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D Troost

Publications and source records attributed to D Troost.

119 records · Page 7Linked to original sources
PubMedDate not supplied

Localization of metallothionein in the mammalian central nervous system.

This review concerns the immunohistochemical localization of metallothionein (MT), a metal-binding protein, in the mammalian central nervous system (CNS). Expression of MT in the mammalian CNS is abundant. In the mouse brain, MT expression is found in some glial cells, whereas in the adult rat brain immunoreactivity varies from no expression at all to abundant reactivity throughout the whole brain. In primates and humans, MT expression is mainly found in astrocytes. Thus, MT expression in the mammalian CNS is found in the pia-arachnoid, ependymal cells and astrocytes. Cells expressing MTs can, in this way, supply essential metals to neurons and may protect neurons against toxic ions.

Aging↗
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Metallothionein in amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disorder characterized by loss of motor neurons in the spinal cord, brainstem and motor cortex. Ten percent of the cases are familial and these have been linked to point mutations in the gene coding for cytosolic copper, zinc superoxide dismutase. The etiology of sporadic ALS is unknown. To further investigate the possible role of metals in causing the disease, we investigated metallothionein (MT) levels in ALS organs and serum. We previously reported significantly increased MT levels in ALS liver and kidney. These are not reflected in serum MT levels, which are normal in ALS. In ALS spinal cord, MT is expressed in gray matter protoplasmic astrocytes. Induction of MT synthesis in ALS may denote increased metal exposure or may result from increased oxidative stress, as in familial ALS.

Aged↗
PubMedDate not supplied

Histopathological changes in the spinal cord after 434 MHz microwave hyperthermia in the cervical region of the rat.

The time-course of thermal damage to the spinal cord was studied after hyperthermia of the cervical region in the rat. Local 434 MHz microwave heating of the spinal cord (cervical 5-thoracic 2) was obtained by using a ring-shaped applicator. Heat treatment at 42.9 degrees C (+/- 0.4 degrees C) for 38 min resulted in neurological symptoms, ranging from uncoordinated use of the forelegs to paralysis and death in 90 per cent (28/31) of the animals. Histological sectioning of the treated part of the spinal cord was performed immediately, 4, 24 h and 3, 7, 14 and 28 days after hyperthermia. Immediately and 4 h after treatment, neurons in the grey matter of the cord were affected and vacuolization was observed in the white matter. In animals with paralysis 1 day after treatment, we noticed neuronal degeneration, myelin pallor and sometimes haemorrhagic foci in white and grey matter. As a reaction to the thermal injury, gliosis was observed and invasion of macrophages and lymphocytes (day 3-14). Animals which had severe neurological symptoms at day 1 after hyperthermia, but had recovered completely 28 days after treatment, showed focal scar formation and demyelination in the spinal cord. The observed neurological complications correlated well with the localization of the observed histopathological changes in the cervical spinal cord.

Animals↗
PubMedDate not supplied

Thermotolerance of the spinal cord after fractionated hyperthermia applied to the rat in the cervical region.

The effects of heat treatment at 42.9 +/- 0.4 degrees C for 30-90 min of rat cervical spinal cord (cervical 5-thoracic 2) were investigated in animals which had received a priming treatment at 42.3 +/- 0.4 degrees for 60 min in the same region 24 hours before. Hyperthermia to the cervical region in the rat was applied by a coaxial double ring radiator, operating at a frequency of 434 MHz. The test heat treatment led to neurological complications, ranging from unco-ordinated use of the forelegs to paralysis of both forelegs. Death was observed, presumably as a result of respiratory paralysis. The animals that received the priming heat treatment were more resistant to heat injury than those without priming. The LD50, 60 days, for animals without and with priming treatment was respectively at 41 +/- 2 min 42.9 degrees C and at 88 +/- 7 min 42.9 degrees C. The TTR calculated from the LD50, 60 days, data is 2.1 +/- 0.2. Almost all animals, without priming, that did not die as a result of the treatment, recovered in the period from day 1 to day 60 after hyperthermia. Animals that had received a priming exposure were less able to recover from neurological symptoms induced by the test heat treatment. For this reason the induced resistance to thermal injury after priming exposure was more pronounced in the data on lethality than on neurological symptoms. Spinal cord histology from animals that did not recover from neurological symptoms showed extensive non-vascular damage to both gray and white matter.

Animals↗
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Ultrastructural changes in the rat sciatic nerve after local hyperthermia.

The rat sciatic nerve was heated over a length of 5 mm for 30 min at 43, 44 or 45 degrees C. Morphological changes were not observed after heating at 43 degrees C. Treatment at 44 degrees C resulted in endoneurial oedema and mild vascular changes, such as contraction and vacuolization of endothelial cells and thickening of the media of the larger vessels. Within 1 week several demyelinated axons were observed. The first changes after heating at 45 degrees C included oedema, blood vessel occlusion and severe endothelial cell damage. Axonal changes, e.g. the accumulation of cell organelles, appeared 8 h after treatment; 24 h after treatment most axons and myelin sheaths showed degenerative changes. Absence of blood flow in the heated area of the nerve was shown 2 h after heating at 45 degrees C. We conclude that hyperthermic treatment directly affects endothelial cells and myelin sheaths in the rat sciatic nerve. Axons degenerate most probably as a consequence of ischaemia.

Animals↗
PubMedDate not supplied

Immunohistological alterations in muscle of patients with amyotrophic lateral sclerosis: mononuclear cell phenotypes and expression of MHC products.

Muscle biopsy specimens from 15 autopsied patients with the isolated form of amyotrophic lateral sclerosis were examined by routine histological and immunocytochemical methods using a panel of monoclonal antibodies directed against differentiation and activation markers of immunocompetent cells. In 12 cases, cellular infiltrates consisting mainly of T-cells and macrophages were seen. Both CD8+ and CD3+ cells, in juxtaposition with OKM1+ macrophages, were particularly seen in the atrophied parts of muscle. The majority of the T-cells appeared to be of the CD4+ T-helper/inducer type, whereas the CD8+ T-suppressor/cytotoxic cells were only rarely and focally present. On the other hand, B-, NK- and K-cells were infrequently seen. Most of the T-cells and macrophages surrounding the atrophied muscle fibers were in an activated state, as indicated by their intense HLA DR expression. In addition, some angulated degenerated fibers showed strong endomysial positivity for HLA DR in the regions where T-cells and macrophages were present in clusters. The immunoreactive changes in ALS-associated muscle atrophy are very similar to those reported for exercise-induced damage and some forms of myositis. The present study shows that the expression of major histocompatibility complex products and the relative numbers of infiltrating immunocompetent cells are closely associated with the extent of destruction of muscle fibers in ALS.

Aged↗
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Lymphocytic infiltration in the spinal cord of patients with amyotrophic lateral sclerosis.

Amyotrophic lateral sclerosis (ALS) is a devastating systemic atrophy affecting the upper and lower motor neurons. The etiology is unknown, but one theory of pathogenesis supposes that the motor system is affected by abnormal immune responses. We have studied the prevalence and extent of lymphocytic infiltration, previously reported as a rare finding in the ALS spinal cord. Application of monoclonal antibodies against macrophages, T- and B-cells to spinal cords from 48 ALS patients disclosed a cellular mononuclear infiltrate in 38 specimens (79%), intense enough to be revealed by routine neuropathological techniques in 6 of them (12.5%); the remaining 10 cords (21%) exhibited no infiltrates. Since duration and clinical signs of the preceeding illness were the same in cases with and without infiltrates, we consider it unlikely that such infiltrates are entirely secondary to atrophy of the cord. As Wallerian degeneration is not accompanied by infiltrates of lymphocytes, their presence in the cord tracts of our material throws doubt on the conventional view that tract degeneration in ALS is exclusively Wallerian.

Adult↗
PubMedDate not supplied

Aberrant myelinated neurites in the anterior horns of a patient with amyotrophic lateral sclerosis.

A case of amyotrophic lateral sclerosis revealed the classical pathologic features of ALS, i.e. neuronal loss in the anterior horns and pyramidal tract degeneration. In addition to the pathological hallmarks of Alzheimer's disease, senile plaques, neurofibrillary tangles and granulovacuolar changes of neurons were also present. Clinically the 67-year-old patient exhibited ALS of the upper extremity and a mild forgetfulness. Two striking pathological features were noted in the spinal cord: first, at several levels in the spinal cord excessive amounts of myelinated neurites were found; second, the microglial proliferation in the anterior horns was very intense and positive for leukocyte common antigen.

Aged↗
PubMedDate not supplied

Malignant glioma after bombshell injury.

A case of post-traumatic glioma is presented. The patient, wounded in the head in World War II by a bombshell, developed symptoms of an intracranial tumor in 1982. Histopathologically the tumor was an astrocytoma grade III. The tumor was in direct continuity with an old abscess membrane.

Brain Injuries↗
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Temporal lobe pathology in amyotrophic lateral sclerosis. Do amyotrophic lateral sclerosis and Alzheimer's disease share a common etiological factor?

An autopsy study was performed on temporal lobe samples from 20 non-demented patients with amyotrophic lateral sclerosis (ALS), 17 age-matched non-demented controls and 4 Alzheimer's disease (AD) patients. Formalin fixed, paraffin embedded sections from the hippocampus with adjacent parahippocampal gyrus and from the superior temporal gyrus were stained with conventional and immunohistochemical stains. Immunohistochemical staining for the A4 protein was enhanced by pretreatment with 0.25% pepsin before 100% formic acid. The incidence and severity of AD-like pathological changes were similar in ALS patients and non-demented controls. In both groups, pathological changes increased with age. This study does not support the hypothesis that ALS and AD share an etiopathogenetic background.

Aged↗