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Biomedical subjects

K W Taylor

Publications and source records attributed to K W Taylor.

At least 37 records · Page 2Linked to original sources
PubMed1988

Pertussis toxin reverses the inhibition of insulin secretion caused by [Arg8]vasopressin in rat pancreatic islets.

When rat pancreatic islets were incubated with 10(-8) M arginine vasopressin in the presence of 15 mM glucose there was a pronounced inhibition of insulin release in comparison with controls. This inhibitory effect appeared to be specific for vasopressin since it was antagonised by vasopressin antibody. Moreover, pertussis toxin (100 ng/ml) reversed the inhibition of insulin release due to vasopressin, indicating the possible involvement of a guanyl-nucleotide regulatory protein in the inhibitory effect. Nevertheless, 10(-8) M vasopressin increased islet concentrations of cyclic AMP even under conditions where insulin release was decreased.

Animals↗
PubMed1986

Coxsackie B4 virus induces short-term changes in the metabolic functions of mouse pancreatic islets in vitro.

Mouse pancreatic islets cultured in vitro were infected with a tissue culture-adapted or a mouse pancreas-adapted strain of Coxsackie B4 (CB4) virus. The effects of the viruses on the islets were assessed by examination of their biochemical functions. It was found that the mouse pancreas-adapted strain of CB4 induced a 'leakage' of insulin from islets incubated at a basal (2 mmol l-1) glucose concentration, both at two and four days following infection. However, at a stimulatory concentration of glucose (20 mmol l-1) the rate of insulin secretion appeared to be normal in these islets. At two days the rate of total protein synthesis in islets infected with mouse pancreas-adapted CB4, incubated at high glucose concentration, was reduced; at four days the degree of inhibition was more severe, the rate at basal glucose concentration falling to half that of the control islets and at the stimulatory glucose concentration to a quarter of the control islets. (Pro)insulin biosynthesis was also inhibited, the rate being reduced to less than half the mean control value in islets infected with mouse pancreas-adapted CB4 virus at 20 mmol l-1 glucose at two days; at four days the rate was greatly reduced at both 2 and 20 mmol l-1 glucose. It is concluded from this study that only certain strains of CB4 virus can infect mouse pancreatic islets in vitro and that infection with strains of virus tropic for the islets leads to an impairment of metabolic functions of the B-cells, and is not necessarily lytic.

Animals↗
PubMed1985

Effect of interferon and double-stranded RNA on B-cell function in mouse islets of Langerhans.

The direct effects of alpha- and beta-interferons on isolated mouse pancreatic islets were investigated in vitro and found to be similar. After 7 h incubation with interferon concentrations above 350 units/ml, glucose-stimulated (pro)insulin biosynthesis was significantly inhibited, with only a slight inhibition of total protein biosynthesis. Inhibition could be abolished in the additional presence of an anti-interferon antibody. Interferon did not affect insulin release, total insulin content, or glucose oxidation of the islets. The stimulation of (pro)insulin biosynthesis by adenosine, D-glyceraldehyde, mannose, N-acetylglucosamine and leucine was also inhibited by interferon, with no effect on insulin release. At concentrations of dsRNA (double-stranded RNA) said to induce interferon (1-100 micrograms/ml), glucose-stimulated (pro)insulin biosynthesis was inhibited without significantly affecting insulin release. The dsRNA may itself inhibit stimulated (pro)insulin biosynthesis or may function indirectly by the induction of interferon.

Animals↗
PubMed1985

2-5A-dependent endoribonuclease activity and effects of A2'p5'A2'p5'A (2-5A core) in mouse pancreatic islets.

Glucose-stimulated (pro)insulin biosynthesis is markedly inhibited is mouse pancreatic islets incubated with micromolar concentrations of 2-5A 'core', (A2'p5'A2'p5'A). Total protein synthesis was also reduced, but to a lesser extent, while insulin release and total insulin content of the islets was untouched by 2-5A 'core'. Evidence is given for the presence of a 2-5A-dependent endoribonuclease which mediates these effects.

Adenine Nucleotides↗
PubMed1985

Biochemical changes induced by Coxsackie B4 virus in short-term culture of mouse pancreatic islets.

Isolated mouse pancreatic islets were infected in vitro with two strains of Coxsackie B4 virus--a tissue culture-adapted strain and a mouse pancreas-adapted strain. Within 48 h of infection changes had occurred in the biochemical activities of islets infected with the mouse pancreas-adapted strain of virus. Basal insulin release was increased two-fold in these islets, while glucose-induced insulin secretion remained unchanged. Insulin biosynthesis was greatly reduced at a stimulatory concentration of glucose (20 mM), thus leading to a reduced insulin content in these islets. These effects are of importance because they demonstrate that certain strains of Coxsackie B4 virus, like encephalomyocarditis virus, may selectively alter beta-cell function in vitro.

Animals↗
PubMed1985

The effect of stimulus significance on relatively sustained (tonic-like) and relatively transient (phasic-like) aspects of electrodermal, heart rate, and eyeblink response.

To examine the influence of stimulus significance on more sustained as well as transient aspects of electrodermal, cardiac (HR), and eyeblink response, a 21-sec tone was sounded in one ear or the other. A click occurred during many tones, and a light followed offset by 9 sec. Four groups were studied: one pressed a pedal immediately on hearing any click; another only on click during tone in a specified ear; a third also responded only to the specified ear, but withheld press until the light; a fourth listened without any response. Results confirmed the important role of stimulus significance in each system whether between- or within-subject comparisons were made. Sustained responses were seen only when a significant signal was sought, involving in each case sustained HR deceleration, slowed blink rate, and heightened electrodermal level. Transient response to click and light also appeared only when there were significant signals. Response to tone-onset gave more ambiguous results. ANOVAs of response magnitude suggested that onset of nonsignificant tones might have elicited ORs, while binomial tests indicated these were not elicited with better than random frequency anywhere but on those trials occurring more frequently at the experiment's onset. Interpretations consistent with both the significance hypothesis and with a distinction between automatic and voluntary ORs can be made only here. Motor response had no effect on electrodermal or eyeblink response, and on HR was associated only with increased acceleration 1-2 sec after pedal-press. Studies using small motor responses to establish stimulus significance are therefore not likely to be substantially biased by the response itself.

Acoustic Stimulation↗
PubMed1985

Effects of glucose and D-3-hydroxybutyrate on human pancreatic islet cell function.

Beta-Cell function in human islets derived from a number of kidney donors was investigated by using various types of islet preparations. With fresh islets, both insulin release and biosynthesis were increased by raising glucose concentrations, although the response was a variable one. In fresh islets, the effects of 5 mmol of glucose/l on release were potentiated by 10 mmol of D-3-hydroxybutyrate/l. Insulin release at 20 mmol of glucose/l was inhibited by adrenaline (0.1 mmol/l), and potentiated by theophylline (10 mmol/l) in the presence of 5 mmol of glucose/l, in islets cultured for 4 days. After culture for 8 days, islets still showed an increase in insulin release and biosynthesis in response to glucose. Pancreas slices derived from fresh human tissue also responded to increasing concentrations of glucose with a sigmoidal curve for insulin release.

3-Hydroxybutyric Acid↗
PubMed1984

Long-term biochemical changes in the islets of Langerhans in mice following infection with encephalomyocarditis virus.

A mild diabetes was induced in mice following the inoculation of a myocardial variant of encephalomyocarditis virus. The majority of infected mice developed a transient hyperglycaemia and only a few mice exhibited a chronic elevation of blood glucose. Infected mice were selected for study if their non-fasting blood glucose levels were above two standard deviations of values in control mice for at least 5 consecutive days. The pancreas from selected inoculated mice and control mice was removed 60 days after infection; random blood glucose levels at this time had returned to normal. Isolated islets of Langerhans from such previously 'diabetic' mice were used to determine the rate of insulin secretion, insulin biosynthesis and cyclic AMP accumulation in response to various glucose concentrations. At glucose (16 mmol/l), both insulin release and biosynthesis were depressed in previously infected animals. At glucose (2 and 10 mmol/l), while insulin biosynthesis was unchanged in infected animals, insulin release was increased. Cyclic AMP accumulation in response to glucose (20 mmol/l) was found to be significantly elevated in islets from infected animals and especially in response to glucose (20 mmol/l) in the presence of isobutyl methyl xanthine (1 mmol/l). Infected mice exhibited a reduction of total pancreatic insulin content in comparison with control mice. The insulin content of isolated islets of Langerhans from infected and control mice was found to be the same. Serum insulin levels, however, from infected mice were higher than in control sera.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Effect of human lymphoblastoid interferon on insulin synthesis and secretion in isolated human pancreatic islets.

Human islets of Langerhans were isolated from the pancreas removed from a 13-year-old female transplant donor. The islets were incubated in a culture medium for 24 h in the presence of human lymphoblastoid interferon (1000 units/ml). Insulin secretion, proinsulin biosynthesis, total protein biosynthesis and total insulin content were assessed at various concentrations of glucose in the presence of interferon. In interferon-treated islets glucose-stimulated insulin secretion was unaltered from that of control islets; however, glucose-stimulated proinsulin biosynthesis was specifically inhibited by interferon (48%, p less than 0.025). Total protein biosynthesis and total insulin content were not significantly affected by interferon.

Glucose↗
PubMed1984

The effectiveness of the thyroid shield in dental radiology.

The effectiveness of the thyroid shield in reducing patient exposure during routine dental radiographic examinations was studied. A nonscreen film and two film-screen combinations were used as dosimeters and to show the spatial distribution of x-ray exposure. The error in the absolute accuracy of the film dosimeter and the error in the reproducibility of the film-screen combinations were less than +/- 10%. Measurements of thyroid exposure and exposure distribution, with and without the shield, were made on a Rando phantom and on patients. In the phantom study, the reduction by the shield of exposure to the thyroid from primary beam and from scatter was found to be highly dependent on the position of the primary beam relative to the thyroid gland but independent of kVp. Exposure reduction by the shield varied from 5% to 56% for a complete-mouth survey, 2% to 18% for a bitewing survey, and 10% to 79% for a panoramic survey. In the patient study, thyroid skin exposures measured on adults were 33% to 84% lower in offices in which the shield was used as compared to offices in which it was not used. Thyroid skin exposures measured on children were 63% to 92% lower. In accordance with the ALARA principle, these results support the routine use of the thyroid shield for all dental radiography.

Adolescent↗
PubMed1984

Dose and quality control (DQC) in diagnostic radiology.

Dose and quality control in diagnostic radiology can play an important role in reducing x-ray exposure and costs whilst maintaining a high level of imaging quality and diagnostic benefit. It can also become very costly. Current government regulations demand unnecessary accuracy in the measurement and performance of certain parameters of x-ray generators whilst ignoring others which are more important. They totally neglect imaging systems. We urge a more critical approach to the requirements for dose and quality control programs. We propose the exchange of information through a user's club and a less regulatory but equally important role for government.

Calibration↗
PubMed1983

Effects of ketone bodies on insulin release and islet-cell metabolism in the rat.

Ketone bodies promote insulin secretion from isolated rat pancreatic islets in the presence of 5 mM-glucose, but are ineffective in its absence. At concentrations of 10 mM or less, the relative abilities of the ketone bodies to potentiate release are in the order D-3-hydroxybutyrate greater than DL-3-hydroxybutyrate greater than acetoacetate. The response curve relating insulin release to D-3-hydroxybutyrate concentration displays a threshold at 1 mM and a maximum at 10 mM. D-3-Hydroxybutyrate (5 mM, but not 10 mM) promotes insulin secretion in the presence of 5 mM concentrations of both L-arginine and DL-glyceraldehyde, but not with L-leucine, L-alanine, L-glutamate or 4-methyl-2-oxopentanoate. The oxidation rates of the exogenous ketone bodies do not correlate well with their capacities to promote insulin release. Moreover, the oxidation of 5 mM-D-3-hydroxybutyrate can be inhibited by 25% with methylmalonate (10 mM) without any diminution of release. The potentiation with D-3-hydroxybutyrate occurs without an observable increase in total islet cyclic AMP. However, a small net efflux matches the relative abilities of the ketone bodies to promote insulin release. With islets from 48 h-starved animals the insulin response is both diminished and less sensitive than in fed animals, since insulin secretion is not significantly raised until a threshold of 5 mM-D-3-hydroxybutyrate is reached. These results suggest that, in the rat at least, there should be a reappraisal of the physiological role of ketone bodies in the promotion of insulin release.

3-Hydroxybutyric Acid↗
PubMed1982

Effects of adenosine, 2-deoxyadenosine and N6-phenylisopropyladenosine on rat islet function and metabolism.

Adenosine (1.0-100 mum). N(6)-phenylisopropyladenosine (0.1-10 mum) and 2-deoxyadenosine (10 mm) all produced a dose-dependent inhibition of glucose-stimulated insulin release. The inhibition of glucose-stimulated insulin release by adenosine and N(6)-phenylisopropyladenosine was abolished by 3-isobutyl-1-methylxanthine (0.1 mm), whereas 2-deoxyadenosine inhibited insulin release even in the presence of 3-isobutyl-1-methylxanthine. These adenosine nucleosides also inhibited the release of insulin induced by 4-methyl-2-oxopentanoate (20 mm), dl-glyceraldehyde (30 mm) and l-leucine (20 mm). Adenosine (10 mum). N(6)-phenylisopropyladenosine (10 mum) and 2-deoxyadenosine (10 mm) did not inhibit insulin biosynthesis or [U-(14)C]glucose oxidation at concentrations of the nucleosides that gave maximal inhibition of insulin release. However, adenosine, 2-deoxyadenosine and N(6)-phenylisopropyladenosine produced marked inhibition of the glucose-stimulated increases seen in islet cyclic AMP accumulation. Similar to its effects on insulin release, 3-isobutyl-1-methylxanthine (0.1 mm) antagonized the inhibitory effects of cyclic AMP accumulation produced by adenosine and N(6)-phenylisopropyladenosine, but had no effect on the inhibition of cyclic AMP accumulation seen with 2-deoxyadenosine. These results show that adenosine and its specifically modified analogues, 2-deoxyadenosine and N(6)-phenylisopropyladenosine, are strong inhibitors of insulin release from rat islets, a function that appears to be the consequence of their ability to inhibit the accumulation of cyclic AMP. It is proposed that the B cells, in common with many other tissues, may possess two different sites at which adenosine nucleosides interact to produce their biological effects; these are the so-called ;P' and ;R' sites first described by Londos & Wolff [(1977) Proc. Natl. Acad. Sci. U.S.A.74, 5482-5486].

Adenosine↗
PubMed1982

The role of metabolism in the control of cyclic AMP efflux, cyclic AMP content, and insulin secretion from rat islets of Langerhans.

Glucose, alpha-ketoisocaproate, and N-acetylglucosamine all initiate insulin release and stimulate cyclic AMP efflux and cyclic AMP accumulation. Mannoheptulose inhibited these islet responses to glucose but not to N-acetylglucosamine or alpha-ketoisocaproate. On the other hand, menadione inhibited these responses to all three secretagogues. Nicotinamide enhanced the insulin release due to glucose and alpha-ketoisocaproate and also enhanced cyclic AMP efflux and intracellular cyclic AMP accumulation. N-acetylglucosamine-mediated insulin release, cyclic AMP efflux, and cyclic AMP accumulation were unaffected by nicotinamide. These results suggest that the metabolic state of the islet is a primary determinant of the ability of a secretagogue to raise cyclic AMP efflux and intracellular cyclic AMP, and these actions may be mediated in part by alterations in the redox state of the pyridine nucleotide system.

Acetylglucosamine↗
PubMed1982

Islet cell function in gold thioglucose-induced obesity in mice.

Blood insulin, blood glucose and the biosynthesis and release of insulin have been studied in mice made obese with a single injection of gold thioglucose. In such mice, blood glucose levels were normal, though serum insulin rose in parallel with the development of obesity. When compared with controls, insulin secretion and synthesis were increased in isolated islets of Langerhans from obese mice, over a wide range of glucose concentrations. However, in obese animals, insulin biosynthesis was augmented above control levels at 2 mmol/l glucose, whilst the increase in insulin secretion accompanying obesity only became evident at glucose concentrations greater than 5 mmol/l. After 2 min incubation, cyclic AMP rose more in islets from obese mice than in controls, though cyclic AMP levels did not significantly differ in either group after 10 min incubation with glucose. Glucose oxidation was also increased in islets of Langerhans from obese mice. It seems possible that changes in glucose oxidation, as well as in cyclic AMP levels, contribute to the alteration in the B cell response in this type of obesity.

Animals↗