[A case of acute autonomic neuropathy].
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to K Mokuno.
Explore the source record for details and available documents.
A sandwich enzyme immunoassay method for measurement of beta subunit of muscle enolase in human serum was developed by use of purified antibodies to enolase beta subunit and beta-D-galactosidase from Escherichia coli as label. The assay was specific to the beta subunit with no cross-reaction with the alpha and gamma subunits of human enolase. The measurable range was from 10 pg to 10 ng per assay tube or 1 to 1000 ng/ml serum. Coefficients of variation within-run and between-run for the assay of serum beta subunit were less than 14%. Normal adult sera contained about 6 ng/ml of the beta subunit, and the levels were significantly elevated in sera of patients with muscular dystrophy and those with myocardial infarction. Serum levels of the beta subunit correlated well with those of creatine phosphokinase, but poorly with those of myoglobin in the same samples. The specific distribution of beta subunit in skeletal muscle and heart was confirmed by measuring the levels in various tissue extracts.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Previous studies indicated that Schwann cells in immature nerves express nerve growth factor (NGF) receptors, and that this expression is down regulated during development but re-induced by Wallerian degeneration. It was also shown that immature Schwann cells are induced to express galactocerebroside and other molecules characteristic of mature Schwann cells by either contact with an axon or treatment with the cyclic adenosine 3',5'-monophosphate (cAMP) analogues dibutyryl cAMP (dbcAMP) and 8-bromo cAMP or the adenylate cyclase activator forskolin. In the present study, NGF receptors on the surface of cultured Schwann cells were demonstrated by binding of an anti-rat NGF receptor monoclonal antibody or of radioiodinated NGF. Treatment of cultured Schwann cells with cAMP analogues or forskolin resulted in a progressive decrease in both immunoreactive NGF receptors and radioiodinated NGF binding. The cultured Schwann cells contained a polyadenylated RNA species homologous with human melanoma NGF receptor mRNA in sequence and size. The amount of this NGF mRNA was lower in cAMP analogue-treated than in untreated Schwann cells.
Serum carbonic anhydrase III (CAIII) levels were determined by means of an enzyme immunoassay method and were compared with serum creatine kinase (CK) and muscle-specific enolase (MSE) levels in 33 patients with myotonic dystrophy. Serum CAIII levels were elevated in all 33 patients, whereas serum CK and MSE levels were elevated in 12 and 10 patients, respectively. Serum CAIII levels showed a good correlation with CK levels, but a poor one with MSE levels. There was no obvious correlation between the serum CAIII level and the duration of illness or the age of the patient. These results suggest that serum CAIII is probably a more sensitive marker than CK and MSE in myotonic dystrophy and may also reflect the type 1 fiber abnormality more predominantly observed in myotonic dystrophy.
Neuron-specific enolase (NSE) and S-100 protein (S-100) levels in cerebrospinal fluid (CSF) were determined in 129 patients with various neurological diseases. The chronological changes of these nervous system-specific proteins in CSF were also examined in 3 patients with acute disorders. NSE and S-100 levels were elevated in many cases with acute conditions. These specific proteins did not increase simultaneously but independently. These results suggested that NSE and S-100 in CSF would be useful markers for damage of the nervous system and that measurement of both NSE and S-100 might positively indicate whether the damage was neuronal, glial or mixed in origin. Moreover, from the serial determination of these substances, they would be better markers than cell counts and total protein in CSF for the active injury for the nervous tissues.
We reported a 44-year-old woman with Guillain-Barré syndrome (GBS) showing elevations of serum anti-GD1a and anti-GT1b antibody levels. A few days after an upper respiratory infection, she felt numbness in her hands and feet, dysphagia and dysarthria, and weakness in her limbs. On admission, examination showed the paralysis of pharynx and neck, moderate weakness of face and upper limbs, and mild weakness of lower limbs. Sensory deficits were minimal on the distal side of extremities. Deep reflexes were decreased or absent. Laboratory examinations revealed the albumino-cytological dissociation in cerebrospinal fluid and the increase of anti-GD1a and anti-GT1b antibodies in serum. Nerve conduction studies demonstrated axonal damage to the motor nerves. With immunoadsorption therapy, she gradually recovered and the anti-GD1a and anti-GT1b antibodies were normalized. It was reported that the anti-GT1a antibody may be associated with a pharyngeal-cervical-brachial (PCB) variant of GBS (Ropper) and the similar cases including the present case. However, in the present case, the serum anti-GT1a antibody level was not increased, whereas those of anti-GD1a and anti-GT1b antibodies did. Therefore, these antibodies may also play a role in the development of PCB signs in GBS.