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H G Jenkins

Publications and source records attributed to H G Jenkins.

10 recordsLinked to original sources
PubMed1992

Diurnal variations in the electroretinographic c-wave and retinal melatonin content in rats with inherited retinal dystrophy.

The inability of retinal pigment epithelium to phagocytose shed photoreceptor disks is a cause of retinal degeneration in the Royal College of Surgeons rat; retinal pigment epithelial phagocytosis and disk shedding are regulated by the diurnal rhythm of retinal melatonin level. The diurnal rhythms of the electroretinogram (particularly that of the retinal pigment epithelial potential, the electroretinographic c-wave) and retinal melatonin content were thus investigated in Royal College of Surgeons rats from postnatal day 17 to 24, the period preceding retinal degeneration. The amplitudes of both the b- and c-waves of the electroretinogram fell significantly during the peak time of rod disk shedding and rose after the time of expected light off in the control and dystrophic rats. While the b-wave rhythms did not differ between the two strains, diurnal changes in the c-wave were significantly less distinct in the dystrophic rats than in controls. This difference may reflect lack of phagocytosis in dystrophic rats. Furthermore, the ERG c-wave was significantly larger and prolonged, and the retinal melatonin content higher, in dystrophic rats of this age group than in controls. It appears that retinal melatonin metabolism may play an important role in the maintenance of retinal pigment epithelial and photoreceptor function.

Animals↗
PubMed1992

Tumour necrosis factor causes an increase in axonal transport of protein and demyelination in the mouse optic nerve.

An increase in fast axonal transport of protein by the optic nerve was found in mice following a single combined injection of human recombinant tumour necrosis factor alpha (rTNF) and [3H]proline into the vitreous chamber. Demyelination was observed in optic nerve fibres arising from the eyes of mice which received a single rTNF injection. No such changes were detected when heat-inactivated rTNF was injected with the label. The effects of intravitreal injection of rTNF on the pathophysiology of mouse optic nerve resembled those found in mice infected with Semliki Forest virus (SFV), an animal model of multiple sclerosis. We suggest that TNF could mediate at least some of the pathophysiological changes found in SFV-infected mice and may provide a clue concerning the disease mechanism in multiple sclerosis.

Animals↗
PubMed1991

Changes in fast axonal transport of glycoproteins in optic nerves of mice infected with Semliki Forest virus.

[3H]fucose incorporation into mouse retinae and subsequent axonal transport of glycoproteins to optic nerve terminals was studied before and during optic nerve demyelination induced by Semliki Forest virus (SFV) infection. As was previously found for [3H]proline-labelled protein, axonally transported glycoprotein was increased before demyelination. Fluorographic analysis of the increased glycoproteins and proteins, after separation by gel electrophoresis, showed particularly large increases in labelling of 2 glycoproteins (38.1 kDa and 45.0 kDa) and 3 protein (15.9 kDa, 23.8 kDa and 27.7 kDa) bands. These increases were due to host-cell rather than viral components. At the time of demyelination, however, [3H]fucose incorporation into retinae of SFV-infected mice was significantly depressed, resulting in reduced label incorporation into axonally transported glycoproteins. Since glycoproteins play a role in axon-glia recognition and adhesion, the early changes in their axonal transport may contribute to the mechanism of demyelination.

Animals↗
PubMed1988

Receptor-mediated uptake of beta-glucuronidase into primary astrocytes and C6 glioma cells from rat brain.

The ability of both primary astrocytes from rat cerebrum and a rat C6 glioma cell line to take up lysosomal enzymes by receptor-mediated endocytosis was compared. The beta-glucuronidase secreted by 3T3 fibroblasts was purified to homogeneity by antibody affinity chromatography, iodinated and used as a typical enzyme to determine the nature of receptors involved in its uptake into glial cells. Both primary astrocytes and C6 glioma cells took up 125I-labelled enzyme in a rapid and saturable manner indicative of specific receptors, while immunostaining with an anti-mouse beta-glucuronidase antibody showed that the enzyme was distributed in a mainly punctate pattern after uptake, characteristic of that of lysosomes. Subcellular fractionation of C6 glioma cells following endocytosis revealed that the enzyme became localised in lysosomes, after first passing through an endosomal compartment. Uptake of enzyme was reduced markedly after its sugar side chains had been removed with N-glycanase, indicating that endocytosis was mediated via a carbohydrate-recognising receptor. A range of carbohydrates and glycoproteins were tested for their ability to inhibit receptor-mediated endocytosis but of these only sialic acid had a notable effect. Further evidence that endocytosis of beta-glucuronidase into primary astrocytes and C6 gliomas may be mediated via sialic acid receptors was provided by the large reduction in rate of uptake observed following removal of this sugar from the enzyme with sialidase.

Animals↗
PubMed1988

Evidence for a T-cell related factor as the cause of demyelination in mice following Semliki Forest virus infection.

Patchy demyelination throughout the central nervous system, including the optic nerve, is known to occur following infection with Semliki Forest virus (SFV) in Swiss/A2G mice. An increase in the fast axonal transport of protein in optic nerves occurred before they showed signs of demyelination in Swiss/A2G mice, heterozygous nude mice and nude mice reconstituted with T-cells. SFV infection, however, caused neither an increase in the fast axonal transport of protein, nor optic nerve demyelination in T-cell-deficient nude mice. Thus, the increase in both axonal transport and demyelination following SFV infection appear to be T-cell-mediated events, rather than direct effects of the virus.

Animals↗
PubMed1988

Developmental and age-related changes in rat brain glycosaminoglycans.

The quantities of each major class of glycosaminoglycan were determined in rat cerebrum from postnatal day 5 to 30 months of age. Chondroitin sulphate, dermatan sulphate, heparan sulphate, heparin, and hyaluronate were found, but no keratan sulphate was detected. Large and rapid changes in glycosaminoglycan content were observed during the period of brain maturation, and thereafter relatively steady levels were maintained until after the age of 12 months. The most remarkable change in the aged rat cerebrum was the ratio by weight of hyaluronate to chondroitin sulphate, which was approximately 1:1 from postnatal day 10 to 18 months but increased to 2.6:1 by the age of 30 months. In immature rats, the proportion of nonsulphated and 6-sulphated disaccharides derived from chondroitinase AC digests of brain glycosaminoglycans was much greater than in adults. In mature rats, chondroitin sulphate was composed almost entirely of 4-sulphated disaccharide subunits. The possibility that these changes could affect the permeability properties of the cerebral extracellular space and ionic equilibria in the brain is discussed.

Aging↗
PubMed1988

Glycosaminoglycans in cortical autopsy samples from Alzheimer brain.

Each of the known classes of mammalian glycosaminoglycans, with the exception of keratan sulphate, was found in cerebral cortex samples from patients with Alzheimer-type dementia and age-matched controls. These molecules were quantitated, after electrophoresis and staining with Alcian Blue dye, by scanning densitometry. No significant differences were found between the mean levels of each of the above glycosaminoglycans in frontal cortex from patients with dementia compared with controls. An increase (26%; p less than 0.05) in the mean level of hyaluronate, but not of other glycosaminoglycans, was found in temporal cortex samples. On the other hand, the uronic acid content of hyaluronate degradation products following Streptomyces hyaluronidase treatment of brain glycosaminoglycans did not reveal any statistically significant changes in Alzheimer's disease. HPLC of disaccharide products from Arthrobacter chondroitinase AC digests did not reveal any significant changes in sulphate substitution of chondroitin sulphate in Alzheimer brain.

Alzheimer Disease↗
PubMed1980

The effect of Escherichia coli endotoxins and adrenocortical hormones on plasma enzyme activities in the domestic fowl.

The intravenous injection of endotoxins isolated from Escherichia coli serogroups O111 and O78 (2 mg/kg) increased the activities of aspartate transaminase and lactate and sorbitol dehydrogenases in the plasma of six- to 11-week-old chickens during the next 24 h. These changes were compared with those produced by adrenocorticotrophic hormone and beta-methasone and were attributed to tissue damage involving the liver followed by increased enzyme synthesis which may have been induced partly by adrenocortical hormones. Further evidence of liver damage was provided by a fall in the activity of cholinesterase. The alkaline phosphatase activity gave no indication of cholestasis.

Adrenocorticotropic Hormone↗
PubMed1969

Hookworm infection.

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Bephenium Compounds↗