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Biomedical subjects

A J Larner

Publications and source records attributed to A J Larner.

At least 109 records · Page 6Linked to original sources
PubMed1995

Pseudohyperphosphatemia.

OBJECTIVE: To review instances of spurious elevation of inorganic phosphate measurements due to interference with analytical methods. METHODS: SElective literature review. RESULTS: Depending on the method used to measure inorganic phosphate, several factors have been reported to produce spurious elevations, including paraproteinemia, hyperlipidemia, hemolysis, and hyperbilirubinemia. Of these, paraproteinemia is probably the commonest. CONCLUSION: Both clinical biochemists and clinicians should be aware of the phenomenon of pseudohyperphosphatemia. Clinically unexplained persistent hyperphosphatemia should initiate a search for potential causes of pseudohypophosphatemia, especially paraproteinemia.

Blood Chemical Analysis↗
PubMed1995

How does garlic exert its hypocholesterolaemic action? The tellurium hypothesis.

The efficacy of garlic as a lipid-lowering agent is being increasingly recognized, but the biochemical mechanisms underlying this action are currently unknown. It is proposed that organic tellurium compounds, which are found in high concentration in fresh garlic buds, may contribute to this action by inhibiting squalene epoxidase, the penultimate enzyme in the synthetic pathway of cholesterol. Weanling rats fed a diet rich in tellurium develop a demyelinating polyneuropathy due to inhibition of this enzyme in peripheral nerves. Chronic exposure to small amounts of tellurium found in garlic might reduce endogenous cholesterol production through inhibition of hepatic squalene epoxidase and so reduce cholesterol levels. Tellurium may also contribute to the characteristic odour of garlic since the most obvious clinical sign of tellurium poisoning is a garlic-like odour.

Animals↗
PubMed1995

Axonal sprouting and synaptogenesis in temporal lobe epilepsy: possible pathogenetic and therapeutic roles of neurite growth inhibitory factors.

Axonal sprouting and synaptic reorganization within the temporal lobe following neuronal injury have been implicated in the pathogenesis of temporal lobe epilepsy (TLE). The molecular species responsible for these structural changes have yet to be fully defined. The recent characterization of molecules whose normal function within the nervous system is to inhibit neurite outgrowth and synaptogenesis prompts the suggestion that a diminution or loss of such molecules might be of relevance to the pathogenesis of TLE. If so, the possibility of developing a novel therapeutic approach to TLE, distinct from currently available symptomatic therapies, to arrest the pathogenetic processes is also raised.

Alzheimer Disease↗
PubMed1994

Myopathy with ragged red fibres following renal transplantation: possible role of cyclosporin-induced hypomagnesaemia.

A 65-year-old man developed a painless proximal myopathy 7 years after commencing cyclosporin therapy following a successful cadaveric renal transplant. Muscle histology showed ragged red fibres and biochemical studies suggested mitochondrial dysfunction. The possible pathogenesis of this mitochondrial myopathy, particularly its relationship to cyclosporin-induced hypomagnesaemia, is discussed.

Aged↗
PubMed1994

Review article: infective complications of therapeutic gastric acid inhibition.

Gastric acid secretion has a non-specific bactericidal action which contributes to gastrointestinal defence mechanisms against micro-organisms. Therapeutic inhibition of acid secretion with histamine H2 receptor antagonists and proton pump inhibitors might therefore be expected to predispose to infection. This article reviews clinical reports of infection occurring during therapeutic gastric acid inhibition, and assesses the risk of infection incurred by such treatment. Non-typhoid salmonelloses, Campylobacter infections, local candidiasis, and possibly Strongyloides hyperinfections may be more prevalent after acid inhibitory treatment, but concurrent impairment of other gastrointestinal defence mechanisms may be necessary to permit infection.

Bacterial Infections↗