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Biomedical subjects

T Tsubaki

Publications and source records attributed to T Tsubaki.

At least 55 records · Page 3Linked to original sources
PubMed1987

[Usefulness of nerve block therapy in patients with herpetic pain].

A retrospective study was performed on 230 patients with Herpes zoster. Among these patients, 156 patients (67.8%) were over 50 years old. Ninety-four percent of the patients who received the nerve block therapy within a month from the onset became ultimately free from pain while only seventy-nine percent of the patients upon whom this therapy was started after 2 months or more were relieved of pain. It was suggested that the earlier the therapy and the younger the patients, the more easily herpetic pain could be controlled. In conclusion, it became apparent that early treatment of Herpes zoster with nerve block therapy, is extremely important for prevention of post-herpetic neuralgia.

Age Factors↗
PubMed1987

5-Chloro-7-iodo-8-hydroxyquinoline (clioquinol) inhibits the nerve growth factor-induced stimulation of RNA synthesis in neonatal rat superior cervical ganglion, in vitro--comparison with effects of methylmercuric chloride and 4-hydroxyaminoquinoline-N-oxide.

The inhibitory effects of 5-chloro-7-iodo-8-hydroxy-quinoline (clioquinol), methylmercuric chloride and 4-hydroxyaminoquinoline-N-oxide(4-HAQO) on DNA, RNA and protein syntheses in the neonatal rat superior cervical ganglion (SCG) were studied in relation to the action of mouse 2.5S nerve growth factor (NGF), using organ cultures. RNA and protein syntheses in SCG were stimulated approximately 3- and 2-fold, respectively, by NGF (1 microgram/ml), but the DNA synthesis was only slightly or not at all stimulated. Methylmercuric chloride and 4-HAQO dose-dependently inhibited DNA, RNA and protein syntheses, either in the presence or in the absence of NGF. On the other hand, clioquinol (up to 100 microM) slightly or not at all inhibited RNA synthesis in the absence of NGF; however, it did abolish the NGF-induced stimulation of RNA synthesis in the presence of NGF. The DNA and protein syntheses were dose-dependently inhibited by clioquinol, either in the presence or in the absence of NGF. We conclude from this study that the interaction between clioquinol and the functions of NGF raises the question of a possible toxicity of the drug on specific neurons.

4-Hydroxyaminoquinoline-1-oxide↗
PubMed1986

[Endogenous inhibitory system in pain].

Electrical stimulation of several brain sites produces profound analgesia in humans, and inhibits nocifensor reflexes in animal studies. Responses of the dorsal horn nociceptive neurons evoked by stimulation onto the receptive fields are also inhibited by brain stimulation. These brain sites are Periaqueductal Gray Matter (PAG), Nucleus Raphe Magnus (NRM), Nucleus Reticularis magnocellularis (NRmc), Locus Coeruleus (LC), Lateral Hypothalamus, and others. We have explained in a general way the mechanism of these stimulation produced analgesia. The mechanism of PAG stimulation analgesia is partly due to an activation of serotonin containing neurons which descend from NRM to the spinal dorsal horn and activated by PAG stimulation. Activation of NRM neurons may produce inhibition of the nociceptive neurons of the dorsal horn by the mechanism of direct postsynaptic inhibition. Currently there is no evidence to support the theory of presynaptic inhibition. Endogenous opioid peptides do not play an important role in PAG stimulation analgesia. On the other hand, the mechanism of NRmc or LC stimulation analgesia may be due to an activation of noradrenaline containing neurons which similarly inhibit the dorsal horn nociceptive neurons in the spinal cord. At present, it still remains unknown whether endogenous opioid peptides play an important role in this type of analgesia.

Analgesia↗
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↗
PubMed1985

Familial Creutzfeldt-Jakob disease in Japan. Three cases in a family with white matter involvement.

Three cases of Creutzfeldt-Jakob disease occurring in one family have been clinicopathologically examined. Although the age at onset, duration, and age at death differed for each case, pathological findings, including diffuse neuronal loss, astrocytosis, spongiform changes and patchy and/or diffuse white matter involvement were similar. Life histories and inheritance patterns of the present 3 cases and 2 other families previously reported in Japan are compared with the general findings for familial cases in western countries.

Aged↗
PubMed1985

Creatine kinase (CK)-linked IgA in Isaacs' syndrome. An immune complex disease?

Electrophoresis of serum from a patient with Isaacs' syndrome revealed an atypical creatine kinase (CK) isoenzyme pattern which contained an extra band migrating between CK2(MB) and CK3(MM). Immunofixation demonstrated that the extra band was a complex of CK3(MM) and IgA. The presence of this complex seemed to correlate with increased serum CK levels which were associated with the aggravation of symptoms. Immunofluorescence studies on muscle biopsy samples revealed the presence of the complex in the muscle fiber membrane and motor endplate. The existence of CK-linked IgA in an Isaacs' syndrome suggests that an immunological abnormality may play a role in the pathological process of this rare syndrome.

Chemical Phenomena↗
PubMed1984

Mitochondrial encephalomyopathy: fluctuating symptoms and CT.

We describe a 29-year-old man with mitochondrial encephalomyopathy. The patient's disorder was characterized by lactic acidosis, hemiparesis, seizures, aphasia, and hemianopia. CT revealed low-density areas that corresponded to the symptoms. His 56-year-old mother is also involved subclinically, demonstrating that muscle biopsy is an important requisite in the final determination of a familial inheritance pattern in mitochondrial myopathy. Neuronal mitochondrial disorders are suggested as the pathogenesis of his neurologic symptoms.

Adult↗
PubMed1984

The Crow-Fukase syndrome: a study of 102 cases in Japan.

Clinical manifestations of 102 cases with the Crow- Fukase syndrome (the syndrome of polyneuropathy, anasarca, skin changes, endocrinopathy, dysglobulinemia, and organomegaly), with or without myeloma, were reviewed. Fifty-six cases with myeloma consisted of 31 with osteosclerotic, 17 with mixed osteosclerotic and osteolytic, and 8 with osteolytic. Forty-six cases without myeloma consisted of 2 with extramedullary plasmacytoma, 33 with M protein alone, and 11 with polyclonal protein alone. There was no significant difference in incidence of the major clinical manifestations between the two groups with and without myeloma. They had a common characteristic histologic finding of the lymph node resembling that of Castleman's disease.

Adult↗