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Biomedical subjects

C C Chang

Publications and source records attributed to C C Chang.

At least 703 records · Page 39Linked to original sources
PubMed1974

Chromosome assignment of the human gene for galactose-1-phosphate uridyltransferase.

Somatic cell hybrids formed between galactose-negative mutant Chinese hamster cells and human lymphocytes were selected in galactose medium and analyzed for the concurrent presence of specific human chromosome(s) and human galactose-1-phosphate uridyltransferase. In one of the hybrid clones only a single human chromosome, A2, was consistently present when the hybrid cells were maintained in the selective medium, suggesting that the location of the structural gene for galactose-1-phosphate uridyltransferase is on this chromosome. Among subclones derived from this cell hybrid in the absence of selection, a complete concordance was demonstrated between the ability or inability to utilize galactose and the concomitant presence or absence of the human transferase and the A2 chromosome.

Animals↗
PubMed1973

N,O-di and N,N,O-tri ( 3 H) acetyl -bungarotoxins as specific labelling agents of cholinergic receptors.

1. alpha-Bungarotoxin isolated from the venom of Bungarus multicinctus was acetylated with [(3)H] acetic anhydride and N-[(3)H] acetyl imidazole. Tri-N-acetyl and hexa-N-acetyl derivatives were obtained from the former, and N,O-di, N,N,O-tri and N,N,N,O-tetraacetyl derivatives from the latter reaction, respectively.2. There were parallel decreases in both neuromuscular blocking action in the phrenic nerve-diaphragm preparation of rats and depression of acetylcholine response of the rectus abdominis muscle of frogs with increased acetylation. Also, a parallel but greater decrease of toxicity in mice was found.3. N,O-Di and N,N,O-triacetyl toxins were localized mostly in the motor endplate region of the rat diaphragm, whereas a slight nonspecific binding along the whole muscle fibre in addition to the peak in the endplate region was observed with N,N,N,O-tetraacetyl and tri-N-acetyl toxins. In contrast, there was a marked nonspecific binding with hexa-N-acetyl toxin and no peak was observed at the endplate zone.4. The specific binding was saturable and irreversible. The number of toxin-receptive sites in one endplate was 1.9-2.2 x 10(7) for all of the labelled toxins irrespective of their potency.5. (+)-Tubocurarine protected effectively against the binding as well as the irreversible neuromuscular blocking effect of the toxins.6. Denervation of the rat diaphragm caused an increase of toxin-receptive sites beginning from the endplate zone at 1-2 days and then along the whole muscle fibre, reaching the maximum at about 18 days. The total receptive sites increased by about 30-fold.7. The significance of the findings is discussed and it is concluded that N,O-di and N,N,O-tri-[(3)H] acetyl alpha-bungarotoxins are specific and irreversible labelling agents for the cholinergic receptors of skeletal muscle.

Acetylation↗
PubMed1973

Influence of chronic neostigmine treatment on the number of acetylcholine receptors and the release of acetylcholine from the rat diaphragm.

1. Rats were treated twice daily for 7 days with neostigmine and the diaphragm was isolated for study of its acetylcholine content, release upon nerve stimulation and the number of receptors in the end-plate.2. While the content of total acetylcholine was unchanged, the release of acetylcholine on stimulation with trains of 500 pulses at 100 Hz every 20 sec was reduced by about 50%. Five days after the end of neostigmine treatment the release of acetylcholine recovered to normal.3. The total number of acetylcholine receptors in the end-plate as measured from the binding of N, O-di[(3)H]acetyl alpha-bungarotoxin was reduced from 2.1 x 10(7) to 1.2 x 10(7) per end-plate.4. The above-mentioned changes are not due to acute pharmacological effects of neostigmine, nor to an immediate effect of cholinesterase inhibition but presumably due to chronic accumulation of acetylcholine at the neuromuscular junction.

Acetylcholine↗