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Biomedical subjects

J C Ng

Publications and source records attributed to J C Ng.

44 records · Page 3Linked to original sources
PubMed1988

Assessment of copper and zinc status of farm horses and training thoroughbreds in south-east Queensland.

The copper and zinc concentrations in the blood of stabled thoroughbred horses and in Australian Stock Horses mares at pasture, either late pregnant or lactating were determined by an atomic absorption spectroscopic method. The plasma concentration of the trace elements in these apparently normal horses were generally below the "normal" range. The plasma copper, caeruloplasmin copper, whole blood copper and plasma zinc concentrations in the stabled thoroughbreds were 0.76 +/- 0.19 micrograms/ml (n = 82), 0.56 +/- 0.14 micrograms/ml (n = 83), 0.75 +/- 0.18 micrograms/ml (n = 82) and 0.47 +/- 0.09 micrograms/ml (n = 83) respectively. The plasma copper and zinc concentrations of all the brood mares at pasture (pregnant and lactating) were 0.56 +/- 0.20 micrograms/ml and 0.47 +/- 0.11 micrograms/ml (n = 30). The plasma copper concentration of the pregnant group of mares (0.64 +/- 0.18 micrograms/ml; (n = 14) was greater than that of the lactating mares (0.49 +/- 0.21; (n = 16). Variation in the plasma copper concentration was also identified between stabled and farm horses, between horses of different stables and between horses of different ages. The proportion of plasma copper bound to caeruloplasmin was 73 +/- 11.8%. These low concentrations of copper and zinc in the plasma of apparently normal horses are of clinical significance since recent evidence has indicated that copper deficiency appears to promote the development of skeletal abnormalities in foals. An alternative to the use of a single plasma sample to identify the copper or zinc deficient horse was discussed.

Age Factors↗
PubMed1986

The nifH gene product is required for the synthesis or stability of the iron-molybdenum cofactor of nitrogenase from Klebsiella pneumoniae.

The MoFe protein of nitrogenase from Klebsiella pneumoniae contains an iron-molybdenum cofactor, FeMoco, the synthesis or processing of which involves the products of at least five genes, nifQ, nifB, nifN, nifE and nifV. We have detected FeMoco activity in extracts of strains which synthesise neither of the MoFe protein subunits, indicating that FeMoco can be synthesised prior to combination with the MoFe protein polypeptides. Expression of the nifH gene (or a large part of it), was essential for FeMoco activity to be observed either in the presence or in the absence of the MoFe protein subunits. The nifH gene product was not involved in the control of the transcription of other nif gene products known to be involved in FeMoco synthesis or processing, nor was it essential for the stability of performed FeMoco before its combination with the MoFe protein polypeptides.

Bacterial Proteins↗
PubMed1982

Some effects of chronic mercuric chloride intoxication on renal function in a horse.

Chronic mercuric chloride intoxication in an aged horse given 0.8 mg Hg/kg/day for 14 weeks was manifest by signs of progressive respiratory difficulty and renal disease. The effects were not self-limiting after mercury was withdrawn, and the animal was destroyed six weeks later. Renal function changes included heavy glycosuria, modest proteinuria, phosphaturia, reduced urine osmolality, gradually increasing urine production, reduced glomerular filtration rate, and terminally, azotemia. The condition bore similarities to the Fanconi syndrome in man. Urinary gamma-glutamyl transpeptidase, alkaline phosphatase and amino-aspartate transferase activities were inconsistent indicators of tubular damage in random samples at this dose rate. The pathologic response was characterized by extensive granulomatous infiltration throughout the lungs, in particular, and to a lesser extent in the kidneys, liver and bone marrow. The renal changes included this marked interstitial reaction and proximal tubular degeneration. Mercury levels were negligible in the lungs and highest in the renal cortex. The granulomatous reaction was not encountered in previous mercury toxicity studies in horses and may indicate an individual sensitivity to the agent.

Animals↗
PubMed1979

Chronic phenylmercuric acetate toxicity in a horse.

Phenylmercuric acetate (PMA) was administered orally to a horse over a period of 27 weeks (190 days) at a dose rate of 0.4 mg Hg/kg per day. The effects produced were consistent with those of chronic inorganic mercury intoxication. The clinical features included masseter muscle atrophy, difficulty in prehension and mastication, malodorous breath, reduced appetite and weight loss, and reflected significant pathological changes involving the buccal, mandibular and dental tissues. Renal dysfunction was evident terminally and there was degeration and necrosis of the proximal tubular epithelium. Necrotic and mineralized foci were found in facial and masticatory msucles, splenic trabecuale and the myocardium. The central nervous system and the intestinal tract were unaffected. The approximate mean plasma inorganic mercury concentration was 500 ng/ml whereas organic mercury levels in blood were much lower. The renal cortex had the highest inorganic mercury content, three times greater than in the liver and cecum, while organic mercury was highest in those tissues and absent from the kidney. The difference in the effects produced in this horse as compared to those in a horse receiving mercuric chloride at the same mercury dose rate, could be attributed to the more rapid and complete absorption of PMA from the gastrointestinal tract.

Animals↗
PubMedDate not supplied

Exercise-induced connective tissue turnover and lipid peroxidation in horses.

Four unfit thoroughbred horses were exercised on a treadmill twice, 5 weeks apart. Exercise consisted of stepwise increments in treadmill speed up to a maximum of 12 m s-1 and then maintained at this speed until the horses were fatigued. Two of the horses were administered phenylbutazone (4.4 mg kg-1) intravenously immediately before the first exercise period and the other two horses immediately before the second exercise period. Clinical observation revealed stiffness of gait and palpable soreness over the lumbar-sacral region in the horses 24 h after the exercise concluded. Mean plasma aspartate aminotransferase and creatine kinase activities and urinary creatinine clearance did not change as a result of exercise. The mean urinary excretion and clearance of hydroxyproline significantly increased in the 24 h following exercise (P < 0.001). A concurrent increase in the urinary excretion of malondialdehyde also occurred (P < 0.001). Prior administration of phenylbutazone did not affect hydroxyproline or malondialdehyde excretion or clearance, nor did it appear to reduce the severity of soreness after exercise. The results indicate that lipid peroxidation and the excretion and clearance of hydroxyproline increase when unfit thoroughbreds are strenuously exercised on a treadmill.

Animals↗