Electron microscopy; proceedings of the Stockholm Conference, September, 1956 . electronmicrosco00euro Year: 1957 Fig. 1. Low power view of several glomerular capillaries in experimental amyloidosis. Arrows indicate nodular protru- sions of the osmiophilic middle layer of the basement mem- brane. i\ capillary lumen; b, cavity of Bowman's capsule. Magnification 5000. Light microscopy showed an amyloidosis of almost all glomcruh. With the periodic acid-silver reaction the capillary wall stained black. The amyloid seemed to be deposited within the space enclosed by the capillary wall. Electron m
Electron microscopy; proceedings of the Stockholm Conference, September, 1956 . electronmicrosco00euro Year: 1957 Fig. 1. Low power view of several glomerular capillaries in experimental amyloidosis. Arrows indicate nodular protru- sions of the osmiophilic middle layer of the basement mem- brane. i\ capillary lumen; b, cavity of Bowman's capsule. Magnification 5000. Light microscopy showed an amyloidosis of almost all glomcruh. With the periodic acid-silver reaction the capillary wall stained black. The amyloid seemed to be deposited within the space enclosed by the capillary wall. Electron microscopy revealed hitherto unknown changes of the basement membrane, in particular of the osmiophilic middle layer. Measurements of the basement membrane in normal mice confirm the findings of Rhodin (18) and Yamada (21). The total thickness of the basement membrane is 1200 A ± 117. The osmiophilic middle layer is 632 A ± 73 thick. The less osmiophilic inner and outer layers are 273 A ±31 thick. In mice with amyloidosis the basement membrane is thickened either continuously or in wavy form (fig. 1). The total thickness is 2200 A ± 116. This increase in thickness is exclusively due to a broadening of the osmiophilic middle layer measuring 1557 A ± 107. The inner and outer less osmiophilic layers are of the same thickness as in normal animals. The difference of the means of the osmiophilic middle layer in sick and normal mice is significant on the 99 level (Student's r-test). The variance of the osmiophilic middle layer in mice with amyloidosis is so much greater than in normal animals (95 'o level; Fisher's F-test) that it cannot be explained as caused by chance alone.' This seems to indicate that the increase in thickness of the middle layer in mice with amyloidosis is caused by a patiiological condition and therefore is varying within relatively broad limits. Apart from the general increase in thickness local protrusions of the middle laser in the shape of knots or mush
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