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J D Balentine

Publications and source records attributed to J D Balentine.

At least 19 recordsLinked to original sources
PubMed1989

Clinical, pathological, and biochemical studies on an infantile case of sulfatide/GM1 activator protein deficiency.

A 28-month-old black male died with severe complications of mental and motor deterioration, seizures, and aspiration. Autopsy demonstrated moderate liver enlargement, normal spleen and kidneys, small testes, and a grossly normal brain. Further examination showed irregular macrogyrae with evidence of a storage or sclerotic process. Thin layer chromatography of the lipids in formalin-fixed tissue demonstrated elevated levels of ceramide trihexoside and possibly sulfatides in liver and a decrease in the ratio of galactosylceramide to sulfatide in brain. Examination of the gangliosides in formalin-fixed brain indicated a slight increase in the percentage of GM1 ganglioside and a clear elevation in GM2 and GM3 gangliosides. Cultured skin fibroblasts had a normal activity for a large number of lysosomal enzymes including arylsulfatase A and galactocerebrosidase. When the cells were loaded with [14C]sulfatide only about 12% of the sulfatide was metabolized after 3 days. Extracts of the cells were subjected to SDS-PAGE and immunoblotting with antisphingolipid activator protein-1 (SAP-1) rabbit antiserum, and no cross-reacting material was detected confirming the diagnosis of metachromatic leukodystrophy caused by SAP-1 deficiency. This patient was clinically more severe than the other patients described previously with this deficiency. Further studies are underway to define the nature of the mutation in this patient.

Autopsy↗
PubMed1988

Spinal cord trauma: in search of the meaning of granular axoplasm and vesicular myelin.

The rapid appearance of selective axonal calcification following experimentally induced spinal cord impact injury has suggested that there is a sudden influx of intracellular calcium which mediates many of the pathological changes subsequent to the trauma. Granular dissolution of axoplasm and vesicular disruption of myelin are the most characteristic alterations in the affected white matter. These changes, which appear early and progress, are identical to those that can be induced by exposing myelinated axons to increased extracellular calcium or to calcium ionophores. These observations have led us to develop the hypothesis that calcium mediates the destruction of traumatized axons in the spinal cord by stimulating calcium-activated neutral proteinases (CANP), which in turn degrade axonal and myelin proteins. A rapid increase in CANP activity has been demonstrated in our experimental rat trauma model and a CANP has been isolated from rat spinal cord myelin which degrades both neurofilament and myelin proteins. However, the interpretation of the role of calcium has been complicated by the fact that granular axoplasm and vesicular myelin can be induced under conditions other than those favorable for CANP enhancement. The ultimate proof of the calcium hypothesis will depend on analyzing early intracellular ionic fluxes and correlating these with the localization of calcium-mediated enzymes and the evolution of pathological events.

Animals↗
PubMed1988

In vitro spinal cord trauma.

Fetal mouse spinal cord explants were harvested and allowed to grow in Maximow chambers. Normal appearing matured cultures were subjected to a brief episode of impact trauma by dropping the flat surface of 25 to 105 mg dressmaker's pins from a height of 10 cm directly onto the exposed surface of the culture. Light and electron microscopic studies at selected posttrauma intervals revealed discrete foci of necrosis preceded or accompanied by nerve fiber changes (granular axoplasm, vesicular myelin, pleomorphic spheroids) identical with those documented in spinal cord trauma in vivo. Although no inherent calcification was observed, calcium was added to some of the traumatized cultures and it was subsequently localized by pyroantimonate in the axoplasm; within mitochondria, adjacent to neurofilaments, and in the cytosol. The study indicates that the morphologic sequence of events of spinal cord trauma in vitro are similar to those observed in vivo, and that the latter may occur in the absence of vascular injury.

Animals↗
PubMed1987

Myelopathy induced by lactic acid.

This study defines the conditions required to provoke myelopathic changes by dripping lactic acid onto the surgically exposed spinal cord of adult male rats. A severe necrotizing myelopathy was observed after 24 h, principally in the posterior half of the cord at the level of lactic acid (pH 1.8) application. A profound early effect on small blood vessel walls, appearing necrotic after 30 min to 2 h, was identified. Nerve fiber alterations (axonal stasis, granular axoplasm, axonal calcification, and vesicular myelin), identical to those appearing early in the myelopathies of trauma and calcium toxicity, were apparent. However, the pathogenesis of these alterations in this model remains unclear, because of the vascular events and the presumed alterations of calcium metabolism by the acid. Further studies are required to elucidate the precise mechanisms of these important reactions of myelinated axons to the injuries provoked by acid, calcium, and trauma.

Acidosis, Lactic↗
PubMed1987

Brain calcium content in ischemic infarction.

Three degrees of focal ischemic infarction in the rat were created in the cerebral cortex supplied by the right middle cerebral artery, by ligation of the right middle cerebral artery and the right common carotid artery and temporary clip compression of the left common carotid artery, in succession. The postischemic accumulation of calcium in cerebral cortex of the right middle cerebral artery territory, determined by atomic absorption spectrometry, correlated with the infarct volume. The results are consistent with the hypothesis that calcium has role as a mediator in the pathogenesis of cerebral infarction.

Animals↗
PubMed1986

Evidence for glycoconjugate in nociceptive primary sensory neurons and its origin from the Golgi complex.

Glycoconjugates with terminal galactose residues were localized in rat spinal cord and spinal ganglia using lectin-HRP conjugates of Griffonia simplicifolia and Glycine max agglutinins. Alternate staining of serial sections with HRP-labelled lectins and an antibody for substance P (SP) showed staining in identical primary sensory neurons with both methods. Similarly, lectin-reactive as well as SP-positive fibers were found in Rexed laminae I and II, Lissauer's tract, the spinal nucleus and tract of the trigeminal nerve, the nucleus commissuralis and a small bundle of fibers just ventral to the central canal. Administration of capsaicin to neonatal rats produced a significant decrease in lectin-reactive fibers of the substantia gelatinosa, and in the number of lectin-reactive sensory neurons. The coexistence of SP with galactose-containing glycoconjugates in spinal ganglion neurons, as well as sensitivity of these cells to capsaicin, provided a basis for classifying the reactive neurons as nociceptive in type. Ligation of dorsal roots resulted in disappearance of lectin reactivity in the spinal cord and caused accumulation of lectin-positive material proximal to the ligature, indicating somatofugal transport of galactose-containing glycoconjugates. Colchicine injection caused an increase in SP reactivity in dorsal ganglion neurons but no change in lectin staining of galactoconjugate. At the ultrastructural level affinity for the lectin conjugates was confined to the Golgi cisternae and the plasmalemma of B-type sensory neurons in the dorsal ganglion. The axolemma of unmyelinated processes stained selectively in dorsal roots and the substantia gelatinosa of the spinal cord. These findings provide evidence for the presence in certain sensory cells of a characteristic galactosylconjugate which may prove to be of significance in nerve function.

Animals↗
PubMed1985

Histochemical localization of galactose-containing glycoconjugate at peripheral nodes of Ranvier in the rat.

Lectin-horseradish peroxidase conjugates were used to study glycoconjugates in paraffin sections of dorsal roots of the rat spinal cord. Griffonia simplicifolia-B4 isolectin (GSA I-B4) and peanut agglutinin (PNA) stained strongly the nodes of Ranvier, localizing, respectively, terminal alpha- and beta-D-galactose. Sialidase digestion did not increase staining with PNA at the node of Ranvier, suggesting the presence of a neutral glycoconjugate. Staining of the nodal but not the internodal axolemma was observed with PNA. The outer surface of the myelin sheath in axons of the dorsal root stained strongly with GSA I-B4 but only weakly with PNA, demonstrating an abundance of terminal alpha-galactose. PNA staining was enhanced in this site by sialidase digestion, showing terminal sialic acid-beta-galactose dimers. The presence of sialic acid here was further evidenced by labeling of these membranes with the lectin derived from the slug, Limax flavus (LFA). Affinity for a high iron diamine-Alcian blue (pH 2.5) sequence demonstrated, in addition, the presence of sulfate esters in glycoconjugates on the outer myelin membrane. GSA I-B4 imparted strong reactivity to nonmyelinated fibers in the dorsal root and the spinal nerve. The present findings appear to reflect several localizations of biochemically described nervous system glycoproteins containing O-glycosidically linked side chains terminated by alpha- and beta-D-galactose.

Animals↗
PubMed1984

Tissue calcium levels in CaCl2-induced myelopathy.

CaCl2-induced myelopathy was produced in rats by the application of a solution of CaCl2 to exposed leptomeninges of lumbosacral spinal cord. Equal lengths of remote cervical and lumbar cord were removed at intervals following Ca2+ application. The total Ca2+ in tissue from lumbar cord was significantly elevated over autologous cervical cord and homologous lumber controls after after 2 h. The maximum Ca2+ increase in lumbar cord was 3.9-fold that of homogolous control and was reached by 8 h post Ca2+ application. The time course for the elevation of Ca2+ as measured by atomic absorption spectrophotometry, resembles that found in spinal cord following direct physical trauma. These findings as well as similar changes in morphology and neural proteins from previous studies suggest that Ca2+ is involved in and may potentiate the degeneration of axons and myelin via Ca2+-activated neutral proteinases.

Animals↗
PubMed1984

Brain calcification in severely stressed neonates receiving parenteral calcium.

Morphologic evidence for calcium salts within the brains of severely stressed neonates at autopsy correlated to the mean daily parenteral dose of calcium gluconate (P less than 0.01). Survival analysis indicated that parenteral administration of calcium contributed a negative effect to predicted survival (P less than 0.05).

Brain Diseases↗
PubMed1984

Changes in myelin and axonal proteins in CaCl2-induced myelopathy in rat spinal cord.

Calcium-induced myelopathy was produced in rats by dripping 1.0 ml of a 10% solution of CaCl2 at pH 7.4 upon exposed spinal cord. Changes in spinal cord proteins were examined following application of calcium. Analysis of proteins by SDS-PAGE revealed progressive losses of neurofilament, microtubular, and glial filament proteins over a period of 8 hours to 5 days. Large losses of myelin proteins were also evident. The protein alterations observed correlate well with ultrastructural changes and resemble those previously found with physical trauma. These observations indicate that Ca2+ plays a pivotal role, possibly by activating proteinase(s), in the degeneration of axons and myelin sheath in both Ca2+-induced myelopathy and spinal cord injury.

Animals↗
PubMed1984

Myxopapillary ependymoma of the cauda equina with extension to the skin of the sacrococcygeal region.

Cutaneous involvement by myxopapillary ependymoma of the cauda equina is described clinically and morphologically. The patient, a young woman, was 12 years old at the time that the neoplasm was diagnosed. Skin involvement developed 12 1/2 years following the initial diagnosis of the primary neoplasm and after the third attempt at surgical extirpation. Involvement of the skin preceded the death of the patient by 11 months.

Adolescent↗
PubMed1984

Ultrastructural pathology of nerve fibers in calcium-induced myelopathy.

Calcium has been proposed as a mediator of nerve fiber degeneration following traumatic injury of the spinal cord. It induces a spongy, necrotizing myelopathy similar in its evolution to that observed in experimental spinal cord trauma. The current study was undertaken to determine the ultrastructural changes in the central nervous system (CNS) nerve fibers associated with calcium-induced myelopathy. A 10% calcium chloride (CaCl2) solution (pH 7.4) was slowly dripped on the dorsal surface of the surgically exposed lower thoracolumbar spinal cord of adult male Sprague-Dawley rats. The posterior and lateral columns of the spinal cords were fixed and processed for electron microscopy. Controls consisted of tissue from normal and sham-operated animals, as well as those receiving equal volumes and osmolarities of sodium chloride (NaCl), magnesium chloride (MgCl2), and potassium chloride (KCl) at the same pH. In the CaCl2 treated animals, spongiosis of increasing severity developed in white matter, as the result of periaxonal, adaxonal and intramyelinic swelling. Vesicular demyelination was consistently observed, beginning within one hour (h) and progressing with increasing severity up to 24-72 h. Axonal changes included pleomorphic spheroids, granular degeneration and intra-axonal calcification. The ultrastructural changes in the nerve fibers provoked by calcium were indistinguishable from those previously reported in experimental spinal cord trauma. These observations strengthen the hypothesis that calcium initiates the nerve fiber degeneration following spinal cord injury.

Animals↗
PubMed1984

Orthostatic hypotension with brainstem tumors.

Three patients with brainstem tumors had orthostatic hypotension as the major presenting manifestation. Two patients had primary tumors that involved the dorsal medulla, pons, and rostral spinal cord; one was a malignant astrocytoma and the other a hemangioblastoma. The third patient had an oat cell carcinoma of the lung with subependymal spread to the medulla, pons, hypothalamus, and thalamus. Evaluation of baroreceptor function in the patient with the malignant astrocytoma showed a defect in the efferent sympathetic limb of the baroreceptor reflex arc.

Adolescent↗
PubMed1984

X-ray microanalysis: identification and quantification of elements in normal and pathologically altered cells.

It is apparent that advanced technology in X-ray microanalysis is rapidly becoming applicable to experimental cellular pathology. Additionally, it has already proven to be of significant value in diagnostic human pathology and clinical research, especially in the areas of environmental toxicology and forensic pathology. Like routine electron microscopy, X-ray microanalysis will soon be a necessary technology for any major medical center practicing 'state-of-the-art' medicine.

Calcinosis↗
PubMed1984

Multimodal assessment of human brain calcification with respect to parenteral calcium gluconate in stressed neonates.

Parenteral calcium may augment the degree of calcification within brains of human neonates (p less than 0.01). This observation is supported by histochemistry, atomic absorption of ashed brain, selected area diffraction, and energy dispersive microanalysis. Survival analysis indicates that a standard replacement dose may have an adverse effect of severely stressed neonates (p less than 0.01). Nuclei within the optic-tract, circumferential pons and temporal lobe showed calcium salt deposits before other cytologic evidence of necrosis was discernible. Most calcification occurred in regions of ongoing necrosis primarily in the neuropil. But Purkinje cell and supraoptic neurons and apparent neurons from the fascia dentata, Ammon's Horn, were densely calcified in several brains. In those infants surviving longer periods both the neuropil and nuclei of glial scar stained for calcium salts.

Brain↗
PubMed1982

Calcium-induced spongiform and necrotizing myelopathy.

Selective axonal calcification has been consistently observed in experimental spinal cord trauma in laboratory animals as well as in human spinal cord injury. A hypothesis of calcium influx resulting in activation of proteolytic and/or lipolytic enzymes has been proposed as a major mechanism of nerve fiber degeneration. The current study was undertaken to determine the effects of calcium influx into nontraumatized spinal cord tissue, utilizing 10 per cent calcium chloride at a pH of 7.4 slowly dripped onto the dorsal surface of the surgically exposed spinal cord of adult male Sprague-Dawley rats. Controls consisted of animals similarly treated with solutions of sodium chloride, magnesium chloride, and potassium chloride at the same pH and osmolarity. Sham-operated and normal animals were also observed. The experimental animals that received calcium chloride consistently developed paraplegia that was evident within 24 hours after treatment. The initial spinal cord lesion consisted of discrete areas of spongiosis in posterior and lateral columns in the segment beneath the application of calcium. The spongiosis progressed in severity and was accompanied or followed by necrosis. The gray matter was relatively spared; however, the posterior horns became consistently necrotic. Calcium was observed histochemically in the areas of spongiosis/necrosis but not in spared areas. Although the topography of the calcium-induced myelopathy differs from that of spinal cord injury, the progression of the clinical and pathologic changes is consistent with the calcium-mediated hypothesis of necrosis in the latter.

Animals↗
PubMed1981

Ca2+-accumulation in experimental spinal cord trauma.

Quantitative measurements of the time course of calcium levels in experimental spinal cord trauma have been made. The injury was produced in rats by dropping a 10 g weight from 30 cm upon exposed dura-invested spinal cord. Lumbar sections of traumatized spinal cord and internal controls from remote cervical cord were excised and analyzed for calcium using atomic absorption spectroscopy. Total calcium levels in the lesioned cord were significantly elevated over control values within 45 min post-trauma (P less than 0.005), with maximal increase at 8 h. The increased levels of calcium in the lesion tissue confirm the previous morphologic finding of calcium deposits within axons in the lesion.

Animals↗