scholarly journals Light and Electron Microscopic Observations of Giant Cells in the Mouse Testis after Efferent Duct Ligation

1987 ◽  
Vol 50 (5) ◽  
pp. 579-585 ◽  
Author(s):  
Shio Kumar SINGH ◽  
Kazuhiro ABE
Keyword(s):  
Giant Cells ◽  
Mouse Testis ◽  
Electron Microscopic ◽  
Efferent Duct ◽  
Duct Ligation

scholarly journals Arrested apoptosis without nuclear fragmentation produced by efferent duct ligation in round spermatids and multinucleated giant cells of rat testis

Reproduction ◽  
2003 ◽  
pp. 879-887 ◽  
Author(s):  
E Anton
Keyword(s):  
Acid Phosphatase ◽  
Nuclear Membrane ◽  
Sertoli Cells ◽  
Giant Cells ◽  
Differential Staining ◽  
Multinucleated Giant Cells ◽  
Nuclear Fragmentation ◽  
Efferent Duct ◽  
Duct Ligation ◽  
Acid Phosphatase Reaction

The apoptotic process evoked by efferent duct ligation in the testes of adult rats was followed for 10 days by differential staining for haematoxylin-eosin, periodic acid-Schiff and a modified trichrome technique in optical microscopy and by ultrastructural localization of acid phosphatase. Round spermatids showed the first effects of efferent duct ligation. At day 3 after ligation, annular clumps of chromatin with typical apoptotic characteristics appeared against the nuclear membrane of these cells. Afterwards, membranous structures and a wide separation between the two layers of the nuclear membrane were observed but nuclear fragmentation did not occur and apoptotic granules were not seen. Cytoplasmic components were also altered, and severely damaged organoids and empty vacuoles lacking acid phosphatase reaction were frequently seen. On day 2 after efferent duct ligation, multinucleated giant cells appeared, which displayed similar characteristics as spermatids and showed no acid phosphatase reaction. Although abnormal spermatids and multinucleated giant cells were surrounded by the cytoplasm of Sertoli cells, neither lysosomal acid phosphatase nor phagocytic activity was detected. It is concluded that efferent duct ligation specifically affects round immature spermatids eliciting a partial nuclear apoptotic response that is not accompanied by autophagic or heterophagic activity and without lysosomal participation in Sertoli cells.

Giant Cell Tumor of Tendon Sheath: Immunohistochemical Study of 20 Cases

1997 ◽  
Vol 83 (5) ◽  
pp. 841-846 ◽  
Author(s):  
Antonio Cavaliere ◽  
Angelo Sidoni ◽  
Emilio Bucciarelli
Keyword(s):  
Giant Cell Tumor ◽  
Giant Cell ◽  
Mononuclear Cells ◽  
Neuron Specific Enolase ◽  
Synovial Cell ◽  
Tendon Sheath ◽  
Giant Cells ◽  
Cell Tumor ◽  
Electron Microscopic ◽  
Filament Bundles

Aims and background Giant cell tumor of tendon sheath (GCTTS) is a common tumor occurring on the tendon sheaths of the fingers. The nature of this lesion is still controversial: some researchers consider it a reactive process arising from chronic inflammation while others regard it as a tumor of presumed synovial cell or monocytic macrophage system origin. In an effort to clarify the histogenesis we decided to further investigate the immunophenotypic profile of this tumor. Study design We studied 20 GCTTS of the fingers using a panel of 18 antibodies, 13 monoclonal and 5 polyclonal. Results The immunohistochemical investigation revealed that the mononuclear cells of this lesion can be divided into two groups. The cells of the first and more numerous group were positive for vimentin, PG-M1 and KP1 but also for muscle actin (HHF35 monoclonal antibody) and neuron-specific enolase. A second population of mononuclear cells, usually arranged around the giant cells, were positive for PG-M1, KP1, LCA and occasionally for alpha-1-antitrypsin and alpha-1-antichymotrypsin. Multinucleated giant cells were also positive for KP1, PG-M1 and LCA monoclonal antibodies. A variable but usually weak positivity for al-pha-1-antitrypsin, alpha-1-antichymotrypsin and lysozyme was also observed. Conclusions Our results suggest a synovial cell origin for GCTTS and do not support the hypothesis that it could be a neoplasm with a true histiocytic origin. The positivity of some cells for the HHF35 antibody, together with electron microscopic evidence of filament bundles with focal dense bodies, suggests that at least part of the mononuclear cells may have a myofibroblastic differentiation.

Changes in testicular blood flow and testosterone production during aspermatogenesis after irradiation

1983 ◽  
Vol 98 (1) ◽  
pp. 35-46 ◽  
Author(s):  
J. Wang ◽  
K. A. A. Galil ◽  
B. P. Setchell
Keyword(s):  
Blood Flow ◽  
Leydig Cells ◽  
Capillary Permeability ◽  
Extracellular Fluid ◽  
Testis Weight ◽  
Γ Irradiation ◽  
Adult Rats ◽  
Efferent Duct ◽  
Duct Ligation ◽  
Testicular Blood Flow

Exposure of the testes of anaesthetized adult rats to 527 rads of γ-irradiation caused testis weight to fall slowly at first and then more rapidly from 21 days afterwards, reaching a minimum at 52 days, when spermatogenesis was severely disrupted. The weights of the accessory organs and the concentrations of testosterone in peripheral blood were slightly reduced; the concentrations in blood from the testicular veins were lower than control at shorter intervals after irradiation, but at later times tended to be similar or greater than control. Testicular blood flow per testis followed testis weight closely, and as a result the production of testosterone by the smaller testes (calculated as the product of plasma flow and the veno–arterial difference in testosterone concentration) was markedly reduced especially when the rats had been stimulated with human chorionic gonadotrophin (hCG). Serum FSH and LH rose appreciably as testis weight fell but there was a proportionately greater rise in FSH than LH, in comparison with surgically castrated animals. Increased amounts of extratubular, extracellular fluid were found in the aspermatogenic testes, but injection of hCG still caused increases in capillary permeability and the amount of fluid in the testis. These results indicate that during aspermatogenesis following irradiation (as with heat and efferent duct ligation) the capacity of the testes to secrete testosterone is severely limited by decreased testicular blood flow, not by the ability of the Leydig cells to release testosterone into their immediate environment.

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