Manual materials handling: a survey of risks, and the selection and training of workers in Singapore.
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Accidents, Occupational↗
Biomedical subjects
T K Tang
Publications and source records attributed to T K Tang.
Effects of thyroidectomy and thyroxine replacement on the responsiveness of the anterior pituitaries from male rats to thyrotropin-releasing hormone in vitro.
Thyroidectomy decreased prolactin concentrations in the anterior pituitary (AP) and serum of the male rat. The amount of basal and thyrotropin-releasing hormone (TRH)-stimulated release of prolactin by AP in vitro was lower in thyroidectomized (Tx) rats than in sham Tx rats. These results suggest that the inhibitory effects of thyroidectomy on pituitary and serum prolactin in male rats are mediated in part by the reduction of the production and spontaneous release of prolactin and the responsiveness of prolactin to TRH.
Animals↗
Amino acid conservation and clinical severity of human glucose-6-phosphate dehydrogenase mutations.
More than a hundred naturally occurring mutations of human glucose-6-phosphate dehydrogenase (G6PD) have been identified at the amino acid level. The abundance of distinct mutation sites and their clinical manifestations make this enzyme ideal for structure-function analysis studies. We present here a sequence and structure combined analysis by which the severity of clinical symptoms resulting from point mutations of this enzyme is correlated with quantified degrees of amino acid conservation within 23 G6PD sequences from different organisms. Our analysis verifies, on a quantitative basis, a widely held notion that clinically severer mutations of G6PD usually occur at conserved amino acids. However, marked exceptions to this general trend exist which are most notably revealed by a number of mutations associated with chronic nonspherocytic hemolytic anemia (class I variants). When mapped onto a homology-derived structural model of human G6PD, these class I mutational sites of low amino acid conservation appear to localize in two spatially distinct clusters, both of which are populated with mutations consisting mainly of clinically severer variants (i.e. class I and class II). These results of computer-assisted analyses contribute to a further understanding of the structure-function relationships of human G6PD deficiency.
Amino Acid Sequence↗
G6PD NanKang (517 T-->C; 173 Phe-->Leu): a new Chinese G6PD variant associated with neonatal jaundice.
Using a non-radioactive PCR-SSCP technique, we identified a novel glucose-6-phosphate dehydrogenase (G6PD) mutation in a Chinese newborn with neonatal jaundice. This new variant (G6PD NanKang) causes a T to C change at nucleotide position 517, producing a Phe173Leu substitution in the human G6PD protein. Since the 517 mutation does not create or remove any known restriction site, we introduced an artificially created site by adding a primer containing a mismatched base to the PCR reaction mixture. The mismatched base accompanying the nearby 517 T-->C mutation generates an XhoI site which is suitable for distinguishing normal from mutant alleles. Using this approach, the 517 mutation can be diagnosed quickly at the DNA level.
Fetal Blood↗