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C Edwards

Publications and source records attributed to C Edwards.

At least 235 records · Page 13Linked to original sources
PubMed1988

Growth hormone (GH) responses to arginine and L-dopa alone and after GHRH pretreatment.

In order to investigate the mechanisms by which arginine and L-dopa cause GH release in humans we measured the GH response to GHRH 1-44 (200 micrograms i.v.), arginine (30 g i.v. over 30 min) and L-dopa (500 mg orally) administered alone and 120 minutes following pretreatment with GHRH 1-44 (200 micrograms i.v.) in normal male subjects. Prior GHRH administration abolished the GH response to subsequent GHRH. Arginine infusion induced a rise in GH levels maximal at 45 min. Following GHRH pretreatment the GH response to arginine was enhanced, with peak values of 19.3 +/- 6.4 vs 53.3 +/- 16.5 mU/l (mean +/- SEM) respectively (P less than 0.02). L-dopa alone induced a rise in GH levels maximal at 90 min (17.6 +/- 7.4 mU/l, mean +/- SEM) but this rise was abolished by pretreatment with GHRH.

Adult↗
PubMed1988

Clinical assessment of an enzyme immunoassay (EMIT) for measurement of serum salicylate.

Salicylic acid concentrations in serum were compared using a homogenous enzyme immunoassay (EMIT) and an automated colorimetric analysis (ACA) technique. Analysis of samples showed similar within-day and day-to-day coefficients of variation (CV): 1.3% and 4.6% by EMIT and 1.0% and 2.6% by ACA, respectively. Quantification of serum containing added salicylate and serum from patients receiving salicylate therapy showed a slight positive bias towards the ACA method over the range of 0-600 mg/l. No significant difference in reliability was found between the two methods. The EMIT assay showed no interference from other antiflammatory drugs being taken by patients who were not taking salicylates. If decisions to alter salicylate dosage are made with due regard to the drug's saturation kinetics, measurements using either EMIT or ACA should allow the clinician to titrate patients' serum concentrations accurately within the narrow therapeutic range.

Colorimetry↗
PubMed1988

Quantitative assessment of factors affecting the recovery of indigenous and released thermophilic bacteria from compost.

Thermophilic actinomycetes and bacilli were recovered from mushroom compost by conventional dilution plating and sedimentation chamber-Andersen sampler methods. Excessive growth of thermophilic bacilli on dilution plates accounted for the poor recovery and limited diversity of actinomycete colonies, and this result was largely unaffected by the use of modified extraction procedures and diluents. Assessment of the actinomycete population was more successfully achieved by applying the sedimentation chamber method, by using selective media, or both. Background resistance of the compost microflora to selective agents (kanamycin, novobiocin, tetracycline, thiostrepton, and NaCl) was extremely varied, but both actinomycetes and bacilli were particularly sensitive to tetracycline. The selective isolation of Thermoactinomyces spp. and Thermomonospora chromogena by novobiocin and kanamycin, respectively, was shown to be reproducible, and the use of high concentrations of kanamycin resulted in the isolation of a novel group of unidentified thermophilic actinomycetes. Comparison of nonselective nutrient media demonstrated that the nutrient-rich protoplast regeneration medium R5 was surprisingly efficient for actinomycete recovery. This medium was found to be particularly appropriate for the recovery of Saccharomonospora viridis BD125, introduced as spores into both sterile and fresh samples of mushroom compost. This stable pigmented variant of the S. viridis strains indigenous to compost was released at concentrations of up to 10 spores g of compost in order to provide information for future experiments on the release and recovery of genetically manipulated strains. The detection limits for this strain were in the region of 10 g from sterilized compost but only 10 g from nonsterile compost. These figures correspond to mean recovery efficiencies of approximately 70% (sterilized compost) and 53% (fresh compost) of viable spores released. Further improvements in the detection and recovery of S. viridis strains released into compost should be achieved by the introduction of selectable markers developed from this information on the antibiotic resistance profile of the indigenous compost microflora.

Journal Article↗
PubMed1988

The effects of different anaesthetic agents on the estimation of uterine vascular permeability in mice.

Vascular permeability in the uterus and other tissues of mice was assessed using the accumulation of 125I-human serum albumin 30 min after its intravenous injection. The anaesthetic agent employed for the 125I-albumin injection differentially affected the estimates of vascular permeability: intraperitoneal (i.p.) tribromoethanol of pentobarbitone sodium produced significantly higher values for the uterus and body wall than ether. The i.p. administration of either Saffan or pentobarbitone sodium reduced estimates of vascular permeability in the duodenum. These results emphasize the importance of the choosing a suitable anaesthetic agent in vascular studies of the uterus and other abdominal tissues.

Alfaxalone Alfadolone Mixture↗
PubMed1988

Induction of luteal regression in the marmoset monkey (Callithrix jacchus) by a gonadotrophin-releasing hormone antagonist and the effects on subsequent follicular development.

Doses of 100 or 200 micrograms of a novel GnRH antagonist ([N-acetyl-D beta Na11-D-pCl-Phe2-D-Phe3-D-Arg6-Phe7-Arg8-D-Ala10]NH2 GnRH) (4 animals/dose) were administered on Days 10/11 of the luteal phase and induced a marked suppression of circulating bioactive LH and progesterone concentrations within 1 day of treatment (P less than 0.01). Thereafter, progesterone concentrations remained low or undetectable until after the next ovulation. Similar results were obtained when 200 micrograms antagonist were given on Days 5/6 of the luteal phase (N = 4). The interval from injection of antagonist (200 micrograms but not 100 micrograms) to ovulation (based on a rise in progesterone above 10 ng/ml) was significantly longer than that from prostaglandin-induced luteal regression to ovulation in control cycles (N = 4/treatment) (range, 13-15 days after antagonist vs 8-10 days after prostaglandin, P less than 0.01). This delay of 4-5 days was equivalent to the duration for which LH concentrations were significantly suppressed by 200 micrograms antagonist when administered to ovariectomized animals (N = 3). Corpus luteum function during the cycle after GnRH antagonist treatment appeared normal according to the pattern of circulating progesterone. These results show that corpus luteum function and preovulatory follicular development in the marmoset monkey are dependent on pituitary gonadotrophin secretion.

Animals↗
PubMed1988

Use of a single-injection tissue-sampling technique to study steroid uptake by the decidualized endometrium of the mouse.

A tissue-sampling paired-tracer method was used to investigate the effect of plasma proteins on uptake by the decidualized endometrium of [3H]progesterone, [3H]oestradiol and [3H]corticosterone. When injected arterially in protein-free Ringer, the extraction of progesterone and oestradiol was 100%, while that of corticosterone was only 60%. The addition of 4% albumin or injection in mouse plasma resulted in significant decreases in progesterone extraction to about 80% and 65% respectively. Injection in pregnant guinea-pig plasma reduced progesterone extraction further (to 33%). While neither 4% albumin nor mouse plasma had any significant effect on the uptake of oestradiol, neonatal rat plasma reduced oestradiol extraction to 40%. These results are consistent with high-affinity binding proteins having a limiting effect on the availability of steroids to target tissues.

Animals↗
PubMed1988

Acarbose. A preliminary review of its pharmacodynamic and pharmacokinetic properties, and therapeutic potential.

Acarbose delays the production of monosaccharides (notably glucose) by inhibiting the alpha-glucosidases associated with the brush-border membrane of the small intestine which are responsible for the digestion of complex polysaccharides and sucrose. In healthy subjects acarbose 100 to 200 mg significantly inhibits postprandial glucose, insulin and triglyceride responses, with some evidence of carbohydrate malabsorption with the higher dose. Clinical trials in patients with non-insulin-dependent diabetes mellitus showed that acarbose improved diabetic control, especially postprandial blood glucose levels, independent of whether the patients were receiving concomitant oral antidiabetic drugs in addition to dietary management. In comparative studies acarbose was significantly superior to placebo, and comparable to biguanides, when used alone or as an adjuvant to sulphonylurea therapy. Trials in patients requiring insulin to control their diabetes demonstrated that acarbose significantly reduced postprandial blood glucose concentrations, resulting in a smoother diurnal blood glucose-time curve and improved symptoms associated with nocturnal hypoglycaemia. Daily insulin requirements were sometimes reduced. In large multicentre trials acarbose up to 600 mg/day for 3 to 12 months improved glycaemic control in approximately 55% of patients with non-insulin-dependent or insulin-dependent diabetes mellitus. Apart from its use in diabetes, encouraging preliminary results have been obtained with acarbose in other therapeutic areas such as dumping syndrome, reactive hypoglycaemia, and types IIb and IV hyperlipoproteinaemias--however, further clinical experience is needed in these settings before clear conclusions can be drawn. No serious side effects have been reported during treatment with acarbose, although it is associated with a high incidence of troublesome gastrointestinal symptoms such as flatulence, abdominal distension, borborygmus and diarrhoea. The incidence of these reactions usually decreases with time. Thus, acarbose represents the first of a new class of oral antidiabetic drugs--the alpha-glucosidase inhibitors. It has proven useful for improving glycaemic control when used as an adjunct to standard therapy involving dietary restriction, oral antidiabetic drugs and/or subcutaneous insulin. That being the case, acarbose should provide the clinician with an interesting treatment option which can be used in a broad range of patients with diabetes mellitus in whom 'traditional' management approaches produce suboptimal glycaemic control.

Acarbose↗
PubMed1988

A possible role for the acetylcholine transport system in non-quantal release of acetylcholine at the rodent myoneural junction.

The effects on the spontaneous, non-quantal release of acetylcholine (ACh) from motor nerve terminals of substances known to inhibit the ACh transport system present in cholinergic synaptic vesicles have been investigated. In mouse diaphragms, the hyperpolarization normally produced by d-tubocurarine (dTC) in muscle endplates that had been treated by an anticholinesterase was partly or completely abolished by 2-(4-phenylpiperidino) cyclohexanol (AH5183, 10(-7)-10(-6)M), quinacrine (10(-7)M) and tetraphenylborate (10(-6) M). Since the sensitivity of the endplate to ACh was not changed, the block of the dTC induced hyperpolarization indicated an inhibition of the spontaneous, non-quantal release of ACh. This was confirmed by direct measurement of the ACh released by rat diaphragm. The release of ACh from the innervated diaphragm was decreased by about 50% by AH5183 (10(-8)-10(-6) M) and by 42% by quinacrine (10(-7)-10(-6) M). The ACh released was presumably neural, since the release of ACh from 4-day denervated diaphragms was not diminished by either AH5183 or quinacrine. The results indicate that the spontaneous release of ACh from the motor nerve terminals is probably mediated by a carrier which may be the vesicular transport system responsible for moving ACh into the vesicle. The transport system is likely incorporated into the membrane of the nerve terminal during exocytosis.

Acetylcholine↗
PubMed1987

Mechanically induced electrical responses in murine mammary epithelial cells in primary culture.

In mouse mammary epithelial cells in primary culture, mechanical stimulation of a cell induced in other cells within the same colony a short depolarization of less than 15 mV with a duration of 1-8 s and a subsequent, prominent hyperpolarization of 6 mV lasting 10-40 s. Epidermal growth factor induces a spontaneous hyperpolarizing response in cultured mammary cells, and in cells treated with EGF mechanical stimulation produced a greater hyperpolarization, while the amplitude of the depolarizing response was not affected. The amplitude of the mechanically induced hyperpolarization was markedly reduced by quinine and tetraethylammonium, blockers of the Ca2+ -dependent K+ channel. The results suggest that the Ca2+ -dependent K+ channel was involved in the hyperpolarization.

Animals↗
PubMed1987

Buoyant density fluctuations during the cell cycle of Bacillus subtilis.

A simple rapid method for preparing synchronous cultures of Bacillus subtilis has been used to investigate changes in density during the cell cycle. Asynchronous cells separated on a stepped Percoll density gradient had a mean cell density of 1.117 g ml-1 +/- 0.004. Samples from a synchronous culture exhibited variation (ca. 1.5%) in mean cell density which was greatest at the onset of cell division. An asynchronous control culture showed little variation in density. These results are discussed in relation to previous work on Escherichia coli.

Bacillus subtilis↗
PubMed1987

A study on early post-denervation changes of non-quantal and quantal acetylcholine release in the rat diaphragm.

The d-tubocurarine (dTC) induced hyperpolarization of antiesterase-treated muscles at the endplate zone, miniature endplate potentials (mepps), resting membrane potentials (RMPs) and the input resistances of single muscle fibres (Rin) were measured in rat diaphragm at various times after denervation. The dTC-induced hyperpolarization decreased in two phases: 2 h after denervation it decreased transiently to 25%, after 4 h it had partially recovered to 60% and from 6 h it progressively decreased up to 12 h after which time it changed to depolarization. The initial fall and recovery were also present in muscles from sham-operated animals. The frequency of mepps decreased by 25% and the amplitude diminished by 10% within the first 2-4 h. After 10 h the frequency had decreased by 35% and the amplitude by 65%. After 12 h no mepps were present. The RMP was not significantly changed during the first 16 h after denervation. From 16 to 24 h the membrane became depolarized at a rate of about 1 mV/h. The input resistance of a single muscle fibre was constant for 12 h after denervation and from 12 to 24 h it increased by 25%. It is concluded that the early decrease in the dTC-induced hyperpolarization is probably due to the desensitization of acetylcholine (ACh) receptors caused by stress-activated non-quantal ACh release. The later decrease of dTC-hyperpolarization reflects a fall in the non-quantal ACh release. The depolarization of the resting membrane after denervation is related to the decrease in passive membrane permeability which is a secondary consequence of transmission failure.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1987

Malignant melanotic schwannoma of the bronchus.

A case of malignant melanotic schwannoma arising in the right upper lobe bronchus of a 27 year old man is presented. Tumours of this type most commonly occur in spinal nerve roots and are generally considered to be benign. The behaviour of those originating elsewhere is less predictable. As far as we are aware this is the first reported case affecting the respiratory tract.

Adult↗
PubMed1987

Uterine blood flow during the development and regression of the decidual cell reaction in ovariectomized, steroid-treated mice.

Uterine blood flow was assessed in mice by measuring organ uptake of intravenously injected [14C]butanol. In ovariectomized mice, injection of 100 ng oestradiol-17 beta increased blood flow 5-fold over that of untreated controls. The injection of oestradiol-17 beta in progesterone-treated mice also increased uterine blood flow at the time of maximal sensitivity to a decidual stimulus, but not 4 days later. Absolute values of blood flow increased during development of the decidual cell reaction in proportion to the increase in uterine weight, reaching maximal values 96 h after decidual induction. When progesterone injections were stopped 72 h after decidual induction, a rapid decrease in absolute and relative blood flow values preceded the decrease in uterine weight. This decrease in uterine blood flow occurred within 12 h of removing a subcutaneous implant containing progesterone. These results are consistent with the view that increased uterine blood flow during decidual development may be necessary to support the rapid increase in uterine weight at implantation and the subsequent decrease in both relative and absolute uterine blood flow on withdrawal of progesterone may promote decidual regression in the mouse.

Animals↗