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Biomedical subjects

W L Maxwell

Publications and source records attributed to W L Maxwell.

48 records · Page 3Linked to original sources
PubMed1989

Axonal injury in the optic nerve: a model simulating diffuse axonal injury in the brain.

A new model of traumatic axonal injury has been developed by causing a single, rapid, controlled elongation (tensile strain) in the optic nerve of the albino guinea pig. Electron microscopy demonstrates axonal swelling, axolemmal blebs, and accumulation of organelles identical to those seen in human and experimental brain injury. Quantitative morphometric studies confirm that 17% of the optic nerve axons are injured without vascular disruption, and horseradish peroxidase (HRP) studies confirm alterations in rapid axoplasmic transport at the sites of injury. Since 95% to 98% of the optic nerve fibers are crossed, studies of the cell bodies and terminal fields of injured axons can be performed in this model. Glucose utilization was increased in the retina following injury, confirming electron microscopic changes of central chromatolysis in the ganglion cells and increased metabolic activity in reaction to axonal injury. Decreased activity at the superior colliculus was demonstrated by delayed HRP arrival after injury. The model is unique because it produces axonal damage that is morphologically identical to that seen in human brain injury and does so by delivering tissue strains of the same type and magnitude that cause axonal damage in the human. The model offers the possibility of improving the understanding of traumatic damage of central nervous system (CNS) axons because it creates reproducible axonal injury in a well-defined anatomical system that obviates many of the difficulties associated with studying the complex morphology of the brain.

Animals↗
PubMed1988

Response of cerebral microvasculature to brain injury.

There is increasing evidence that there is a direct response of the cerebral microvasculature to head injury. We have investigated using SEM and TEM the response of microvessels within the white matter of the baboon brain to lateral head acceleration. There is rapid endothelial disruption and swelling of perivascular astrocytes near the sites of petechial haemorrhage. The formation of microvilli in all vessels reaches a peak at 6 h and extends at least 5 mm from the site of haemorrhage. The astrocyte response suggests a partial recovery by 6 h. The endothelial response is most marked in arterioles and venules and is maintained for 6 days after injury. We suggest there is a biphasic cerebrovascular response to brain injury. First there is rapid astrocytic swelling possibly correlated with transient disruption of the blood-brain barrier. This is followed by morphological changes in the endothelium of all vessels which are most marked in arterioles and venules and extend considerable distances throughout the neuropile. This response is discussed in the light of disruption of the blood-brain barrier.

Animals↗
PubMed1988

Freeze-fracture studies of reactive myelinated nerve fibres after diffuse axonal injury.

We have studied the axonal and myelin sheath response in diffuse axonal injury after angular acceleration using the freeze-fracture and thin section techniques. It was found that the glial-axonal junction was intact until 1 h after injury. But upon loss of the nodal axolemma specialisations, after 3 to 4 h, the dimeric particles of the glial-axonal junction (GAJ) were lost and, by 6 h, the myelin lamellae became separated from the axonal remnant. There was a correlated loss of glial membrane specialisations of the GAJ during this separation. In the internodal region a suggestion of membrane damage occurred after 20 min but discrete myelin dislocations (particle-free areas) were not found until 1-h survival and were extensive by 6 h. Areas of loosely organised myelin occurred between intact axons at 7-28 days after injury. No evidence for growth cone formation was obtained.

Animals↗
PubMed1988

Response of intraventricular macrophages after a penetrant cerebral lesion.

The response of epiplexus and supraependymal cells to extravasated blood after a penetrant cerebral lesion was investigated. Epiplexus cells respond more actively than supraependymal cells. The epiplexus cells tend to aggregate near areas of extravasation of erythrocytes, this being most marked 6 hours after injury. Epiplexus cells lose their smooth surface appearance, retract their filopodia and adopt a more spherical form, with short microvilli or blebs. Numerous inclusion vesicles develop; some contain disrupted erythrocytes 6-12 hours after injury and these are still present 24-30 hours after injury. By 8-16 days after injury epiplexus cells resume a smooth surface appearance and the number of inclusion vesicles is much reduced. This suggests reversion to a quiescent state, from an earlier active state.

Animals↗
PubMed1984

The distribution of types I, III, IV and V collagens in penetrant lesions of the central nervous system of the rat.

The presence and distribution of types I, III, IV and V collagens within open lesions in the rat cerebrum have been demonstrated by immunofluorescent techniques. In the adult animal, types I and III collagens can be identified in the cicatrix from eight days onwards. Types IV and V collagens occur in the basement membrane of the glia limitans formed between the neuropile and the cicatrix and in the basement membranes of the blood vessels. In neonatal animals, less than eight days old at operation and allowed to recover for eight days, no type I or III collagens occur in the lesion and no types IV and V are present along the edge of the neuropile, because a glia limitans is not formed. In animals operated on when eight days old, the adult response is found in the cortex only, but when 16 days old the full adult response occurs in all parts of the lesion.

Animals↗
PubMed1983

Deposition of scar tissue in the central nervous system.

Standard parasagittal lesions were placed stereotactically in the cerebral hemispheres of neonatal and adult rats in order to compare scarring in the immature and mature animal. Lesions were examined by light and electron-microscopy and immunofluorescence to study the astrocyte reaction, collagen deposition, and the formation of the basement membrane of the glia limitans. Normal mature scarring characterized by the deposition of collagen, astrocyte end-feet alignment over a glia limitans, and the permanent presence of mesodermal cells (fibroblasts and macrophages) in the core of the lesion, does not occur in wounds before 8-10 days post-partum (dpp). Instead there is no deposition of collagen, and only a transitory astrocyte response occurs with the formation of an interrupted glia limitans. These latter features disappear with time so that the wound is ultimately obliterated by the growth of axons and dendrites through the lesion. Mature scarring is attained over 8-12 dpp when increasing amounts of collagen are deposited and a continuous permanent glia limitans is formed. The acquisition of the mature response to injury from 8-12 dpp may be correlated with the presence of increasing titres of a fibroblast growth factor (FGF), derived from autolytic digestion of injured brain tissue. We have investigated FGF activity using a 3 T 3 fibroblast tissue culture assay to detect mitogenic activity in brain extracts from rats lesioned at different ages and from leukodystrophic mice which have no myelin. Our results show that high titres of FGF are present in the developing brain long before myelination commences, and that normal levels of FGF are found in the brains of leukodystrophic mice which have no myelin. Scarring in brain lesions in these mutants is quite normal.

Animals↗
PubMed1982

The acrosomal zonule.

A structure associated with the developing acrosome during spermiogenesis in the rat and the Chinese hamster is described. The acrosomal zonule first appears in the cap phase of spermiogenesis and can be detected at all stages of development until after spermiation. The role of the acrosomal zonule is discussed.

Acrosome↗
PubMed1981

Ultrastructure of the seminiferous tubules in magnesium-deficient rats.

The ultrastructure of the seminiferous tubule in the testis of magnesium-deficient rats is described. The boundary tissue was normal. Cells in the basal compartment were shrunken with large intercellular spaces except where desmosome-like junctions occurred. Cellular relations in the intermediate and adluminal compartments appeared normal but the SER in spermatids was less organised than in the control. There is extensive vesiculation of th SER in Sertoli cells. The role of the Sertoli cell in the maintenance of differences in the ionic compartments of the extratubular and intratubular milieu is discussed.

Animals↗
PubMed1980

Light microscopic and ultrastructural changes of the exocrine pancreas in magnesium deficient rats.

In magnesium deficient rats with a clinical picture of protein malnutrition, pancreatic changes typical of protein malnutrition were expected. However, in rats fed for four weeks on a low magnesium diet (protein content 25%), light and electron microscopic studies revealed that the acinar cells of the pancreas were packed with zymogen granules, suggesting a disturbance in the discharge (rather than in the production) of the pancreatic enzymes. The mitochondria and the lumina of the RER were swollen. The nuclei had an irregular outline, the chromatin was aggregated into irregular granules and the nucleolemma of the nucleolus was fibrillar. It was suggested that the disturbance in the release of pancreatic enzymes might cause a maldigestion of the dietary protein, which eventually would lead to the condition of protein malnutrition in the magnesium deficient rats. The disturbance of exocytosis in the pancreas of magnesium deficient rats might be due to the preferential use of all the available magnesium for protein (enzymes) synthesis so that there were no magnesium ions left for the energy dependent discharge of the zymogen granules.

Animals↗
PubMedDate not supplied

Experimental intracerebral haematoma in the rat: sequential light microscopical changes.

In a small animal model of controlled intracerebral haemorrhage, changes within the haematoma and surrounding tissues were examined by light microscopy in toluidine blue stained semithin sections. Groups of animals were killed at 2, 6, 15, 24 and 48 hours, 2, 4, 8 and 14 days, and 3 months survival. Sequential changes in neurons, glia and leucocytes, together with the gradual absorption of the blood clot and its replacement by an astrocytic scar are described.

Animals↗