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Biomedical subjects

Y Murai

Publications and source records attributed to Y Murai.

At least 91 records · Page 5Linked to original sources
PubMed1994

[Comparative studies on the evaluation of vibratory perception thresholds using three different instruments, vibratron II, TM-31A and SMV-5--reliability, correlation with age and interrelationship].

Vibratory perception thresholds of 40 (13 males and 27 females) subjects without sensory disturbances were evaluated using three different instruments, Vibratron II, TM-31A and SMV-5, successively three times every third or fourth day to compare their reliability, correlation with age and interrelationship. The intraclass correlation coefficients of the threshold, obtained at the palmar distal phalanx of the index finger of the predominant hand by using Vibratron II and SMV-5 were 0.77 and 0.88, respectively, and those at the radial styloid process on the same side by using TM-31A and SMV-5 were 0.62 and 0.84, respectively. There was a similarity of the intraclass correlation coefficients in the measurement at both sites between the subjects of ages < or = 40 and those of ages > 40, when different instruments were used. However, the thresholds were lower among the subjects of ages < or = 40 than among those of ages > 40. A significantly positive correlation was found between the threshold and the age at both sites when using different instruments. A significantly positive correlation was also found between the thresholds obtained by Vibratron II and SMV-5 at the palmar distal phalanx and between those obtained by TM-31A and SMV-5 at the radial styloid process. The above data indicate that each instrument is applicable not only for diagnosing and evaluating the vibratory sensation disturbances, but also for the follow-up study and evaluation of the efficacy of the specific treatment for the patients with sensory disturbances. They are likewise applicable for the screening and diagnosis of peripheral neuropathy in the occupational and environmental medicines. However, the reliability was lowest in the evaluation by TM-31A, and the correlation coefficient was smallest in the relationship between the age and the threshold obtained by TM-31A.

Adolescent↗
PubMed1994

Greater number of microtubules per axon of unmyelinated fibers of mutant quails deficient in neurofilaments: possible compensation for the absence of neurofilaments.

Morphometric evaluations were performed on the peroneal nerve from mutant quails deficient in neurofilaments (NF) to elucidate the effect of an absence of NF on unmyelinated axons. The diameter frequency distribution of unmyelinated axons was similar between controls and mutants. The mean transverse axonal area, axonal circumference and circularity index of the unmyelinated axons were also similar in controls and mutants. However, the number of microtubules (MT) per axon was greater (P < 0.01) in the mutants than in the controls. The regression analysis relating the number of MT per axon to the diameter of unmyelinated axons indicated a greater number of MT in the mutants than in the controls (P < 0.05-0.01). A significantly greater number of MT per axon in the mutants may suggest a compensatory increase of MT in the absence of NF. This may conserve the size and transverse circular profile of the unmyelinated axons which are probably maintained by both MT and NF in the controls. The number of MT may be increased at the expense of the soluble fraction of tubulin.

Animals↗
PubMed1994

Differential up-regulation of voltage-dependent Na+ channels induced by phenytoin in brains of genetically seizure-susceptible (E1) and control (ddY) mice.

We investigated the effect of in vivo administration of an antiepileptic drug, phenytoin, on the saxitoxin binding capacity of receptor site 1 of the Na+ channel alpha-subunit, and the expression activity of the channel messenger RNA in epileptic El mouse brains, as compared with parental ddY mice. Subchronic treatment with phenytoin (25 mg/kg per day) for 14 days increased the [3H]saxitoxin binding to brain-derived synaptic membranes of both El and control ddY mice in a time dependent manner. This increase plateaued at 21 +/- 4% in El mice and 28 +/- 3% in ddY control mice after administration of phenytoin for seven days. After cessation of treatment with phenytoin, [3H]saxitoxin binding capacity returned to the basal level within two weeks in both ddY and El brains. Scatchard plot analysis revealed that the phenytoin treatment caused a 20-30% increase in maximum binding capacity of [3H]saxitoxin binding without any change in equilibrium dissociation constant in the brain cortical synaptic membranes of both epileptic El and control ddY mice. A single injection of phenytoin (25 mg/kg) elevated the level of Na+ channel messenger RNA within 1 h in ddY mouse brains. The increase in Na+ channel messenger RNA reached a peak (about 80% increase) after 5 h of phenytoin administration in a concentration-dependent manner (6.25-50 mg/kg). On the other hand, in El mouse brains, Na+ channel messenger RNA was not elevated until more than 5 h after phenytoin injection, and was increased by only about 33%.(ABSTRACT TRUNCATED AT 250 WORDS)

Amphibian Proteins↗
PubMed1994

[A case of chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) with bilateral recurrent nerve palsy and primary alveolar hypoventilation--comparative studies of the histological findings of the two sural nerve biopsies with 9 years interval].

A 27-year-old man noticed a tingling sensation in his fingers and toes in early 1982, at the age of 18 years, and his symptom gradually progressed in the following several months. In December 1982, based on neurological and laboratory examinations including the first sural nerve biopsy on the right side, a diagnosis of axonal sensory neuropathy of unknown etiology was made. During the following years, muscle weakness in the distal limbs and hoarseness developed and progressed, and the sensory impairments became gradually evident. On the second neurological examination in July 1991, he showed soft palate palsy and bilateral recurrent nerve palsy. The intrinsic muscles of hands and feet were atrophic, and pes cavus was noted bilaterally. There was mild to moderate weakness in the distal muscles of both limbs. Ankle jerk was absent and other tendon reflexes were decreased in both limbs. A mild to moderate decrease of both superficial and deep sensations with mild paresthesia was noted in both hands and feet. Routine laboratory findings were unremarkable. In blood gas analysis, hypercapnea and respiratory acidosis were found. Spirometry showed an increase of residual volume, and alveolar CO2-pulmonary ventilation response test suggested the presence of primary alveolar hypoventilation caused by hypofunction of the medullary respiratory center. In nerve conduction studies, motor nerve conduction velocities were moderately reduced in bilateral median and ulnar nerves. Distal latencies of M-waves were prolonged in bilateral median nerves. Temporal dispersion of M-wave was found in the left tibial nerve. The amplitudes of sensory action potentials were moderately reduced in bilateral median and sural nerves.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1994

[A case of acute cholinergic dysautonomia].

A 52-year-old man with hypohidrosis and selective parasympathetic peripheral autonomic nerve disturbances of acute onset is described. In April 1991, he noted a feeling of dryness in the eyes and the oral cavity, disturbance of taste, difficulty in micturition and a feeling of dryness at the distal extremities with acute onset, which were followed by alternating diarrhea and constipation. Clinical and laboratory autonomic examinations revealed decreased sweating in the distal extremities, decreased lacrimation and salivation, a decrease in the average urinary flow with residual urine and hypersensitive pupillary constriction to the instillation of methacholine. On the other hand, the results of upright tilt testing, the Valsalva test and cold pressor test were all normal, and the plasma noradrenaline level was also normal. Therefore, the diagnosis of acute cholinergic dysautonomia was made. He resumed his clerical work without medication 3 months after the onset. One year and 4 months after the onset, clinical and laboratory examinations showed that hypohidrosis in the distal lower extremities remained unchanged. We found ten patients of acute cholinergic dysautonomia in the literature, and concluded that our patient should be classified as a typical case of this disease. Clinical reports of acute cholinergic dysautonomia are relatively rare, and our patient is the oldest among the reported patients.

Acute Disease↗
PubMed1993

[A case of acute polyradiculoneuropathy with autonomic disturbances following rubella infection].

A 32-year-old man developed a rash on his body and extremities following acute fever of a few days duration, and also noticed pain and spontaneous tingling sensations in his lower extremities. Because severe pneumonia with dyspnea and low arterial blood oxygen concentration were found on examination, he was admitted and treated. After recovering from pneumonia in two months, he complained of abdominal symptoms, such as constipation, nausea and vomiting, spontaneous tingling sensations in the lower extremities, and orthostatic dizziness and fainting. On neurological examination, a mild to moderate muscle weakness was found in the distal muscles of both extremities. The ankle jerk was absent. Both superficial and deep sensations were moderately to severely decreased in the feet with positive Romberg's sign. Constipation and vomiting with nausea were noted. Clinical and laboratory examinations revealed marked orthostatic hypotension and hypohidrosis. Motor and sensory conduction studies indicated the presence of axonal degeneration and segmental demyelination and remyelination in the limbs nerves. CSF examination indicated that protein was 150 mg/dl and the cell count to be 18/mm3. Titer of antibody to rubella virus was significantly elevated. There were no other abnormalities to indicate the cause of motor, sensory and autonomic neuropathies. Therefore, the diagnosis of acute polyradiculoneuropathy with autonomic disturbances after rubella infection, which is rare in the literature, was made.

Acute Disease↗
PubMed1993

A basic transthyretin variant (Glu61-->Lys) causes familial amyloidotic polyneuropathy: protein and DNA sequencing and PCR-induced mutation restriction analysis.

A new mutation of transthyretin (TTR) has been identified in a patient with late-onset familial amyloidotic polyneuropathy (FAP) of Japanese origin. Peptide mapping by reverse-phase high performance liquid chromatography to compare the patient's TTR with normal TTR showed the presence of an abnormal peptide. Amino acid sequence analysis of the peptide (residues 49-61) showed a lysine-for-glutamic acid substitution at position 61. This substitution, verified by direct DNA sequencing, was the result of a guanine to adenine change on exon 3 of the TTR gene. A polymerase chain reaction-induced mutation restriction analysis (PCR-IMRA) system was established to rapidly detect the missense mutation. TTR-Lys61 is the first variant TTR with a replacement of the acidic with basic amino acid to be found in the amyloid precursor proteins of FAP.

Aged↗
PubMed1993

Mutation of the myelin P0 gene in Charcot-Marie-tooth neuropathy type 1.

We had previously reported that the myelin P0 gene was responsible for Charcot-Marie-Tooth neuropathy type 1B (CMT1B). In this study we found a different mutation of the P0 gene in a family of Charcot-Marie-Tooth neuropathy type 1 without a DNA duplication in chromosome 17p11.2. The mutation, a histidine substitution for arginine at amino acid position 98, is located in the extracellular domain of P0 like as the mutations in the three pedigrees with CMT1B. The extracellular domain forms an immunoglobulin domain responsible for the function of P0 as an adhesion molecule. Alterations in the tertiary structure of the extracellular domain of P0 would modify the function of P0, resulting in an impairment of peripheral myelin compaction.

Adult↗
PubMed1993

[Japanese translation of profile of mood states (POMS)--interpretation of the fifty-six items of mood factors and their application in a manufacturing automotive parts factory].

As in Europe and the USA, POMS is now going to be widely used in the area of occupational health in Japan. However, the Japanese translation of POMS is still not well established. Therefore, in this study, we translated the POMS into Japanese, and using 261 medical students in their last three years of study, we analyzed whether the fifty-six items of the mood factors of POMS are correctly or differently interpreted compared with the classified mood states in the original POMS. The number of the items, differently interpreted at a higher frequency than 20% among the students, was about 20 on the average of three years. Many of the items fell under the heading of "depression-dejection" and "tension-anxiety". The number of items, differently interpreted at a lower frequency than 5% among the students, was about 15 on the average of three years. Many of these items belonged to "vigor". The Japanese translation of POMS was applied to 106 workers engaged in manufacturing automotive parts. Among male and female workers exposed to organic solvents, a positive correlation (P < 0.05) was found between the urinary hippuric acid level and the score of "anger-hostility". Negative correlations (P < 0.05-0.001) were found between the age and each score of "tension-anxiety", "depression-dejection", "anger-hostility", "fatigue" and "confusion". However, no significant difference in the score of any mood factors of POMS was found between the group of sixty-one workers exposed to organic solvents and the group of forty-five workers unexposed.(ABSTRACT TRUNCATED AT 250 WORDS)

Affect↗
PubMed1993

Characterization of asbestos fibers in lungs and mesotheliomatous tissues of baboons following long-term inhalation.

Changes in the dimensions of inhaled asbestos fibers in the lung and translocation of intrapulmonary asbestos fibers into mesothelial tissues were investigated in 17 baboons (5 exposed to amosite, 4 to chrysotile, 5 to crocidolite, and 3 unexposed). The animals received different cumulative doses of asbestos by inhalation, followed by varying recovery periods (0-69 months). All asbestos types induced pulmonary asbestosis with severity directly related to the cumulative dose. There were a larger number of asbestos bodies in the lung of the amphibole-exposed animals than in those exposed to chrysotile. A tissue burden study, using transmission electron microscopy on 25-microns paraffin sections, ashed in a low-temperature asher, was performed. Intrapulmonary amosite fibers were shorter in geometric mean length compared with a standard amosite sample (UICC) (3.3 microns). In explanation, it was considered that long fibers might not be able to reach the lower respiratory tract and/or long fibers might be fragmented into shorter fibers. Further, in the amosite-exposed group, the mean length of intrapulmonary fibers increased with the extension of recovery period, suggesting that shorter fibers had been cleared from the lung. The chrysotile standard sample (UICC) had a shorter geometric mean length (1.1 microns) than amosite. The mean length of intrapulmonary chrysotile did not noticeably change with the extension of inhalation and recovery periods; however, the mean width decreased with the extension of these periods. This finding strongly suggested that separation of thick chrysotile fibers had occurred in the lung. The crocidolite standard sample (Transvaal) had a shorter geometric mean length (1.4 microns) than amosite.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Axonal sprouting of motor nerve in acrylamide-intoxicated rats with progressive weakness.

Quantitative morphologic studies on the motor axons in endplates of extensor digitorum longus muscle (EDL M) and soleus muscle, and on the myelinated fibers of the nerve to EDL M and other lower limb nerves were made on rats showing progressive weakness, intoxicated with acrylamide for 4 weeks (test), using silver staining. Terminal sproutings were significantly greater in frequencies in test compared with control in both muscles. In addition, morphologic changes in test consisted of a significant increase in the number of axon terminal branches and in the frequency of swellings of the preterminal, terminal, and ultraterminal axons and in an increase of myelinated fibers showing axonal degeneration in the nerve to EDL M. Such findings were in contrast with the previous report that cumulative doses of acrylamide inhibit sprouting of motor axons in endplates.

Acrylamide↗
PubMed1993

Polyneuropathy due to ethylene oxide, propylene oxide, and butylene oxide.

Axonal neuropathy occurs due to occupational ethylene oxide (EtO) exposure. The experimental model of human EtO neuropathy was established. In addition, the neurotoxic effects of propylene oxide (PpO) and butylene oxide (BtO) were demonstrated in rats. Although no human neuropathy due to PpO or BtO is reported, both chemicals must be considered to be neurotoxic, based on this study.

Animals↗
PubMed1993

Smaller number of large myelinated fibers and focal myelin thickening in mutant quails deficient in neurofilaments.

The peripheral nervous system of a mutant of a Japanese quail deficient in neurofilaments (mutant) and of a normal Japanese quail (control) was morphometrically evaluated to characterize the morphological findings, especially those of the myelinated fibers of the mutant. In the proximal peroneal nerves, the frequency of the teased myelinated fibers showing the focal myelin thickening was higher in mutant than in control (P < 0.001) without obvious ongoing axonal degeneration and segmental demyelination. The total numbers of the myelinated fibers in the proximal and distal peroneal nerve, and in the tibial nerve branch to gastrocnemius muscle (pars medialis) were similar between control and mutant, although the number of the large myelinated fibers was less (P < 0.01) and the number of the small myelinated fibers was greater (P < 0.01) in mutant compared with control. The median diameters of neuronal cell bodies of the sacral dorsal root ganglia were similar in control and mutant. The percentages of light, dark and unclassified cells evaluated based on the histologic cytoplasmic features were also similar in control and mutant. Therefore, morphometric alterations were more pronounced in the peripheral myelinated nerve fibers compared with those in the cell bodies of the spinal dorsal root ganglia. We concluded that a smaller number of large myelinated fibers with a greater number of small myelinated fibers and the presence of focal myelin thickening are the main morphologic findings in this mutant, probably due to the arrest of radial growth or maturation of the axons of the myelinated fibers in the absence of ongoing myelinated fiber degeneration.

Animals↗
PubMed1993

Sulfhydryl drugs reduce neurotoxicity of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in the mouse.

Striatal levels of dopamine and its metabolites 3-methoxy-4-hydroxy-phenylacetic acid (DOPAC) and homovanillic acid (HVA) decreased 7 days after subcutaneous injection of MPTP (20 mg/kg) to the mouse. Striatal GSH contents decreased and GSSG/GSH ratios increased one hour after subcutaneous administration of MPTP. Pretreatments of both cysteamine (200 mg/kg, s.c.) and dimercaprol (20 mg/kg, i.m.) reduced the MPTP-induced decreases in striatal dopamine, DOPAC and HVA, and also prevented the MPTP-induced decreases in GSH levels and increases in GSSG/GSH ratios. On the other hand, injection of cysteamine did not modify the MPTP-induced decreases in striatal levels of dopamine and its metabolites when it was done 2 hours after MPTP administration. Moreover, pretreatment of cysteamine did not affect striatal concentrations of MPP+ in MPTP-treated mice. These results suggest that sulfhydryl drugs such as cysteamine and dimercaprol may reduce neurotoxicity of MPTP probably via changes in redox cycle of glutathione in the brain.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed1993

Cortical somatosensory potentials evoked by magnetic stimulation of thoracic and lumbar roots.

We applied twin coil magnetic stimulation to thoracic and lumbar roots to evaluate the posterior column function in 50 normal subjects and 34 patients with neurologic disorders. In all nine patients with cervical myelopathy, there were abnormal somatosensory evoked potentials (SEPs) with stimulation of upper thoracic levels. In 14 patients with thoracic or lumbar myelopathy, there were normal SEPs with stimulation of spinal roots above the lesions and abnormal SEPs with stimulation below the lesions. In a patient with girdle sensation between T-3 and T-6, the peak latencies of P2 were significantly delayed with stimulation of T-2 and T-4, but peak latencies were normal with T-6, T-10, and L-3 stimulation. Ten patients with polyneuropathy had normal SEPs recorded with thoracic and lumbar root stimulation. SEPs by twin coil stimulation at thoracic and lumbar root levels are useful in detecting lesions of spinal cord or roots and for following their clinical course noninvasively.

Adolescent↗
PubMed1993

Sudomotor potential evoked by magnetic stimulation of the neck.

We studied the sudomotor potential in the palm of the hand, evoked by magnetic stimulation of the neck, in 15 normal subjects and five patients with dysautonomia. The potentials consisted of two positive peaks (S1, S2), with mean (+/- SD) onset latencies of 408.5 +/- 31.8 and 619 +/- 61.4 msec. The sudomotor potential was clearly obtained only from the palm and was influenced by stimulus intensity, coil position, current direction in the coil, atropine or pilocarpine iontophoresis, and motor effort. With this method, we estimated the postganglionic sympathetic conduction time and the central reflex time, the mean values (+/- SD) of which were 408.5 +/- 31.8 and 323.3 +/- 45.2 msec. In three patients with severe dry skin, the sudomotor potential and the sympathetic skin response were not obtained. A patient with OPCA had a prolonged central reflex time, and a patient with alcoholic polyneuropathy showed a delayed sudomotor potential. Sudomotor potential is a noninvasive and useful method for evaluating sympathetic sudomotor function in patients with central and peripheral nervous system disorders.

Adult↗