Search PubMed⌕ Search

Biomedical subjects

H Tsukagoshi

Publications and source records attributed to H Tsukagoshi.

At least 199 records · Page 11Linked to original sources
PubMed1985

Cortical cerebellar degeneration with testicular neoplasm.

Cortical cerebellar degeneration was found in a 28-year-old man with testicular neoplasm. The patient, who had undergone a left orchidectomy for the testicular tumor, developed progressive cerebellar symptoms with mental changes 7 months later. The autopsy revealed the spread of a malignant germ cell tumor of the testis, and cortical cerebellar degeneration in the central nervous system (CNS) which was characterized by almost complete loss of Purkinje cells and degeneration of the both dentate nuclei and superior cerebellar peduncles. The present case is the first of cortical cerebellar degeneration combined with testicular neoplasms.

Adult↗
PubMed1985

Gastrointestinal amyloid deposition in AL (primary or myeloma-associated) and AA (secondary) amyloidosis: diagnostic value of gastric biopsy.

Gastrointestinal amyloid deposition was investigated in 21 autopsy cases of nonhereditary systemic amyloidosis, 18 of the AL (primary or myeloma-associated) type and three of the AA (secondary) type. Vascular deposition of amyloid, most apparent in the submucosa, was found in all cases. Parenchymal deposition was observed mainly in the muscularis mucosae and muscularis externa in the AL type, and in the lamina propria mucosae in the AA type. Comparison of amyloid deposition in the stomach and rectum revealed no differences for the AA type. In the AL type, however, deposition in the lamina propria mucosae and muscularis mucosae was more frequent and marked in the wall of the stomach than in the rectum. Thus, gastric biopsy would be more valuable than rectal biopsy in the diagnosis of AL amyloidosis.

Adult↗
PubMed1984

An autopsy case of acute porphyria with a decrease of both uroporphyrinogen I synthetase and ferrochelatase activities.

An autopsy case of a 37-year-old woman with acute porphyria is reported. The patient began to complain of severe menstrual pains, and later developed serious peripheral neuropathy and various autonomic nervous symptoms. The autopsy revealed a marked loss and degeneration of axons and myelin sheaths in the peripheral nervous system (PNS), and prominent central chromatolysis of the spinal anterior horn cells. The predominant process of the peripheral neuropathy appeared to be axonal degeneration. Biochemical analysis showed a marked increase of delta-aminolevulinic acid (ALA), porphobilinogen, uroporphyrin, and coproporphyrin in the urine, and an increase of coproporphyrin and protoporphyrin in the stools and blood. In the analysis of the enzymatic activities of the liver and bone narrow, the activity of ALA synthetase (ALA-S) was markedly increased, and the activities of both uroporphyrinogen I synthetase (URO-S) and ferrochelatase were decreased. It was characteristic in this case that the enzymatic abnormalities found in both acute intermittent porphyria (AIP) and variegate porphyria (VP) coexisted. Biochemical analysis of the sciatic nerve showed an increase of ALA-S activity and a decrease of both URO-S and ALA dehydrase activities. This was the first report that indicated the presence of abnormal activities of the heme biosynthetic enzymes in the peripheral nerves of porphyric patients. The possibility was discussed that these enzymatic abnormalities of the heme biosynthesis in the peripheral nerve itself might be strongly related to the pathogenesis of the porphyric neuropathy.

Adult↗
PubMed1984

Fine structure of the synaptic endings between sympathetic axons and skeletal muscle cells and of the varicosities in the bundles of neurites in tissue culture.

In cocultures of skeletal muscle and sympathetic ganglia from chick embryos, synaptic boutons on skeletal muscle cells and varicosities in the neuritic bundles were observed electron microscopically. Synaptic endings on skeletal muscles were bulbous. Most synaptic boutons simply made contact with muscle fibers, but some boutons appeared as concave invaginations into the sarcolemma. In the neuritic bundles, numerous varicosities were observed. Close approximations were found between the synaptic boutons and skeletal muscles and between the varicosities and neurites (dendrites or axons), but no membrane thickening nor subsynaptic infolding was observed in either synapse; in our cultures the contacts were characteristic of the autonomic nervous system. In both synapses, three variations were demonstrated by KMnO4 fixation after 5-hydroxydopamine incubation: (i) containing predominantly small dense-core vesicles (noradrenergic type), (ii) predominantly small clear vesicles (cholinergic types), and (iii) a mixture of both small dense-core and small clear vesicles (mixed type). Cytochemically, the varicosities in the neuritic bundles were predominantly noradrenergic at 1 week in culture, and both the synaptic boutons on skeletal muscles and the varicosities in the neuritic bundles contained a mixed population of small dense-core and small clear vesicles at intermediate times, with a gradual shift to cholinergic characteristics. These findings strongly suggest that in this culture system some sympathetic neurons or fibers become cholinergic (neuronal plasticity).

Animals↗
PubMed1984

Peripheral and autonomic nerve lesions in systemic amyloidosis. Three pathological types of amyloid polyneuropathy.

Twenty autopsy cases of systemic amyloidosis, consisting of 10 cases of primary systemic amyloidosis, 6 cases of myeloma-associated amyloidosis, 2 cases of secondary amyloidosis, and 2 cases of hereditary amyloidosis, were studied clinically and pathologically with special reference to peripheral and autonomic neuropathy. The peripheral nerves of 8 cases with clinical manifestations of polyneuropathy showed deposition of amyloid in the endoneurium, capillaries within the nerve fascicles, perineurium, and epineurium with a loss and degeneration of the nerve fibers. In the peripheral nerve lesions of these cases, there appeared to be three types: I. Endoneurial deposition of amyloid--loss of unmyelinated and small myelinated fibers, II. vessel wall deposition of amyloid in the vasa nervorum--loss of large myelinated fibers; and III. a mixed type of I and II. While the peripheral nerves of 12 cases without neuropathy mainly showed deposition of amyloid in the epineurium and perineurium with well preserved nerve fibers. The possibility was considered that the pathogenesis and variety of peripheral and autonomic nerve lesions might be related to the various molecular features of amyloid proteins or their precursors in systemic amyloidosis.

Adult↗
PubMed1984

Distal myopathy of Gowers: a reappraisal.

This article argues against the general idea that the patient described by Gowers as distal myopathy in 1902 may have suffered from myotonic dystrophy. A case of distal myopathy with markedly atrophic sternocleidomastoids is presented. Patients of distal myopathy with absence of sternocleidomastoids, sometimes accompanied by facial weakness, are recorded in the literature. All these cases are sporadic and may be called distal myopathy of Gowers, which is different from Welander's cases.

Adult↗