Biomedical subjects

K N Ham

Publications and source records attributed to K N Ham.

At least 37 records · Page 2Linked to original sources

PubMed1979

The effects of temporary fluid restriction in clip-nephrectomized rats.

Constriction of the remaining renal artery in unilaterally nephrectomized rats is associated with a high mortality in the early post-operative phase before hypertension has developed. The high mortality is accompanied by increased vascular permeability, mesenteric and pancreatic oedema. Temporary post-operative water restriction reduces this mortality and also modifies subsequent blood pressure elevation, heart weight and cardiac index in surviving animals.

Animals↗

PubMed1978

Lead-loaded ion-exchange resin bead as a calcergen.

Several heavy metals have direct calcifying effects in connective tissues; most notable among them is lead (Pb), whether administered topically (1) or systemically with local injury (2). The mechanisms of metal-induced soft tissue calcification have been studied by injecting salts of known in vitro calcifying potential into subcutaneous connective tissue (3); of the metals used, only lead and holmium produced an early accumulation of minerals on collagen in vivo. Lead is also claimed to accelerate bone healing in the rabbit leg with no toxic effects (4). Lead-loaded ion-exchange resin beads, implanted into surgically prepared subcutaneous pouches in rats, rapidly induced subcutaneous calcification which has been studied by microradiography and electron-probe microanalysis.

Animals↗

PubMed1978

Toxic effects of dental amalgam implants. Optical histological and histochemical observations.

Dental amalgam and porcelain control discs were implanted in the subcutaneous tissue of rats. Amalgam implants exerted a toxic effect caused by release of metal ions which was characterized by prolonged inflammation, delayed granulation and disordered collagen formation. Dental porcelain was found to be a suitable biocompatible control which provided a bulk similar to that of dental amalgam but induced only an uncomplicated granulation response.

Animals↗

PubMed1978

Liver and kidney damage induced by N-hydroxyparacetamol.

1. Liver and kidney glutathione are depleted in rats and mice following administration of N-hydroxyparacetamol. 2. Centrilobular hepatic necrosis and necrosis of renal proximal convoluted tubules were also found, the liver lesion predominantly in mice and the renal lesion predominantly in rats. Glutathione depletion was not responsible for this species difference. 3. These results indicate that N-hydroxyparacetamol is the metabolic precursor of the reactive toxic intermediate of paracetamol. They are also relevant to the pathogenesis of the renal damage associated with long term abuse of phenacetin containing compound analgesics.

Acetaminophen↗

PubMed1977

Acute silicoproteinosis.

A case of alveolar lipoproteinosis associated with silicosis is reported. A 58-year-old man had been exposed to silica for seven years and died three years after the onset of symptoms. Light microscopy of biopsy and necropsy material showed small silicotic nodules, silica particles, and alveolar lipoproteinosis, and ultrastructural studies were performed to define changes in alveolar epithelium and macrophages. The case provides a further example of alveolar lipoproteinosis developing as a response of the lung to injury by an external agent.

Acute Disease↗

PubMed1977

An experimental model of analgesic-induced renal damage--some effects of p-aminophenol on rat kidney mitochondria.

1. p-Aminophenol, a known nephrotoxin, has been studied as a model for phenacetin-induced renal damage. 2. Respiration, oxidative phosphorylation and ATPase activity were inhibited in mitochondria isolated from the kidneys of treated rats; this could not be reversed by the addition of exogenous loosely bound cofactors and bovine serum albumin to the assay medium. 3. After treatment the mitochondrial levels of sodium and calcium were increased, potassium decreased and magnesium unaltered. 4. Mitochondria isolated from treated rats showed ultrastructural damage. 5. The results are interpreted to indicate that renal tubular cell mitochondrial injury is important in triggering cortical analgesic renal damage.

Adenosine Triphosphatases↗

PubMed1976

Neoplasia in the rat induced by N-hydroxyphenacetin, a metabolite of phenacetin.

N-hydroxyphenacetin, a phenacetin metabolite, was fed to rats as a 0.05-0.5% dietary supplement. After 9 months, tumours of the liver were found in 36 of 64 animals. One animal also developed a renal tumour. No tumours were found in control animals. The findings implicate phenacetin as a carcinogen and suggest that N-hydroxyphenacetin may be the metabolite responsible.

Animals↗

PubMed1975

Nephrotoxicity and molecular structure.

The nephrotoxicity of a number of aminophenols, quinols and catechols has been assessed from the extent of necrosis of proximal convoluted tubules produced by intravenous injection in rats, and the toxicity correlated with the oxidation-reduction potentials of the compounds.

Aniline Compounds↗

PubMed1974