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E H Choy

Publications and source records attributed to E H Choy.

42 records · Page 3Linked to original sources
PubMedDate not supplied

Modulation of blood glucose by melatonin: a direct action on melatonin receptors in mouse hepatocytes.

Melatonin receptors were studied in isolated mouse hepatocytes using the 2[(125)I]iodomelatonin binding assay. The binding of 2[(125)I]iodomelatonin to hepatocytes isolated from the mouse using collagenase was stable, saturable, reversible and of high affinity. The equilibrium dissociation constant (K(d)) obtained from saturation studies was 10.0 +/- 0.4 pmol/l (n = 16), which was comparable to the K(d) obtained from kinetics studies (6.9 +/- 1.2 pmol/l, n = 3), and the maximum number of binding sites (B(max)) was 2.9 +/- 0.4 fmol/mg protein (n = 16). The relative order of potency of indoles in competing for 2[(125)I]iodomelatonin binding was 2-iodomelatonin > 2-phenylmelatonin > 6-chloromelatonin > melatonin > 6-hydroxymelatonin > N-acetylserotonin, indicating that the binding was mediated by the ML(1) receptor subtype. The linear Rosenthal plots, the close proximity of the Hill coefficient to unity and the monophasic competition curves suggest that a single class of 2[(125)I]iodomelatonin binding sites is present in the mouse hepatocytes. Guanosine 5'-O-(3-thiotriphosphate) dose-dependently inhibited 2[(125)I]iodomelatonin by lowering the affinity of binding, while no inhibitory effects of adenosine nucleotides were observed, suggesting that the binding sites are G-protein linked. Western immunoblotting was used to identify the melatonin receptor subtype in mouse hepatocytes using anti-Mel(1a) and anti-Mel(1b). Hepatocyte membrane extract reacted with anti-Mel(1b) but not anti-Mel(1a) giving a peptide-blockable band of 36 kD, supporting the hypothesis that the melatonin receptors in mouse hepatocytes are of the Mel(1b) subtype. Melatonin injection and a high plasma glucose level affected 2[(125)I]iodomelatonin binding in the whole mouse liver homogenates. Plasma glucose was elevated by mid-light intraperitoneal injection of melatonin (4 and 40 mg/kg body weight) in a dose-dependent manner with maximum elevation achieved 1 h after injection. 2[(125)I]Iodomelatonin binding at this time showed increased K(d) with no changes in B(max). When the plasma glucose returned to normal within 2 h, the binding remained lowered with increased K(d) but no changes in B(max). Elevation of plasma glucose by 2-deoxyglucose injection (500 mg/kg), on the other hand, decreased the binding by decreasing the B(max) without affecting the K(d). Suppression of plasma glucose by insulin injection (3 IU/kg) did not change the binding. Thus, melatonin may act directly on the liver to elevate the plasma glucose level, and changes in plasma glucose level itself may in turn affect hepatic melatonin binding.

Adenine Nucleotides↗
PubMedDate not supplied

The consequences of rheumatoid arthritis: quality of life measures in the individual patient.

Despite conventional treatment, RA still has many deleterious consequences. From the patients' perspective, these include persistent pain, functional disability, fatigue, and depression modified by health beliefs and underlying psychological problems. Disability is a consequence of pain, active synovitis and joint damage. It is usually assessed by self-reported questionnaire; the Health Assessment Questionnaire (HAQ) remains the dominant disability measure, although generic health measures such as Short Form-36 and Nottingham Health Profile provide similar information. Treatment with disease modifying drugs and biologic agents improves pain, fatigue and disability. We specifically evaluated the effects of both these drugs and also disease duration on disability assessed by HAQ scores, as there is most information on this topic and it is of fundamental importance to patients. In early RA HAQ gives a 'J-shaped' curve; the initial fall is due to the immediate benefits of treatment and the subsequent gradual rise due to the inability of therapy to fully suppress the disease or prevent progressive joint damage. In established RA HAQ scores increase by about 1% annually and over 25 years average HAQ scores increase by 1.0. Disease modifying drugs and biologics both significantly reduce HAQ scores and the reduction is maintained for 2-5 years. This reduction is seen in both early and established disease. Early steroid therapy has immediate symptomatic treatment, but does not have long-term benefits. Over 5 years the impact of aggressive therapy with disease modifying drugs declines and there is evidence that insufficient treatment is given to many patients with RA. The outcome of RA is greatly improved by current treatment with disease modifying drugs and biologic agents. However, more needs to be done and achieving better results is enhanced by routinely measuring the impact of the disease in routine practice.

Arthritis, Rheumatoid↗
PubMedDate not supplied

Synovial fluid lymphocyte proliferation to tuberculin protein product derivative: a novel way of diagnosing tuberculous arthritis.

We report a case of tuberculous arthritis in which the diagnosis was aided by lymphocyte proliferation assay to a panel of bacterial antigens. It illustrates that the lymphocyte proliferation assay may be a useful diagnostic tool in patients with tuberculous and reactive arthritis. It also supports the notion that there is a selective accumulation of antigen specific T cells at the site of inflammation in both septic and reactive arthritides.

Adult↗