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Transmission Electron Microscopic Study (transmission + electron_microscopic_study)
Selected AbstractsLysosomal abnormalities during benzo(a)pyrene-induced experimental lung carcinogenesis , defensive role of capsaicinFUNDAMENTAL & CLINICAL PHARMACOLOGY, Issue 1 2009P. Anandakumar Abstract The objective of the present study was to investigate whether lysosome is a target in benzo(a)pyrene-induced, oxidative stress-mediated lung cancer in Swiss albino mice and the plausible role of the phytochemical substance capsaicin in mitigating lysosomal damage. Oxidative stress was assessed based on the level of carbonyl content. The activities of lysosomal proteases like cathepsin-D, cathepsin-B, ,- d -glucosidase, ,- d -galactosidase, ,- d -glucuronidase, ,- d - N -acetylglucosaminidase and acid phosphatase were assessed to evaluate lysosomal function. Administration of benzo(a)pyrene (50 mg/kg body weight) to mice induced a increase in the activities of lysosomal enzymes and oxidative stress was evident by the increase in carbonyl content. Treatment with capsaicin (10 mg/kg body weight) decreased carbonyl content and restored the activities of lysosomal enzymes to near normalcy. Transmission electron microscopic study of lysosomes further showed the defensive action of capsaicin against the lysosomal damage caused in benzo(a)pyrene-induced lung cancer. From the present study, it can be concluded that lysosomal damage is an indispensable event in benzo(a)pyrene-induced lung cancer, and capsaicin was able to effectively prevent it, which proves the chemoprotective effect of capsaicin against benzo(a)pyrene-induced experimental lung carcinogenesis. [source] Regression of blood vessels in the ventral velum of Xenopus laevis Daudin during metamorphosis: light microscopic and transmission electron microscopic studyJOURNAL OF ANATOMY, Issue 2 2000H. BARTEL Structural changes of the ventral velum of Xenopus laevis tadpoles from late prometamorphosis (stage 58) to the height of metamorphic climax (stage 62) were examined by light and transmission electron microscopy. Special emphasis was given to the blood vessel regression. Early changes of velar capillaries were formation of luminal and abluminal endothelial cell processes, vacuolation, and cytoplasmic and nuclear chromatin condensation. At the height of metamorphic climax, transmission electron microscopy revealed apoptotic endothelial cells with nuclear condensation and fragmentation, intraluminal bulging of rounded endothelial cells which narrowed or even plugged the capillary, and different stages of endothelial cell detachment (,shedding') into the vessel lumen. These changes explain the ,miniaturisation' of the velar microvascular bed as well as the typical features found in resin-casts of regressing velar vessels which have been observed in a previous scanning electron microscopy study of the ventral velum. [source] Pathology of lumbar nerve root compression Part 1: Intraradicular inflammatory changes induced by mechanical compressionJOURNAL OF ORTHOPAEDIC RESEARCH, Issue 1 2004Shigeru Kobayashi Study design: This study is to investigate the intraradicular inflammation induced by mechanical compression using in vivo model. Objectives: The relationship between the intraradicular edema and nerve fiber degeneration induced by mechanical compression was determined in the nerve root. Summary of background data: Recently some studies reported that mechanical compression increased microvascular permeability of the endoneurial capillaries and resulted in an intraradicular inflammation. These changes may be an important factor of the pathogenesis of radiculopathy. However, the natural courses of the intraradicular inflammation after mechanical compression are still poorly understood. Methods: In dogs, laminectomy was performed at L7 and the seventh nerve root was exposed to compression at 7.5 gram force (gf) clipping power. The animals were evaluated at 1 and 3 weeks after clipping. After the appropriate period of nerve root compression, Evans blue albumin (EBA) was injected intravenously. The nerve root sections were divided into two groups. The sections were used to investigate the status of the blood,nerve barrier function under the fluorescence microscope. The other sections were used for light and transmission electron microscopic study. Results: After 1 and 3 weeks, intraradicular edema was observed not only at the site of compression but also in the peripheral zone of a compressed anterior root and in the central zone of a compressed posterior root. The evidence of active Wallerian degeneration was also seen in the area of intraradicular edema. In addition, the nerve roots showing Wallerian degeneration were infiltrated by inflammatory cells, such as macrophages and mast cells. Conclusions: Inflammatory reaction, such as Wallerian degeneration, breakdown of blood,nerve barrier and appearance of macrophage, may be deeply involved in radiculitis arising from mechanical compression, and these factors seem to be important in the manifestation of radiculopathy. © 2003 Orthopaedic Research Society. Published by Elsevier Ltd. All rights reserved. [source] Ultrastructural changes in feline dental pulp with periodontal diseaseMICROSCOPY RESEARCH AND TECHNIQUE, Issue 5 2003Jamileh Ghoddusi Abstract A light and transmission electron microscopic study was conducted on dental pulp on cats suffering periodontal disease. After extraction, pulp tissues were fixed and embedded in Epon-Araldite. Thick layers of predentin (50 ,m) and odontoblasts (30 ,m) were observed. In thin sections, odontoblasts showed many mitochondria and secretary vesicles. Some capillaries with several fenestrations were located within the odontoblastic layer. All the sections of pulp examined displayed a generalized infiltration of chronic inflammatory cells. Fibroblasts displayed lytic changes in some areas. These findings imply that the pulp is significantly affected by periodontal disease and furcation-involved teeth should be a carefully considered factor when dental treatment is planned. Microsc. Res. Tech. 61:423,427, 2003. © 2003 Wiley-Liss, Inc. [source] | |||||||||||||