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Biomedical subjects

M Tsujihata

Publications and source records attributed to M Tsujihata.

At least 109 records · Page 6Linked to original sources
PubMed1988

Role of the macrophage in the pathogenesis of experimental autoimmune myasthenia gravis.

To clarify the role of Ia antigen positive macrophages which invade motor end-plates in the induction of the chronic phase, experimental autoimmune myasthenia gravis (EAMG) rats were injected intraperitoneally with silica dust on day 6 after immunization. Silica injection partially inhibited the invasion of motor end-plates with macrophages as compared with a saline injection. The titer of antibodies to the Narke acetylcholine receptor (AChR) in the chronic phase did not differ in either the saline or the silica groups, while the titer of antibodies to rat-AChR (non-crossreactive antibodies) was lower in the silica group than in the saline group. The silica group survived longer than the saline group. These results suggest that Ia antigen positive macrophages in the acute phase act as antigen-presenting cells and play an important role in the production of antibodies to self-AChR in the chronic phase.

Animals↗
PubMed1987

Ultrastructural study of the motor end-plate in botulism and Lambert-Eaton myasthenic syndrome.

The motor end-plate fine structure was studied in 3 patients with type A botulism and compared with that in 4 patients with Lambert-Eaton myasthenic syndrome (LES). In the botulism cases a biopsy of the biceps brachii muscle was performed at the chronic stage. The skeletal muscle showed a neurogenic change. The nerve terminal area had decreased and the postsynaptic regions had been denuded of their nerve terminals in 16% of the regions (9.8% in control). No highly simplified postsynaptic regions were observed. The findings are consistent with those observed at the motor end-plates in motoneuron diseases. By contrast, in LES no changes were observed in the presynaptic region. In the postsynaptic region, the postsynaptic membrane length and membrane density decreased and hypertrophy of the junctional folds was not observed.

Action Potentials↗
PubMed1986

Ultrastructural study of the effect of calcium ionophore, A23187, on rat muscle.

The present study was undertaken to investigate changes in the muscle fiber when treated with calcium ionophore. Muscles treated with ionophore showed disruption of the plasma membrane of the muscle fiber, delta lesions, marked contraction of the myofibrills, and dissolution of Z lines and I bands. Black granules of calcium pyroantimonate were observed inside the plasma membrane in ionophore-treated muscle fibers without alteration of the other muscle organelles. The density of the intramembranous particles was less in muscle treated with calcium ionophore than in the control muscle. These results support the previous hypothesis that the increased concentration of intracellular calcium activates calcium-activated neutral protease and induces necrosis of the myofiber. The mechanism for the decrease in the density of intramembranous particles is unsolved. However, the disruption of the plasma membrane may not be a direct effect of calcium ionophore on it, but a secondary phenomenon which occurs after the calcium-induced necrosis of the muscle fibers.

Animals↗
PubMed1986

A new method of detection of islet cell antibodies (ICA) using peroxidase-labeled protein A, and incidence of ICA in type 1 (insulin-dependent) diabetes.

We have developed a new method of detecting islet cell antibodies using peroxidase-labeled protein A, and have determined the incidence of ICA in Type 1 (insulin-dependent) diabetes in Japan. In our method, fresh frozen sections of human pancreas and serum samples were incubated and then treated with peroxidase-labeled protein A at room temperature. Conjugates of peroxidase and protein A were subjected to Sephadex G-200 column chromatography, and only the 80,000 dalton peak was employed. The treated sections were allowed to react with haematoxylin and eosin (HE) to confirm the localization of islet cells. With this method, human pancreatic tissues can be used regardless of age and blood type, and the stained sections can be stored for more than 5 years. Serum samples obtained from 52 patients with Type 1 diabetes, 54 with Type 2 (non-insulin-dependent) diabetes and 100 control subjects were examined. In patients with Type 1 diabetes, islet cell antibodies were detected in 14 of 14 (0.5 years after onset), 3 of 6 (0.5-1 years after onset), 7 of 16 (1-5 years after onset) and 2 of 16 (more than 5 years after onset). In contrast, only 4 of 54 patients with Type 2 diabetes and none of the controls were ICA positive. It is concluded that, with our newly developed method using peroxidase-labeled protein A, ICA is present in all Japanese Type 1 diabetic patients whose diabetic manifestations are less than 0.5 years duration from onset.

Adult↗
PubMed1985

[A family of von Recklinghausen's neurofibromatosis complicated by mononeuritis multiplex, bilateral acoustic neurinomas, and falx and spinal meningiomas].

A family of von Recklinghausen's disease complicated by multiple diverse primary brain tumors was reported. Case 1. The proband, born in 1923, was admitted to the Nagasaki University Hospital on March 11, 1974, for evaluation of headache and hearing loss. Neurological examination disclosed: decreased visual acuity on the right: bilateral choked discs; anisocoria, right pupil wider than left; right blepharoptosis; artificially fixed right eye; right facial palsy; markedly impaired hearing with negative vestibular responses to caloric test; paralysis of the right soft palate and vocal cord; atrophy of the right side of the tongue; right claw hand with positive Froment's sign; left drop foot; loss of deep reflexes on the left arm and legs; positive Babinski on the right. Nerve conduction studies revealed failure to evoke muscle action potential in response to electric nerve stimulation on the left ulnar and right superficial peroneal nerves. Needle electromyography showed no motor unit potentials in the left first dorsal interosseus and right anterior tibial muscles. Sensory nerve action potentials could not be evoked on any nerves tested. X-ray films showed enlargement of the internal auditory passages, falx tumor on brain scan and carotid angiography, and spinal tumor on myelography. At craniotomy, a 7 X 5.5 X 4 cm falx meningioma was removed. At suboccipital craniotomy performed five weeks later, right acoustic neurinoma measuring 1.5 cm in diameter was removed. Case 2. This relative, born in 1945, was the son of the proband. A spinal meningioma at C 7-T 1 was removed in 1957. However, he could not walk after operation and died of pneumonia two years later.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Adult type beta-galactosidase and neuraminidase deficiency in three siblings.

In recent years, there have been described a number of patients with beta-galactosidase and neuraminidase deficiency of juvenile onset. The clinical features in these patients are myoclonus, cherry-red spots, insidious visual loss, corneal clouding, gargoyle like appearance and ataxia. The condition appears to be transmitted as an autosomal recessive trait. Pathologically it has been characterized that there are vacuolation of lymphocytes, and inclusion bodies such as concentric membranous bodies in the ganglion cells of the rectum. Here we report a patient with beta-galactosidase and neuraminidase deficiency of juvenile onset in whom unusual "fingerprint" profiles were obtained in the submucosal ganglion cells in the rectum and will discuss the clinical significance of the inclusion bodies.

Humans↗
PubMed1984

[A case of spongiform encephalopathy with ataxia and amyloid plaques].

CASE: A 63-year-old man was admitted to our hospital because of gait disturbance. His daughter died of the same disorder at age 29. In 1974, at age 59, the patient noticed mild recent memory disturbance and clumsiness in handwriting. In 1976, his gait was markedly unstable, but he could walk without assistance, and his speech became dysarthric. In spring, 1977, he was unable to walk without assistance. From Jan. 9, 1978, through Feb. 14, 1978, he was hospitalized in our hospital. Neurological examination revealed an ataxic gait and scanning speech. Deep tendon reflexes of the upper extremities and ankle jerks were normal, but knee jerks were absent. Pathological reflexes were not elicited. Both superficial and deep sensations were normal. He was alert and showed no overt dementia. Laboratory data including CSF, EEG and brain CT were normal except positive TPHA in serum. Thereafter, he was followed up with the diagnosis of spinocerebellar degeneration. In 1979, he developed a limb ataxia. In spring, 1980, he became very irritable and was easily excited. He gradually developed dementia and urinary incontinence. In 1981, his illness progressed to an akinetic mutism and died of pneumonia on July 19, 1981. Myoclonus and periodic synchronous discharges in EEG were not observed until his death. The brain was 1,075 g in weight after formalin fixation and the cerebrum was generally soft. The gyri showed no evidence of abnormalities or atrophy, while the cerebellum and brain stem, especially the pons, were atrophic. The arterial and venous systems showed no remarkable changes. The spinal cord was externally unremarkable. The ventricles were dilated.(ABSTRACT TRUNCATED AT 250 WORDS)

Akinetic Mutism↗