[Ultrastructural study of experimental cerebrocortical necrosis in calves (author's transl)].
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Abstract:
Cerebrocortical necrosis (CCN) was experimentally induced in three calves with the thiamine antagonist Amprolium. The calves were followed clinically. At the time of development of typical clinical signs of CCN the calves were killed and necropsied and a complete histopathologic examination was performed. The light microscopic lesions of the cerebral cortex were those of middle laminar necrosis and deep laminar edema. The necrotic zone consisted of fine vesicles and differed only slightly from the edema zone. In the former some neurons were morphologically normal, others showed signs of injury, while in the latter all neurons were injured. The lesions are consistent with those found in natural cases of CCN. Biopsies from the cerebral cortex were taken at the time of early clinical signs. Ultrastructural studies of these biopsies showed no clear difference between the zones of necrosis and edema observed light microscopically. The ultrastructural changes were characterized by dilatations in the neuropil. The cytoplasm and foot plates of the astrocytes had a "watery" appearance and contained dilated mitochondria and large vesicles. The vesicles were continuous with the granular endoplasmic reticulum. It was concluded that the initial morphologic changes in CCN in calves were indicative of a cytotoxic edema of the astrocytes. This may be due to a cytotoxic edema with subsequent loss of cell volume control. The primary astrocytic changes could then lead to neuronal injury.Keywords:
Neuropil
Cerebral edema
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Cerebrocortical necrosis (CCN) was experimentally induced in three calves with the thiamine antagonist Amprolium. The calves were followed clinically. At the time of development of typical clinical signs of CCN the calves were killed and necropsied and a complete histopathologic examination was performed. The light microscopic lesions of the cerebral cortex were those of middle laminar necrosis and deep laminar edema. The necrotic zone consisted of fine vesicles and differed only slightly from the edema zone. In the former some neurons were morphologically normal, others showed signs of injury, while in the latter all neurons were injured. The lesions are consistent with those found in natural cases of CCN. Biopsies from the cerebral cortex were taken at the time of early clinical signs. Ultrastructural studies of these biopsies showed no clear difference between the zones of necrosis and edema observed light microscopically. The ultrastructural changes were characterized by dilatations in the neuropil. The cytoplasm and foot plates of the astrocytes had a "watery" appearance and contained dilated mitochondria and large vesicles. The vesicles were continuous with the granular endoplasmic reticulum. It was concluded that the initial morphologic changes in CCN in calves were indicative of a cytotoxic edema of the astrocytes. This may be due to a cytotoxic edema with subsequent loss of cell volume control. The primary astrocytic changes could then lead to neuronal injury.
Neuropil
Cerebral edema
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Cerebral edema
Morphology
Brain Edema
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A 51-year-old woman who had been given cobalt therapy for nasopharyngeal carcinoma was seen three years later with a mass in the left frontotemporal region of the brain. Biopsy specimen of the lesion showed the classic features of delayed radiation necrosis on light microscopy. In addition, several blood vessels showed endothelial cell proliferation. Transmission electron microscopical study demonstrated numerous alterations of the endothelial cell, such as intraluminal infoldings of the plasma membrane, an increased amount of cytoplasmic organelles, and the frequent occurrence of tubular bodies in addition to degenerative and reactive changes in the neuropil.
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Organelle
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The pathology of Ictaclurus punctatus with the typical symptoms bacterial septicemia was studied.The results demonstrated that the main pathological changes of bacterial septicaemia in Ictaclurus punctatus were as follows:Gill lamellae showed proliferation and fusion as a plate,tumefaction and degeneration in the epithelial cells.Intestine showed degeneration,necrosis,loss in epithelial cells,expansion and congestion in capillary of lamina propria and submucosa.Liver cells showed tumefaction,vacuolar degeneration and even necrosis,and hepatic cord arranged irregularly.The stomach showed degeneration,necrosis,loss in epithelial cells,expansion and congestion in capillary of lamina propria and part of the lamina propria exposed.The kidney showed swelling,degeneration,necrosis in renal tubular epithelial cell,atrophy and even necrosis,collapse in glomerular,edema,hemorrhage in interstitial.The muscle fibers were swelled and fractured,with cloddy,homogenizing degeneration or irregular dissolution.
Lamina propria
Degeneration (medical)
Submucosa
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Ultrastructural findings in three cases of gastric carcinoma with coagulative necrosis are reviewed with special emphasis on microvascular changes. Intratumoral microvasculature revealed more or less stabilized vessels. Some were characterized by a close association between pericytes and endothelial cells, whereas others showed laminated basement membrane, with a loose association between pericytes and endothelial cells. Some mural cells exhibited ultrastructural signs of regressive changes, including lipofuscin granules, swollen mitochondria, and cytoplasmic lucency. These findings are discussed in relationship to a number of recent studies of the microvascular injury caused by hypoxia and reoxygenation, in humans and animals.
Coagulative necrosis
Lipofuscin
Pericyte
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Immunostaining
Neuropil
Brain Edema
Human brain
Immunofluorescence
Cerebral edema
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The ultrastructure of the fibrous sheath, the layer of ganglionic cell bodies and the neuropil of brain ganglion of Oncomelania hupensis was first observed under transmission electron microscope. Ultrastructural changes were found in the brain ganglion after immersing the snails in sodium pentachlorophenate. The mitochondria of nerve fibers and neurons showed denaturation and necrosis, and glycogen in neurones was markedly reduced; the neuropil also exhibited denaturation and necrosis. The ultrastructural findings may explicate in some way the mechanism of molluscicidal action of NaPcP on Oncomelania hupensis via its action on the nervous system (Figs. 1-6).
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Oncomelania hupensis
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S INCE postoperative cerebral edema remains an important cause of morbidity and mortality in neurosurgery there is need for an experimental model that closely resembles this clinical condition. Prados et al. 4 exposed the cerebral cortex of cats to air; edema of moderate degree, permitting closure of the dura mater, usually followed but rarely and unpredictably there was marked swelling. Luse and Harris 1 reported swelling of the brain following craniotomy in the rabbit; they stated that this technique was not a suitable method for the consistent production of cerebral edema. This communication reports a method for the consistent production of a marked degree of postoperative cerebral edema together with some observations on the edema thus produced.
Cerebral edema
Brain Edema
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Objective To observe the ultrastructural changes of damaged lung induced by ischemic acute kidney injury(IAKI) in rats.Methods Transmission Electron Microscopy and morphometric analysis were used in this study.Results Both type I and II alveolar cells undergoing necrosis could be seen in the lungs damaged by IAKI.Disappeared osmiophilic multilamellar bodies of damaged type II cells could be found.In addition,endothelial cells undergoing apoptosis were also noted in the lungs damaged by IAKI.Neutrophilic leukocyte infiltration was evident in alveolar septum with IAKI.Conclusions Both necrosis and apoptosis are involved in the lungs damaged by IAKI,but necrosis is more evident than apoptosis.Leukocyte infiltration is also involved in the lungs of RIRI animals.
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Dysembryoplastic neuroectodermal tumor (DNT) is a rare brain neoplasm. Although the tumor pathology is relatively well charactererized, its full clinicopathological spectrum is still discussed, and ultrastructural data on it are very limited. Here, the authors describe detailed ultrastructural pathology of 7 cases of DNT. Each tumor consisted of 3 major elements: neoplastic cells (oligodendroglial-like cells, OLC), elongated processes forming neuropil-like structure, and expanded "mucoid" extracellular space, the latter giving an impression of cellular elements floating within it. Neoplastic cells had round, oval, or elongated nuclei, no discernible nucleoli, and a relatively narrow rim of cytoplasm. Some nuclei were irregular and invaginated, and pseudoinclusions (invaginations of cytoplasm penetrated into toroid-like nuclear formations) were observed. Part of the cytoplasm sequestrated within pseudoinclusions often appeared degenerated with large blebs and electron-lucent vesicles, and some of these contained, in turn, semicircular profiles of unknown significance. Chromatin was clustered below the nuclear membrane. The cytoplasm contained a few mitochondria, round rather than elongated, a few stacks of rough endoplasmic reticulum, and scanty microtubules and clear vesicles. The second element consisted of innumerable cellular processes. Some of these were elongated and formed stacks connected by symmetric or asymetric adhesive plaque junctions. Others had shorter "neck" containing microtubules extending into bulbous extensions. Dense-cored vesicles were occasionally observed, both in the cytoplasm of neoplastic cells and within processes. In one cell, cross-sectioned annulate lamellae were found. In the cytoplasm of a few cells, unusual inclusions reminiscent of ribosome-lamellae resembled "laboratory tubes" with cone-like endings. At higher power, walls of the "tubes" resolved into layered structures composed of several laminae; between these, ribosome-like structures were visible. The authors conclude that OLC exhibit clear-cut characteristics of neuronal cells and not true oligodendocytes.
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