodermatic skin and nail dystrophy as signs of systemic amyloidosis 1 year before an IgG myeloma of the lambda type was diagnosed. The skin lesions appeared at mechanically irritated locations on the trunk and at the tensor sites of the extremities. Histology showed a subepidermal blister and necrotic keratinocytes in the epidermis. There were amyloid deposits in the papillary dermis perivascular, and in the deep dermis around eccrine glands and in arrectores pilorum muscles. Polyclonal antibodies allowed classification of the deposits as amyloid composed of lambda light-chain immunoglobulins. Electron microscopy revealed globoid deposits of non-branching filaments typical of amyloid. The blister was formed at the level of the lamina lucida, with the lamina densa at the base of the bottom of the bulla. So far, junctional blister formation in bullous amyloidosis of the skin has been described only once. Our case is the second report of this blister type, and to our knowledge the first published report of a junctional blister in myeloma-associated systemic amyloidosis.

The present study concerned 16 human menisci: light, transmission (TEM) and scanning electron microscopic (SEM) techniques were used in addition to histochemical examinations, to define the microstructure of their collagenous fibre systems. A characteristic arrangement of the fibrils was noted. The diameters of the collagen fibrils ranged between 20 and 190 nm in the medial meniscus, the mean value being 67.5 nm (lateral: 70 nm). Many collagen type VI fibrils were detected, and collagen type IV was present. Such an organization has implications for knee joint stability, the variability of the fibril diameters and the characteristic arrangement giving the tissue great tensile stiffness and allows adaptation to all physiological loading conditions. On the surface of the menisci openings of canal-like structures were noted. Their characteristic distribution indicates that they carry nutrients from the synovial fluid to the normal avascular areas of the menisci.

Traumatic haemorrhagic shock in male rats caused an increase of cytoskeletal, especially filaments, in the numerous endothelial cells of the mesenteric microvessels during an examination period of 15 minutes to 2 hours. The filaments become ultrastructurally visible especially in endothelial cells with an enhanced "activity", in case of attachment of cells and in narrow capillaries with stasis. Additional investigations of these findings with other results will be carried out.

Cell adhesion to an extracellular matrix or other suitable substrata is correlated with the formation of adhesion plaques and the bundling of microfilaments. A model of the structure of the adhesion plaque is given, considering some recent data on proteins which are involved: adhesion proteins (collagen, fibronectin, laminin etc.), receptors of adhesion proteins (e.g. integrin), components of the membrane skeleton (talin, vinculin etc.), and cytoskeletal proteins. Furthermore, the structure of microfilaments, their interaction with the membrane skeleton and other elements of the cytoskeleton as well as their role in cell flattening are discussed. Several results from literature are presented which hint at the significance of the cytoskeleton in growth regulation. From experiments on growth regulation of lens epithelial cells the following conclusion were drawn: Cell substratum contact is a precondition for the organization of microfilaments. Intact microfilaments and a rigid substratum are necessary for the development of isometric traction forces. Traction forces produced by the microfilaments alter the shape and structure of the cell nucleus and may be involved in inducing a replication competent chromatin structure.

The platelet cytoskeleton is composed of microfilaments, microtubules and intermediate filaments (vimentin is only a minor component). Since actin is the major platelet protein, this review is restricted to aspects of the microfilamental system. The first part is devoted to the description of actin and of proteins thought to be associated with actin in platelets. The review will then focus on the organization of the microfilaments in unstimulated and stimulated platelets. Finally, the role of the microfilaments in maintaining unstimulated platelets in a functional form and in directing the responses of platelets to activation is discussed.

Poorly differentiated laryngeal carcinomas, which light microscopically are made up of anisomorphic nuclei, undifferentiated cytoplasm and hardly visible cell membranes, show electronmicroscopically a remarquable polymorphism. The tumor cells, which form solid or trabecular groups of different sizes often with poorly defined borderlines to the stroma, are subdivided according to their ultrastructural features in spinosa, secretory and stemcell types. Lymphocytes, plasmacells and reticular cells may show distinct focal proliferation or may be completely absent. In some cases, there was a transition between tumour tissue and metaplastic ciliated and glandular epithelium with concomitant reduction of normal glands. By comparison, besides hyperplastic and metaplastic squamous and ciliated epithelium, normal mucosal biopsies reveal invaginations of pseudostratified ciliated epithelium.

A 19-year-old patient suffering from Jadassohn's anetoderma with progressive dermatrophia showed positive reaction to treatment with chloroquin diphosphate.

Surgically-obtained tissue specimens from 41 patients with ventricular aneurysm were studied electron microscopically. The tissue from the resected aneurysms showed substantially varied morphological differences. In some, there were extensive regions of scar containing increased fibrotic material and few cells, in others there were also larger contiguous regions of myocardium with an essentially normal appearance. In the preserved myocardial regions, the cardiac cells showed moderate hypertrophy. There was an increase in contractile substance in parallel with an increase in mitochondria and enlargement of the nucleus with frequent waves and invaginations in the cell membrane. The cells at the marginal regions between fibrous tissue and preserved myocardium were frequently isolated from adjacent cells. In particular, when the isolated cells were completely surrounded by fibrous tissue, clear degeneration was apparent. These cells showed mainly a fibrillolysis with dissolution of the cross-bands and loss of the entire contractile apparatus. In compensation, occasionally there was proliferation of other cell structures, especially the free sarcoplasmatic reticulum. The hypertrophy of the still intact myocardial cells is considered compensatory for the infarct-incurred loss of tissue. The degenerative appearance is mainly attributable to fibrous tissue invasion. The diminished oxygen supply, compromised or abolished impulse conduction, loss of function and passive stretch during systole may be regarded as causes of the degeneration.

We give a review of the maturation and aging processes of elastic fibers. Elastic fibers of adult human skin are composed of elastin (amorphous matrix) and surrounded by microfibrils (structural glycoproteins). The physiological aging of elastic fibers is a continuous process starting at the age of 40 or 50 and reaching its final state in the senium. This process is characterized by the following morphological changes: (1) decreasing number of microfibrils, (2) occurrence of osmiophilic inclusions, and (3) fragmentation and disintegration of the fibers. These alterations are due to reduced synthesis of elastin and increased deposits of lipids and calcium. As a result, the elastic fibres show increased susceptibility towards proteolytic enzymes.

A total of 455 enucleated globes were examined for a pseudoexfoliation syndrome. The typical alterations could be diagnosed most clearly from the ciliary processes. The diagnosis is frequently missed in first examinations of routine sections. Among 323 nonselected eyes with secondary glaucoma, which had to be enucleated following painful amaurosis, pseudoexfoliation syndrome was found in 3.4%. On the other hand, in 132 eyes with intraocular tumors it was found only once. Our examinations provide indications that pseudoexfoliation syndrome possibly causes an unusually high incidence of deleterious secondary changes which render enucleation necessary.

A testicular gonadal stromal tumor with Leydig cells and mesenchymal cells resembling to Sertoli cells is presented. At the ultrastructural level most of the tumor cells could only be classified as endocrine differentiated cells. Because of their uncharacteristic organelles no Sertoli cells could be demonstrated by means of electron microscopy. The labelling of fibrillary actin underlines the cellular heterogeneity and the different cellular functional state of the tumor cells. These findings are interpreted as an evidence of a multidirectional differentiation potential of the gonadal stroma mesenchyme. These observations support the classification of these neoplasia as gonadal stromal tumors particularly in light of the clearly visible differentiation. Problems of evaluating the malignant potential of gonadal stromal tumors are also discussed.

We give a retrospective survey on the clinical, histological, biochemical, and pathogenetical aspects of sclerodermiform changes rarely accompanying porphyria cutanea tarda (PCT). Sclerodermiform changes were seen in 12 patients (2% of all our PCT cases). In these patients, no correlation was found between the severity of the dermatological signs and symptoms and the degree of disturbance in the porphyrin metabolism. Biochemical remission was not accompanied by improvement of the sclerodermiform changes. The proportion of porphyrins with 4 or 5 COOH-groups was higher than that of PCT patients without sclerosis. The findings are consistent with the view that the development of sclerodermiform changes cannot be merely explained by phototoxic reactions, but the "dark-effect" of the porphyrins may also play an important role in the pathogenesis.