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M Theron

Publications and source records attributed to M Theron.

10 recordsLinked to original sources
PubMed2006

A quantitative model of error accumulation during PCR amplification.

The amplification of target DNA by the polymerase chain reaction (PCR) produces copies which may contain errors. Two sources of errors are associated with the PCR process: (1) editing errors that occur during DNA polymerase-catalyzed enzymatic copying and (2) errors due to DNA thermal damage. In this study a quantitative model of error frequencies is proposed and the role of reaction conditions is investigated. The errors which are ascribed to the polymerase depend on the efficiency of its editing function as well as the reaction conditions; specifically the temperature and the dNTP pool composition. Thermally induced errors stem mostly from three sources: A+G depurination, oxidative damage of guanine to 8-oxoG and cytosine deamination to uracil. The post-PCR modifications of sequences are primarily due to exposure of nucleic acids to elevated temperatures, especially if the DNA is in a single-stranded form. The proposed quantitative model predicts the accumulation of errors over the course of a PCR cycle. Thermal damage contributes significantly to the total errors; therefore consideration must be given to thermal management of the PCR process.

Base Sequence↗
PubMed2004

Pressure and temperature interactions on cellular respiration: a review.

Thermodynamic equations show that pressure and temperature can, theoretically, act in synergy or in opposite directions depending on their respective variations. Hence, they interact to establish rates of biological processes (pressure/temperature interactions, PTI). For such studies, it is interesting to use aquatic ectotherms, in particular fish, because it is easy to submit them to temperature and/or pressure changes. This review focuses on the effects of temperature and pressure changes on the energy metabolism of fish, mitochondrial oxygen consumption and functioning, showing that the observed effects do not always match the predictions made by equations or models. Unpublished results concerning the mitochondrial function of eels acclimatised at two temperatures and two pressures show that the mitochondrial targets of pressure and temperature are probably not the same. The possible mechanisms and consequences of PTI are discussed.

Animals↗
PubMed2001

Why can the eel, unlike the trout, migrate under pressure.

In order to elucidate the difference between pressure resistance in trout (Onchorhyncus mykiss) and eel (Anguilla anguilla), oxygen consumption of red muscle permeabilised cells and mitochondria were measured at 101 ATA hydrostatic pressure per se. Such an experiment involved the setting up of a special system allowing measurements under high pressure. The results show that hydrostatic pressure strongly alters the oxidative phosphorylation in trout but not in eel, which exhibits mitochondrial pressure resistance. It is hypothesised that the eel has a supranormal mitochondria functioning at atmospheric pressure in order to cope with the high pressure environment encountered during its migration.

Journal Article↗
PubMed2000

Improvement in the efficiency of oxidative phosphorylation in the freshwater eel acclimated to 10.1 MPa hydrostatic pressure.

Previous studies have suggested that the efficiency of oxidative phosphorylation in the freshwater eel (Anguilla anguilla) is increased after acclimation to high hydrostatic pressure. Analysis at atmospheric pressure of the respiratory chain complexes showed that, after 21 days at 10.1 MPa, the activity of complex II was decreased to approximately 50 % (P<0.01) of the control value and that cytochrome c oxidase (complex IV) activity was significantly increased to 149 % of the control value (P<0.05). ADP/O ratios calculated from mitochondrial respiration measurements were significantly increased after acclimation to high hydrostatic pressure (2.87 versus 2.52, P<0.001) when measured in the presence of pyruvate plus malate at atmospheric pressure. These results clearly show an increased oxidative phosphorylation efficiency in response to high-pressure acclimation.

Adaptation, Physiological↗
PubMed2000

In vitro reactivity of ventral aorta to acetylcholine and noradrenaline in yellow freshwater eel (Anguilla anguilla L.) acclimatized to 10.1 MPa hydrostatic pressure.

We examined in vitro vascular reactivity of eels previously acclimatized to 10.1 MPa hydrostatic pressure (HP) for 21 days. The isometric tension developed by ventral aortic rings was measured at atmospheric pressure. Dose-response curves for either acetylcholine (ACh) or noradrenaline (NA), as well as contractions evoked by 80 mM K+, were compared with time-matched experiments conducted on rings obtained from control eels. Results showed that neither the optimal tension nor the maximal force of the K+-evoked contraction were significantly modified, suggesting that acclimatization to high HP did not change the vascular smooth muscle contractile machinery. The dose-response curve to ACh was not significantly changed. Conversely, although NA always relaxed aortic rings, the response of acclimatized eels was significantly reduced over the entire range of the agonist concentration tested (10(-8) to 10(-3) M), except for the lowest one (10(-9) M). The maximal amplitude of the NA-induced relaxation was significantly reduced in aortic rings from acclimatized eels as compared with non-acclimatized samples (339.3 +/- 86.5 vs. 744.3 +/- 72.1 mg x mg(-1) dry weight, P < 0.005). Our results suggest that acclimatization to high HP could selectively alter the control of vascular tone by catecholamines.

Acclimatization↗
PubMed1997

Amisulpride versus placebo in the medium-term treatment of the negative symptoms of schizophrenia.

BACKGROUND: Amisulpride is a substituted benzamide with high selectivity for dopamine D2 and D3 receptors. The purpose of the study was to evaluate the effect of 100 mg amisulpride in patients with predominantly negative symptoms of schizophrenia. METHOD: This was a multi-centre, randomised, parallel-group, double-blind study. Patients received either amisulpride (100 mg/day) or placebo over a six-month treatment period. RESULTS: A total of 141 patients were included, 69 received amisulpride, 72 placebo. Fifty-eight patients (41%) had received neuroleptic treatment prior to inclusion. The percentage of amisulpride patients completing the study (55%) was significantly higher than that with placebo (32%), and drop-out rates due to lack of efficacy were 27% with amisulpride and 47% with placebo. All efficacy assessments were statistically in favour of amisulpride compared with placebo. The overall incidence of extrapyramidal symptoms was comparable in both groups; only five patients started anti-Parkinsonian treatment during the study (one in the placebo and four in the amisulpride group). CONCLUSION: Amisulpride is effective in the medium-term treatment schizophrenic patients with predominantly negative symptoms.

Adult↗
PubMed1996

Efficacy of mizolastine, a new antihistamine, compared with placebo in the treatment of chronic idiopathic urticaria.

A two-centre, double-blind, randomized, placebo (P)-controlled, parallel-group study was conducted in the UK to examine the efficacy and safety of mizolastine (M), a new H1-receptor antagonist, as a once-daily 10-mg dose in chronic idiopathic urticaria. Fifty-six outpatients (M: n = 28; P: n = 28) with a mean age of 38 +/- 15 years, a duration of disease of more than 3 years, and symptoms of urticaria at least twice a week in the absence of treatment were recruited. After a single-blind placebo run-in period, patients were allocated to one of two treatment groups and were evaluated after 7 and 28 days. The main characteristics (age, duration of disease, number of urticarial episodes, and total score) of the two groups were comparable at inclusion. Mizolastine was shown to improve the urticaria symptoms: at the end of the study, mizolastine produced a significantly greater decrease in the global symptom score comprising itch, wheals, and erythema (M: 2.1 +/- 2.1 vs P: 0.4 +/- 2.0; P = 0.002). The patient-rated global discomfort from symptoms measured by visual analog scale was significantly improved with mizolastine (M: 31.4 +/- 36.7) compared to placebo (P: 5.4 +/- 27.6; P = 0.003), with respectively more M responders (74.1%) than P responders (28.6%, P = 0.001), a responder being a patient with a > or = 50% decrease in VAS. Premature dropouts due to lack of efficacy and loss to follow-up mainly occurred at the first evaluation (day 7) and were more often observed in patients in the placebo group (n = 17) than in the mizolastine group (n = 8) (P = 0.031). No serious adverse events were recorded. Somnolence was reported in two mizolastine patients, one of whom discontinued the study. Thus, mizolastine may be considered a new treatment option for the symptoms of chronic urticaria.

Adult↗
PubMed1983

Cardiovascular effects of AQ-A 39 in healthy volunteers.

Ten healthy male volunteers performed maximal exercise tests on a bicycle ergometer. A control reading was obtained; at a second session propranolol 80 mg was given, and then placebo, 100 mg or 200 mg AQ-A 39 were administered in a randomised double-blind manner. At peak exercise, the heart rate averaged 191.6 beats/min during the control test, 185.8 beats/min after placebo, 172.4 beats/min with 100 mg of AQ-A 39 (-10%), 166.0 (beats/min) with 200 mg of AQ-A 39 (-13.4%); with 80 mg of propranolol, the heart rate averaged 132.8 beats/min and the workload accomplished was substantially lower than that accomplished with AQ-A 39 and placebo which remained the same as in the control test. No effect on blood pressure was observed. The rate pressure product was significantly reduced with AQ-A 39.

Adult↗