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Biomedical subjects

R H Scott

Publications and source records attributed to R H Scott.

88 records · Page 5Linked to original sources
PubMed1971

Influence of temperature of incubation and type of growth medium on pigmentation in Serratia marcescens.

Maximal amounts of prodigiosin were synthesized in either minimal or complete medium after incubation of cultures at 27 C for 7 days. Biosynthesis of prodigiosin began earlier and the range of temperature for formation was greater in complete medium. No prodigiosin was formed in either medium when cultures were incubated at 38 C; however, after a shift to 27 C, pigmentation ensued, provided the period of incubation at 38 C was not longer than 36 hr for minimal medium or 48 hr for complete medium. Washed, nonpigmented cells grown in either medium at 38 C for 72 hr could synthesize prodigiosin when suspended in saline at 27 C when casein hydrolysate was added. These suspensions produced less prodigiosin at a slower rate than did cultures growing in casein hydrolysate at 27 C without prior incubation at 38 C. Optimal concentration of casein hydrolysate for pigment formation by suspensions was 0.4%; optimal temperature was 27 C. Anaerobic incubation, shift back to 38 C, killing cells by heating, or chloramphenicol (25 mug/ml) inhibited pigmentation. Suspensions of washed cells forming pigment reached pH 8.0 to 8.3 rapidly and maintained this pH throughout incubation for 7 days. Measurements of viable count and of protein, plus other data, indicated that cellular multiplication did not occur in suspensions of washed cells during pigment formation. By this procedure utilizing a shift down in temperature, biosynthesis of prodigiosin by washed cells could be separated from multiplication of bacteria.

Anti-Bacterial Agents↗
PubMedDate not supplied

Activation of a G protein promotes agonist responses to calcium channel ligands.

The activation of a guanine nucleotide binding (G) protein is an essential step in coupling certain receptors to the inhibition of voltage-activated calcium channels. We have previously observed that analogues of GTP potentiate the effect of receptor agonists and inhibit calcium currents in cultured dorsal root ganglion (DRG) neurones. A residual sustained 'L-type' component of the calcium channel current is resistant to inhibition by internal guanosine 5'-O-3-thiotriphosphate (GTP-gamma-S). Because calcium channel antagonists such as D600, nifedipine and diltiazem inhibit L currents, we examined their effect on GTP-gamma-S-modified currents. These compounds all produced a rapid and very marked potentiation of calcium channel currents in the presence of internal GTP-gamma-S and this effect was prevented by pertussis toxin which ADP ribosylates the G proteins Gi/Go (for review see ref. 10). We suggest that this potentiation indicates that activated G protein can interact with the calcium channel, and that this enhances the action of calcium channel ligands at their agonist sites on the channel in its resting state. These results represent the first electrophysiological evidence that guanine nucleotides are able to influence cellular responses to calcium channel ligands.

Animals↗
PubMedDate not supplied

A heat-treated factor VIII concentrate prepared by controlled-pore glass adsorption chromatography.

Four years' experience with a method for preparing a high-purity, low-fibrinogen, heat-treated factor VIII concentrate is reported. The process, batch adsorption of a cryoprecipitate extract with controlled-pore glass granules, removes 77 percent of the cryoprecipitate fibrinogen, resulting in a final concentrate-specific activity of 0.74 IU factor VIII per mg of protein at a yield of 194 IU factor VIII per kg of starting plasma. Heat treatment of the lyophilized concentrate for 72 hours at 60 degrees C results in less than 10 percent loss of factor VIII activity. This process does not require expensive fractionation equipment, is suitable for small-to medium-scale batch concentrate production and could be adopted by moderately well-equipped regional blood processing laboratories for the decentralized production of a high-quality, heat-treated factor VIII concentrate.

Absorption↗
PubMedDate not supplied

Metabotropic glutamate receptor activation and intracellular cyclic ADP-ribose release Ca2+ from the same store in cultured DRG neurones.

The whole cell patch clamp technique has been used to record Ca(2+)-activated cation and chloride conductances evoked by release of Ca2+ from intracellular stores of cultured neonatal dorsal root ganglion neurones. The aim of this study was to investigate metabotropic glutamate receptor (mGluR) mechanisms and evaluate a possible role for cyclic ADP-ribose as an intracellular signalling molecule. Glutamate and the metabotropic glutamate receptor agonist (1S, 3R)-ACPD-evoked transient depolarizations, Ca(2+)-activated inward currents and rises in intracellular Ca2+. The (1S, 3R)-ACPD-activated currents were insensitive to InsP3 signalling inhibitors, heparin and pentosan polysulphate. Intracellular application of ryanodine alone activated currents in this study and proved a difficult tool to use as a potential inhibitor of cyclic ADP-ribose-mediated responses. However, intracellular dantrolene did attenuate both (1S, 3R)-ACPD and cyclic ADP-ribose responses. Intracellular photo-release of cGMP and cyclic ADP-ribose mimicked the responses to mGluR receptor activation. Intracellular application of nicotinamide and W7 inhibited the responses to photo-released cGMP but did not prevent responses to mGluR activation. The cyclic ADP-ribose receptor antagonist 8-amino cyclic ADP-ribose attenuated responses to (1S, 3R)-ACPD, cGMP and cyclic ADP-ribose, but some Ca(2+)-activated inward currents were still observed in the presence of this antagonist. In conclusion, mGluR receptor activation, cGMP and cyclic ADP-ribose release Ca2+ from intracellular stores. Some evidence suggests that pharmacologically related pathways are involved.

Adenosine Diphosphate Ribose↗
PubMedDate not supplied

Acute and chronic cardiovascular effects of doxorubicin in the dog: the cardiovascular pharmacology of drug-induced histamine release.

We evaluated the acute hemodynamic effects of doxorubicin in the open-chest dog. Doxorubicin at doses of 1-4 mg/kg administered over 2 min produced profound hemodynamic changes that were similar to those produced by histamine. These changes persisted despite administering the drug as a slow infusion. Histamine release in peripheral tissues was documented by a marked increase in venous histamine levels following doxorubicin administration. The heart extracted histamine during a period when arterial levels were increased, as indicated by consistently low coronary sinus/aortic ratios. Secondary catecholamine release occurred in response to histamine and histamine-mediated hemodynamic effects. Immunoreactive prostaglandins E and F were increased in coronary sinus blood beginning 30 min after the initiation of a continuous infusion of doxorubicin, and increased slowly thereafter. H1- and H2-receptor blockade with diphenhydramine and cimetidine prevented the early (2-30 min postinfusion) effects of doxorubicin, and combined histaminergic and adrenergic blockade prevented the late effects. A dose of doxorubicin (1 mg/kg) that released histamine and catecholamines produced primary cardiac effects acutely and a cardiomyopathy when administered chronically. The release of vasoactive substances could be part of the pathogenetic mechanism of anthracycline cardiomyopathy.

Animals↗
PubMedDate not supplied

Inhibition of high voltage-activated Ca2+ currents from cultured sensory neurones by a novel insect peptide.

PMP-D2, a novel 35 amino acid peptide isolated from the brain of the locust Locusta migratoria, is localised specifically in neurosecretory cells and nerve tracts of the Pars intercerebralis. When PMP-D2 is applied onto rat sensory neurones it blocks high voltage-activated inward Ca2+ currents at concentrations ranging from 0.1 mu M to 10 mu M. The inhibitory effect of PMP-D2 is more marked on the sustained inward Ca2+ current measured at the end of 100 ms voltage step commands than on the maximum inward Ca2+ current. These results suggests that PMP-D2 may differentially inhibit the two components of the high voltage-activated inward Ca2+ currents of rat sensory neurones.

Animals↗