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Biomedical subjects

E Satoyoshi

Publications and source records attributed to E Satoyoshi.

At least 19 recordsLinked to original sources
PubMed1992

Therapeutic trials on progressive muscular dystrophy.

The special medical care in the National Sanatorium prolonged the life span of the patients with progressive muscular dystrophy from 15.8 years to 20.4 years over the last 20 years. Various new drug trials for muscular dystrophy have been implemented in the last 12 years in Japan. Bestatin and Loxistatin, protease inhibitors, showed definite improvement on dystrophic mice or hamsters, animal models of muscular dystrophy. However clinical application of these drugs failed to prove the effects on patients with Duchenne muscular dystrophy. The difficulty of clinical evaluation and judgement of effects in progressive neurological diseases is discussed.

Animals↗
PubMed1992

[Divergence paralysis due to a lesion of the lateral tegmentum of the midbrain caused by thalamic hemorrhage].

A 66-year-old diabetic and hypertensive man suddenly developed right hemiplegia. Examination revealed right hemiplegia including his face, vertical gaze palsy, and divergence paralysis. The cranial CT scan disclosed a left thalamic hemorrhage as large as 40 mm in diameter, which extended to the midbrain. He was treated medically and his divergence paralysis improved. But all other symptoms remained for the next 11 months and he eventually died of acute retroperitoneal hemorrhage. The autopsy revealed spongy state and gliosis extending from the left thalamic nuclei to the left midbrain. In the tegmentum, dorsolateral part around the left oculomotor nucleus was involved. The precise location of the human divergence center of the eyes is still unknown. According to previous reports, the divergence center may locate in the tegmentum of the midbrain or pons. Recently, animal experiments detected the neurons which fire for divergent in the mesencephalic reticular formation just dorsal and lateral to the oculomotor nuclei. Our case had a lesion of gliosis and spongy state, namely the old hematoma, in the same portion. Therefore, we considered that the human divergence center of the eyes might exist in the lateral tegmentum of the midbrain, just lateral and dorsal to the oculomotor nucleus.

Aged↗
PubMed1990

1-[11C]pyruvate turnover in brain and muscle of patients with mitochondrial encephalomyopathy. A study with positron emission tomography (PET).

We examined pyruvate turnover using 1-[11C]pyruvate in the brain and epicranial muscle of 6 patients with mitochondrial encephalomyopathy (MEM), diagnosed by muscle biopsy and mitochondrial enzyme assay. The radioactivity was measured by positron emission tomography (PET). The time-activity curve for 11C in both brain and muscle generated after i.v. injection of 1-[11C]pyruvate consisted of 2 components in normal subjects and patients, i.e. a fast and a slow component which were assumed to represent the aerobic (mitochondrial) and anaerobic (glycolytic) metabolism of pyruvate, respectively. In the brain and muscle of patients, the aerobic component was smaller and the anaerobic larger than in normals. The extent of this abnormality seemed to reflect the severity of the disease. The same slight abnormality for [11C]pyruvate turnover was also observed in the brain of MEM patients who were without cerebral symptoms. Cerebral blood flow (CBF) and cerebral oxygen consumption (CMRO2) of most patients were lower than those of normals, and the oxygen extraction fraction (OEF) was decreased in many patients.

Adult↗
PubMed1990

Distal myopathy.

Various types of the distal myopathy except Welander's late distal myopathy of Swedish type were described. There were many reports in the past concerning the varieties of the distal myopathy. Distal myopathy is a rather rare disorder and it may be difficult to diagnose these cases. Among these various distal myopathy, an emphasis was made upon the clinical and pathological characteristics of the diseases, particularly distal muscular dystrophy of Miyoshi, Distal myopathy with rimmed vacuole formation of Nonaka and ours, and Oculo-pharyngo-distal myopathy. All these diseases show the distal muscle involvement but the clinical features, heredity, course and pathological features are quite different, and prognosis is also different. Accordingly when we examined these distal myopathy cases, clinical characteristics and histo-pathological findings should be carefully studied. It should be also emphasized that the level of serum CPK dose not indicate the severity of the myopathy. In muscular dystrophy or myositis, serUm CPK elevates remarkably and we can consider the level of CPK as a sign of the severity or condition of the disease. However, in myopathy as "rimmed vacuole distal myopathy" serum CPK remains in normal level even though weakness is severe. This is due to absence of the membrane abnormalities of muscle cells. Leakage of the CPK from muscle cells, therefore, does not reflect the degree of the cell destruction. In this point we have to remember the fact that serum CPK is not a indicator of all muscle diseases and even if the CPK is normal, we have to consider the presence of myopathy.

Adolescent↗
PubMed1989

Catecholamines increase nerve growth factor mRNA content in both mouse astroglial cells and fibroblast cells.

Previous studies have shown that catecholamines increase the nerve growth factor (NGF) content in medium conditioned by mouse L-M fibroblast cells and mouse astroglial cells. In this study, the NGF mRNA levels in these cells were measured by Northern blot analysis. In astroglial cells treated with epinephrine (EN), the cellular NGF mRNA level increased prior to accumulation of NGF in the culture medium. 3-Hydroxytyramine (DA) and norepinephrine (NE) also increased the cellular NGF mRNA content. An increased level of NGF mRNA elicited by EN was also observed in mouse L-M cells. These results indicate that catecholamines enhance NGF synthesis of L-M fibroblast cells and astroglial cells by increasing the cellular content of NGF mRNA. The present results also indicate that the effects of catecholamines are not mediated by adrenergic receptors.

Albuterol↗
PubMed1989

Positron emission tomography using pyruvate-1-11C in two cases of mitochondrial encephalomyopathy.

Positron emission tomography (PET) using pyruvate-1-11C was carried out to investigate the in vivo metabolism of pyruvate in the brains of patients with mitochondrial encephalomyopathy and Leigh's disease. Two epileptic patients were studied as control subjects. Radioactivity was eliminated from the brain tissue of the epileptic patients soon after injection of pyruvate-1-11C. PET images of mitochondrial encephalomyopathy patients showed an increase in radioactivity in the cerebral cortex, basal ganglia and thalamus, with elimination of radioactivity being slower than that of epileptic patients. One patient with Leigh's disease showed similar PET images. PET using pyruvate-1-11C is useful for the evaluation of mitochondrial energy metabolism in the brain.

Brain Diseases↗
PubMed1989

Neurotoxicity of human eosinophils towards peripheral nerves.

The toxicity of eosinophils towards peripheral nerves was examined using cultures of posterior ganglion cells from chick embryos. Eosinophils were also derived from a patient with significant "hyper-eosinophilia", peripheral neuropathy, bronchial asthma, myocardial damage and skin involvement. A sural nerve biopsy showed a severe to almost complete loss of myelinated fibers without pathological changes suggesting necrotizing vasculitis. Surviving neurons in a culture containing the patient's eosinophils or serum were markedly decreased in number as compared with those in normal subjects. These results support the possibility that the peripheral neuropathy in the patient caused by toxic agents derived from eosinophils.

Adult↗
PubMed1989

Distal myopathy with rimmed vacuole formation. A follow-up study.

A long-term follow-up study of patients with familial distal myopathy with rimmed vacuole formation and a review of the literature indicates that the prognosis of the disorder was extremely poor as to daily life. Although the initial symptom appearing in early adulthood was muscular wasting and weakness in the legs, especially the distal muscles, severe generalized skeletal muscle involvement with sparing of the facial, extraocular, bulbar, intercostal and diaphragm muscles was recognized in the advanced stage. The disease is probably inherited as an autosomal recessive trait, while there is a considerable female preponderance, the female-to-male ratio being 2:1. The disorder is distinguishable from various types of distal myopathy on the basis of clinical and pathological findings, and other myopathies with rimmed vacuole formation, including inclusion body myositis, from a prognostic viewpoint.

Adult↗
PubMed1989

[Two cases of mitochondrial myopathy (focal cytochrome c oxidase deficiency), long-term follow-up on a diagnosis of ocular type myasthenia gravis].

Two patients (a 50-year-old and a 35-year-old men) with focal cytochrome c oxidase deficiency, manifesting ptosis and external ophthalmoplegia of 13 and 6 years' duration, respectively, were reported. Patient 1 (a 50-year-old male) had also slight muscular weakness of the proximal limb and neck flexor muscles. Diagnosis of myasthenia gravis had been made on the clinical findings including ptosis and external ophthalmoplegia, diurnal fluctuation of symptoms, and equivocal positive Tensilon test. However, waning phenomenon on repetitive nerve stimulation or elevation of titer of the anti-acetylcholine receptor antibody was not detected on both patients. Needle EMG showed mild myopathic changes. Finally, pathological and biochemical analyses of the biopsied muscles confirmed the diagnosis of mitochondrial myopathy (focal cytochrome c oxidase deficiency).

Adult↗
PubMed1989

[A case of symptomatic adrenoleukodystrophy heterozygote manifested by spastic paraparesis of late onset].

A case of symptomatic adrenoleukodystrophy (ALD) heterozygote, manifested by spastic paraparesis, was reported. The patient's 9 year-old grandson had ALD, and her 34 year-old daughter, who was the mother of the case of ALD, was asymptomatic but accompanied by elevation of serum very long chain fatty acid (VLCFA). The patient's gait disturbance appeared at age 62 and that gradually worsened. On admission, she showed spasticity on the lower limbs with bilateral Babinski's reflexes, muscle weakness of the lower limbs and interossei muscles of the hand, and mild sensory disturbance on the distal part of all limbs. Serum VLCFA was markedly elevated. There was no abnormal adrenal function. Sensory and motor nerve conduction velocities were within normal limits. A needle EMG examination disclosed long-duration and high-amplitude potentials. Auditory brainstem response (ABR) revealed elongation of III-V wave intervals bilaterally, and somatosensory evoked potential (SEP) showed delayed N20. Brain CT scan revealed no abnormality but MRI (T2 weighted image) showed mild high intensity areas in the capsula interna and cerebral peduncles. The abnormality of MRI suspected that spastic paraparesis may result from involvement of the corticospinal tract of the cerebrum or brainstem though the symptom has been considered due to the lesion of the spinal cord. Examinations of ABR, SEP and MRI were useful methods to make a diagnosis of symptomatic ALD heterozygote.

Adrenoleukodystrophy↗
PubMed1989

[Positron emission tomography in two cases of transient global amnesia].

We encountered two cases of typical transient global amnesia (a 53-year-old woman and a 50-year-old man). Both cases showed no evidence of abnormal findings which caused the attack on examinations of CSF, EEG, brain CT, brain MRI and cerebral angiography. Examinations of positron emission tomography, using 15O labeled CO2 and O2, were performed on 14 and 8 days after the attack in the female and male cases, respectively, and those disclosed decreased regional blood flow (CBF), increased oxygen extraction ratio (OER), and decreased oxygen metabolic ratio (CMRO2) in the bilateral medial temporal and occipital lobes, which were supplied by the bilateral posterior cerebral arteries. PET, performed on about one month after the attack, revealed normalized values of CBF, OER, CMRO2 in both cases. These findings strongly suggested that transient global amnesia in our cases may be related to ischemia of the bilateral posterior cerebral arteries.

Amnesia↗
PubMed1988

Antibodies against saline-soluble components of skeletal muscle in myasthenia gravis.

Antibodies against phosphate-buffered-saline extracts (SE) of non-acetylcholine receptor (AChR) skeletal muscle antigens were found in patients with myasthenia gravis (MG). The antigenicity of SE was distributed in three fractions with molecular masses of over 200 kDa, 90-150 kDa and 7-14 kDa on gel filtration. These fractions shared common antigenicities. Further analysis of 90-150 kDa fractions on sodium dodecyl sulphate polyacrylamide gel electrophoresis showed five major bands, ranging from 105 kDa to 275 kDa. The antibodies against SE were detected in 52% (58/112) of the MG patients; incidence and titres were higher in the thymoma group (n = 21; 90% and 0.872 respectively) than in the non-thymoma group (n = 91; 43% and 0.200, P less than 0.001). In patients without a thymoma, these antibodies were frequently observed in late-onset disease and the severe generalized form (P less than 0.01). In 4 of 7 ocular MG patients without anti-AChR antibodies, low but appreciable levels of anti-SE antibodies were found. In 73% (11/15) of generalized MG patients treated with prednisolone and thymectomy, anti-SE antibody titres changed in association with those of anti-AChR antibodies and with the clinical course. Both antibody titres increased synchronously in patients who developed crises.

Adult↗
PubMed1987

Regulation of nerve growth factor synthesis/secretion by catecholamine in cultured mouse astroglial cells.

The nerve growth factor (NGF) synthesis/secretion by cultured mouse astroglial cells was modulated by catecholamine. In quiescent cells, epinephrine (EN) and dopamine (DA) markedly increased the NGF content in the conditioned medium (CM). Conversely, EN, DA, and norepinephrine (NE) decreased the NGF content in growing cells. Cholinergic agonists, metacholine and carbamylcholine, slightly increased the NGF content in quiescent cells, but showed no effects on growing cells. Other neurotransmitters tested had no effects on either growing or quiescent cells. These results suggest that catecholamine is one of the molecules responsible for regulation of NGF synthesis/secretion in the mouse brain.

Animals↗
PubMed1987

Synthesis/secretion of nerve growth factor is associated with cell growth in cultured mouse astroglial cells.

Astroglial cells cultured from 8-day-old mouse brain synthesized and secreted nerve growth factor (NGF). An increase in cell density or the withdrawal of serum from the culture medium caused a drastic decrease in the rate of NGF secretion which could be reversed by reculturing at a low cell density or by refeeding with serum-containing culture medium. The cells cultured for two weeks without serum entered the quiescent phase without loss of the activity of an astroglial marker enzyme, glutamine synthetase. These results suggest that NGF secretion by astroglial cells in vitro is regulated in a growth phase-dependent manner. Evidence is also presented to show that NGF secretion is not phase-specific in the cell cycle.

Animals↗