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Biomedical subjects

K H Lu

Publications and source records attributed to K H Lu.

At least 55 records · Page 3Linked to original sources
PubMed1984

A critical evaluation of some problems associated with clinical caries trials by computer simulation.

Unbiased examiners' errors have little effect on the outcome of a clinical trial, provided that they are not larger than 10%. Unbiased error greater than 10% would tend to make the variance larger than expected. Demonstration schemes as discussed in this paper may show spurious positive effects, due to attempts by examiners to avoid reversals in diagnosis. Professional intervention is mostly responsible for the SU component - the direct transition from sound surface to DMF. These surfaces are lost for reasons other than caries activities per se. It should not be included in the measure of caries experience in clinical trials. The component UU represents the surfaces that show incipient caries at two consecutive examinations. It represents mostly past history and has little bearing on current caries activities. Since the DMFS = IU + SU + UU, and the contributions of IU as a rule are small, the use of DMFS as a measure of caries experience in clinical trials is unjustified. The NCI = SI + IU deals directly with the stage where the cariostatic agent is supposed to be working. There is a definite advantage to using this index as the caries experience measure in clinical trials.

Child↗
PubMed1981

Effect of cimetidine on serum prolactin in normal women and patients with hyperprolactinaemia.

In normal women, intravenous injection of the H2-antihistamine, cimetidine, provoked a 3-4 fold rise in serum prolactin, without changes in serum growth hormone, thyrotrophin, or gonadotrophins. Hyperprolactinaemic patients with pituitary tumours, idiopathic hyperprolactinaemia or hypothalamic lesions demonstrated little or no rise in serum prolactin (expressed as a percentage increment) in response to cimetidine; these responses were significantly more blunted than the prolactin responses to intravenous TRH in the same subjects. Post-partum women also demonstrated blunted percentage prolactin responses to cimetidine, although responses to TRH were, in most patients, normal. Dynamic testing of prolactin secretion with cimetidine is no more useful than TRH in distinguishing tumourous from non-tumourous hyperprolactinaemia.

Adolescent↗
PubMed1980

The effect of an antiserum to luteinizing hormone-releasing hormone on the progesterone-induced luteinizing hormone surge in ovariectomized, estrogen-primed rats.

A rabbit antiserum to synthetic LHRH was shown to be specific to rat hypothalamic LHRH, as revealed by binding studies (RIA). The present study was undertaken to determine the effects of this antiserum (LHRH-AS) on the progesterone-induced LH surge in ovariectomized rats primed with estrogen on the proestrous LH surge in cycling females. An ip injection of 0.2 ml LHRH-AS at 1200 h on proestrus completely inhibited the preovulatory rise in serum LH from 1700-1800 h. In long term ovariectomized rats, a sc injection of estradiol benzoate reduced serum LH levels by 50% at 1200 h on the third day. Subsequent administration of progesterone elicited a LH surge, with peak LH value 4-6 h after progesterone. However, concurrent administration of LHRH-AS effectively prevented the increase in LH release by progesterone, and an iv injection of LHRH-AS was shown to be more effective than ip administration in inhibiting the progesterone stimulation of LH release. Although estrogen and progesterone may induce a change in pituitary responsiveness to hypothalamic LHRH in ovariectomized rats, the present study provides evidence that tonic and/or increased LHRH release is required for the acute increase in LH release caused by progesterone.

Animals↗