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  • 1
    Digitale Medien
    Digitale Medien
    Topical application of dynorphin-A antibodies reduces edema and cell changes in traumatised rat spinal cord
    Amsterdam : Elsevier
    Regulatory Peptides 53 (1994), S. S91-S92 
    Details
    ISSN: 0167-0115
    Quelle: Elsevier Journal Backfiles on ScienceDirect 1907 - 2002
    Thema: Medizin
    Materialart: Digitale Medien
    URL: http://linkinghub.elsevier.com/retrieve/pii/0167-0115(94)90256-9
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  • 2
    Digitale Medien
    Digitale Medien
    Changes in the sympathetic nervous system in diabetes mellitus (1968)
    Springer
    Journal of neural transmission 31 (1968), S. 86-95 
    Details
    ISSN: 1435-1463
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Beschreibung / Inhaltsverzeichnis: Zusammenfassung Es wird über die Resultate einer vorläufigen Untersuchung der pathologischanatomischen Veränderungen am peripheren autonomen Nervensystem in vier Fällen von Diabetes mellitus berichtet. Stückchen von präganglionären Rami communicantes, vom thoracalen orthosympathischen Grenzstrang und vom Ganglion coeliacum wurden histologisch untersucht. Die wichtigsten Resultate waren folgende: 1. Die präganglionären Rami communicantes nach dem thoracalen Grenzstrang zeigten eine klare Degeneration und eine Destruktion der Markscheiden, teilweise von segmentalem Charakter. 2. Paravertebrale wie prävertebrale Ganglia zeigten neuronale Läsionen mit schlechter Färbbarkeit der Nissl-Substanz, Neuronolysis begleitet von Proliferierung der Kapselzellen, Vakuolisierung des Zytoplasmas und degenerative Veränderungen der Ausläufer. 3. Die trophischen Gefäße der Rami communicantes sowie die der Ganglia wiesen Läsionen auf, die durch eine klare Verdickung ihrer Wände, die sich mit der PAS-Methode nach McManus stark rot färben ließen, gekennzeichnet waren. Es hat sich also gezeigt, daß allgemein verbreitete, histologisch nachzuweisende Läsionen des peripheren autonomen Nervensystems in Fällen von Diabetes mellitus vorkommen können.
    Notizen: Summary A preliminary study on the patho-anatomical changes of the peripheral autonomic system in diabetes mellitus is reported. Pieces from preganglionic communicating rami, thoracic sympathetic trunks and ganglion coeliacum obtained at autopsy from four diabetics were examined. The main findings were as follows: 1. Preganglionic communicating rami to thoracic sympathetic trunks displayed marked axonal degeneration and myelin destruction, partly of segmental characteer. 2. Paravertebral and prevertebral ganglions showed neuronal lesions including poor staining of Nissl substance, neuronolysis accompanied by proliferation of capsule cells, vacuolization of the cytoplasm and degenerative changes of processes. 3. Nutrient blood vessels of both communicating rami and ganglions displayed lesions characterized by a marked thickness of the walls staining intensely red with PAS according to McManus. Thus, widespread histologically detectable lesions of the peripheral autonomic nervous system may occur in cases of diabetes mellitus.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF02239177
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  • 3
    Digitale Medien
    Digitale Medien
    Effects of p-chlorophenylalanine on microvascular permeability changes in spinal cord trauma (1990)
    Springer
    Acta neuropathologica 79 (1990), S. 595-603 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Trauma ; Spinal cord injury ; Microvascular permeability ; Serotonin ; p-Chlorophenylalanine (p-CPA)
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The possibility that serotonin can take part in the initiation of the increased microvascular permeability occurring in a spinal cord trauma was investigated in a rat model with 131I-sodium and lanthanum as tracers. We influenced the serotonin content in the tissue pharmacologically by treating animals with a serotonin synthesis inhibitor, p-chlorophenylalanine (p-CPA), before the production of the injury and compared the results with injured, untreated controls. A small incision was made in the dorsal horn of the lower thoracic cord. It caused a progressive extravasation of 131I-sodium in the damaged segment, measured after 1,2 and 5 h. Rostral and caudal segments also showed a significant but lower accumulation of 131I-sodium. Lanthanum added to the fixative was used as an ionic tracer detectable by electron microscopy. The endothelial cells of microvessels removed from the perifocal region after 5 h showed a marked increase in the number of lanthanum-filled vesicles. Many endothelial cells had a diffuse penetration of the tracer into the cytoplasm and the basement membrane. However, the tight junctions usually remained closed to lanthanum. Pretreatment with p-CPA markedly reduced the extravasation of 131I-sodium measured at 5 h in the traumatized cord. At the cellular level, the endothelial vesicles filled with lanthanum approached the condition of uninjured animals. The diffuse infiltration of lanthanum into endothelial cells and its spread into the basement membrane of the vascular wall were usually absent. Our results indicate that serotonin plays a role in the initiation of the increased microvascular permeability which occurs in spinal cord injuries.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00294236
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  • 4
    Digitale Medien
    Digitale Medien
    Edema formation and cellular alterations following spinal cord injury in the rat and their modification with p-chlorophenylalanine (1990)
    Springer
    Acta neuropathologica 79 (1990), S. 604-610 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Trauma ; Spinal cord injury ; Edema ; Serotonin ; p-CPA
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The possibility that serotonin can modify the early pathological sequences occurring in spinal cord trauma was investigated in a rat model. To that end we took advantage of the possibility of influencing serotonin pharmacologically by treating animals with a serotonin synthesis inhibitor, p-chlorophenylalanine (p-CPA) before the production of the injury and compared the results with injured, untreated controls. A unilateral incision was made into the dorsal horn of the lower thoracic cord (about 2.5 mm deep, 4.5 mm long) and the trauma. The injured region from untreated animals showed macroscopically at that time a pronounced swelling and the water content had increased by 3.5% as compared to intact controls. The segments rostral and caudal to the lesion also exhibited a profound increase in water content. Light microscopy revealed a significant expansion of the spinal cord as compared to controls. The swelling was most pronounced in the gray matter on the injured side. Electron microscopy showed distorted neurons, swollen astrocytes and extracellular edema in the gray matter in and around the primary lesion. There was also a sponginess in the surrounding white matter with disruption of myelin, collapsed axons and widened periaxonal spaces. Pretreatment of the rats with p-CPA significantly reduced the swelling of the injured spinal cord and there was no visible expansion. The ipsilateral edema in the central gray matter was considerable less pronounced as compared to that in untreated animals. The increase in water content was less than 1% in these animals. The neuronal and glial cell changes were also markedly reduced in the drugtreated rats. The disruption of myelin and the vacuolation of the gray matter were much less severe. Our results show that p-CPA can markedly modify the edema and the cellular changes occurring in the traumatic spinal injury and indicate that serotonin is somehow involved in the production of the early, and thus important, pathological events.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00294237
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  • 5
    Digitale Medien
    Digitale Medien
    Immunohistochemical evidence of endothelin-1 in human choroid plexus (1992)
    Springer
    Acta neuropathologica 84 (1992), S. 457-460 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Choroid plexus ; Choroid plexus papilloma ; Endothelin-1 ; Human brain ; Immunohistochemistry
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary An immunohistochemical investigation was carried out on 17 specimens of human choroid plexus obtained post mortem, 1 biopsy of normal choroid plexus including part of the lateral ventricle and 1 papilloma of the choroid plexus removed surgically. The material was fixed in formalin. Paraffin and cryostat sections were used. A polyclonal antiserum to endothelin-1 served as a primary antibody. The avidin-biotin-peroxidase method was applied to demonstrate the immunoreaction. The epithelial cells of the choroid plexuses, the choroid papilloma and most ependymal cells of the lateral ventricle showed a distinct brown reaction product in their cytoplasm indicating antigenic sites to endothelin-1. The reaction was of lesser intensity in the ependymal cells. The connective tissue in choroid plexus was unstained. A positive immunoreaction was present in the walls of some vessels in the choroid plexus in cryostat sections. This is the first report on the presence of antigenic sites to endothelin-1 in the epithelial cells of the human choroid plexus. The role of endothelin in these cells should be investigated to ascertain if the cells synthesize this biologically active peptide or if it is merely bound to receptors in them.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00227676
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  • 6
    Digitale Medien
    Digitale Medien
    Binswanger's disease in the absence of chronic arterial hypertension (1992)
    Springer
    Acta neuropathologica 83 (1992), S. 434-439 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Binswanger's disease ; White matter lesion ; Arteriolosclerosis ; Dementia
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary The cerebral changes are described in a woman of 54 who suffered from Binswanger's encephalopathy: there were no signs or symptoms of chronic arterial hypertension. The disease presented as dementia of about 3 years duration. Computed tomography of the brain 2. 5 years before her death showed bilateral widespread hypodense lesions in the cerebral white matter. She died of an asthmatic attack. Autopsy disclosed extensive bilateral degeneration of the central white matter, lacunes and gliosis. Severe obliterative arteriolosclerosis occurred in the meningeal vessels and those supplying the affected parts of the brain. Light microscopy showed that the most severe lesions occurred in the arterioles. Immunohistochemistry demonstrated profound extravasation of plasma proteins chiefly albumin, indicating dysfunction of the blood-brain barrier. Thus, the lesions characteristic of Binswanger's encephalopathy may develop in the absence of chronic arterial hypertension. Additional pathogenic factors, possibly genetic predisposition to vascular injury may play a role in the development of this condition.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00713538
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  • 7
    Digitale Medien
    Digitale Medien
    Increased expression of growth-associated protein 43 immunoreactivity in axons following compression trauma to rat spinal cord (1996)
    Springer
    Acta neuropathologica 92 (1996), S. 19-26 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Key words Growth-associated protein 43 ; Immunohistochemistry ; Rat ; Spinal cord ; Trauma
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract Growth-associated protein 43 (GAP43) is one compound used to indicate growth of axonal endings during development and regeneration, particularly of peripheral neurons. Using immunohistochemistry, we have studied the expression of GAP43 in the spinal cord of rats subjected to mild, moderate or severe compression injury and used neurofilament immunostaining to demonstrate axonal injuries. Samples removed from the compressed T8–9, the cranial T7 and the caudal T10 segments were studied at 4 h, 24 h, 4 days and 9 days after injury. Control rats showed a moderate immunostaining of neurons in dorsal root ganglia, weak staining of ventral motor neurons and, with the exception of the corticospinal tracts, a weak staining in some axons of the longitudinal tracts of the cord. Injury in the compressed region led to increased GAP43 immunoreactivity in axons of normal and expanded size. This occurred particularly 1–4 days after injury and normalized 9 days thereafter. More marked immunostaining was present in the cranial and caudal segments. The corticospinal tracts never showed such staining. The increase of GAP43 immunostaining is presumably caused by disturbed axonal transport from neurons with the capacity to synthesize and transport the GAP43 antigen. Transported material may thus be available for regeneration of axons, but this source of material may vary between different classes of axons within the cord.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/s004010050484
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  • 8
    Digitale Medien
    Digitale Medien
    Accumulation of β-amyloid precursor protein and ubiquitin in axons after spinal cord trauma in humans: immunohistochemical observations on autopsy material (1996)
    Springer
    Acta neuropathologica 92 (1996), S. 49-55 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Key wordsβ-Amyloid precursor protein ; Ubiquitin ; Human ; Spinal cord ; Trauma
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Abstract We evaluated by immunohistochemistry the presence of β-amyloid precursor protein (ßAPP) and ubiquitin-like material which may accumulate in axons of the human spinal cord subjected to injury. Autopsy material was obtained from nine cases with different types of trauma: breech delivery with neonatal spinal injury, compression of the cord induced by fractures of the vertebral column, haematomas or intradural meningioma. The post-trauma period ranged from 10 days to several years. The spinal cord of six control cases without evidence of injury presented βAPP immunoreactivity in nerve cell bodies and in a few axonal profiles but not in dendrites. Seven of the nine cases with spinal cord trauma showed an accumulation of βAPP-immunoreactive material in axons of the longitudinal tracts at the site of the injury. Five cases presented similar axonal immunoreactivity in the grey matter of the cord. Ubiquitin-like immunoreactivity was present in expanded axons in cases with spinal cord injury. Cases with spinal cord trauma thus present βAPP-immunoreactive axons particularly of the longitudinal tracts in the same way as in trauma to rat spinal cord and in various brain injuries. The aggregation of βAPP-immunoreactive material indicates disturbed axonal transport of βAPP. Accumulation of ubiquitin-like immunoreactive material in expanded axons at the site of trauma may be one prerequisite for degradation of abnormal proteins by the ubiquitin-mediated proteolytic pathway.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/s004010050488
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  • 9
    Digitale Medien
    Digitale Medien
    Bicuculline-induced epileptic brain injury (1983)
    Springer
    Acta neuropathologica 62 (1983), S. 87-95 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Status epilepticus ; Nerve cell injury ; Bicuculline ; Rat cerebral cortex
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary It was earlier shown that bicuculline-induced status epilepticus gives rise to profound acute changes in the rat cerebral cortex, i.e. edema and neuronal alterations. In the present study, we explored to what extent interruption of the seizure activity reverses the changes observed. To that end, status epilepticus of 1 and 2 h duration was induced by bicuculline before the seizures were arrested by i.v. injection of diazepam. The brain was then fixed by vascular perfusion either 5 min (1 h of seizures) or 2 h (1 and 2 h of seizures) of recovery and cerebral cortical tissue was studied by light (LM) and electron microscopy (EM). Already 5 min following the arrest of seizure activity most of the astrocytic edema had disappeared, and the number of injured neurons was clearly reduced. After 2 h of recovery, following 1 h of status epilepticus, the edema was virtually absent, and only few injured cells were found (only about 1% of the neuronal population). When recovery was instituted after 2 h of status epilepticus, numerous dark, triangular neurons were found. In the last group an adequate blood pressure could not be obtained. Therefore, the cellular alterations observed were probably not the result of the seizure activityper se. After 5 min of recovery, EM studies showed condensed, dark-staining injured neurons, similar to those previously observed in non-recovery animals. However, an increased incidence of swollen mitochondria was observed. After 2 h of recovery a few severely injured neurons remained which showed signs of progressive injury with fragmentation of the cell body.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00684924
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  • 10
    Digitale Medien
    Digitale Medien
    Hypoglycemic brain injury (1980)
    Springer
    Acta neuropathologica 50 (1980), S. 31-41 
    Details
    ISSN: 1432-0533
    Schlagwort(e): Hypoglycemia ; Nerve cell injury ; Biochemistry ; Light microscopy ; Rat cerebral cortex
    Quelle: Springer Online Journal Archives 1860-2000
    Thema: Medizin
    Notizen: Summary Profound hypoglycemia causing the disappearance of spontaneous EEG activity was induced by insulin in rats. For analysis of cerebral cortical concentrations of labile phosphates, glycolytic metabolites and amino acids, the brain was frozen in situ. For microscopic analysis of the corresponding cerebral cortical areas the brain was fixed by perfusion. Hypoglycemia with an isoelectric EEG for 30 and 60 min caused severe perturbation of the cerebral energy metabolites. After both 30 and 60 min of isoelectric EEG, two microscopically different types of nerve cell injury were seen. Type I injury was characterized by angulated, darkly stained neurons with perineuronal vacuolation, mainly affecting small neurons in cortical layer 3. Type II injured neurons, mainly larger ones in layers 5–6, were slightly swollen with vacuolation or clearing (depending on the histotechnique used) of the peripheral cytoplasm, but had no nuclear changes. Recovery was induced by glucose injection. Improvement in the cerebral energy state occurred during the 30 min recovery period even after 60 min of hypoglycemia. However, the persisting reduction in the size of adenine nucleotide and amino acid pools after 30 or 180 min recovery suggested that some cells remained damaged. In confirmation many type I injured neurons persisted during the recovery suggesting an irreversible injury. The disappearance of virtually all type II injuries indicated reversibility of these histopathological changes. The microscopic changes in hypoglycemia were different from those in anoxia-ischemia suggesting a dissimilar pathogenesis in these states despite the common final pathway of energy failure.
    Materialart: Digitale Medien
    URL: http://dx.doi.org/10.1007/BF00688532
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