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W F Blakemore

Publications and source records attributed to W F Blakemore.

At least 145 records · Page 8Linked to original sources
PubMed1980

Biochemical studies on a case of feline mannosidosis.

Evidence is presented for the biochemical diagnosis of the first case of feline mannosidosis. A marked deficiency of acidic alpha-D-mannosidase in the brain, kidney and liver and excessive excretion of mannose-rich oligosaccharides in the urine were found in a kitten suffering from a nervous disorder. Residual acidic alpha-D-mannosidase, ranging from 2 to 5.5% of the normal activity, was observed in the tissues of the affected kitten. It has similar kinetic and physicochemical properties to the normal activity. The amount of mannose in the urine of the affected kitten was 19-fold greater than in a comparable control, and the molar ratio of mannose to N-acetylglucosamine was approx. 6 : 1. High concentrations of neutral oligosaccharides were detected in the urine. The predominant oligosaccharide appeared to be a hexasaccharide. The biochemical features of bovine, feline and human mannosidosis are compared, and it is concluded that feline mannosidosis may be a useful animal model for studying the human disease.

Animals↗
PubMed1980

Ataxia and spinal cord degeneration in llama, wildebeeste and camel.

Clinical and pathological findings from instances of ataxia in a group of wildebeeste (Connochaetes taurinus), two llamas (Llama glama) and one Arabian camel (Camelus dromedarius) are presented. Clinically, all the affected animals showed a non-febrile, progressive ataxia. Neuropathologically, Wallerian degeneration was diffuse in the spinal cord of the camel and llamas but was focal in the wildebeeste. Degeneration was present in the cervical dorsal roots in the wildebeeste and in the ventral nerve roots at all levels of the cord in the llamas. Peripheral nerve were affected in all the species. The possible roles of copper deficiency and plant poisons in the aetiology of the condition are discussed.

Animals↗
PubMed1980

The relationship between internodal length and fibre diameter in the spinal cord of the cat.

The relationship between internodal length and external fibre diameter in the spinal cord was examined on glutaraldehyde perfused material from a number of cats. The relationship in all samples was highly significant and there was no significant difference either between animals or between the lateral and dorsal columns. However, there was considerable variability, some internodes being twice and others less than half as long as the length predicted by the regression equation. Our results showed that the relationship between internodal length and fibre diameter was essentially a linear function. No internodes shorter than 100 micrometers were seen.

Animals↗
PubMed1980

Acute nicotinamide deficiency in the pig induced by 6-aminonicotinamide.

Pigs given intraperitoneal injections of 6-aminonicotinamide developed a syndrome similar to a natural disease found in Queensland. Focal lesions, involving mainly destruction of glial cells, developed in the intermediate grey matter of the cervical and lumbar enlargement of the spinal cord. There was widespread vacuolation of spinal cord white matter. The glial cell loss was repaired. We suggest that natural acute nicotinamide deficiency can occur if a threshold dose of an antimetabolite of nicotinamide is absorbed over a short period of time.

6-Aminonicotinamide↗
PubMed1978

Suppression of remyelination in the CNS by X-irradiation.

Rat and cat spinal cords were exposed to 2000, 3000 or 4000 rads of x-irradiation prior to producing an area of primary demyelination in the dorsal columns by the injection of lysolecithin. In animals irradiated with 4000 rads no remyelination by either Schwann cells or oligodendrocytes occurred. With 2000 rads both types of remyelination occurred, but when compared to unirradiated controls, central remyelination was less extensive, while Schwann cells remyelinated a greater percentage of axons. With 3000 rads the results were variable, some animals responded similarly to those in the 4000 rad group, whereas others responded as the 2000 rad animals. Oligodendrocytes were found among the persistently demyelinated axons in the 4000 rad animals and their processes were associated with, but only rarely formed a myelin sheath round, the demyelinated axons. It was concluded that irradiation damage to local cells was responsible for the inhibition of remyelination but it could not be determined if this was due to its effect on the oligodendrocytes alone. The origin of the oligodendrocytes found among the demyelinated axons is discussed in this context.

Animals↗
PubMed1978

Lesions in the cat spinal cord following local injections of 6-aminonicotinamide.

Lesions were made in the spinal cord of cats by means of local injections of 6-aminonicotinamide. The concentration needed to induce primary demyelination also caused extensive axonal death. In the early stages following injection there was evidence of astrocyte and oligodendrocyte destruction and with longer survival times most of the surviving demyelinated axons were remyelinated by Schwann cells. This experimental system indicates that Schwann cell remyelination of central axons follows astrocyte destruction, but it was not considered a suitable model system for the study of cellular relationships in remyelination because of the extensive concomitant axonal damage.

6-Aminonicotinamide↗
PubMed1978

Decompression sickness in the goat: nature of brain and spinal cord lesions at 48 hours.

An investigation was undertaken to determine whether permanent damage to the central nervous system (CNS) is associated with transient decompression sickness in the goat. Twelve goats were compressed in air at 100 fsw for one hour. After decompression over a period of 2.5 min, seven animals showed signs of decompression sickness and four of these were treated by recompression in oxygen. Residual clinical signs after 12 h were present in one animal only. The seven affected goats were killed 48 h after decompression. Lesions in the CNS (other than hemorrhage) were confined to the spinal cord of three animals that had shown paralysis, and consisted of infarction of white matter with occasional microthrombi and perivascular proteinaceous edema of the gray matter. In all seven animals, there was hemorrhage in the spinal cord and in four, hemorrhage in the brain. Infarction of the spinal cord was not present in the four animals that had shown only slight clinical signs (limping); one of these goats had been treated by recompression in oxygen.

Animals↗
PubMed1977

Remyelination in the spinal cord of the cat following intraspinal injections of lysolecithin.

Intraspinal injections of small volumes of lysolecithin were made in the cat. These produced a local area of primary demyelination at the site of injection and all the demyelinated axons were subsequently remyelinated either by oligodendrocytes or Schwann cells. In general the type of remyelination depended on the position of the axon relative to the point of injection; those near the centre of the lesion were remyelinated by Schwann cells while those at the edges were remyelinated by oligodendrocytes. At the very centre of the lesion there was fairly extensive axonal degeneration. Oligodendrocyte-remyelinated axons were enclosed within astrocyte processes which were usually covered by basement membrane on the surface next to Schwann cells. The pattern of remyelination in the cat was compared with similar lesions in the rat and it was concluded that the more vigorous astrocytic response in the cat was responsible for the differences observed in the lesions in the 2 species.

Animals↗
PubMed1975

The ultrastructure of normal and reactive microglia.

Normal microglia have a distinct morphology. In rapidly, but now in slowly evolving pathological states the features used to identify the resting cell are often lost. When there is invasion by haematogenous monocytes, phagocytes develop whose origin - cerebral or haematogenous- cannot be ascertained on morphological features alone. These observations stress that microglia are part of the reticulo-endothelial system.

Animals↗