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Biomedical subjects

H Fukunaga

Publications and source records attributed to H Fukunaga.

At least 91 records · Page 5Linked to original sources
PubMed1985

Structure-activity relationship of bufotoxins and related compounds for the inhibition of Na+, K+ -adenosine triphosphatase.

Forty kinds of bufotoxins and related compounds were tested for inhibition of Na+, K+ -adenosine triphosphatase from guinea pig heart, and the structure-activity relationship has been discussed. The inhibitory activities of bufotoxins were dependent upon the dicarboxylic acid and amino acid components. The compounds having both the arginine and suberic acid moieties showed the higher inhibitory activities. The sulfates and glucuronides of cardiac steroids exhibited much less potency than the parent genins. The mode of inhibition was determined by means of the Dixon and Lineweaver-Burk plots.

Animals↗
PubMed1984

Intranuclear inclusions in muscle, nervous tissue, and adrenal gland.

A 30-year-old man had had chronic progressive wasting and weakness of muscles for 17 years. A muscle biopsy 5 years prior to death revealed myopathic changes were rimmed vacuoles and intranuclear inclusions which corresponded to "inclusion body myositis". At autopsy, intranuclear inclusions were observed in neurons, oligodendroglia, and in parenchymal cells of the adrenal medulla. Ultrastructurally, the inclusions in muscles, nervous tissue, and adrenal medulla were identical and consisted of abnormal tubulolinear structures measuring 10-20 nm in diameter. Similar inclusions have been reported in muscles with "inclusion body myositis" and in the nervous system with "neuronal intranuclear hyaline inclusion disease", respectively. Absence of clinical symptoms related to the CNS and adrenal gland, and well-preserved parenchymal cells in these organs of our patient suggest a benign nature of the disease except in the muscular system. Attempts to isolate a virus from the brain were fruitless . This patient may serve to connect both diseases in muscles and the nervous system, and to disclose the etiology of these inclusions.

Adrenal Glands↗
PubMed1984

Alzheimer's disease with widespread presence of Lewy bodies.

Progressive mental deterioration associated with parkinsonism was observed in a 68-year-old patient in the senile period. Pathologically, evidence of senile changes was obtained consisting of degeneration of the neurons and numerous senile plaques with classical and perivascular types. Further, neuronal degeneration in the form of Lewy bodies was evidently observed in the hypothalamus, substantia nigra et innominata, locus caeruleus of the vagus nerve, some nuclei in the reticular formation of the brainstem and neurons in the cerebral cortex. The clinical and pathological manifestations were those of Alzheimer's disease and Parkinson's disease. It is suggested that some common etiological factors may cause those lesions as Alzheimer's disease and Parkinson's disease.

Aged↗
PubMed1983

Passive transfer of Lambert-Eaton myasthenic syndrome with IgG from man to mouse depletes the presynaptic membrane active zones.

In the Lambert-Eaton myasthenic syndrome (LEMS), there is a decreased release of acetylcholine quanta from the nerve terminal by nerve impulse. Recently, an autoimmune origin of LEMS was documented by passive transfer of its electrophysiologic features from man to mouse with IgG. Freeze-fracture electron microscopy of LEMS neuromuscular junctions has revealed a paucity of presynaptic membrane active zones. Thus, the active zones might be the targets of the pathogenic autoantibodies in LEMS. To test this assumption, freeze-fracture electron microscopic studies were done in mice injected with 10 mg of IgG daily from each of three LEMS patients and in control mice treated with normal human IgG or no IgG. IgG from patients 1 and 2 impaired neuromuscular transmission in mice, but IgG from patient 3 failed to do so. After 52-69 days of treatment, diaphragm or anterior tibial muscles were removed and coded. Paired muscles from control mice and mice receiving LEMS IgG were studied "blindly." Satisfactory freeze-fracture replicas of 185 presynaptic membrane P-faces were analyzed by stereometric methods. In mice treated with LEMS IgG that was pathogenic by electrophysiologic criteria, there was a selective depletion of active zones and active-zone particles but not of other membrane particles and there was a concomitant increase of large membrane particles aggregated into clusters. These findings provide additional evidence that the active zones facilitate quantal transmitter release by nerve impulse, lend further support to the assumption that the active-zone particles are Ca2+ channels, and establish mediation of the membrane lesions in LEMS by IgG.

Action Potentials↗
PubMed1983

Parkinson's disease of post-encephalitic type following general paresis--an autopsied case.

A clinico-pathological report is given of a case of Parkinson's disease following a general paresis. A 66-year-old male, with no previous history of febrile disease or viral encephalitides, developed a dementing illness. The general paresis was diagnosed from serological studies at the age of 45. He underwent a series of penicillin plus fever therapies as treatment for neurosyphilis. He also developed generalized rigidity and slow mobility 12 years after the diagnosis of general paresis. An anti-Parkinson drug was given. Finally he fell in a state of muteness and became bedridden. He had been hospitalized for 21 years and died from bronchopneumonia. The pathological findings were strikingly similar to post-encephalitic parkinsonism in addition to a healed state of general paresis. They consisted of a widespread nerve cells loss, gliosis and the presence of Alzheimer's neurofibrillary tangles in the substantia nigra. In the cerebral cortex, a diffuse loss of nerve cells and the presence of a weak positive iron reaction were observed. The coexistence of general paresis and post-encephalitic parkinsonism is unusual and the authors discussed the etiological relationship between the two different conditions.

Aged↗
PubMed1980

A case of nemaline myopathy with ophthalmoplegia and mitochondrial abnormalities.

A case of nemaline myopathy with ophthalmoplegia is reported. The patient was a 35-year-old man born of consanguineous parents. He had a myopathic face, high-arched palate, nasal voice, scoliosis, very thin trunk and marked muscle weakness involving face, neck, limbs and trunk. He also had ptotis of the left eyelid and mild bilateral ophthalmoplegia, also detected by electrooculogram. Biopsy of gastrocnemius muscle revealed nemaline rods. At the ultrastructural level, the rods appeared to have axial and cross striations, and in cross-sections at high magnification they seemed to have a crystal lattice structure. Intranuclear rods were also observed. In addition to the rods, abnormal mitochondria including a number of paracrystalline inclusions were seen.

Adult↗
PubMed1979

Dectection of spinal cord lesion using skin electrode recordings of spinal evoked potential.

The multi-channel recording of somatosensory spinal evoked potential (SSEP) was carried out on 30 patients with various neurological disorders. In some cases, SSEP changes corresponded well with the lesioned level. In general, the lesions of thoraco-cervical level were difficult to detect, because the appearance rate of SSEP peaks are reduced over the thoraco-cervical spine even in normal controls. In cases with spinal type of MS, SSEP revealed marked changes and subclinical sensory demyelinating lesions were detectable. Chronological SSEP recording in patients with acute transverse myelitis revealed functional improvements corresponding with clinical recovery. Surface and non-invasive SSEP recording is useful for detecting lesions in the spinal cord or peripheral nerves. It also offers valuable information about chronological modification of the lesions, and may reveal subclinical changes in certain neurological disorders.

Adolescent↗