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Biomedical subjects

N Fukuhara

Publications and source records attributed to N Fukuhara.

At least 73 records · Page 4Linked to original sources
PubMed1988

An autopsy case of mitochondrial encephalomyopathy: biochemical and electron microscopic studies of the brain.

A 29-year-old single woman had recurrent stroke-like episodes. She developed loss of consciousness, myoclonic seizures, and lactic acidosis. She died at the age of 30. A muscle biopsy study revealed mitochondrial myopathy, and the postmortem biochemical analysis demonstrated decreased cytochrome c oxidase activity in the skeletal muscles by 20% of normal control. The brain had multiple ischemic lesions in the cerebral cortex without major vascular occlusions. We present this case as an autopsy case of mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) with a partial deficiency of cytochrome c oxidase. The analytical electron microscopic study of the calcified small vessels in the globus pallidus revealed increased calcium, phosphorus and iron. No accumulation of chromium, nickel or zinc was noted in this case, which was different from the previously reported cases of basal ganglia calcification.

Adult↗
PubMed1988

Role of VP3 in human rotavirus internalization after target cell attachment via VP7.

A cell lysate prepared from MA104 cells that had been infected with human rotavirus KUN strain (HRV-KUN) contained a 35-kilodalton protein capable of binding to MA104 cells. The binding of the 35-kilodalton protein was inhibited by a serotype 2-specific antiserum but not by antisera to other serotypes. Not only trypsin-treated, infectious HRV-KUN but also untreated, noninfectious virions effectively competed with the 35-kilodalton protein for the same cell surface binding sites. One monoclonal anti-VP7 (AH6) absorbed the 35-kilodalton protein from the HRV-KUN-infected cell lysate, whereas another monoclonal anti-VP7 (S2-2G10) inhibited the virions to compete with the 35-kilodalton protein for the cell surface binding sites. Both anti-VP7 (S2-2G10) and anti-VP3 (K-1532, K-376) monoclonal antibodies had the virus-neutralization activity, but only anti-VP7 inhibited virus adsorption. On the other hand, anti-VP3 monoclonal antibodies were capable of completely inhibiting the infection of preadsorbed HRV-KUN as long as virions were not yet internalized. Subsequent studies with [35S]methionine-labeled and purified HRV-KUN showed that not only trypsin-treated, infectious virions but also untreated, noninfectious virions were capable of efficient target cell binding and internalization. The internalization modes of these two HRV-KUN preparations were, however, quite different. Only the components of the inner capsid were internalized from trypsin-treated virions, whereas no such selective internalization was seen with untreated virions. Furthermore, anti-VP3 inhibited this selective internalization of the inner capsid from the infectious virions. From these results we conclude that VP7 is the HRV-KUN cell attachment protein and that adsorption of HRV-KUN via VP7 is independent of trypsin treatment, whereas the limited cleavage of VP3 by trypsin, which is essential for the development of HRV-KUN infectivity, is needed for the selective internalization of the inner capsid components, a process that is apparently essential for HRV-KUN infection.

Adsorption↗
PubMed1988

[Sensori-motor neuropathy associated with congenital bilateral club feet: histological and ultrastructural study of the sural nerve].

A 53-year-old female with sensori-motor neuropathy associated with bilateral club feet was reported. She was admitted because of numbness in the bilateral feet and gait disturbance. Her parents were not related. There was no family history of any neurological diseases. She had bilateral club feet which were present at birth to developed in early childhood. She could walk, but could not run. Since 5 years prior to the admission she noted gradually increasing disturbance of gait. Neurological examination revealed muscular weakness and wasting in the distal parts of the lower extremities and decreased deep tendon reflexes. There were hypesthesia, hypalgesia and dysesthesia in the lateral portions of the bilateral feet. Deep sensation was normal. There was no weakness or wasting in the upper extremities. Motor nerve conduction velocities were normal and sensory nerve conduction velocities were reduced in the median nerve. No action potentials could not be elicited in the bilateral tibial and peroneal nerves. A sural nerve biopsy showed a markedly hypertrophic perineurium, 28-150 micron thick, a large Renaut body measured 140 micron by 200 micron in diameters and a markedly reduced number of the myelinated fibers. Fiber size histogram showed many unmyelinated fibers larger than 1 micron, despite loss of fibers of the usual size. Therefore, a part of the unmyelinated fibers might be demyelinated. There were no axonal degeneration and onion-bulb formation. Segmental demyelination was found in approximately 30% of the myelinated fibers.(ABSTRACT TRUNCATED AT 250 WORDS)

Clubfoot↗
PubMed1987

Serologic characteristics of a human rotavirus isolate, AU-1, which has a "long" RNA pattern and subgroup I specificity.

An unusual human rotavirus (HRV) isolate, designated AU-1, has a "long" RNA electrophoretic pattern and subgroup I specificity, in contrast to properties common to HRVs previously isolated. Hemagglutination activity of the AU-1 strain was demonstrated using erythrocytes of 1-day-old chicken. Neutralization assays revealed that the AU-1 strain was crossneutralized by hyperimmune antisera against the MO strain (serotype 3). However, antiserum directed against a reassortant in which the gene for Vp7 was replaced by the corresponding AU-1 gene neutralized the AU-1 strain to a significantly higher titer than the MO strain.

Hemagglutination Tests↗
PubMed1987

Evidence for endocytosis-independent infection by human rotavirus.

The effects of five lysosomotropic drugs (NH4Cl, chloroquine, methylamine, amantadine and dansylcadaverine) and cytochalasin B on human rotavirus (HRV KUN strain) and vesicular stomatitis virus (VSV Indiana strain) infection in monkey MA 104 cells were examined. These drugs had little effect on HRV yield but greatly reduced VSV yield. The results strongly suggest that HRV does not require endocytotic activity and intracellular acidic vesicles for the initial stage of infection and support our postulate that HRV enters the target cell by direct penetration of its nucleoid through the cell membrane.

Amantadine↗
PubMed1987

[An autopsy case of myoclonus epilepsy associated with ragged-red fibers (Fukuhara disease)].

In 1980, Fukuhara et al. have reported two patients with "myoclonus epilepsy associated with ragged-red fibers" (MERRF), which is at present accepted as a distinctive clinical entity among the mitochondrial encephalomyopathies. We describe here postmortem findings of the case whose clinical findings were reported in detail by Fukuhara et al. (1980) as Case 1. The neuropathological findings were summarized as follows: 1) degeneration of dentate nucleus, red nucleus, globus pallidus, subthalamic nucleus and pontine tegmentum, 2) degeneration of the Clarke's column, spinocerebellar tract, posterior column and corticospinal tract, as well as of the posterior spinal nerve root and sural nerve, and 3) degeneration of substantia nigra, locus ceruleus, cerebellar cortex and inferior olivary nucleus. The lesions were degenerative in nature, and their distribution was different from those of dentato-rubropallidoluysian atrophy, Joseph's disease or Friedreich's ataxia. It was concluded that MERRF is a single disease entity also from pathological point of view.

Adult↗
PubMed1987

Local control rate of split-course irradiation combined with chemotherapy for head and neck cancer.

Between 1976 and 1984, 99 patients were treated with radical external irradiation (RT) for squamous cell carcinoma of the head and neck excluding the glottis and paranasal cavity. Twenty-six out of 55 patients (47%) on chemotherapy (CT) were treated by split-course (split) RT, mainly because of acute mucositis. Only 8 out of 44 patients (18%) not on CT were treated by split RT. Although the group given split RT alone rested for 14 days and received 35 Gy, the split RT + CT group rested for 16 days and received a lower dose (30.5 Gy). The mean total doses for each treatment modality were 64 Gy in the continuous course (contin.) of RT alone, 63 Gy in contin. RT + CT, 67 Gy in split RT, and 62 Gy in split RT + CT. The observed/predicted (by a Radiation Therapy Oncology Group) control ratios of primary lesions at 2 yrs were 61/80 (0.76), 72/83 (0.87), 75/73 (1.03), and 69/71 (0.97), respectively. Among patients with a predicted rate of over 80%, the observed rates were almost identical (72%, 74%, 4/4, and 75%, respectively). However, for patients with predicted rates of 50-80%, the observed rate was 71% (12/17) in the group given combined therapy against 50% (5/10) in RT alone group. Among patients with predicted rates under 50%, the observed rate was 57% (4/7) in split RT + CR and only 25% (1/4) in contin. RT; there were no cases in contin. RT + CT. Split RT + CT is considered to be favorable for patients with poor prognostic factors.

Aged↗
PubMed1986

Characterization of monoclonal antibodies against human rotavirus hemagglutinin.

Three monoclonal antibodies capable of specifically inhibiting hemagglutination of human rotavirus were produced. Their hemagglutination inhibition (HI) activity was specific to the homologous strain (KUN) used for immunization. The monoclonal antibodies with HI activity were highly effective in neutralizing the infectivity of the KUN strain. These antibodies reacted with Vp80, and 80,000 molecular weight (MW) protein present in the viral outer shell. It was confirmed by immunoblotting assay with the monoclonal antibodies that the antigenic site of human rotavirus hemagglutinin (HA) resides on Vp80 and on its smaller trypsin cleavage products Vp30 (MW 30,000) and Vp24 (MW 24,000). Immunofluorescence studies using the antibodies revealed that the HA antigen of the KUN strain developed at the final stage of virus maturation.

Animals↗
PubMed1986

Structural polypeptides of the murine coronavirus DVIM.

The structural polypeptides of the murine coronavirus DVIM (diarrhoea virus of infant mice) have been analysed in comparison with other strains MHV-2, MHV-3, MHV-4 (JHM) and MHV-S by SDS-PAGE. In the presence of 2-mercaptoethanol, three major glycopolypeptides, gp180, gp69, gp25 (as a group of similar species) and one major non-glycosylated polypeptide p58 were detected. The gp69 is a DVIM specific glycopolypeptide, in which the glycosidic moieties are linked to the core polypeptide through N-glycosidic bonds, and hence may be correlated with the short projections of the viral envelope. Further gp140, which appears in the absence of reducing agents, is apparently a dimer of gp69 held together by disulfide linkages. The gp25 family, on the other hand, consists of four polypeptides, two of which are not metabolically inhibited by tunicamycin suggesting that they are O-linked glycopolypeptides. DVIM seems to be serologically closely related to the MHV-S strain as shown by neutralization.

Animals↗
PubMed1986

Experimental neuropathy induced by methyl mercury compounds: autoradiographic study of GABA uptake by dorsal root ganglia.

Methyl mercury chloride (MMC, 10 mg/kg body weight/day) was subcutaneously injected into rats for 1 week. Animals were killed at 5 or 14 days (at the onset of clinical symptoms) after injection of MMC. Morphologically, most of the myelinated fibers in peripheral nerves showed axonal degeneration. Ganglion cells showed histopathological changes similar to those in previous reports. The cytoplasm of satellite cells stained dark with toluidine blue and was narrow, and sometimes showed focal disappearance of rough endoplasmic reticula, ribosomes or filaments. Autoradiography in the control rats showed that 3H-GABA was exclusively localized within the satellite cells and Schwann cell cytoplasm of the myelinated fibers and was not revealed within the ganglion cells. The number of silver grains markedly decreased in the satellite cells of the MMC-treated rats. 14C-GABA uptake by dorsal root ganglia also decreased to 75.0% of the control on the 5th day and to 49.2% on the 14th day. Therefore, MMC was found to inhibit greatly the GABA uptake into the satellite cells in the earlier stage of poisoning, and was considered to affect primarily the satellite cells and Schwann cells as well as the ganglion cells.

Animals↗
PubMed1986

[Distant metastases from carcinoma of the oral cavity and pharynx].

Distant metastases were detected clinically in 25 (14%) of 173 patients with squamous cell carcinoma of the oral cavity and pharynx admitted from 1975 to 1982. The probability of distant metastases was higher in patients with advanced tumor (stages III and IV: 21%; T4: 27%; N3: 37%), lymphoepithelioma (57%) and in patients with a decreased lymphocyte count in the peripheral blood at presentation (less than 1300/microliter; 58%). The incidence of metastases in advanced cases was 45% in the oropharynx, 24% in the nasopharynx and 20% in the oral cavity. Whether the regional tumor had been controlled or not in advanced cases, there was no difference between the incidence and the period of detection of distant metastases.

Adolescent↗
PubMed1985

Ultrastructural studies on the neuromuscular junctions of Becker's muscular dystrophy.

Ultrastructural studies on muscle biopsies from three patients with Becker's muscular dystrophy showed that the i.m. nerves presented loss or disarrangement of the neurofilaments and an increased number of glycogen granules and/or myelin figures not infrequently in the myelinated and unmyelinated nerve fibers. The neuromuscular junctions showed markedly widened sole-plate areas, and several terminal axons frequently abutted and formed neuromuscular junctions on the same fiber. The secondary synaptic clefts were markedly decreased in number and short in length in type I fibers but not in type II fibers. Most terminal axons showed no degenerative changes. Therefore, the participation of a neural factor might be suggested as the cause of Becker's muscular dystrophy, although it does not mean denervation in the conventional sense of an axonal degeneration.

Adolescent↗