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Biomedical subjects

T Mitsuma

Publications and source records attributed to T Mitsuma.

At least 217 records · Page 12Linked to original sources
PubMed1990

Type I familial amyloid polyneuropathy. A pathological study of the peripheral nervous system.

The neuropathological changes were examined in 2 cases of type I familial amyloid polyneuropathy (FAP), confirmed by a genetic study with human transthyretin (prealbumin) cDNA. These cases were from different foci of type I FAP in Japan, but showed a similar pathology in the peripheral nerves. Loss of dorsal root and sympathetic ganglion neurons, predominantly those of small size, was prominent, whereas ventral horn cells were well preserved. Distally accentuated axonal loss with marked axonal sprouting was the principal feature. Fibre sprouts were ubiquitous throughout the nerves and affected the fibre size distribution. Segmental demyelination and remyelination were prominent in the proximal portions of nerves, but axonal degeneration was more conspicuous in the distal portions. The centrally-directed branches of the primary sensory neurons did not show distally-accentuated axonal loss in the dorsal columns. Amyloid deposits were present universally in the endoneurial spaces of the peripheral nerves, but more prominently in the dorsal root ganglia, sympathetic ganglia and more proximal portions of the nerves, and the distribution correlated well with the occurrence of the pathology of peripheral nerves. Neurofilamentous accumulation was frequent in the proximal axons and neuronal cell bodies of the sensory and sympathetic neurons. Schwann cells and satellite cells to which amyloid deposits were attached frequently showed disappearance of basement membrane and proliferation of distorted processes. The findings in the present cases suggest that the Schwann and satellite cells may be directly affected by the amyloid deposits, but the pathogenetic mechanism of marked axonal and neuronal involvement still remains to be elucidated.

Adult↗
PubMed1990

[Spatial distribution of the peripheral nerve lesion in polyarteritis nodosa].

We have examined the peripheral nerves in four patients with polyarteritis nodosa. They were consisted of two males and two females with the age of 70, 49, 65 and 75 years respectively. The sciatic and posterior-tibial nerves, sural nerves, ventral and dorsal spinal nerve roots, dorsal ganglia and spinal cord were removed at autopsy. Particularly, the sciatic and posterior-tibial nerves were removed as a whole and suspended in a glass cylinder with a weight and fixed in 1.5% glutaraldehyde and 0.05 M phosphate buffer, pH 7.4 for 16 hours. The nerve fragments of every 3 to 3.5 cm along the sciatic and posterior-tibial nerve were examined on conventional paraffin-embedded and epon-embedded sections, and osmicated teased-fibers. Necrotizing angitis was commonly present in the epineurium of the sciatic and posterior-tibial nerves in all four patients. Although necrotizing angitis was diffusely distributed in the proximal to distal portions of the nerve, loss of myelinated fibers, occurred only in the distal to mid-lower portions of the sciatic nerve. There was no substantial myelinated fiber loss in the proximal part of the sciatic nerve in three of four cases. Myelinated fiber loss in the fascicle was central fascicular or multiple-focal in pattern in the proximal portions of the nerve, but was diffuse in more distal portion of the posterior tibial nerve. Segmental demyelination and myelin irregularity in the teased-fiber preparation were more prominently observed in the proximal portions, but fibers with axonal degeneration were more frequent in the distal portions of the nerve.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1990

Failure to demonstrate the effect of various pre-pro-TRH fragments on TSH and PRL release from rat pituitary in vitro.

The effects of Pro-thyrotropin-releasing hormone (TRH), pre-pro-TRH (53-74), pre-pro-TRH (83-106), pre-pro-TRH (115-151), pre-pro-TRH (160-169), pre-pro-TRH (178-199) and TRH on thyrotropin (TSH) and prolactin (PRL) release from the rat anterior pituitary were studied in vitro. The rat anterior pituitary was incubated in medium 199 (pH 7.4) with 1.0 mg/ml of bacitracin (medium) for 30 min. The amount of TSH and PRL release into the medium was measured by radioimmunassay. TSH and PRL release from the anterior pituitary was stimulated with the addition of TRH or pro-TRH in a dose-related manner, but not with other peptides. The findings suggest that TRH and pro-TRH stimulate TSH and PRL release from the anterior pituitary in vitro.

Animals↗
PubMed1990

Effects of thyroid hormone, TRH and TSH on pro-TRH concentrations in various organs of rats.

The effects of large doses of thyroid hormone, thyrotropin (TSH) or thyrotropin-releasing hormone (TRH) on pro-TRH concentrations in the rat hypothalamus, cerebrum, cerebellum, brain stem, stomach and eye were studied. The rats were administered T4 (2.5 mg/kg), T3 (375 micrograms/kg), TRH (1.0 mg/kg) or bovine TSH (1.25 IU/kg) i.p. and seven rats in each subgroup were decapitated at 4 or 24 h after the injection. Pro-TRH, TRH, TSH and thyroid hormone were measured by each radioimmunoassay. Immunoreactive pro-TRH (ir-pro-TRH) and immunoreactive TRH (ir-TRH) were found in the hypothalamus, cerebrum, brain stem, stomach and eye. Ir-pro-TRH concentrations in the hypothalamus decreased significantly after T4 and T3 injection and tended to decrease after TRH and TSH injection, but not significantly. In contrast, ir-pro-TRH concentrations in other tissues showed no changes after T4, T3, TRH or TSH injection. Ir-TRH concentrations in tissues did not change significantly after these hormone injection. The plasma TSH levels decreased significantly, while these of thyroid hormone increased significantly after thyroid hormone injection. Elution profile of acetic acid extracts of hypothalamus, stomach or eye was identical to that of synthetic pro-TRH. The findings suggest that the large dose of thyroid hormone inhibits pro-TRH synthesis in the hypothalamus, and that TRH synthesis in the tissues except the hypothalamus may not be regulated by thyroid hormone.

Animals↗
PubMed1990

[Autonomic dysfunction in vasculitic neuropathy--special reference to sudomotor function].

We examined autonomic functions in 14 patients with peripheral neuropathy caused by necrotizing vasculitis. These patients consisted of three allergic granulomatous angitis (Churg-Strauss syndrome, AGA), two systemic lupus erythematosus (SLE), two progressive systemic sclerosis (PSS), one mixed connective tissue disease (MCTD), one polyarteritis nodosa (PN) and five nonsystemic vasculitis. All of them were proven to have a vasculitis by sural nerve, muscle or skin biopsy. Sixteen age- and sex-matched healthy volunteers were also examined. Local sweating induced by intradermal injection of pilocarpine and nicotine (a concentration of 10(-4) g/dl, 0.1 ml) was measured with ventilated capsular method on the forearm and lower lateral leg at 23 degrees C of room temperature and 40% of relative humidity. Other autonomic functions including skin temperature at rest and after cold loading (15 degrees C, 6 minutes), variation in the R-R interval of heart beat (CV%), orthostatic hypotension and bladder dysfunction were also monitored. A decrease in sweat rate and recovery rate of skin temperature after cold-loading was seen more frequently in patients with necrotizing vasculitis than normal volunteers. Abnormality in the local sweat response against nicotine and pilocarpine was more frequently present in the involved area of somato-sensory and motor nerves as compared with those in the non-involved area. An occurrence of decrease in recovery rate of skin temperature after cold-loading also well correlated to the region of somato-sensory- and motor involvement. So far other autonomic dysfunction, only one patient had orthostatic hypotension, impotence and bladder dysfunction.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

[Myasthenia gravis associated with tonic pupil].

A 41 year-old female patient with acquired autoimmune myasthenia gravis (MG, IIa type) and tonic pupil (Adie's pupil) of the right side was reported. Adie's pupil was pointed out at the same time of the clinical diagnosis of MG in September, 1988. She had the solitary thymoma identified by pneumo-mediastinograph and mediastinal CT scan. Results of the positive anti-nicotinic AChR antibody titer, the positive edrophonium test and the electrophysiological examination gave unambiguous evidences of acquired autoimmune MG with thymoma. Instillations to the eyes of cocaine, pilocarpine and epinephrine, and the pupillary response to the intravenous injection of edrophonium revealed the postganglionic abnormality mainly in the parasympathetic system. There were no other overt symptoms due to dysautonomia. She refused thymectomy. Her myasthenic and pupillary signs became gradually improving without any immunosuppressive medications. It is concluded that two diseases of the patient may be probably caused by multiple organ- or tissue-specific autoantibodies, in addition to pathogenetic significance of Adie's pupil.

Adie Syndrome↗
PubMed1989

Low uptake of [3H]2-deoxy-D-glucose by cultured rat Schwann cells.

[3H]2-Deoxy-D-glucose (2-DG) was used to investigate the glucose uptake in cultured rat Schwann cells from postnatal Sprague-Dawley rat sciatic nerves. The glucose uptake of Schwann cells slightly increased in a time- and dose-dependent manner. However, the maximal uptake level was much lower than that of ethylnitrosourea (ENU)-induced transformed rat schwannoma-like cells and fibroblasts. By autoradiography of the cultured system, we were able to visualize the accumulation of [3H]2-DG grains in the schwannoma-like cells and fibroblasts, but not in Schwann cells.

Animals↗
PubMed1989

Nerve growth factor receptor immunoreactivity in human benign peripheral nerve sheath tumor.

In situ expression of nerve growth factor (NGF) receptors in human dermal and plexiform neurofibroma, schwannoma and traumatic neuroma was examined by an immunohistochemical method using a monoclonal anti-human NGF receptor antibody. Immunoreactivity for the NGF receptor was observed on the principal cells of both neurofibroma and schwannoma. Immunostaining by the anti-S-100 beta protein antibody in adjacent sections suggested that the vast majority of NGF receptor-positive cells were also positive for S-100 beta protein. In traumatic neuroma, staining for the NGF receptor was more intense in the perineurium than in the endoneurial cells.

Adult↗
PubMed1989

Radioimmunoassay for thyrotropin-releasing hormone precursor peptide, Lys-Arg-Gln-His-Pro-Gly-Arg-Arg.

A radioimmunoassay for thyrotropin-releasing hormone (TRH) precursor peptide Lys-Arg-Gln-His-Pro-Gly-Arg-Arg (pro-TRH), has been developed. Anti-pro-TRH antibody was raised in rabbits immunized with a conjugate of synthetic pro-TRH analog, Cys-Lys-Arg-Gln-His-Pro-Gly-Arg-Arg-Cys (pCC10) to bovine serum albumin. This antibody did not cross-react with TRH, TRH-OH, His-Pro-diketopiperazine, neuropeptides, pituitary hormones and peptides which are included in prepro-TRH. Radioiodination of pCC 10 was performed by chloramin T method, followed by purification of radioiodinated material on Sephadex G-25 column. Pro-TRH was extracted from tissues, using 1.0 N acetic acid. The assay was performed with a double antibody system. The values are expressed as an equivalent of pCC 10. The dilution curves of acetic acid-extracts of rat hypothalamus and stomach in radioimmunoassay system were parallel to the standard curve. The recovery of tissue pro-TRH was 80%, the intra-assay and interassay variation was 5.2% and 8.9%, respectively. The elution profiles of acetic acid-extracts of the rat hypothalamus and stomach on Sephadex G-50 showed a single peak corresponding that of pCC 10. Immunoreactive pro-TRH was found in the rat brain, spinal cord, eye, stomach, intestine, pancreas and adrenal gland. These data suggest that this assay system is a suitable to measure pro-TRH in the tissues, and that pro-TRH is widely distributed in the rats.

Adrenal Glands↗
PubMed1989

Effects of acetylcholine on thyrotropin-releasing hormone release from the rat caecum in vitro.

Effects of acetylcholine on the release of thyrotropin-releasing hormone (TRH) from the rat caecum in vitro were studied. The rat caecum was incubated in medium 199 with 1.0 mg/ml of bacitracin and 100 micrograms/ml of ascorbic acid (pH 7.4) (medium). The amount of TRH release into the medium was measured by radioimmunoassay. The immunoreactive TRH (ir-TRH) release from the rat caecum was enhanced significantly in a dose-related manner with the addition of acetylcholine, but not changed with atropine. The stimulatory effect of acetylcholine on ir-TRH release from the rat caecum was blocked with an addition of atropine. Elution profile of acid-methanol-extracted rat caecum on Sephadex G-10 was identical to that of synthetic TRH. The findings suggest that the cholinergic system stimulates TRH release from the rat caecum in vitro.

Acetylcholine↗
PubMed1989

Effects of opioid peptides on thyrotropin-releasing hormone release from the rat caecum in vitro.

Effects of opioid peptides (beta-endorphin, dynorphin (1-13). alpha-neoendorphin, beta-neoendorphin, leucine-enkephalin, methionine-enkephalin) on the release of thyrotropin-releasing hormone (TRH) from the rat caecum were studied in vitro. The rat caecum was incubated in medium 199 with 1.0 mg/ml of bacitracin (pH 7.4) (medium). The amount of TRH release from the rat caecum into the medium was measured by radioimmunoassay. The immunoreactive TRH (ir-TRH) release from the rat caecum was inhibited significantly in a dose-related manner with the addition of opioid peptides. The inhibitory effects of opioid peptides on ir-TRH release from the rat caecum were blocked with an addition of naloxone. The elution profile of acid-methanol-extracts of rat caecum on Sephadex G-10 was identical to that of synthetic TRH. The findings suggest that opioid peptides inhibit TRH release from the rat caecum in vitro.

Animals↗
PubMed1989

X-linked recessive bulbospinal neuronopathy. A clinicopathological study.

A clinicopathological study on X-linked recessive bulbospinal neuronopathy was undertaken on 9 cases, with morphological observations on 3 autopsied cases and sural nerve biopsies from 6 patients. Both lower motor and primary sensory neurons were involved. Lower motor neurons were markedly depleted through all spinal segments and in brainstem motor nuclei except for the third, fourth and sixth cranial nerves. Primary sensory neurons were less severely affected. A quantitative study of primary sensory axons at several levels in the peripheral nervous system suggested that a distally accentuated axonopathy was the salient pathological process. Segmental demyelination and remyelination clustered on individual fibres, and g ratios (axon diameter: total fibre diameter) in the sural nerve showed an increased scatter in some cases. Evidence of regeneration was inconspicuous. Unmyelinated fibres were well preserved throughout all the nerves examined. Neurons in the Onufrowicz nuclei, in the intermediolateral columns and in Clarke's columns of the spinal cord were generally well preserved. These observations indicate that a lower motor and primary sensory neuronopathy is a major neurological manifestation in this disease.

Aged↗
PubMed1989

Nerve growth factor receptor immunoreactivity in the neuronal perikarya of human sensory and sympathetic nerve ganglia.

We examined immunohistochemically the dorsal root ganglia, sympathetic ganglia, spinal cord, ventral and dorsal roots, and sciatic nerves obtained at autopsy from adult humans, using a monoclonal antibody against the human nerve growth factor receptor. We observed labelling in a granular pattern in the neuronal perikarya of dorsal root and sympathetic nerve ganglia. Ventral horn cells and axons were not labelled.

Antibodies, Monoclonal↗
PubMed1989

Myoinositol inhibits proliferation of cultured Schwann cells: evidence for neurotoxicity of myoinositol.

To determine whether so-called uraemic toxins exhibit direct toxic effects on Schwann cells, the latter were cultured in a monolayer with the addition of uraemic toxins. Proliferation of Schwann cells was estimated with [3H]-thymidine incorporation into DNA synthesis. Myoinositol, methylguanidine, guanidinosuccinic acid, parathyroid hormone, phenol, p-cresol, 4-hydroxyphenylacetic acid, 4-hydroxybenzoic acid, and 3-carboxy-4-methyl-5-propyl-2-furanpropionic acid were added at various concentrations to the culture medium. Addition of myoinositol at concentrations between 50 and 100 micrograms/ml, values analogous to those in in a dose-dependent way. Myoinositol also inhibited axolemma-stimulated proliferation of Schwann cells. The other compounds at concentrations occurring in uraemic serum did not show any toxic effect on Schwann cells. These results suggest that myoinositol has a neurotoxic effect on Schwann cells, and uraemic polyneuropathy seemed to be caused by a defect in maintaining normal myelin due to accumulation of myoinositol.

Animals↗
PubMed1989

[Migrating multiple mononeuritis and nonsystemic angitis].

Multiple mononeuritis of migrating nature at onset occurs in a variety of disease conditions. "Migrant sensory neuritis" without a systemic underlying disorder described by Wartenberg (1958) is the most distinctive form of this type of neuropathy. Its pathomechanism is not uniform, but angiopathy has been suggested by Matthews et al. (1981). In this report, we describe five cases of sensory-dominant multiple mononeuritis with migrating nature and without systemic visceral involvement. The patients consisted of four females and one male between 26 and 71 years of age. All showed recurrent episodes of sensory involvement along the distal branches of the cutaneous nerve. The patients presented with sudden onset of numbness or pain radiating along the cutaneous branches of the involved nerves often followed by persistent sensory deficit. In mild episodes, the sensory symptom with numbness almost completely subsided. The frequency of these episodes ranged from 7 times in 6 months to 6 times in 9 years. The clinical manifestations were similar or identical to those of migrant sensory neuritis reported by Watenberg and Matthews et al. Cranial nerve involvement and less frequent episodes in the present series differed from those in the previous reports. Laboratory examinations did not disclose any underlying disorder, suggesting systemic collagen vascular disease. Sural nerve biopsy study in two patients revealed vasculitis in small or medium-sized arteries in the epineurium as well as reduced population of large myelinated fibers. Small myelinated fibers were slightly increased in number, probably to regenerating fibers. Sensory action potentials were low or not evoked in the nerves examined.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗