Histology and histopathology Vol. 1, nº 1 (1986)

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http://hdl.handle.net/10201/177649

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Encephalopathy with astrocitic residual bodies. Report of a case and rewiev of the literature
(Murcia : F. Hernández, 1986) Figols, J.; Cervós-Navarro, J.; Wolman, M.
Biopsy and autopsy findings in a girl who died at 7% months after having suffered from progressive axial hypotonia, myoclonus, EEG changes and retarded psychomotor development. Inclusions consisting of lamellar profiles, situated in membrane-bound cytosomes were found mainly in astrocytes, but also in neurones and in axons of peripheral nerves. Lipofuscin bodies were also increased in number. The patient belongs in the same category as cases studied by Towfighi et al. (1975) and Martin et al. (1977). Etiology and pathogenesis of this syndrome remain unknown. It is suggested, however, that the pathological changes observed might have been caused by the administration soon after birth of anti-epileptic dmgs (diphenylhydantoin, clonazepam and nitrazepan).
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Oxygen toxicity in the infant rhesus monkey lung. Light microscopic and ultrastructural studies
(Murcia : F. Hernández, 1986) Ainsworthl, Dorothy M.; Keithl, lngegerd; Lobas, Jeffrey G.; Farrel, Philip M.; Eicker, W.
Eight monkeys were anesthetized with ketamine hydrochloride and positive pressure ventilated with >95% oxygen (tests) or room air (controls) for 24 hours. Two test monkeys and one control were treated with E. col; endotoxin (500 pg/kg) 1V at the start of the study and after 12 hours. Histopathological changes in the lung parenchyma were evaluated using light and electron microscopy. Interstitial edema was detected as early as 24 hours after the onset of hyperoxia but there was no significant increase in the alveolar-capillary distance (blood-air barrier). Morphologic signs of oxygen toxicity further included swelling and disruption of vascular endothelium, and swelling of alveolar Type I1 pneumocytes. There was no difference in the number of macrophages per high power field between the four groups but significant differences were observed in the number of neuroepithelial bodies (NEBs) per cmL and mast cells per high power field at the light microscopic level. Treatment with endotoxin did not protect against oxygen toxicity and was associated with an exacerbation of the morphological alterations in the lung parenchyma and swelling of alveolar Type 1 pneumocytes.
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Postnatal development of dendritic reticulum cells and their immune complex trapping ability.
(Murcia : F. Hernández, 1986) Yukata Imai; Michi Dobashi; Kazuo Terashima
The postnatal development of dendritic reticulum cells in the rat popliteal lymph nodes was electron microscopically investigated in relation to the appearance of immune complex trapping capacity. The popliteal lymph nodes of neonatal rat consisted of loosely arranged fibroblastic reticulum cells. In the following stage, the ueripheral cortex and paracortex became distinguishable. The former was made up of an accumulation of small lymphocytes, scattered within a framework of reticulum cells. On te 28 th day, the first primary follicle appeared in the peripheral cortex. Simultaneously the immune complex could be trapped on the cytoplasmic membrane of reticulum cells, which were located in the central portion of the primary follicles. The early image of germina1 centers appeared corresponding to immune complex trapping areas. In the well-developed secondary follicles, the immune complex trapping cells were mainly localized in the cap area. Their cytoplasmic membranes formed the dendritic processes, on which the distinct ability of trapping of the immune complex was recognized. It was dernonstrated that the fibroblastic reticulum cells, forming the stromaof lymph nodes, were transformed into the typicai dendritic reticulum cells with labyrinth structures in the cap area. Desmosomal junctions were often found, not only between the dendritic reticulum cells themselves, but aiso between the dendritic reticulum cells and lymphocytes. We suggest that the desmosomal junctions play a role as the channel for a transmission of immunological information.
Open Access
Primary malignant fibrous histiocytoma of the breast.
(Murcia : F. Hernández, 1986) Sigurd, Lunde; Nesland, Jahn M.; Holm, Ruth; Johannessen, Jan Vicents
Clinical, light microscopic, electron microscopic and immunocytochemical features of 4 cases (3 women and 1 man) of primary malignant fibrous histiocytoma (MFH) of the breast are presented. The literature is reviewed and the diagnosis and treatment discussed. The good outcome is stressed and local excisioo or simple mastectomy recommended as appropriate treatment .
Open Access
Ultrastructure of pancreatic exocrine cells of the rat during starvation.
(Murcia : F. Hernández, 1986) Takashi Kitagawa; Kazuyuki Ono
Ultrastructural changes of the pancreatic exocrine cells after 3, 7, 14, 21, 28, 35 and 42 days of starvation were observed in male rats aged from 16 to 18 months weighing between 600 and 700 grams. The number of zymogen granules after starvation decreased to less than about 70 per cent of that of the control. Changes in the rough endoplasmic reticulum were hardly seen up to 14 days of starvation as compared with the control, but were observed in the apical and basal cytoplasm of the cell from 21 days after starvation. Particularly in 35- and 42-day starved rats, the rough endoplasmic reticulum was frequently shortened and dilated, and changed to disorganized membranous structures. The lysosomes in the apical cytoplasm of the cell gradually increased in number after starvation, and contact or fusion between the zymogen granules and lysosomes (viz. so-called crinophagy) was often seen at 35 and 42 days of starvation. Large autolysosomes especially those containing zymogen granules and rough endoplasmic reticulum were also marked in the basal cytoplasm of the cell after 35 and 42 days of starvation. Alterations in the basal cytoplasm of the cell appeared later than those in the apical cytoplasm. It was considered that, owing to its role in protein synthesis, the basal cytoplasm of the pancreatic exocrine cells in starved rats might be protected as far as possible during long-term starvation.

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