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Biomedical subjects

M Deshimaru

Publications and source records attributed to M Deshimaru.

At least 37 records · Page 2Linked to original sources
PubMed1979

The effect of hyperthyroidism induced by thyroideum siccatum on the central nervous system: an electron microscopic study.

Ten adult male rats were administered orally with thyroideum siccatum every day to produce a hyperfunctional state of thyroid hormone. They were examined electron microscopically for the fine structure of the brain. Clinically, experimental rats lost in weight, manifested a hyperactive, irritative attitude, and were in an aggressive state. Electron microscopically, the nerve cells showed a slight increase in the number of mitochondria in the frontal cortex, spiral and petaloid variation of ER in the thalamus. The specific findings in the experimental rats were variations of synapse observed in the frontal and temporal cortex, gyrus hippocampi, and thalamus, centering around the hypothalamus. They included meandering of the presynaptic membrane, formation of vacuoles by the presynaptic membrane, saccate projection of this membrane to the postsynapse, and changes in vacuoles which were torn off and fell into the dendrite. These variations occurred in the synaptic membrane and ER, probably because synthesis of the membrane had been accelerated remarkably by the action of thyroid hormones. They were considered to have brought about abnormalities to the conductive and transmission system. They seemed to be closely related with emotional disturbances and psychic symptoms, since such variations were particularly apparent in the hypothalamus.

Aggression↗
PubMed1977

Mechanism of histopathological changes of nerve cells experimentally induced by chronic alcohol poisoning.

Experimental alcoholism was produced in rats by supplying them with 15% ethanol as the only source of liquid for a whole year. Histopathological examination revealed that Purkinje cells and granule cells in the cerebellum mainly showed such changes as decrease of ER, ribosomes and severe atrophy of the nerve cells. It might be speculated that these changes were caused by the disturbance of protein synthesis in the nerve cells induced by chronic alcohol effect.

Alcoholism↗
PubMed1977

Electron microscopic study of experimental thallotoxicosis.

To adult male rats 2 mg per rat of thallium acetate: CH3 COOT1 was given orally daily for six months. Clinically, the experimental rats revealed only alopecia and showed no neurological signs. Pathological findings were noted in muscle and cerebrum. Marked changes were observed in muscles and were as follows: swelling and vacuolation of mitochondria, destruction of cristae, ruptures of mitochondrial membranes, degeneration of sarcoplasmic reticulum and destruction of myofilaments. In the cerebrum, there were vacuolation of mitochondria, dilatation of Golgi cisterns in hypothalamus and thalamus. Sciatic nerve, liver and kidney were intact. From this, we consider that T1+ ions selectively affect the muscle and its mitochondria.

Animals↗
PubMed1977

[An autopsy case of head injury with a manic-depressive states (author's transl)].

M. M. a man aged 49. He suffered from a head injury at the aged of 41. At that time he lost consciousness for a few minutes and he was diagnosed as a consquassatio cerebri. The sequelaes of his head injury were a change of character and a disturbance of autonomic nerve function. The changes of character were decreased of activity, lie-down for all day, decrease of speech and depressive mode, and occasionally he was ill-humored, restless and irritative. Periodically he became euphoris, talkative and childisch. He had a disturbance of autonomic nerve function which became worse in parallel to the depressive states. We speculated that character changes, such as manic-depressive states and disturbances of autonomic nerve function were due to the bruising of the bilateral orbital surfaces of frontal lobes.

Bipolar Disorder↗
PubMed1976

Late changes in human sural nerves in Minamata disease and in nerves of rats with experimental organic mercury poisoning.

The sural nerves of 2 human cases with Minamata disease and poisoned rats were examined histopathologically. Both showed similar findings: the myelinated nerve fibres were decreased in number, but small myelinated nerve fibres were increased: The latter were irregular in shape and their Schwann cells showed regressive changes, with high electron density of the cytoplasms and many glycogen granules. Onion bulb formation was not found. According to fibre diameter histograms, the ratio of small myelinated nerve fibres of 2-5 mum showed a high percentage. A large number of the small myelinated nerve fibres were presumed to be regenerated nerve fibres. These findings are different from other peripheral neuropathies and may be characteristics of the late changes of the sural nerve induced by organic mercury compound.

Adolescent↗
PubMed1976

Neuro-Behcet's disease showing severe atrophy of the cerebrum.

A 38-year-old female died 6 years after the onset of what was, clinically and histopathologically, consistent with neuro-Behcet's disease. Pathologically the cerebrum showed severe atrophy. The main changes were observed in the grey and white matter, the diencephalon and the basal ganglia by light microscopy. All these changes originated in softenings around blood vessels, especially small vessels or capillaries. These foci fused together to form large regions of softening. Glial or mesenchymal reactions were minimal. In the white matter there was slight perivascular-infiltration, mainly consisting of lymphocytes. In view of these findings, it is suggested that these changes were caused by an allergic vasculitis. The present case of Neuro-Behcet's disease is the first one showing general atrophy of the cerebrum. It is very important in relation to demyelinating encephalitis.

Adult↗
PubMed1976

[Olivo-ponto-cerebellar atrophy with personality changes and slight disturbance of intelligence].

H. I., a housewife aged 55 years, began feeling a gait disturbance at 48 years old. After this she had incoordination of arms, dysarthria and tremor of hands. Aged 54 years, she could not stand up by herself. In addition to these neurological signs she had a change of character, such as losing control of herself, unreservedness and unceremoniousness, and slight disturbance of intelligence. She died at the age of 55 years about seven years after the onset. Histopathologically, noticeable changes were observed on the medulla oblongata, pons and cerebellum; the severe neuronal loss of the pontine nuclei and the olivary nuclei with demyelination and gliosis of the cerebellopetal fibers. Especially a great deal of lipofuscin granules in the nerve cells of the frontal and temporal lobe were observed. In the substantia nigra some pigmented cells were deleted. This case was diagnosed as olivo-ponto-cerebellar atrophy clinico-histopathologically. We discussed conserning the etiology of the changes of personality and slight disturbance of intelligence in relation to histopathological changes. It is speculated that the mental disorders are due to the degeneration of the nerve cells in the frontal and temporal lobes.

Atrophy↗
PubMed1976

[Histopathological findings of the nerve and muscles in familial primary amyloidosis, with special reference to the mechanism of amyloid fibril production].

T. I., a male aged 38, had a hereditary primary amyloidosis over four generation in his family history. He had peripheral neuropathy with dissociated sensory disturbances in the lower limbs, impotence, gastrointerstial dysfunction and orthostatic hypotention. N. suralis and M. quadriceps femoralis taken from him were examined by light and electron microscopy. N. suralis contained a lot of amyloids reacting with congo-red in the nerve fibres. Amyloid fibrils were remarkably observed around the blood vessels. They were continuous with the basement membrane of the endotherial cells. A few deposites were observed around the Schwann cell and fibroblasts. In M. quadriceps femoralis, amyloid like fibrils were noted in the perivascular spaces. Especially, a great deal of amyloid fibrils were continuous with the basement membranes. From this finding, it might be speculated that the basement membrane may play an important role in the production of amyloid fibrils.

Adult↗
PubMed1976

[Peripheral nerve disease associated with acute renal failure due to bromate poisoning].

A case of 21 year old male with neuropathy caused by renal insufficiency was present. He had taken bromate (mixed powder of potassium bromate and sodium bromate) for the purpose of suicide and suffered from acute renal insufficiency and hard of hearing. Renal dysfunction improved gradually by peritoneal dialysis and hemodialysis. However, on the 32th day after the onset, burning pain appeared in the bilateral feets. Following this, he began to complain of the disturbances of superficial and deep sensory below the ankle jerks and the weakness of his toes. Considering the clinical features, we supposed that the disturbance of the peripheral nerve was caused by uremia due to taking bromate. N. suralis was biopsied on the 80th day after the onset and examined electron microscopically. Electroscopical findings was as follows. Degeneration of the Schwann cells and irregularity or destruction of the myelin sheaths were observed. The axoplasm of the myelinated nerve fiber were relatively preserved as compared with the changes of the myelin sheaths. In the unmyelinated nerve fibers, cavity formations were observed. The findings of regeneration were not observed. From the electron microscopical findings, we speculate that the changes of the Schwann cells and the myelin sheaths are primary resulting from the disturbance of the metabolism of the Schwann cells. We speculate that anemia and hypoproteinemia caused by bromate disturbed regeneration.

Acute Kidney Injury↗