J. R. Rüttner

The ultrastructural localization of fibronectin in the lining layer of rheumatoid arthritis synovium: the synthesis of fibronectin by type B lining cells.

SummaryThe distribution of fibronectin in the lining layer of inflamed rheumatoid arthritis (RA) synovium has been ultrastructurally investigated using an anti-human plasma fibronectin antibody.The hyperplasia of lining cells was prominent in the lining layer of the inflamed RA synovium. A high level of fibronectin was localized in this region. Ultrastructurally the fibronectin was observed on the surface of both type A (type M) and type B (type F) cells, and in the extracellular fibrin-like material. This glycoprotein was detectable in rough endoplasmic reticulum (RER), some Golgi apparatus, and peripheral vesicles of type B cells. On the other hand, RER and Golgi apparatus of type A cells failed to be immunostained with the antibody. Type A cells occasionally contacted each other with interdigitation of cytoplasmic processes, and a high amount of fibronectin was localized in this region.These findings indicate that fibronectin is synthesized along the classic secretory pathway through RER and Golgi apparatus of type B cells. On the contrary, type A cells seem not to be associated with the local synthesis of the glycoprotein. Fibronectin may play a structural role in organizing these proliferated lining cells by promoting cell adhesion. The synthesis of fibronectin by proliferated type B cells may be responsible in part for the local increase of this glycoprotein in the lining layer of RA synovium.

Diagnostic and prognostic value of monoclonal antibodies in immunophenotyping of angioimmunoblastic lymphadenopathy/lymphogranulomatosis X

Summary. Immunophenotyping of frozen lymph node sections from seven patients with morphologically defined angioimmunoblastic lymphadenopathy (AILD) was performed with a panel of 20 monoclonal antibodies (MoAb). MoAb for identification of dendritic reticulum cells showed remnants of follicular structures in all cases. In four cases these ‘burnt out’ follicular structures were associated with clusters of polyclonal B‐cells. Vascular proliferation and small amounts of intercellular collagenous fibrils were reliably revealed by MoAb CIV22 against basement membrane collagen. Cellular infiltrates of T4 + cells prevailed in four cases, of T8+ cells in one case. In one case conventionally identified blasts were of T‐and B‐cell origin. Expression of cell proliferation associated nuclear antigen identified by MoAb Ki‐67 was present in more than 25% of lymph node cells in three patients with fatal outcome, but in less than 10% of cells in two patients with a better clinical course. Therefore MoAb Ki‐67 may represent a valuable prognostic marker in AILD.

The localization of fibronectin in rheumatoid arthritis synovium by light and electron microscopic immunohistochemistry.

SummaryThe distribution of fibronectin in rheumatoid arthritis (RA) synovium has been investigated by light and electron microscopic immunohistochemistry using an antihuman fibronectin antibody. Heavy accumulation of fibronectin was observed in the lining layer and the areas of proliferation of fibroblasts. Rough endoplasmic reticulum (RER) and peripheral vesicles of proliferated type B lining cells and fibroblasts contained large amounts of fibronectin. Thus these cells seem to participate actively in the local synthesis and secretion of this glycoprotein. Type A lining cells and migrated mononuclear phagocytes contained many phagolysosomes in some of which dense accumulation of fibronectin was observed. Some of the materials in the phagolysosomes, with dense accumulation of fibronectin, resembled the fibrinous material-fibronectin complexes frequently seen in the pericellular spaces. Accordingly fibronectin seems to play a role in the clearance of fibrinous materials by these phagocytes.The proliferated capillaries and small vessels possessed multilamellated basement membranes with heavy accumulation of fibronectin. However, RER or Golgi apparatus of the endothelial cells contained no detectable amounts of fibronectin. This indicates that these cells do not actively participate in the synthesis of fibronectin and that the majority of this glycoprotein in the basement membranes originates in fibronectin from blood vessel exudate. Fibrinous material-fibronectin complexes were frequently seen on the endothelial cell surfaces. Circulating platelets and mononuclear cells occasionally came in contact with these complexes, suggesting an association of fibronectin with the formation and clearance of thrombi in the vascular lumina at the inflammatory sites of RA synovium.

Diagnostic and Prognostic Value of Monoclonal Antibodies in Immunophenotyping of T Cell Lymphomas

6 cases of post-thymic T cell lymphoma (PTCL) and 4 cases of T lymphoblastic lymphoma were investigated with a panel of 21 monoclonal antibodies (MoAb). The PTCL group was composed of 2 by 2 cases of lymphoepithelioid cell lymphoma, T zone lymphoma and T immunoblastic lymphoma. In lymphoepithelioid cell lymphoma, the cell proliferating activity was low, and a malignant clone was not identifiable by the methods used. In the cases of T zone lymphoma and T immunoblastic lymphoma, malignant populations were detectable on the grounds of immunologic marker profile combined with cytologic particularities. The 4 cases of T lymphoblastic lymphoma were of a common cortical thymic phenotype (T4+, T8+, T6+) and presented with a mediastinal mass. In 3 of them, cell proliferation marker (Ki-67) was expressed by most tumor cells. Cell proliferating activity, however, did not inversely correlate with survival.

The Localization and Secretion of Type IV Collagen in Synovial Capillaries by Immunohistochemistry Using a Monoclonal Antibody against Human Type IV Collagen

The localization and the secretion of type IV collagen in synovial capillaries have been investigated by detecting the antigenic determinant of the major triple helix of human type IV collagen. Type IV collagen was indicated to be localized mainly in the lamina densa of basement membranes (BM) and to be secreted by both endothelial cells and pericytes. The pericytes secreted this collagen to both surfaces facing endothelial cells and the interstitial connective tissue. On the contrary, the direction of type IV collagen secretion by the endothelial cells was strictly confined to one side, namely towards the surface facing the BM. The absence of the antigenic determinant in rough endoplasmic reticulum and Golgi apparatus of the endothelial cells and pericytes indicated that the major triple helix of type IV collagen is mainly formed in the secretory vesicles after budding from the Golgi apparatus.

Establishment and Characterization of an Epstein-Barr Virus Nuclear Antigen-Negative Hairy Cell Line

Continuous cell lines have been established from spleen cells of patients with confirmed hairy cell leukemia (HCL). One cell line, HCL-Z1, lacks Epstein-Barr virus nuclear antigen (EBNA), grows attached to the substratum and retains typical features of hairy cells as revealed by transmission and scanning electron microscopy. HCL-Z1 differs morphologically from the three other EBNA-positive lymphoblastoid cell lines obtained (HCL-Z2, HCL-Z3, HCL-Z4) as well as from normal spleen cells or lymphocytes. The three lymphoblastoid cell lines derived from HCL patients show similar surface features as a line from a myeloma patient. Therefore, not all cell lines derived from HCL patients may be considered as representative of the patients leukemia cells.

The thickening of basement membrane in synovial capillaries in rheumatoid arthritis.

SummarySynovial tissues from seven rheumatoid arthritis (RA) patients were used for the ultrastructural investigation of capillary cellular components and basement membranes (BM). Attention has been specially paid to the mechanism of BM thickening of the capillaries in the inflammatory sites.The capillary BM were multilamellated in the inflammatory sites. The multilamellation was characteristic not only in the BM surrounding the endothelial cells and pericytes but also in the BM between these two types of cells. Cell debris was frequently encountered between the multilamellated BM. The hyperplasia and various stages of degeneration of the endothelial cells were observed in these regions. Some endothelial cells were activated and occasionally located in capillaries containing degenerated endothelial cells. The high incidence of these findings indicates the following hypotheses.The accelerated rate of death and replenishment of capillary cellular components may play a role in BM thickening in the inflammatory sites of RA synovium. These cells may not only produce one layer of BM in their life-time but may also be activated to produce excessive amounts of BM components to make several layers.

Lungenkrebshäufigkeit und Todesalter bei den Silikosetodesfällen der SUVA, 1960–1978

The frequency of lung carcinoma among the deaths of silicotics registered by the Swiss National Accident Insurance Fund from 1960 to 1978 has been compared with the causes of death of all Swiss males during the same period. The PMR, while underestimating the true risk, is significantly raised among foundry workers. SMRs for lung cancer (estimated by comparing the numbers of pulmonary and non-pulmonary malignancies) are elevated among foundry workers, miners, workers in ceramic and miscellaneous industries. Only the stone/slate industry has not yielded a significant excess of lung cancers.

Morphologie der Knorpeldestruktion bei experimentellen Kaninchenarthritis

Bei der morphologischen Analyse von Gelenkdestruktionen bei rheumatoider Arthritis hat bis anhin unbestritten die zerstorende Wirkung des synovialen Pannusgewebes im Vordergrund gestanden (1–7). Zwei Hauptangriffsrichtungen des Pannus werden unterschieden, namlich: 1. Die zungenformige Proliferation des Pannusgewebes uber den Gelenkknorpel, der sogenannte Knorpelpannus, und 2. der Markpannus, d.h. das Einwachsen des Pannusgewebes in die subcorticalen Markraume (8–10).

Erratum zu: Krebsmortalität 1980/81 und Krebsinzidenz 1980 im Kanton Zürich

Redaktlon / R~klactlon Prof. Dr. mad. F. H. Epstein (Chefredaktor), Institut for Sozialund Pr&ventivmedizin der Universitht ZOrich, Gloriastrasse 30, CH-8006 Z~irich PD Dr. med. R. Bruppacher, Abteilung fLir Sozialund Pr&ventivmedizin der Universitht Basal, St. Albanvorstadt 19, CH-4052 Basel Dr mdd. J. Martin, M6decin cantonal adjoint, Rue Cita-Devant 11, CH-1005 Lausanne (r(~claction francophone) Wissenschaftllcher Belrat Consell sclentlflque Dr. mad. Th. Abelin, Professor ffir Sozialund Pr&ventivrnedizin, Universil~.t Bern (Pr&sident) Dr. mad. Dr. h.c.U. Frey, Direktor Bundesamt ffir Gesundheitswesen, Bern Dr. mad. E. Grandjean, Professor for Hygiene und Arbeitsphysiologie, ETH ZOrich Dr m6d. F. Gutzwiller, Professeur de M(~decine sociale at pr(~ventive, Universit~ de Lausanne Dr mdd. O. Jeanneret, Professeur de M~decine sociale et pr6ventive, Universit6 de Geneva Dr m6d. B. Junod, PD Institut de M6decine sociale at preventive, Universit6 de Lausanne Dr. mad. G. Ritzel, Professor for Sozialund Pr&ventivmedizin, Universit~t Basel Dr. mad. M. Sch&r, Professor for Sozlalund Pr~tventivmedizin, Universit,~t Z0dch Prof. Dr. mad. F. H. Epstein, Institut f(Jr Sozialund Pr&ventivmedizin, Universit&t Z(irich Dr. mad. dent. Th. Marthaler, Professor for orale Epidemiologie und Pr~ventivzahnmedizin, Universit&t Z0rich Dr. med. H. Schlegel, Professor for Arbeitsmedizin, Schweizerische Unfallversicherungsanstalt, Luzern