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Biomedical subjects

A H Bretag

Publications and source records attributed to A H Bretag.

At least 19 recordsLinked to original sources
PubMed1994

Immunolabelling for VDAC, the mitochondrial voltage-dependent anion channel, on sarcoplasmic reticulum from amphibian skeletal muscle.

Patch-clamp studies of ion channels in the sarcoball membrane, a relatively pure preparation of sarcoplasmic reticulum, had earlier revealed a high-conductance anion channel with some properties similar to the mitochondrial voltage-dependent anion channel (VDAC). Using post-embedding immunolabelling, the presence of VDAC was investigated in sarcoball preparations from the semitendinosus muscle of the cane toad Bufo marinus. As expected, the outer membrane of mitochondria found within the interior of skinned fibres was decorated with gold label. Surprisingly, sarcoplasmic reticulum membrane was also labelled. The sarcoball membranes, which could arise from either the sarcoplasmic reticulum or from mitochondria, were also labelled. These results indicate the presence of a VDAC-like protein in the sarcoplasmic reticulum.

Animals↗
PubMed1994

Carbohydrate-reactive, pore-forming outer membrane proteins of Aeromonas hydrophila.

Two outer membrane proteins of Aeromonas hydrophila A6, isolated in a one-step affinity chromatography process based on carbohydrate reactivity, were found to be pore-forming molecules in artificial planar bilayer membranes. These carbohydrate-reactive outer membrane proteins (CROMPs; M(r)s, 40,000 and 43,000) were subjected to amino acid analysis. The amino acid profiles for these two outer membrane proteins were almost identical. A partial protein sequence of a 14-amino-acid fragment of the 40,000-Da protein revealed homology with outer membrane porins of Escherichia coli and A. hydrophila. CROMPs were compared with carbohydrate-reactive porins also extracted from outer membranes of A. hydrophila A6. These porins were isolated by using standard porin purification techniques (insolubility in 2% sodium dodecyl sulfate, solubility in 0.4 M NaCl, and Sephacryl S-200 gel filtration), and then Synsorb H type 2 affinity chromatography was done. The physical and functional properties of the carbohydrate-reactive porins and CROMPs were found to be identical. On the basis of pore-forming properties in planar lipid bilayers and channel inhibition with maltotriose solutions, a nonspecific, general diffusion porin and a LamB-like maltoporin were identified in both CROMP and carbohydrate-reactive porin preparations. To our knowledge, the use of carbohydrate reactivity to isolate channel-forming proteins from bacterial outer membranes has not been reported previously.

Aeromonas hydrophila↗
PubMed1994

Benign familial disease with muscle mounding and rippling.

Four members of a family in three generations exhibited unusual clinical features of localised transient swelling of muscle induced by percussion (muscle mounding or myoedema) and were able, voluntarily, to induce rhythmic waves of contraction in certain muscles (muscle rippling or rolling). All had raised serum creatine kinase activity. Muscle biopsy in two members showed no specific abnormality. Experimental studies performed on excised intercostal muscle showed that abnormal "after-contractions" and increased sarcolemmal excitability could be demonstrated in vitro.

Action Potentials↗
PubMed1993

Modification of the transient outward current of rat atrial myocytes by metabolic inhibition and oxidant stress.

1. A putative function of the transient outward current (ITO) in cardiac myocytes is to modulate the shape of the action potential and, consequently, cardiac contractility. In addition, it has been suggested that this current may help protect against arrhythmias during periods of cardiac ischaemia. In our investigation of the possible anti-arrhythmic action of ITO, we have examined its response to metabolic inhibition and oxidant stress. 2. Whole-cell recordings were obtained from rat atrial myocytes using standard patch-clamp techniques. Inhibition of metabolism, using 10 mM 2-deoxy-D-glucose (2-DG) to block glycolysis with or without the addition of 2 mM cyanide to block oxidative phosphorylation, led to inhibition of ITO at a holding potential of -70 mV. Shifting the holding potential to -80 mV restored ITO, suggesting that metabolic inhibition had shifted the inactivation curve of ITO in a negative direction. 3. Quasi steady-state inactivation curves revealed a shift in ITO inactivation induced by complete metabolic inhibition with 2-DG and cyanide. Myocytes typically contracted shortly after the shift was observed. In the presence of Ruthenium Red, contraction was delayed and myocytes could undergo several exposures to the metabolic inhibitors, each time displaying a shift in ITO inactivation. The shifts ranged between -7 and -20 mV. 4. Recovery from inactivation was determined using a two-pulse protocol. The time constant of recovery at a holding potential of -80 mV reversibly shifted from 48 +/- 8 to 129 +/- 21 ms during metabolic inhibition (n = 4). 5. The activation of ITO from a holding potential of -100 mV shifted in a negative direction during metabolic inhibition, from a half-activation voltage of 0.3 +/- 3.0 to -14.7 +/- 2.5 mV (n = 5). Such a -15 mV shift increases the amplitude of ITO by approximately 30% at 0 mV. 6. A shift in ITO inactivation similar to that produced by metabolic inhibition could be shown when myocytes were subjected to oxidant stress induced by either 1 mM t-butyl hydroperoxide (TBHP) or the photoactivation of 100 nM Rose Bengal. Furthermore, an increase in pipette concentration of free Ca2+ from 20 to 200 nM also shifted ITO inactivation in a negative direction. 7. These results raise the possibility that the rise in intracellular [Ca2+] occurring during both metabolic inhibition and oxidant stress modifies activation and inactivation of ITO.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1988

Membrane channels and muscle disease.

Membrane channels so far characterized at the single channel level and their possible involvement in muscle dysfunction are reviewed. Experiments using isolated external intercostal muscle from a patient with Torbergsen syndrome and isolated rat muscles with chemically induced myotonia suggest further involvement of membrane channels in muscle disease. Both the presence of unusual channels and the absence of normal channels can confer properties on the sarcolemmal and sarcoplasmic reticular membranes which give rise to peculiar and distinctive defects in muscle behaviour.

Adult↗
PubMed1986

Ovine congenital progressive muscular dystrophy: clinical syndrome and distribution of lesions.

The distribution and severity of lesions in the skeletal muscles of 37 Merino sheep with congenital progressive muscular dystrophy (CPMD) are described. An explanation for the clinical signs is offered on the basis of functional defects in regional muscle groups. Lesions in the extensors of the hip, stifle and hock joints and flexors of the digits are primarily responsible for the progressive abnormality of hind limb gait that is characteristic of the clinical syndrome. Lesions in extensors of the elbow and flexors of the shoulder, carpus and digits affected fore limb function in advanced cases. The tendency for some affected sheep to develop ruminal tympany is probably caused by lesions in the diaphragmatic crus. Clinically affected sheep had higher resting and post-exercise concentrations of serum creatine phosphokinase and lactic dehydrogenase than unaffected control sheep. The rise in serum creatine phosphokinase after exercise was greater in affected sheep than in controls. Myotonia was not demonstrated in electromyographic studies in one sheep.

Animals↗
PubMed1981

The progression of Duchenne muscular dystrophy: clinical trial of allopurinol therapy.

A 12-month clinical study of Duchenne muscular dystrophy was carried out during a double-blind trial of allopurinol therapy. The disease was monitored by assessment of muscle power and function, pulmonary function tests, and electrocardiography. Biochemical assessments were made of plasma creatine kinase, pyruvate kinase, uric acid, and urinary excretion of 3-methylhistidine and creatinine. Allopurinol did not alter the progression of the disease.

Adolescent↗
PubMed1980

Chemically induced myotonia in amphibia.

Frogs and toads treated with high doses of anthracene-9-carboxylic acid (A-9-C) develop prolonged muscular contractions and 'divebomber' electromyograms characteristic of myotonia. Hitherto, myotonia has been considered peculiar to homeotherms where it is associated with several hereditable diseases and can be induced by specific treatments, most of which seem to act by decreasing membrane chloride conductance. Our work indicates that myotonia can be induced in amphibia by similar means. We offer possible reasons why others have missed seeing myotonia in amphibia.

Amphibians↗
PubMed1980

Myotonia as a side effect of diuretic action.

1. Commonly used loop diuretics produce side effects in man which are similar to chemically induced myotonia. These diuretics have structural affinity with known myotonic agents. 2. We have observed EMG myotonia in vivo in leg muscles of rats treated with intravenous frusemide. 3. In the presence of several different diuretics, rat isolated diaphragm, soleus and extensor digitorum longus muscles as well as frog sartorius muscles produce typically myotonic contractions with relaxation times up to several seconds. 4. Intracellular recording of action potentials from diuretic-treated muscles reveals long lasting after-discharges following a brief electrical stimulus, again typical of chemically induced myotonia. 5. Having demonstrated a myotonic action of several diuretics we suggest a need for caution in using these drugs in persons with hereditary myotonia and a need to be aware of possible provocation of myotonia in subclinical cases. Myopathies and neuropathies which are known to result from chronic exposure to myotonic agents also need to be considered. 6. In our study, the diuretic, acetazolamide, unmasked subthreshold myotonia. This seems to be at variance with reports of its usefulness in the treatment of myotonia. 7. Diuretics should probably not be employed in the treatment of herbicide intoxication where their myotonic activity would be expected to add to the known myotonic activity of the herbicide.

Animals↗
PubMed1975

Differences in action potentials and accommodation of sensory and motor myelinated nerve fibres as computed on the basis of voltage clamp data.

1. Voltage clamp experiments were performed on sensory and motor nerve fibres of the frog using a digital computer for automatic experiment control and data recording. 2. Rates of rise and maximum amplitudes of potassium currents were determined in both sensory and motor fibres, so that comparative values of n infinity and tau-n could be obtained. 3. The results indicate that the n infinity-V curve for sensory fibres is displaced from the curve for motor fibres in a depolarising direction. The potassium kinetics are similar in both for voltage steps up to about - 20 m V, beyond which tau-n becomes progressively smaller for sensory than for motor fibres. 4. These comparative values of n affinity and tau-n have been used to calculate alpha-n and beta-n values for a model "motor" action potential by considering the Frankenhaeuser-Huxley computed action potential to be "sensory". This modification of the potassium system, together with some alteration to the sodium inactivation system produces a satisfactory model "motor" action potential. 5. The model sensory and motor action potentials behave quite similarly to their experimentally recorded counterparts with respect to action potential shape and relative duration, repetitive firing, accomodation and the simulated action of T.E.A.

Action Potentials↗