TRANSMISSION ELECTRON MICROSCOPY Sample Clauses

TRANSMISSION ELECTRON MICROSCOPY. 1.7.1 Analysis will be performed using the analysis method set forth in the AHERA Regulation 40 CFR Part 763 Appendix A. 1.7.2 Asbestos Structures referred to in this Section include asbestos fibers, bundles, clusters or matrices, as defined by method of analysis.

TRANSMISSION ELECTRON MICROSCOPY. (A to C) Glomerular segments with an increase of epithelial cells in Xxxxxx’x capsule without prominent sclerosis (early lesions). Podocytes appear activated with extensive foot process effacement, microvillous transformation, and enlarged nuclei (A). Locally, the parietal epithelium appeared damaged and denuded segments Xxxxxx’x capsule were present (A, arrow). Segmentally, there appeared to be an increased number of nuclei along Xxxxxx’x capsule (B). We sometimes observed bridging epithelial cells between activated podocytes and Xxxxxx’x capsule (C). The insert shows the cell contact between the podocyte and the bridging cell with apparent fusion of cell membranes. Amorphous extracellular matrix (ECM) was sometimes present surrounding the epithelial cells in Xxxxxx’x space (B, ). In lesions with more advanced sclerosis (D) we did see denuded glomerular basement membrane (GBM) segments and sometimes remnants of podocytes (arrowhead) appeared to be present. Amorphous ECM was sometimes deposited on top of the naked GBM (∗) [(A and B) ×7000; (C and D) ×5000]. of lesions in each of 137 whole glomeruli contained in the kidney segment. For each glomerulus three to five PAS-stained sections could be studied. Lesions were cat- egorized in four different groups. The first group con- tained only normal or ischemic quadrants sometimes as- sociated with wrinkling or even collapse of the capillaries of the glomerular tuft, without cellular hypertrophy or hy- perplasia. Second group showed early lesions defined by collapse of the capillaries, accompanied by hypertrophy and epithelial proliferation (hyperplasia) of glomerular epithelial cells and early adhesions between the glomeru- lar tuft and Xxxxxx’x capsule. The third contained more advanced lesions, characterized by collapse of the capillaries of the glomerular tuft, with foam cells, ECM accumulation, sclerotic segments, and various degrees of hypercellularity. The last group consisted of quadrants of glomeruli with advanced sclerosis. To analyze the distribution of the various marker pro- teins and to determine the cellular origin, consecutive sections were used for incubations with the various anti- bodies as described in Table 1. Using our system, two consecutive profiles of the same glomerulus could be viewed simultaneously. In addition, we have performed double staining using different sets of marker proteins to strengthen our findings.