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Biomedical subjects

J Cook

Publications and source records attributed to J Cook.

At least 235 records · Page 13Linked to original sources
PubMed1983

Amino-acid sequence of two trypsin isoinhibitors, ITD I and ITD III from squash seeds (Cucurbita maxima).

The amino-acid sequences of two trypsin isoinhibitors, ITD I and ITD III, from squash seeds (Cucurbita maxima) were determined. Both isoinhibitors contain 29 amino-acid residues, including 6 half cystine residues. They differ only by one amino acid. Lysine in position 9 of ITD III is substituted by glutamic acid in ITD I. Arginine in position 5 is present at the reactive site of both isoinhibitors. The previously published sequence of ITD III has been shown to be incorrect.

Amino Acid Sequence↗
PubMed1983

The effect of H1 and H2 receptor antagonists on the dermographic response.

The effect on dermographic wealing of an H1 and H2 receptor antagonist was studied separately and in combination. a double-blind protocol was used and dermographism was measured as the diameter of weal response to a measured force. Both H1 and H2 antagonists had a small but non-significant effect, but the combination of H1 plus H2 antagonist had an approximately additive effect which was significant. Although this indicates a role for H2 receptors in dermographism it does not establish the degree of involvement, nor whether H2 antagonists necessarily have any advantage over a potent H1 blocker alone in the treatment of dermographism.

Adult↗
PubMed1983

The human C3b receptor.

The cellular receptor for the C3b fragment of the third component of complement is a 205,000 molecular weight glycoprotein expressed by erythrocytes, polymorphonuclear leukocytes, monocytes, B lymphocytes, a subset of T lymphocytes and glomerular podocytes. The receptor molecule is a potent inhibitor of complement activation by both the alternative and classical pathways. It serves as a cofactor in the proteolytic degradation of C3b bound to immune complexes. On neutrophils and monocytes, the receptor enhances immunoglobulin-dependent phagocytosis of opsonized particles and triggers internalization of soluble ligands bearing C3b. The number of C3b receptor molecules expressed on erythrocytes is genetically determined and was found to be low in patients with systemic lupus erythematosus: these abnormalities when associated with a low number of receptors in the kidney of patients with non-systemic lupus erythematosus nephritis may predispose to immune complex diseases.

Animals↗
PubMed1982

The varying tissue distribution of L-glutamic acid labelled at three different sites.

Methods using 5 and 6 enzymes were devised to synthesize L-[11C]glutamic acid (GA), labeled on the carboxyl group of either the alpha-(AGA) or gamma-(GGA) carbon atom. The distribution of the 11C-labeled AGA or GGA in rabbits was compared with that of L-[13N]glutamic acid. The results show that AGA was rapidly decarboxylated with loss of the 11C-label, and that GGA was also decarboxylated, but to a lesser degree. Thus, the radiolabel distribution may not reflect the distribution of the original compound. The results also demonstrate that positron labeled pharamaceuticals may be rapidly synthesized via complex enzymatic pathways.

Animals↗
PubMed1982

Blockade of 3-carbomethoxy-beta-carboline induced seizures by diazepam and the benzodiazepine antagonists, Ro 15-1788 and CGS 8216.

The benzodiazepine antagonists Ro 15-1788 and CGS 8216 blocked the clonic and tonic convulsions elicited by 3-carbomethoxy-beta-carboline (beta-CCM). The PD50 values for Ro 15-1788, CGS 8216, and diazepam were: 2.0, 0.6, and 2.0 mg/kg, respectively. Neither Ro 15-1788 nor CGS 8216 potentiated the effect of a threshold convulsant dose of beta-CCM. Moreover, these benzodiazepine antagonists neither attenuated nor potentiated the tremorigenic actions of another beta-carboline, harmaline. Diazepam, however, considerably reduced the tremorigenic actions of this drug.

Animals↗
PubMed1980

Histamine weal formation and absorption in man.

1 The weal and flare response to intradermal histamine was measured over a range of doses in forearm skin of man. 2 The use of calipers to measure weal thickness was validated by measurement of observer and method errors. Repeated measurements at intervals of 5 min or more compressed the weals by 6% per reading. 3 Flare response reached a maximum at 5 min compared with 20 min for weal thickness and the sensitivity of the flare response was greater than the weal response at lower doses of histamine. 4 Sensitivity, lambda was comparable for the measurement of flare, weal diameter and thickness or volume. The advantage of weal thickness was in the measurement of weal formation and resorption. 5 The time course of histamine weal formation and disappearance was measured and found to have a T1/2 of 5.4 min and 87 min, respectively. 6 The T1/2 of disappearance of comparable 09% w/v NaCl solution and serum weals were 18 and 28 min respectively. 7 It is suggested that persistence of histamine weals is due to a vasoactive agent other than histamine.

Adult↗