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D Webster

Publications and source records attributed to D Webster.

At least 91 records · Page 5Linked to original sources

A second activation peptide from bovine cationic trypsinogen.

1. Although only one activation peptide of bovine cationic trypsinogen has been reported previously, the peptide fraction obtained from activation mixtures shows several bands on paper electrophoresis at pH 6.5. 2. The major band was the peptide previously described. The band second in intensity of staining with ninhydrin (10-20% of that of the main band, as judged by eye) had an electrophoretic mobility consistent with its being related to the main peptide. It appeared on activation both of bulk commercial samples of trypsinogen and, as the Appendix shows, of samples prepared from pancreases obtained at the local abattoir. 3. The second peptide proved to be Phe-Pro-Val-Asp-Asp-Asp-Asp-Lys, and we conclude that it is another activation peptide. We discuss briefly the genetic and phylogenetic implications of our findings.

Amino Acid Sequence↗

The immediate reaction between bromcresol green and serum as a measure of albumin content.

I investigated the immediate ( less than 30s) reaction between bromcresol green and serum, as a measure of albumin content. Fifty sera were analyzed in duplicate for albumin by electrophoresis on cellulose acetate by a procedure previously shown to give results in good agreement with two immunoprecipitation techniques, and by a bromcresol green method with the absorbance being read as soon as possible after mixing. Results by the dye method were 3.0 g/liter higher than those by electrophoresis; this difference was independent of the albumin content of the serum. Slight turbidity, jaundice, or added hemoglobin did not significantly interfere with albumin determination. Aparently the immediate reaction between serum and the dye reagent provides a simple, reliable measure of albumin content when 3.0 g/liter is subtracted from the result obtained.

Bromcresol Green↗

Phosphonomethyl analogues of hexose phosphates.

The analogue of fructose 1,6-bisphosphate in which the phosphate group, -O-PO3H2, on C-6 is replaced by the phosphonomethyl group, -CH2-PO3H2, was made enzymically from the corresponding analogue of 3-phosphoglycerate. It was a substrate for aldolase, which was used to form it, but not for fructose 1,6-bisphosphatase. It was hydrolysed chemically to yield the corresponding analogue of fructose 6-phosphate [i.e. 6-deoxy-6-(phosphonomethyl)-D-fructose, or, more strictly, 6,7-dideoxy-7-phosphono-D-arabino-2-heptulose]. This proved to be a substrate for the sequential actions of glucose 6-phosphate isomerase, glucose-6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase. Thus seven out of the nine enzymes of the glycolytic and pentose phosphate pathways so far tested catalyse the reactions of the phosphonomethyl isosteres of their substrates.

Fructose-Bisphosphatase↗

Cell-mediated immunity to intrinsic factor in autoimmune disorders.

Evidence of cell-mediated immunity to gastric intrinsic factor was present in 86% of patients with pernicious anaemia and in at least 13% of patients with hyperthyroidism, 21% of patients with atrophic gastritis, and four out of nine (46%) patients with hypogammaglobulinaemia. Controls gave negative results. The four patients with hypogammaglobulinaemia and cell-mediated immunity to intrinsic factor had evidence of impaired gastric function.

Agammaglobulinemia↗

Extinction following intracranial reward: the effect of delay between acquisition and extinction.

Rats trained to press a bar for intracranial reinforcement gave as many responses during extinction as did water-reinforced controls, when extinction came immediately after an acquisition session. However, the experimental animals gave fewer responses in extinction than water-reinforced animals when extinction was delayed for 1 hour after acquisition. The activity level of the experimental animals was high immediately after acquisition but declined markedly over the delay period, which suggests that resistance to extinction after intracranial reinforcement is primarily a function of activity level.

Analysis of Variance↗