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T Kohriyama

Publications and source records attributed to T Kohriyama.

49 records · Page 3Linked to original sources
PubMed1987

Characterization of sulfated glucuronic acid containing glycolipids reacting with IgM M-proteins in patients with neuropathy.

In some patients with neuropathy and plasma cell dyscrasia, the serum IgM M-proteins are known to bind to the myelin associated glycoprotein and to peripheral nerve glycolipids. We have isolated two acidic glycolipids which bind to the M-protein from human cauda equina by DEAE-Sephadex, Iatrobeads, and high performance liquid column chromatographies. The major acidic glycolipid migrated between GM1 and GD1a and the minor acidic glycolipid migrated between GD1a and GD1b. Their structures were elucidated by sugar analysis, enzymatic digestion, mild acid hydrolysis, permethylation, fast atom bombardment mass spectrometry, and NMR studies. Their core structure was confirmed to be paragloboside by high performance thin-layer chromatography-immunostaining using anti-paragloboside monoclonal antibody. Both acidic glycolipids lacked sialic acid but contained sulfated glucuronic acid as their acidic moiety. The sulfate group in the glucuronic acid was established by periodate oxidation and permethylation studies to be attached to the 3 position. The structures of the two acidic glycolipids are therefore consistent with the following: IV3GlcUA(3-sulfate)nLcOse4Cer and VI3GlcUA(3-sulfate)nLcOse6Cer. Additionally, the free carboxyl group on the glucuronic acid residue was shown to be necessary to bind the IgM M-proteins from neuropathy patients.

Antibodies, Monoclonal↗
PubMed1987

Subcellular localization of sulfated glucuronic acid-containing glycolipids reacting with anti-myelin-associated glycoprotein antibody.

Peripheral nerve glycolipids, with which anti-myelin-associated glycoprotein (MAG) antibodies from patients with demyelinating neuropathy and plasma cell dyscrasia cross-react, proved to be novel glycosphingolipids containing a sulfated glucuronyl residue. Consequently, there has been much interest in the immunological role that these sulfated glucuronyl-glycosphingolipids (SGGLs) may play in the pathogenesis of this disorder. For the determination of the distribution of these glycolipids in various nervous tissues and, thereby, the elucidation of their pathogenicity, a quantitative immunostaining-TLC method for their detection has been devised. Using this method, we demonstrated that these glycolipids were distributed in greatly different amounts in the peripheral nerves from human, bovine, chicken, rat, and rabbit. Subcellular localization studies of bovine peripheral nerve also demonstrated that they were enriched in the axolemma-enriched fraction and present in glial-related membranes in lower concentrations. In addition, these glycolipids were present in bovine dura mater and transformed rat Schwann cells. These biochemical results suggest that not only myelin but also axons could be involved as targets of the anti-MAG antibody in macroglobulinemia neuropathy, and it may also be necessary to examine anti-SGGL activity in patients with axonal neuropathy associated with plasma cell dyscrasia.

Animals↗
PubMed1987

Neuropathy and IgM paraproteinemia: differential binding of IgM M-proteins to peripheral nerve glycolipids.

Two patients with neuropathy and IgM paraproteinemia displayed different immunoreactivity to acidic peripheral nerve glycolipids. In one patient, immunostaining on thin-layer chromatographic plate revealed binding of the IgM to sulfated glucuronosyl paragloboside (SGPG) and sulfated glucuronosyl lactosaminyl paragloboside (SGLPG). The other IgM bound SGPG, SGLPG, and a new third glycolipid. Immunoreactivity of the IgM varies in this syndrome.

Aged↗
PubMed1985

Electron-microscopic and immunohistochemical studies on endomyocardial biopsies from a patient with eosinophilic endomyocardial disease.

Light- and electron-microscopic studies and immunohistochemical procedures were carried out on blood eosinophils and left ventricular endomyocardial biopsies from a 68-year-old man with an eosinophilia of 8.2 X 10(9)/l and congestive cardiac failure due to eosinophilic endomyocardial disease. Some blood eosinophils were vacuolated and degranulated, and reversal of the normal staining pattern of eosinophil granules was seen by means of electron microscopy. The biopsies showed degenerative changes in the cardiac myocytes, with interstitial fibrosis and infiltration by numerous eosinophils, mast cells, and macrophages. Eosinophils infiltrating the myocardium showed a decrease in the number of granules, many of which were indistinct or contained dissolving crystalloids, which occasionally were seen to be discharged onto the surface of adjacent cardiac myocytes. Immunohistochemical studies of the endomyocardial biopsies with a monoclonal antibody, which is specific for activated eosinophils and binds to the secreted forms of eosinophil cationic protein (ECP) and eosinophil protein-X (EP-X), demonstrated that the lesions contained numerous activated eosinophils and secreted ECP and EP-X. These findings support the concept that in eosinophilic endomyocardial disease, activated eosinophils infiltrate and degranulate in the myocardium, releasing eosinophil cationic proteins which then damage adjacent myocardial cells.

Aged↗
PubMedDate not supplied

Age-related change in peripheral nerve conduction: compound muscle action potential duration and dispersion.

BACKGROUND: We investigated the effect of age on nerve conduction parameters with special reference to the compound muscle action potential (CMAP) duration and duration ratio. METHOD: We examined 295 subjects (aged 15-85 years old) with no previous history or present signs of peripheral neuropathy. The subjects were divided into 3 groups: young (15-34 years old); intermediate (35-64 years old), and old (65-85 years old). RESULTS: CMAP amplitude was lower in the old group than in the young group; however, the CMAP ratio (proximal CMAP/distal CMAP) did not change with age. The CMAP duration and duration ratio did not differ among the 3 groups. The CMAP area was smaller in the old group, but the area ratio was almost constant among the 3 groups. CONCLUSION: We suggest that age-related changes in CMAP amplitude, duration or area may occur uniformly, at least in the forearm and the calf segment, in routine nerve conduction studies. The present findings also provide useful and reliable information, regardless of age, in diagnosing peripheral neuropathy.

Action Potentials↗
PubMedDate not supplied

[Age-related changes in amplitude ratio, duration ratio and area ratio in nerve conduction studies].

We investigated the effect of aging on nerve conduction parameters in 184 subjects (aged 10-75 years) without any history or signs of peripheral neuropathy, in order to clarify the diagnostic parameters of demyelinating neuropathies in the aged. The CMAP amplitude ratio (proximal CMAP/distal CMAP), duration ratio and area ratio remained unchanged throughout the second to eighth decades. The lower limits of normal CMAP amplitude ratio (mean -3SD) were 0.79 (median nerve), 0.74 (ulnar nerve), 0.59 (peroneal nerve), and 0.48 (tibial nerve). The upper limits of normal CMAP duration ratio (mean 11+ 3SD) were 1.22 (median nerve), 1.19 (ulnar nerve), 1.35 (peroneal nerve), and 1.32 (tibial nerve). The lower limits of normal CMAP area ratio (mean -3SD) were 0.84 (median nerve), 0.78 (ulnar nerve), 0.61 (peroneal nerve), and 0.62 (tibial nerve). There were no age-related changes in amplitude ratio or duration ratio of SNAP, although the standard deviations increased with age. Since the amplitude ratio, duration ratio and area ratio are simple and age-independent, they can provide useful and reliable information for routine nerve conduction studies for aged patients with demyelinating neuropathies.

Action Potentials↗
PubMedDate not supplied

Ratios of nerve conduction parameters in proximal to distal limbs remain constant through the second to the eighth decades.

We investigated the effect of age on nerve conduction parameters to establish a diagnostic validity in demyelinating neuropathies of the aged. We evaluated 257 subjects (age 10-76 years old) with no history or signs of peripheral neuropathies. The CMAP amplitude ratio (proximal CMAP/distal CMAP), duration ratio, and area ratio were almost the same throughout the second to eighth decades. The respective lower limits of the normal CMAP amplitude ratio (mean-3 SD) were 0.79 (median nerve), 0.75 (ulnar nerve), 0.57 (peroneal nerve), and 0.45 (tibial nerve). The upper limits of the normal CMAP duration ratio (mean +3 SD) were 1.21 (median nerve), 1.22 (ulnar nerve), 1.37 (peroneal nerve), and 1.35 (tibial nerve). The lower limits of the normal CMAP area ratio (mean-3 SD) were 0.81 (median nerve), 0.78 (ulnar nerve), 0.60 (peroneal nerve), and 0.57 (tibial nerve). No age-related changes were observed in the amplitude ratio or duration ratio SNAP, although the standard deviation increased with age. Since the amplitude, duration and area ratios are easily calculated and age-independent, they can provide useful and reliable information on aged patients with demyelinating neuropathies by conventional nerve conduction studies.

Adolescent↗