Cytogenetic findings in a metastasizing primary testicular chondrosarcoma.

The first case of a primary chondrosarcoma of the testis is reported. The testicular tumor, 2.5 cm in diameter, metastasized to the retroperitoneal lymph nodes in a 24-year-old male. Histologically, the testicular tumor and the lymph node metastases revealed a well-differentiated chondrosarcoma. Cytogenetic analysis of the retroperitoneal metastases showed a complex chromosomal aberration with two copies of the isochromosome of the short arm of chromosome 12. This is a specific chromosomal anomaly in testicular germ cell tumors. Thus, the cytogenetic analysis proved the germ cell origin of tumor cells as opposed to a possible paratesticular mesenchymal histogenesis. Moreover, the triploid modal chromosomal number of tumor cells confirmed the relationship between polyploidization and a high degree of differentiation in germ cell tumors. These findings stress the clinical relevance of the cytogenetic analysis in at least a subset of cytogenetically well-characterized solid tumors.

Adhesion and spreading of corneal endothelial cells on collagens type I and IV in vitro: a model to study mechanisms of endothelial repair.

In vitro assays using endothelial cells (EC, bovine corneal) were performed to study adhesion and spreading on collagen types I and IV. Adhesion was quantitatively analyzed by counting the EC under a light microscope. Spreading was determined by measuring cell area using a scanning electron microscope (SEM). Collagen types I, IV, and IV-F, a mixture of 70, 120, and 140 KD fragments of type IV, all promoted EC adhesion, Types IV and IV-F showed evidence of giving a more marked adhesion than type I. A study of cell area, carried out under identical conditions, such as those in the adhesion assay, showed that types I and IV-F, but not type IV, promoted cell spreading. This provides evidence that cell adhesion and spreading are indeed separate biological phenomena. Furthermore, the ability of fragments of type IV collagen to promote both cell adhesion and spreading may represent an inherent repair mechanism in damaged endothelium.

[Comparative studies on collagen expression of chondrocytes in monolayer and spheroid culture]. / Vergleichende Untersuchungen über die Kollagenexpression von Chondrozyten in Monolayer- und Sphäroidkultur.

Dedifferentiation of cells is well known in cell culture biology. This phenomenon is examined in comparative studies on collagen expression of chondrocytes in monolayer and spheroid culture. Immunohistochemical studies were carried out by the indirect peroxidase technique. In the differentiated state a positive reaction for collagen type II was found. This was lost as dedifferentiation took place, in which case positivity for collagen types I, III, and V increased.

Differential expansion of human endothelial monolayers on basement membrane and interstitial collagens, laminin and fibronectin in vitro.

In this study the ability of a human endothelial cell monolayer to expand over specific components of the basement membrane and extracellular matrix was investigated over a 5-day period. The method was intended as a model to study the mechanisms of endothelial regeneration. All components were coated onto sterile coverslips at a concentration of 10 micrograms/ml. The highest expansion was obtained on fibronectin, laminin and collagen type III, all three being statistically significantly greater than on the uncoated control surface (0.002 greater than p greater than 0.0001). Collagens types I and IV and a high molecular weight fragment mixture of type IV (IV-F, consisting of 75, 120 and 140 kD fragments) elicited approximately similar expansion rates, significantly higher than the control (0.02 greater than p greater than 0.003), although significantly lower (approximately 15%) than collagen type III, fibronectin and laminin (p less than 0.001). The high monolayer expansion on collagen type III is surprising, as it is a relatively minor biosynthetic product of the endothelial cell. It could, however, be of significance in wound healing, in which endothelial cells come into contact with this interstitial collagen. In addition, the similar results obtained with collagens IV and IV-F indicate that expansion of the endothelial monolayer is not dependent on the integrity of the tetrameric structure of type-IV collagen.

In vitro studies on the expansion of endothelial cell monolayers on components of the basement membrane.

The purpose of the present study was to observe the expansion of a monolayer of endothelial cells over specific components of the basement membrane. This was performed in vitro in a monolayer expansion assay over 5 days. The control surface was uncoated glass in the form of coverslips. Test substances were coated at a concentration of 10 micrograms/ml. The highest expansion was obtained with a high molecular weight fragment mixture of collagen type IV (IV-F, consisting of 75, 120 and 140 KD fragments), followed by fibronectin. Collagens type I, III and IV tetramer gave similar results, less than fibronectin or collagen type IV-F, although all of the above basement membrane coatings promoted expansion significantly above that of the control (P less than 0.01). The poorest expansion was obtained with laminin, which was significantly less than the control. The pentapeptide GRGDS, related to the fibronectin cell binding region, gave expansion significantly below that of the intact fibronectin molecule, as did the intact collagen type IV molecule compared with type IV-F (P less than 0.025). This indicates that sequences of the fibronectin molecule other than the cell binding sequence may be involved in promoting endothelial cell expansion. In addition, the integrity of the collagen type IV molecule does not appear necessary for this effect. On the contrary, the higher movement on IV-F may represent an inherent repair mechanism in damaged endothelium. Autoradiographic studies show that endothelial cell proliferation at the expanding front is involved in the migration assay.

Interaction between endothelial cells and basement membrane components. In vitro studies on endothelial cell adhesion to collagen types I, III, IV and high molecular weight fragments of IV.

Understanding the mechanisms involved in maintaining the integrity of the vascular endothelium is fundamental to studies on atherosclerosis, thrombosis, inflammation and tumor invasion. One of the essential aspects is the relationship between the endothelial cell (EC) layer and the underlying components of the basement membrane (BM). The importance of the biological role of the individual components of the BM in the promotion of EC adhesion is investigated. In this study suspensions of bovine corneal ECs (BCECs; 5 x 10(4)/ml) were used to investigate the adhesion of EC to collagen type IV and a mixture of fragments of the tetrameric molecule (IV-F, consisting of 75, 120 and 140 kD fragments), as well as collagen types I and III, coated at a 10-micrograms/ml concentration onto glass coverslips in vitro. Adhesion was quantified after 2 h of interaction by direct counting in the light microscope following fixation of the adherent cells. Collagens type IV and IV-F markedly promoted BCEC adhesion both in the presence or absence of 10 or 50% fetal calf serum, indicating that the integrity of the tetrameric molecule is not required for EC adhesion to collagen type IV, but can be replaced by high molecular weight fragments. Collagens type I and III increased EC adhesion in the absence of serum, although not in the presence of serum. Indirect evidence for a possible role of fibronectin in EC adhesion to type-IV collagen is given by the ability of the tetrapeptide (Arg-Gly-Asp-Ser (10 micrograms) to temporarily block (15-30 min) the adhesion-promoting effect of type-IV collagen. The nature of the adhesion sequences on the fragments of type-IV collagen remains to be elucidated.

Topography of the inferior rectal artery: a possible cause of chronic, primary anal fissure.

The authors believed that it might be possible to explain the local frequency of the anal fissure at the posterior commissure by an anatomic relationship, and examined the blood supply of the anus. The inferior rectal artery is demonstrated by postmortem angiography and by manual preparations (N = 41) and histologic study after angiography of the vessels (N = 10). The blood supply at the different sites of the anal canal are demonstrated by a morphometric study (N = 20). The inferior rectal artery presents two variants in the postmortem angiographies, type 1 (85.4 percent) and type 2 (14.6 percent). In type 1, the posterior commissure is less perfused than the other sections of the anal canal. In addition, the blood supply may be more compromised by contusion of the vessels passing vertically through the muscle fibers of the sphincter ani internus muscle during increased sphincter tone. The role of topography in the pathogenesis of the primary anal fissure is illustrated in a model.