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Biomedical subjects

J D Balentine

Publications and source records attributed to J D Balentine.

At least 37 records · Page 2Linked to original sources
PubMed1979

Selective mitochondrial degeneration in renal tubules following hyperbaric oxygen exposure.

To study the ultrastructural effects of hyperoxia on the kidney, young adult Sprague Dawley rats were exposed to 3 atmospheres absolute (ATAs) of pure oxygen for 5 hours and were killed in a time sequence varying from immediately to 30 days after exposure. Their renal cortices were processed for electron microscopy. Selective mitochondrial changes were observed within sublethally and transiently altered proximal tubular epithelial cells. The most consistent finding was the accumulation of 0.08 mu to 0.5 mu round to ovoid homogeneous matrical inclusions which frequently formed larger confluent amorphous masses. The inclusions stained intensely with lead and uranium but appeared homogeneously electron-lucent in unstained sections. Energy-dispersive x-ray analysis revealed that they did not contain calcium or phosphorus. The inclusions were different from the innately electron-opaque flocculent densities commonly found in pathologically altered mitochondria. Since the mitochondria containing them were removed by autophagocytosis, it is suggested that the inclusions were associated with selective mitochondrial degeneration induced by hyperoxia. No glomerular lesions were found.

Animals↗
PubMed1978

Recurrent meningitis due to an intracranial epidermoid.

The association of intracranial dermoids and epidermoids and recurrent meningitis is usually related to the presence of dermal sinuses that allow bacterial entry. Epidermoid cysts rarely discharge their contents into subarachnoid space to cause meningitis, except after surgical removal. We describe a child who had 10 separate episodes of chemical meningitis between age 13 months and her death at age 2 years 9 months. Death was caused by an intra-axial epidermoid in the ventral pons which had ruptured into the subarachnoid space, as shown at autopsy. There was no evidence of sinus tracts, and radiographic studies revealed no mass.

Brain Neoplasms↗
PubMed1978

Electron microscopy of peroxidase and acid phosphatase in leprous and uninfected armadillo macrophages: a macrophage subpopulation contains peroxisomes and lacks bacilli.

Lepromatous tissue from armadillos inoculated 24--36 months earlier with Mycobacterium leprae was obtained for electron microscopic studies. Cytochemically stained lepromas revealed a subpopulation of macrophages containing peroxisomes. These peroxidase reactive macrophages were not infected with bacilli. Acid phosphatase was present in macrophages and many of these were infected with bacilli and contained vacuoles and lipid globules. Within the membrane-bound vacuoles, acid phosphatase surrounded bacilli. However, the reaction product ended abruptly at a 15--40 millimicron thick zone of low electron density surrounding intact bacilli. Acid phosphatase was more intensely reactive and localized less precisely in heavily infected and vacuolated macrophages than in lightly and non-infected cells. The effectiveness of this bacillary barrier and the numerous infected macrophages with substantial acid phosphatase argue against the ability of acid phosphatase to protect host cells from leprosy bacilli. Evidence suggests a protective action of peroxidase or the rapid turnover of macrophages within lepromas. Granular and membranous debris were commonly seen within vacuoles of infected macrophages. A portion of the debris was ultrastructurally similar to bacillary matrix and was nonreactive for peroxidase and acid phosphatase. Following homogenization and centrifugation, similar materials banded with bacilli above 60% sucrose. Another portion of the debris was ultrastructurally similar to host lysosomal matrix and was reactive for acid phosphatase. Results support the concept of dual host and parasitic origins of the debris found in phagolysosomes of infected macrophages. Transparent, oval Epon defects remained eccentric to the majority of intact bacilli in centrifuged fractions. Apparently, an intrinsic property of leprosy produced these Epon defects.

Acid Phosphatase↗
PubMed1978

Lysosomal activity in experimental spinal cord trauma: an ultrastructural cytochemical evaluation.

The possible role of lysosomal activity in the early post-trauma phase of severe experimental spinal cord trauma was assessed utilizing an acid phosphatase cytochemical ultrastructural study. The results indicate that there is no evidence for lysosomal alteration prior to the development of cellular degeneration or necrosis. No diffuse cytoplasmic staining was observed. This study indicates that physical lysosomal injury resulting in release of hydrolases into spinal cord cells is not a tenable hypothesis as a primary initiating event in the development of spinal cord necrosis following trauma. However, the data are consistent with the general theory that lysosomal activity is important in the secondary degradation of cells following their being altered beyond recovery.

Acid Phosphatase↗
PubMed1978

Macrophages migration through the brain parenchyma to the perivascular space following particle ingestion.

Forty-eight rats received intracerebral injections of sterile colloidal carbon. At intervals between 10 minutes and 31 days after carbon injection, the rats were perfused with glutaraldehyde, and autopsies were performed. Between 10 minutes and 3 hours after injection, carbon particles were extracellular and located strictly within the needle track. During the first few days the carbon was ingested by macrophages. Initially absent, carbon-laden macrophages spread to the neuropil immediately surrounding the injection site at 7 to 31 days following injection. These carbon-laden macrophages frequently were elongated within the neuropil and resembled microglia. Carbon-laden macrophages eventually accumulated around local vessels and in perivascular spaces. Many macrophages containing carbon remained in the injection site at the longest sampling interval of 31 days. Results indicate two macrophage responses to colloidal carbon in the central nervous system: a) an indolent population remains in the injection site for at least 1 month and b) a second population of macrophages emigrates through the neuropil. They eventually surround local vessels and enter the perivascular space. The migrating macrophages offer an explanation for the peculiar perivascular cells in Krabbe's disease and may provide a link between the CNS parenchyma and immunocompetent cells.

Animals↗
PubMed1978

Pathology of experimental spinal cord trauma. I. The necrotic lesion as a function of vascular injury.

Adult Sprague Dawley rats were subjected to spinal cord trauma at the lower thoracic-lumbar levels utilizing a weight dropping technique onto the surgically exposed dorsal surface. The experimental conditions of trauma consistently produced severe paraplegia without spontaneous movement of the hindlimbs, a sensory level, and neurogenic bladder dysfunction. Changes in blood vessels and the development of tissue necrosis were studied in a posttrauma time sequence by light and electron microscopy. Fibrinoid necrosis and disruption of major arteries as well as veins were observed immediately after impact, antedating the evolution of parenchymal necrosis. A fusiform zone of spinal cord necrosis, involving the complete cross-sectional area beneath the site of impact, evolved over a period of 8 to 24 hours, being initially complete in the gray matter by 4 hours and thereafter in the white matter. Ultrastructural observations revealed that the evolution of necrotic cellular constituents was piecemeal. Except for the occurrence of intracellular calcification and heterophagocytosis in the traumatized tissue, the electron microscopic features of cellular necrosis were comparable to those of postmortem spinal cord autolysis, studied in parallel. The observations are consistent with trauma producing ischemic necrosis, resulting from major blood vessel disruption occurring at the moment of impact.

Animals↗
PubMed1978

Pathology of experimental spinal cord trauma. II. Ultrastructure of axons and myelin.

Adult male Sprague Dawley rats were subjected to spinal cord trauma of the lower thoracic-upper lumbar spinal cord using a weight dropping technique onto the surgically exposed dorsal surface. This experimental model, which results in severe paraplegia and development of complete segmental necrosis, was studied in a time sequence varying from immediately to 30 days afterward by electron microscopy, in order to characterize the pathologic changes in axons and myelin in the area of impounding. The results revealed tubulovesiculation within axons immediately posttrauma. Axonal fragmentation, axonal and adaxonal swelling accounted for the progressively increasing spongy appearance of the white matter. Beginning at 30 minutes and progressing until completion of tissue necrosis at 8 to 24 hours, axonal necrosis characterized by a finely granular alteration gradually evolved. Spheroids containing increased mitochondria, neurofilaments, lysosomes, and smooth endoplasmic reticulum appeared both in and peripheral to the zone of necrosis. Axonal calcification, rarely observed within 30 minutes, appeared maximally after the evolution of tissue necrosis. Two basic abnormalities of myelin were found: vesicular degeneration and intramyelinic vacuolization. These characteristically occurred late and involved fibers with abnormal axoplasm and were interpreted as being secondary in origin.

Animals↗
PubMed1977

Calcification of axons in experimental spinal cord trauma.

Selective discrete intraaxoplasmic deposits of hydroxyapatite crystallites were observed in adult male rats subjected to experimental trauma to the lumbosacral spinal cord. Although previously unreported in spinal cord trauma, the presence of these deposits in minimally altered axons and during the early posttrauma period suggests that such selective calcification may be of more than secondary significance. In view of the current emphasis on cytotoxicity of calcium, especially in relation to axonal degeneration, an evaluation of the role of calcium in augmenting traumatic spinal cord necrosis is warranted.

Animals↗
PubMed1977

Complex oligodendroglial invaginations within myelinated nerve fibers of the central nervous system during axonal degeneration.

Ultrastructural studies of spinal cord in rats subjected to hyperbaric oxygen exposure and experimental spinal cord trauma have resulted in frequent degeneration of axons. In both experimental situations central nervous system myelinated fibers containing complex cytoplasmic interdigitations of electron lucent, normal appearing cytoplasm, and dense cytoplasm, interpreted as degenerative, were observed. In some of the complex profiles the electron lucent cytoplasm could be traced back to the inner mesaxon, where its relation to the latter indicated a glial origin. Cytochemical evaluation of acid phosphatase activity in the complex cytoplasmic interdigitations revealed that both components contain significant lysosomal activity. The complex structures are interpreted as being sequestrations of degenerating axoplasm by distal adaxonal oligodendroglial processes, possibly representing an unusual form of heterophagocytosis.

Acid Phosphatase↗
PubMed1976

Retroperitoneal ganglioneuroblastoma: a kaleidoscope of neuronal degeneration. A light and electron microscopic study.

The light and electron microscopic features of an unique retroperitoneal ganglioneuroblastoma in a four-year-old female are described. The unprecedented concurrence of Hirano, zebra, membranous cytoplasmic (MCB), and Pick bodies in the same population of neoplastic, sympathetic ganglion cells provides further evidence for their non-specificity. Although the pathogenesis of the membranous cytoplasmic bodies in this tumor is unclear, they ostensibly arise within endoplasmic cisterns, similar to the proposed origin of membranous cytoplasmic bodies in Tay-Sachs disease. Both the apparent continuum between argyrophilic bodies and central chromatolysis, and the incorporation of various cytoplasmic constituents within neurofilamentous proliferations reflect some of the dynamic factors involved in the formation of Pick bodies.

Cell Count↗
PubMed1976

Infection of armadillos with Mycobacterium leprae. Ultrastructural studies of peripheral nerve.

Peripheral nerves of armadillos were studied 16 to 30 months after intradermal or intravenous inoculation with Mycobacterium leprae. Numerous bacilli were found within macrophages, Schwann cells, and perineurial cells; endothelial cells, pericytes and fibroblasts were involved as well. The bacilli were characteristically contained in membrane-limited vacuoles that were interpreted as being phagosomes. Some of the phagosomes contained granular, membranous, and vesicular debris considered to be bacillary degradation products, suggesting that lysosomal activity was present within the phagosomes. Multivesicular bodies, a few of which contained bacilli, were abundant in macrophages and perineurial cells. An unusual proliferation of irregular tubulovesicular profiles was noted, especially in Schwann and perineurial cell cytoplasm, surrounding and within phagosomes containing bacilli. The pattern of cellular involvement of neural structures with M leprae was similar to that observed in lepromatous leprous neuritis in humans.

Animals↗
PubMed1975

Central necrosis of the spinal cord induced by hyperbaric oxygen exposure.

Seventy-six adult rats were exposed to 60 psig of oxygen on consecutive days until death. At autopsy, 17 of the animals segmental foci of central necrosis of the spinal cord gray matter, often associated with small ball- and flame-shaped hemorrhages in either the cervical and/or lumbosacral enlargements. Paraplegia or quadriplegia were clinically observed prior to death. The oxygen-induced spinal cord lesions are similar though not identical to those observed in experimental and human spinal cord trauma. These observations indicate that the therapeutic use of hyperbaric oxygen in patients with spinal cord injury has a potential danger of causing central spinal cord necrosis.

Animals↗
PubMed1975

Oxygen tension in spinal cord gray matter during exposure to hyperbaric oxygen.

Adult female rats were exposed to 60 psig of 100% oxygen for 60 minutes. Oxygen tensions in the gray matter of the lumbosacral enlargement of the spinal cord, electroenecephalograms, electrocardiograms, and respirations were monitored before, during, and after the compression periods. Oxygen tensions were found to rise sharply to as high as 1050 mm Hg during compression and remained at significantly high levels throughout the entire hour of exposure. These data support the hypothesis that spinal cord lesions induced by exposure to hyperbaric oxygen are the result of excessive tissue oxygenation.

Animals↗