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Biomedical subjects

F Wegener

Publications and source records attributed to F Wegener.

10 recordsLinked to original sources
PubMed1990

Wegener's granulomatosis. Thoughts and observations of a pathologist.

The clinical entity now known as Wegener's granulomatosis was first reported in 1936. Since then the disease's histopathology has been clarified, although its etiology remains unknown. Treatment requires immuno-suppressant therapy and careful following of affected patients. The present report reviews the historical background for the discovering of Wegener's granulomatosis and current clinical considerations.

Granulomatosis with Polyangiitis↗
PubMed1990

[50 years of Wegener's granulomatosis].

Wegener's granulomatosis (WG) was discovered as an independent "new" disease in 1936. The author describes in retrospect the conditions, favorable circumstances and lucky coincidences that chanced to lead to this discovery. Subsequently, a detailed impression of the morphology of the disease is given, portraying especially the unusual diversity of the microscopic anatomy, both of the granuloma and of the vasculitis and nephritis. In conclusion the author shows the progress that has been made in clinical research on diagnostic techniques, knowledge of the stages and courses of WG and accordingly adapted treatment and in understanding the immunology of this disease.

Granulomatosis with Polyangiitis↗
PubMed1980

Concanavalin A capping in polymorphonuclear leukocytes.

Various polymorphonuclear leukocyte (PMN) functions are dependent on an intact intracellular cytoskeleton consisting of the microtubules and the microfilaments. To investigate the microtublule system in PMNs we observed the spontaneous, Colchicine and Diamide induced cap-formation by fluorescence microscopy ion PMNs obtained from children with bacterial and viral infections demonstrated with 47 +/- 1% a significantly increased number of spontaneous capped PMNs compared to 22 +/- 1% capped cells obtained from controls. Furthermore, 52 +/- 2% PMNs of patients on immunosuppressive therapy exhibited spontaneous surface capping. There was no significant elevation in the number of capped PMNs (30 +/- 2%) obtained from children with viral infections. Colchicine and Diamide increased the number of capped cells in control PMNs as well as in PMNs from patients to 69 +/- 1% and 67 +/- 1%, respectively. Since the increased spontaneous cap formation in PMNs is associated with a defect of microtubule assembly, the various leukocyte function defects described in patients with bacterial infections, bronchial asthma or on immunosuppressive therapy may have to be considered the consequence of an altered microtubule system.

Asthma↗