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Biomedical subjects

J J Harding

Publications and source records attributed to J J Harding.

At least 91 records · Page 5Linked to original sources
PubMed1989

Risk factors for cataract in Oxfordshire: diabetes, peripheral neuropathy, myopia, glaucoma and diarrhoea.

423 cataract patients and 608 controls between the ages of 50 and 79 were interviewed in a case-control study in Oxfordshire. Diabetes, myopia, glaucoma, peripheral neuropathy and severe diarrhoea were identified as risk factors. The excess risk experienced by females with diabetes was confirmed. The trauma of surgery for glaucoma may be largely responsible for the appearance of glaucoma as a risk factor. Severe diarrhoea has now been identified as a risk factor in England and in India. The risk associated with peripheral neuropathy may indicate a common aetiology at least for some proportions of the two conditions.

Aged↗
PubMed1989

Protection against cataract by aspirin, paracetamol and ibuprofen.

Results of a case-control of 423 cataract patients and 608 controls in Oxfordshire shows that the protective effect against cataract associated with consumption of aspirin-like analgesics (aspirin, paracetamol and ibuprofen family) is manifest even at low doses. Less than 150 g total dose was associated with a halving of the risk of cataract extraction.

Acetaminophen↗
PubMed1988

The major metabolite of bendazac inhibits the glycosylation of soluble lens proteins: a possible mechanism for a delay in cataractogenesis.

Glucose-6-phosphate and galactose react non-enzymically with lens proteins. The rates of these reactions are decreased by 5-hydroxybendazac but not by its parent compound, bendazac. Both bendazac and its major metabolite bind to lens proteins, mostly by non-covalent interactions. These results are discussed in relation to the use of bendazac as an anti-cataract drug.

Animals↗
PubMed1988

Non-enzymic glycosylation (glycation) of lens proteins by galactose and protection by aspirin and reduced glutathione.

Radioactive galactose becomes attached covalently to lens proteins in the same way as glucose. Simultaneous incubation with aspirin inhibits the reaction with galactose in a dose-related manner. Incubation with aspirin before incubation with galactose in the absence of aspirin showed that aspirin can modify crystallins permanently to prevent the binding of galactose. The galactosylation was also inhibited by glutathione at physiological concentrations. All major groups of lens proteins reacted with galactose but a higher level of modification of protein in the material of high molecular weight may indicate that galactosylation has induced aggregation of the proteins. The modification of all major crystallin groups was confirmed by isolating the galactosylated proteins by affinity chromatography. The results are discussed in relation to glycosylation of lens proteins in diabetes and galactosaemia and the role of glycosylation in cataract.

Acetylation↗
PubMed1988

A case-control study of cataract in Oxfordshire: some risk factors.

Three hundred patients with cataract and 609 control subjects with the same age-sex distribution were interviewed in a study of cataract in Oxfordshire, England. The risks associated with severe diarrhoea, glaucoma, and work on a military base have been demonstrated. Population attributable risks were calculated for those and other risk factors.

Aged↗
PubMed1988

Drugs, including alcohol, that act as risk factors for cataract, and possible protection against cataract by aspirin-like analgesics and cyclopenthiazide.

A case-control study of cataract in Oxfordshire explored the risks and benefits associated with a variety of drugs. Steroids including the diuretic spironolactone, nifedipine, heavy smoking, and beer drinking were associated with a raised risk. On the other hand aspirin-like analgesics (paracetamol, ibuprofen, aspirin, etc. appeared to protect against cataract. Cyclopenthiazide appeared to provide a similar protection.

Aged↗
PubMed1987

Conformational changes induced in lens alpha- and gamma-crystallins by modification with glucose 6-phosphate. Implications for cataract.

There is good evidence that the non-enzymic chemical modification of proteins plays a role in the aetiology of cataract and diabetic sequelae. This paper presents new evidence that glycosylation of two major lens structural crystallins, alpha- and gamma-crystallins, by glucose 6-phosphate (G6P) induces conformational changes in the proteins. In addition the surface charge on the molecules is altered. These changes would affect protein-protein and protein-water interactions within the lens and could lead to disruption of the short-range order of the lens proteins which is essential for lens transparency. Conformational changes to lens proteins are known to occur in human cataractous lenses but their cause in vivo is not established. Cumulative chemical modification of proteins, over a period of decades, is a strong candidate as a causal agent.

Circular Dichroism↗
PubMed1987

High-molecular-weight crystallin aggregate formation resulting from non-enzymic carbamylation of lens crystallins: relevance to cataract formation.

Incubation of mixed bovine lens crystallins with 100 mM potassium cyanate causes almost all the protein to form large aggregates. These aggregates are not dispersed by powerful chaotropic agents and are held together by disulphide bonds. Experiments with beta L-crystallin show that carbamylation of this one protein class can bring about the aggregation of other unmodified crystallins. The carbamylated crystallin served as a nucleus for aggregation of other crystallins. These changes are related to the chemical modification of crystallins and the ensuing conformational changes in cataractogenesis.

Animals↗
PubMed1987

Epidemiology and risk factors for cataract.

Cataract is the major cause of blindness worldwide. It is a greater problem in third world countries than in the West and several attempts have been made to explain the excess in these countries. This paper provides an overview of the literature especially on studies designed to identify risk factors for cataract. There is an association between poverty and cataract and, more specifically, between cataract and a history of severe diarrhoea-dehydration. Recent results from a case-control-led study of cataract in Oxford are also presented with the quantitation of risks associated with a number of factors including diarrhoea, renal failure and diabetes. In this study an apparently protective effect of aspirin, paracetamol and similar drugs was observed. This protective effect applies to the risk associated with diabetes.

Cataract↗
PubMed1986

Do aspirin-like analgesics protect against cataract? A case-control study.

The results of a case-control study of 300 cataract patients and 609 controls indicate that long-term use of aspirin-like analgesics halves the risk of cataract. Myopia and the use of nifedipine were found to carry a significant risk of cataract, and renal failure appeared to carry a high risk, though few patients were affected. The results also confirm diabetes, glaucoma, and use of steroids as risk factors for cataract.

Acetaminophen↗
PubMed1986

Bendazac prevents cyanate binding to soluble lens proteins and cyanate-induced phase-separation opacities in vitro: a possible mechanism by which bendazac could delay cataract.

The reaction of lens proteins with cyanate (carbamylation) causes many changes seen in human cataract including disruption of the protein conformations. Bendazac, a putative anti-cataract drug, decreases the binding of cyanate to lens proteins and prevents the cyanate-induced elevation of the phase separation temperature in incubated rat lenses. Its major metabolite, 5-hydroxybendazac, also inhibits the binding of cyanate to lens proteins even when it is present only during a pre-incubation period. The metabolite is more effective than the parent compound.

Animals↗