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Biomedical subjects

M Tsujihata

Publications and source records attributed to M Tsujihata.

At least 127 records · Page 7Linked to original sources
PubMed1983

Fatal neonatal nemaline myopathy: a case report.

A fatal neonatal nemaline myopathy in a Japanese girl was described. The patient was hypotonic at birth and failed to establish effective respiration. Rod-like structures were observed within a variety of skeletal muscles, particularly in the diaphragm. This is the first case of fatal neonatal nemaline myopathy in which many satellite cells were observed.

Biopsy↗
PubMed1983

Myasthenia gravis associated with Satoyoshi syndrome: muscle cramps, alopecia, and diarrhea.

We studied a woman who had evidence of myasthenia gravis at age 17. At age 19, she gradually developed alopecia and painful muscle spasms (Satoyoshi disease). Deposition of immune complexes (IgG, C3, and C9) was demonstrated at the motor endplates of limb muscle (biceps brachii); primary synaptic clefts were widened, and postsynaptic folds were simplified. This is the first case of myasthenia and Satoyoshi disease in the same patient.

Adult↗
PubMed1982

Fatal neonatal nemaline myopathy.

Nemaline myopathy was first reported in 1963 and has been considered to be a congenital, non-progressive myopathy with weakness since birth. However, severe forms leading to death in infancy have been rarely reported. Recently we necropsied a female infant with fatal neonatal nemaline myopathy who required mechanical ventilatory support immediately following delivery. She had suffered from recurrent pneumonia and died at five months of age. Light and electron microscopic studies on both muscle biopsy and autopsy specimens were diagnostic of nemaline myopathy. Characteristic rod-like structures were demonstrated within skeletal muscles, and accumulations of thin filaments were seen in numerous muscle fibers. The origin of these structures in the Z-disks and other morphologic features were the same as those of the rods occurring in congenital cases of rod myopathy. No involvement was observed in the cardiac muscle or in the smooth muscle of the gastrointestinal tract. It is likely that involvement of the skeletal muscles of the pharyngeal areas, intercostal spaces, and diaphragm might have contributed to the difficulty in swallowing and respiratory distress.

Abnormalities, Multiple↗
PubMed1981

Pharmacophysiological study on muscle treated with calcium ionophore A23187.

Muscle treated with A23187, which raises intracellular free Ca2+ concentration, was studied to elucidate effects on membrane properties. The mean resting membrane potential was reduced; it was normally depolarized by ouabain but not significantly hyperpolarized by epinephrine and insulin. In the presence of ouabain, membrane depolarization was not provoked by insulin. The results imply a defect of active Na+-transport of the membrane after exposure to a calcium ionophore.

Animals↗
PubMed1981

Effects of long-term administration of ambenonium chloride on motor end-plate fine structure and acetylcholine receptor in rat.

Ambenonium chloride was administered orally in a dosage of 6 mg/kg/day to rats for 14-360 days. Motor end-plate fine structure and junctional AChR were quantitatively analyzed and red (soleus) and white (EDL) muscle fibers. In treated animals, degeneration and simplification of postsynaptic folds and widening of synaptic clefts were often observed in soleus end-plates, but infrequently in EDL end-plates. On the other hand, the postsynaptic AChR was reduced markedly in both soleus and EDL end-plates. No presynaptic changes were observed. These results show that long-term administration of Anti-ChE agents in myasthenia gravis may have an adverse effect on neuromuscular transmission.

Ambenonium Chloride↗
PubMed1981

Contractile and chemosensitive properties of muscle treated with calcium ionophore A23187. Comparison with dystrophic muscle.

Rat diaphragms were treated with calcium ionophore, A23187, for 60 min at 37 degrees C, and twitch, tetanus and their derivatives were studied on the basis of the active state concept. Results were than compared with those of human dystrophic muscle. Like dystrophic muscle, maximum tetanic force and maximum velocity of tetanus development were markedly reduced. Changes in twitch parameters, which tend to appear in an early stage of muscular dystrophy, were not noted after the treatment with this ionophore, except alterations relating to prolongation of the active state. Twitch/tetanus ratio was thus increased, while it was decreased in dystrophic muscle. Isoproterenol-induced change of twitch was normally seen in the A23187-treated muscle, while dystrophic muscle responded to catecholamine in a manner different from control. Therefore, the muscle treated with calcium ionophore is not wholly similar to dystrophic muscle.

Animals↗