Search PubMed⌕ Search

Biomedical subjects

H Miyano

Publications and source records attributed to H Miyano.

At least 73 records · Page 4Linked to original sources
PubMed1981

Frequency analysis of surface EMG to evaluation of muscle fatigue.

A theory concerning the spectral density of surface electromyogram (EMG) in isometric contraction is described and herein, a conduction velocity measure, which was derived from a surface EMG model, is suggested. In order to confirm the validity of this measure, the spectral modification with respect to muscle fatigue is studied experimentally. The EMG signals were obtained from the biceps brachii and the rectus femoris in four subjects. The spectral modification shifted to a lower frequency as fatigue developed. The conduction velocity measure decreased linearly in both the biceps brachii and rectus femoris, but this tendency was more pronounced in the biceps. It is suggested that the spectral shift was concerned with conduction velocity of action potential along the muscle fibres. From these experimental results, we believe that we are justified in claiming that our conduction velocity measure is a useful index to estimate motor function.

Action Potentials↗
PubMed1979

Theoretical analysis of surface EMG in voluntary isometric contraction.

A new stochastic model of the surface EMG is suggested and the spectral density of the surface EMG is studied theoretically and experimentally to confirm the validity of this model. Theoretical results show that while the contraction level is not so high, the shape of the spectral density (distribution) does not change and its amplitude is directly proportional to the motor unit firing frequency and recruitment. To illustrate the theoretical results, experiments were carried out for rectus femoris and biceps brachii. The surface EMG was lead off by bipolar surface electrodes. And the spectral density of the surface EMG was calculated using FFT algorithm. From these experimental results, it was confirmed that our theoretical results were almost valid.

Electromyography↗
PubMed1976

Specific action of 4-nitropyridine 1-oxide on Excherichia coli K-12 pro+ strains leading to the isolation of proline-requiring mutants: isolation and characterization of pro-mutants.

A specific action of 4-nitropyridine 1-oxide on Escherichia coli K-12 Pro(+) strains leading to highly efficient, selective isolation of Pro(-) mutants is described. Incubation of Pro(+) cells with a sublethal concentration of 4-nitropyridine 1-oxide in Penassay broth gave Pro(-) mutants, which lacked either the biosynthetic pathway of proline from glutamic acid to glutamyl gamma-phosphate (proB(-)) or the pathway from glutamyl gamma-phosphate to glutamic gamma-semialdehyde (proA(-)) or both. Pro(-) mutants, which have the metabolic block between Delta(1) pyrroline-5-carboxylate (the cyclized dehydration product of glutamic gamma-semialdehyde) and proline (proC(-)) were not found among survivors. Treatment of Pro(+) cells with N-methyl-N'-nitro-N-nitrosoguanidine led to isolation of all three types of Pro(-) mutants, suggesting that the action of 4-nitropyridine 1-oxide on Pro(+) cells is apparently distinct from the action of N-methyl-N'-nitro-N-nitrosoguanidine. F-duction and interrupted mating experiments led to determination of the correlation between proline loci and the biosynthetic pathway of proline from glutamic acid.

Culture Media↗
PubMed1976

Specific action of 4-nitropyridine 1-oxide on Escherichia coli K-12 Pro+ strains leading to the isolation of proline-requiring mutants: mechanism of action of 4-nitropyridine 1-oxide.

Possible mechanisms involved in the action of 4-nitropyridine 1-oxide (4NPO) on Escherichia coli K-12 pro(+) cells in Penassay broth leading to the selective isolation of proA(-) and/or proB(-) mutants but not proC(-) mutant were studied. Reconstruction experiments between pro(+) and pro(-) cells, together with experiments on the bactericidal action of 4NPO on pro(+) and pro(-) cells, indicated that 4NPO is more toxic for pro(+) and proC(-) cells than for proA(-) and proB(-) cells. These results, coupled with data indicating little mutagenicity of 4NPO on E. coli cells, led us to conclude that the selection of proA(-) and/or proB(-) cells that arose spontaneously in the pro(+) culture is a possible mechanism for the action of 4NPO. Examination of 4NPO sensitivity of pro(+) transductants derived from proA(-) and proB(-) cells with P1 vir phage and pro(+) cells as donor and of pro(+) spontaneous revertants derived from those pro(-) cells suggested that 4NPO-sensitive gene(s) should be on, or very close to, the proA and proB loci and that both products of proA and proB genes may be involved in the sensitivity of bacteria to 4NPO. The fact that the 4NPO-sensitive allele is dominant over the 4NPO-resistant allele further indicated the possible correlation between gene products of proA and proB and the 4NPO sensitivity of bacteria. Experiments on metabolic conversion of 4NPO with bacterial cells proved that the major metabolic pathway of the agent is reduction to (possibly via 4-nitroso-) 4-hydroxylamino- and 4-amino-pyridine 1-oxides, and then to 4-aminopyridine. Investigation of the effect of structural modification of 4NPO on the elective selection of Pro(-) mutants in Pro(+) culture further suggested that the structural feature indispensable for the action of the agent is the hydroxyl-amino or its more oxidized state at the 4 position and the N-oxide moiety at the 1 position on the pyridine skeleton. Action of 4NPO in minimal medium was found to be bacteriostatic on pro(+) cells but not on pro(-) cells, leading to the formation of long nonseptate multinucleate filament cells on pro(+) cells. Possible biochemical mechanisms of the selective toxicity of 4NPO for pro(+) and pro(-) cells are discussed.

Escherichia coli↗
PubMed1972

[Stroke care units].

Explore the source record for details and available documents.

Cerebrovascular Disorders↗
PubMed1971

[Big medicine].

Explore the source record for details and available documents.

Nuclear Medicine↗