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Biomedical subjects

T Ibi

Publications and source records attributed to T Ibi.

67 records · Page 4Linked to original sources
PubMed1985

Acute predominantly sensory neuropathy.

An account is given of an unusual patient with acute sensory neuropathy, leading within a few weeks to almost generalized sensory loss. Generalized sensory deficits were involved in the face, tongue, and palate. He had a drug allergy from chemotherapy during an early stage of illness. An albuminocytological dissociation of the cerebrospinal fluid was noted in a few months. A sural nerve biopsy after 2 months showed a marked reduction of fibers, and extensive invasion of phagocytes throughout the endoneurium. This patient recovered poorly with profound sensory ataxia of the limbs and tongue. A possible explanation for the clinico-pathological findings may be that acute idiopathic polyradiculoneuritis (Guillain-Barré syndrome) and toxic neuropathy exert an etiological role in the extramedullary sensory system.

Acute Disease↗
PubMed1985

Immunohistochemical demonstration of carbonic anhydrase III and muscle-specific enolase in paraffin-embedded human skeletal muscle sections.

We have demonstrated the histochemical fiber types of human skeletal muscle in paraffin sections by the immunohistochemical method, together with compatible observations previously made in frozen sections that carbonic anhydrase III is mainly localized in type 1 fibers (Shima et al. 1983), and muscle-specific enolase in type 2 fibers (Ibi et al. 1983). This method is useful to analyze the fiber types when frozen muscle samples at biopsy or autopsy cannot be obtained.

Animals↗
PubMedDate not supplied

Immunohistochemical demonstration of beta-enolase in human skeletal muscle.

We have localized beta-enolase activity in human skeletal muscle fiber using the immunohistochemical method (two-step method). The first immunoreagent was rabbit anti-human beta-enolase serum raised in New Zealand white rabbit, and the second was peroxidase conjugated staphylococcal protein A. The immunohistochemical reaction for beta-enolase was noted higher in type 2 fiber, which demonstrates the low oxidative and high glycolytic enzyme activity, than in type 1 fiber.

Histocytochemistry↗
PubMedDate not supplied

[Clinico-pathological analysis of vesiculotubular myopathy of adult onset].

The patient was a 50-year-old house wife. There were complicated consanguineous marriages in the family tree. Since 30 years of age, she had suffered from progressive limb muscle weakness, but without myalgia and myasthenia. At present, she was wheelchair-bound. Physical examinations showed obesity, congenital livedo racemosa, epicanthus palpebrae and left renal defect. Neurologically, facial, anterior cervical, and iliopsoas muscles were well preserved, but others were severely involved. Laboratory examinations revealed mildly elevated myogenic serum enzymes, and myogenic changes on needle EMG. In her muscle biopsy from the left rectus femoris muscle, there were no inflammatory changes, but marked variations of the fiber size as well as adipose tissue replacement were recognized. Strickingly, basophilic masses located in the center of the sarcoplasm were present in about 10% of the fibers. Histochemically, the masses were present in both type 1 and 2 fibers, and exhibited almost similar stained patterns to the tubular aggregates, but were dystrophin-, GRP78- and clathrin-positive. Under electron microscopy, the masses consisted of aggregates of the vesiculotubular structure, measuring approximately from 60 nm to more than 6 microns in diameter, which were continuous with T system/sarcoplasmic reticulum and were clearly segregated from myofilaments. This is a chronic progressive muscular disorder of adult onset with the peculiar pathological finding of vesiculotubular structure.

Age of Onset↗