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P Cheung

Publications and source records attributed to P Cheung.

99 records · Page 6Linked to original sources

A simple method for "reference range" estimation from routine laboratory data.

A simplified method is presented to estimate reference ranges from hospital laboratory data. It is based on a combination of graphical estimation of relative sizes of normal and abnormal populations and the "mode-center" concept in which the mode of the total population centers on the 50% cumulative frequency of the normal population. This method can be applied to determine reference ranges even though the data source contains abnormally high and/or low values. The reference ranges obtained for BUN and calcium from in-patient and out-patient sources by this method were found to be similar to those reported for "healthy" subjects.

Blood Urea Nitrogen↗

Patterns of phonological disability in Cantonese-speaking children in Hong Kong.

Tone, vowel and consonant production are described for a large group of Cantonese-speaking children assessed in speech and language therapy clinics in Hong Kong. The patterns of disability follow predictions made on the basis of work on normal phonological development in Cantonese, and on psychoacoustic factors in acquisition: consonants account for more disability than vowels, and tones are least problematic. Possible articulatory and auditory contributions to explanation of the observed patterns are discussed.

Articulation Disorders↗

Intraadrenal steroid metabolism in the guinea pig: guinea pig adrenal microsomes metabolize androstenedione in a manner distinct from liver microsomes.

Several immunochemical homologs of hepatic cytochromes P450 (CYPs) capable of steroid catabolism have been identified in the guinea pig adrenal cortex. Their predominance in males suggests a role in sex-differentiated metabolism of androgens. Therefore, we examined the ability of microsomes from male guinea pig adrenals and liver to metabolize androstenedione. Microsomes were incubated in the presence of radiolabeled steroids, the products of the reaction extracted, separated by TLC, and visualized by autoradiography. Metabolites were identified by comigration with commercially available standards in several solvent systems, in one and two dimensional TLC. Microsomes from both tissues metabolized androstenedione. However, the products formed differed markedly in the two tissues. Liver microsomes formed one major metabolite, testosterone. It represented 85% of the metabolized androstenedione. 6 beta-Hydroxylated androstenedione and testosterone each comprised 3-4% of the liver metabolites. In addition, at least 10 other products were formed, but taken together they constituted less than 8% of the metabolized androdostenedione. Adrenal microsomes, on the other hand, produced several major metabolites: 16 alpha-, 16 beta-, and 6 beta-hydroxy-androstenedione, plus one unidentified product constituted 93% of the metabolized androstenedione. 16 alpha-Hydroxylation of androstenedione was 60 fold, 16 beta-hydroxylation 12 fold, and 6 beta-hydroxylation 2.5 fold greater in adrenal than in liver microsomes. The unidentified product, which was the least polar, was formed exclusively by adrenal microsomes. The hydroxylation reactions performed by adrenal tissue are consistent with the presence in adrenal microsomes of immunochemical homologues of members of the CYP1A, 2B, 2C and 3A families which have known steroid hydroxylation functions in liver. The Kms of the formation of 16 alpha-, 16 beta- and 6 beta-hydroxyandrostenedione by adrenal microsomes are in the range reported for steroid hydroxylation reactions in rat liver tissue. Their distinct values suggest that these hydroxylation steps are performed by different CYPs. However, assignment of site-specific steroid hydroxylation reactions to individual hepatic CYP homologs in the adrenal requires further investigation and is being pursued using combined techniques of biochemistry and molecular biology.

Adrenal Glands↗

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