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Biomedical subjects

A Dixon

Publications and source records attributed to A Dixon.

15 recordsLinked to original sources
PubMed1991

Training issues.

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Acquired Immunodeficiency Syndrome↗
PubMed1990

Zoladex plus tamoxifen versus Zoladex alone in pre- and peri-menopausal metastatic breast cancer.

Phase II studies examining the endocrinological and clinical efficacy of Zoladex and Zoladex plus tamoxifen have been examined in pre- and peri-menopausal women with advanced breast cancer. No adverse endocrinological interaction between the drugs have been observed. Although a higher proportion of static disease was observed with the combination of the drugs, which possibly occurred at the expense of partial remissions, the time to disease progression was extended in women who received Zoladex plus tamoxifen. Remissions were primarily restricted to patients whose tumours were ER positive. Only occasional responses were seen in ER negative disease. This was especially evident where the ER negative tumours were EGF-R positive and showed high rates of cell proliferation.

Adult↗
PubMed1990

Inhibition of palmitoyl co-enzyme A hydrolase in mitochondria and microsomes by pharmaceutical organic anions.

Rat microsomes and mitochondria were isolated and incubated with selected pharmaceutical organic anions at concentrations of 0, 0.2, 0.5, 1.0, and 2 mM. Activity of palmitoyl CoA hydrolase (PCAH) was shown to be reduced in a dose-dependent manner in microsomes by ibuprofen, valproate, acetyl salicylate, 2,4-dichlorophenoxyacetate (2,4-D), and 4-pentenoate, but not salicylate. Mitochondrial PCAH activity was inhibited by clofibrate, ibuprofen, valproate, and 2,4-D. Mitochondrial oxidative phosphorylation was impaired or uncoupled by each of the mitochondrial PCAH inhibitors. The inhibition of PCAH by some of these agents may lead to fatty acyl CoA accumulation. Very low concentrations of fatty acyl CoA are known to cause mitochondrial uncoupling and increase permeability. This action may play a role in the mitochondrial injury caused by some of these agents or related disease processes.

Animals↗
PubMed1988

Corneal elastosis within lattice dystrophy lesions.

Corneal buttons of two patients with lattice corneal dystrophy were studied by light and electron microscopy. They showed elastotic degeneration within the amyloid deposits. The amyloid deposits displayed characteristic staining; the elastotic material (elastin) within the deposits stained positive with Verhoeff-van Gieson and Movat pentachrome stains and showed autofluorescence. The characteristic ultrastructural findings of amyloid and elastotic material were also demonstrated. The possibility of the associations of these two materials in the cornea is discussed.

Amyloidosis↗
PubMed1988

Mutual feelings.

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Economics, Nursing↗
PubMed1985

Perforated granulomatous colitis caused by Histoplasma capsulatum.

A 57-year-old man who presented with an acute abdomen and clinically was thought to have perforated colonic diverticulitis, was found to have transmural granulomatous inflammation and perforation of colon that was caused by Histoplasma capsulatum. Although involvement of any part of the gastrointestinal tract may occur with disseminated histoplasmosis, the complication of intestinal perforation requiring emergency surgery (particularly in the colon) is extremely rare and warrants this case report with discussion of the various clinicopathologic features of gastrointestinal histoplasmosis and the occurrence of primary intestinal histoplasmosis.

Colon↗
PubMedDate not supplied

Biochemical relationships between Reye's and Reye's-like metabolic and toxicological syndromes.

Reye's syndrome is a hepatic encephalopathy with fatty infiltration of the liver and is due to mitochondrial dysfunction. Knowledge of the mechanisms causing Reye's syndrome has been gained from the study of Reye's syndrome-like diseases, including inborn errors of mitochondrial energy production, viral disease and toxicological injury. Entry of fatty acids into mitochondria or beta-oxidation itself may be impaired. Toxins such as hypoglycin, pentanoate, valproate, salicylate, and their metabolites inhibit beta-oxidation pathways and can produce Reye's syndrome-like presentations. Biochemical manifestations of the diverse causes of Reye's syndrome-like disorders are similar and include: hypoglycaemia due to impaired gluconeogenesis, accumulation of fatty acids, fatty acyl CoAs, and acyl carnitines with depletion of free CoA and carnitine. Accumulated products may further injure mitochondria and exacerbate impaired beta-oxidation, uncouple oxidative phosphorylation or increase mitochondrial permeability. Mitochondrial swelling and steatosis of hepatic cells are the histological result. With the advances of biochemical techniques for the study of organic acid excretion patterns, serum fatty acid patterns and identification of enzymatic deficiencies in cells from patients with Reye's syndrome-like presentations, it is clear that Reye's syndrome is, in part, a collection of various inborn errors and toxicological states. Circumstances such as viral disease, prolonged fasting and drugs may precipitate clinical expression of these deficiencies as Reye's syndrome. As work progresses, further causes of Reye's syndrome will be identified.

Animals↗
PubMedDate not supplied

Hydranencephaly.

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Adult↗