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T Mitsuma

Publications and source records attributed to T Mitsuma.

At least 91 records · Page 5Linked to original sources
PubMed1996

Expression of glial cell line-derived growth factor mRNA in the spinal cord and muscle in amyotrophic lateral sclerosis.

The steady-state expression levels of glial cell line-derived growth factor (GDNF) mRNA was studied in the post mortem spinal cord and muscle of patients with amyotrophic lateral sclerosis (ALS), by reverse transcription followed by polymerase chain reaction (RT-PCR). GDNF mRNA levels in the lumbar cord were significantly increased in ALS as compared with controls. On the other hand, GDNF mRNA levels were significantly lower in the muscle in ALS patients. The increase of GDNF mRNA in the spinal cord mostly reflected an increase in the anterior horn, anterior and lateral columns, where the pathological involvement was severe. In the posterior column and posterior horn with less pathological involvement, the increase was less. These results suggest that GDNF mRNA levels are inversely regulated between the spinal cord and muscle in ALS, increased in the spinal cord and lowered in the muscle, in correlation with the pathological severity.

Aged↗
PubMed1996

Possible mechanism of anhidrosis in a symptomatic female carrier of Fabry's disease: an assessment by skin sympathetic nerve activity and sympathetic skin response.

Fabry's disease, X-linked alpha-galactosidase deficiency, features a variety of autonomic abnormalities including anhidrosis. In this study, we measured the skin sympathetic nerve activity (SSNA), skin potential and sweat rate in a symptomatic female carrier to investigate the underlying pathophysiology of anhidrosis. The basal activity and responsiveness of SSNA were both fairly well preserved, although slightly reduced compared with the control levels. However, sweating was completely absent, despite the normal skin potential change in response to SSNA bursts. These results suggest that anhidrosis in Fabry's disease is a result of sweat gland dysfunction as well as abnormal SSNA.

Adult↗
PubMed1996

Abnormal neuropeptide concentration in rectal mucosa of patients with inflammatory bowel disease.

Regulatory neuropeptides are widely distributed in the gastrointestinal tract, where they play an important role in motility, secretion, and immune and inflammatory responses. In this study, the rectal mucosal content of somatostatin (SOM), substance P (SP), beta-endorphin (BE), and thyrotropin-releasing hormone (TRH) was measured by radioimmunoassay in 56 patients with ulcerative colitis (UC), 15 patients with Crohn's disease (CD), 15 patients with acute infectious colitis (AIC), and 11 controls, who showed no inflammation of the rectal mucosa, nor abnormal bowel movements. The content of immunoreactive (ir)-SOM was decreased in UC patients, especially in those with persistent disease activity, while the levels of ir-SP, BE, and TRH were increased in such patients. Some changes of ir-peptide levels were also observed in CD and AIC patients. The changes in neuropeptide levels were analyzed in relation to histological grades of inflammation in UC patients, grades 4-5 showing the most significant changes. The levels of ir-SOM, SP, BE, and TRH showed no significant change in chronic persistent UC when measured 6-12 months after the initial examination. In contrast, in patients with remitting intermittent UC, the levels of SP and BE decreased during remission. Abnormal intestinal neuropeptide content may be implicated in the continued mucosal immune and inflammatory responses that are manifested in patients with inflammatory bowel disease.

Adult↗
PubMed1996

Expression of mRNAs for neurotrophic factors (NGF, BDNF, NT-3, and GDNF) and their receptors (p75NGFR, trkA, trkB, and trkC) in the adult human peripheral nervous system and nonneural tissues.

The steady-state mRNA levels of the four neurotrophic factors of nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3) and glial cell line-derived neurotrophic factor (GDNF) and their receptors (p75NGFR, trkA, trkB and trkC) in the adult human peripheral nervous system (PNS) as well as nonneural tissues were examined using quantitative reverse transcription-polymerase chain reaction (RT-PCR). NGF and BDNF mRNA levels were high in the heart and spleen as well as in the dorsal root ganglia (DRG) and spinal cord, showing similar spatial expression patterns, while NT-3 mRNA levels were more pronounced in the liver and spleen. In contrast to these neurotrophins, GDNF mRNA expression occurred at the highest levels in the muscle, and it was also comparatively high in the spinal cord. p75NGFR mRNA was expressed extensively throughout the PNS tissues and in the spleen. The spatial expression patterns differed among trkA, and trkB and trkC mRNAs. trkA mRNA was greatly expressed in the DRG, sympathetic ganglia and spleen, while the trkB and trkC mRNA levels were high in the DRG, spinal cord and brain. The levels of trkB and trkC mRNAs with tyrosine kinase domain, compared to those with extracellular domain, were relatively high in the DRG, whereas they were low in the spinal cord and brain. The spatial patterns of the distributions of neurotrophic factors and their receptors mRNA levels in the adult human PNS and nonneural tissues are largely similar to those reported in other mammals, but these findings provide further, more specific, understanding relevant to the therapeutic approach to human diseases.

Adult↗
PubMed1996

Age-related changes in human spinal ventral horn cells with special reference to the loss of small neurons in the intermediate zone: a quantitative analysis.

A cytoarchitectonic study of spinal ventral horn cells was performed to identify age-related changes. The diameter distribution of ventral horn neurons of the fourth lumbar segment of the spinal cord and their size and topographical distributions were investigated in 14 autopsy cases. These cases represented patients of 18-100 years of age who had died of non-neurological diseases. The results indicate that small neurons widely distributed in the intermediate zone of the ventral horn significantly diminished with aging (P < 0.0005, r = -0.898), whereas medium-sized and large neurons located in the medial and lateral nuclei showed only a slight decrease with advancing age. The total number of neurons in the whole ventral horn was also noted to decrease significantly with aging (P < 0.0005, r = -0.899). While small neurons in the intermediate zone of the ventral horn are thought to be mostly interneurons, their physiological function still remains obscure in many respects. The findings of this study provide insight into age-related cell loss in terms of size and location.

Adolescent↗
PubMed1996

Differential pattern in tissue-specific somatic mosaicism of expanded CAG trinucleotide repeats in dentatorubral-pallidoluysian atrophy, Machado-Joseph disease, and X-linked recessive spinal and bulbar muscular atrophy.

We investigated the somatic mosaicism of trinucleotide repeat expansion in the neural and nonneural tissues of a dentatorubral-pallidoluysian atrophy (DRPLA), Machado-Joseph disease (MJD), and spinal and bulbar muscular atrophy (SBMA) patient and their correlation to the topographical distribution of the pathological involvement. The spatial pattern of tissue-specific somatic mosaicism in the CAG repeat size was significantly different among the DRPLA, MJD and SBMA patients. The size of the major bands of the mutant CAG repeat allele was significantly smaller in the cerebellar cortex in both DRPLA and MJD patients by 6 and 2 repeat units respectively and larger in the colon and liver of DRPLA by 5 repeats or more. There were also 1-2 repeat-sized small variations of major band size among the neural tissues in DRPLA. In contrast, there was no tissue-specific variation of major bands of CAG repeats and diversity of extra bands among the examined tissues including the cerebellum in the SBMA patient. There was no parallel occurrence of tissue-specific CAG instability and severity of neuropathological involvement in the neural and nonneural tissues of DRPLA, MJD and SBMA patients. Lack of significant tissue-specific somatic mosaicism in SBMA including the cerebellar cortex may suggest that CAG repeat expansion in the mutant androgen receptor gene is far more stable compared with that in DRPLA and MJD as well as those reported in Huntington's disease.

Adult↗
PubMed1996

Demonstration of slow acetylator genotype of N-acetyltransferase in isoniazid neuropathy using an archival hematoxylin and eosin section of a sural nerve biopsy specimen.

The genotype for N-acetyltransferase was analyzed in five Japanese patients with isoniazid neuropathy by using the allele specific polymerase chain reaction for a single slice of the 30-year-old paraffin-embedded and hematoxylin-eosin stained sural nerve biopsy specimens. We found slow acetylator genotypes for N-acetyltransferase in all isoniazid neuropathy patients. This result confirmed that patients with the slow acetylator genotype tend to develop neuropathy after administration of isoniazid.

Acetylation↗
PubMed1996

Effects of serotonin on the release of thyrotropin-releasing hormone from the rat retina in vitro.

Effects of serotonin on the release of thyrotropin-releasing hormone (TRH) from the rat retina were studied in vitro. The retina was incubated in medium 199 (pH 7.4) with 1.0 mg/ml of bacitracin and 100 micrograms/ml of ascorbic acid (medium) for 20 min. The amount of TRH release into the medium was measured by radioimmunoassay. The TRH release from the rat retina was inhibited significantly in a dose-related manner with the addition of serotonin and enhanced with cyproheptadine. The inhibitory effect of serotonin on TRH release from the retina was blocked with the addition of cyproheptadine. The elution profile of methanol extract of the rat retina was identical to that of synthetic TRH. The findings suggest that the serotonergic system inhibits TRH release from the rat retina in vitro.

Animals↗
PubMed1996

Short stature due to growth hormone deficiency associated with Cushing's disease and ulcerative colitis.

We report a rare case of Cushing's disease associated with ulcerative colitis in a patient primarily treated with growth hormone due to short stature. At the age of fifteen years, the patient had a short stature due to GHD and was treated with the extracted GH for a short period. At the age of twenty-one years, his body weight gradually increased and, based on the results of several tests, he was diagnosed with Cushing's disease and GHD was observed in our patient. The excess secretion attenuation of pituitary hormones with reduced secretion periods as well as the relation between ulcerative colitis and elevated plasma cortisol concentrations is briefly discussed in this paper.

Adult↗
PubMed1996

Founder effect in spinal and bulbar muscular atrophy (SBMA).

We analyzed the polymorphic (CAG)n and (GGC)n repeats of the androgen receptor gene in 113 unrelated X-linked spinal and bulbar muscular atrophy (SBMA) X chromosomes and 173 control X chromosomes in Japanese males. The control chromosomes had an average CAG repeat number of 21 +/- 3 with a range from 14-32 repeat units, and SBMA chromosomes had a range from 40-55 with a median of 47 +/- 3 copies. The control chromosomes had seven different alleles of the (GGC)n repeat with the range of 11 to 17; the most frequent size of (GGC)n was 16 (79%), while (GGC)17 was very rare (1%). However, in SBMA chromosomes only two alleles were seen; the most frequent size of (GGC)n was 16 (61%) followed by 17 (39%). (GGC)n size distribution was significantly different between SBMA and control chromosomes (P < 0.0001), indicating the presence of linkage disequilibrium. There was no allelic association between the (CAG)n and (GGC)n microsatellites among control subjects as well as SBMA patients, which suggests that a founder effect makes a more significant contribution to generation of Japanese SBMA chromosomes than new mutations.

Genetic Linkage↗
PubMed1996

Infarction of superior cerebellar artery presenting as cerebellar symptoms.

BACKGROUND: MRI of the brain has facilitated the diagnosis of cerebellar infarction in the territory of the superior cerebellar artery (SCA). We analyzed the data on patients with SCA infarction who presented with only cerebellar symptoms in an attempt to define its underlying pathophysiology. SUMMARY OF REPORT: Ten patients with SCA infarction who presented with cerebellar symptoms were studied by brain MRI, angiography, and underlying pathology. Brain MRI demonstrated an infarct in the SCA territory in the anterior rostral cerebellum of all patients. None had abnormalities in the brain stem. In four patients, a hemorrhagic infarct was present in the same region. Cerebral angiography revealed no obvious SCA occlusion or atherosclerotic vascular disease in any patient. Eight of the 10 patients had heart disease, such as atrial fibrillation or old myocardial infarction. The presumed diagnosis was occlusion of the SCA in its periphery due to cardiogenic embolism. CONCLUSIONS: When a patient presents with only cerebellar symptoms and has cerebellar infarction demonstrated by brain MRI, the SCA branch is probably occluded by cardiogenic embolism.

Aged↗
PubMed1996

Selective loss of small myelinated fibers in the lateral corticospinal tract due to midbrain infarction.

Small myelinated fibers in the lateral corticospinal tract (LCST) were selectively diminished as compared with large myelinated fibers in a patient with an old paramedian midbrain infarct involving the red nuclei, oculomotor nuclei, and inferior olivary pseudohypertrophy. Although the physiologic function of small myelinated fibers in the LCST is unknown in humans, we hypothesize that some of these fibers may include the rubrospinal tract.

Cerebral Infarction↗
PubMed1996

Distribution of somatostatin receptor type 2 in the rat: immunohistochemical study.

Somatostatin receptor type 2 (SSTR-2) was identified immunohistochemically in the rat tissues using specific antipeptide antiserum raised in New Zealand white rabbits immunized with a conjugate of synthetic SSTR-2 peptide (31-41) with bovine serum albumin. Immunohistochemical analysis was performed by avidin-biotin complex method. SSTR-2 immunoreactivity was visualized in the central nervous system and anterior pituitary thus supporting previous investigations of SSTR-2 distribution using in vitro autoradiographic ligand binding. Significant stain was detected in neural perikarya, axons and dendrites as well as in many cells of retina, adrenal medulla, gastric and duodenal mucosa, Auerbach's nervous branch and Meíssner's nervous branch of the stomach, small intestine and colon. When using antiserum preincubated with synthetic SSTR-2 peptide (31- 41) or rat anterior pituitary homogenate which contains SSTR-2 peptide, no significant stain of the anterior pituitary or neurons in the hypothalamus was detected. These findings suggest that SSTR-2 is widely distributed and that the method used is valuable in studying the distribution of SSTR-2 in rats.

Journal Article↗
PubMed1996

Effect of anti-TRH-receptor antibody on corticosterone release from rat adrenal gland in vitro.

The effect of anti-thyrotropin-releasing hormone (TRH) receptor antibody on corticosterone release from the rat adrenal gland in vitro was studied. The adrenal glands were incubated in medium 199 with 1.0 mg/ml bacitracin (pH 7.4, medium) for 20 min and the release of corticosterone into the medium was measured by radioimmunoassay. TRH inhibited corticosterone release from the adrenal gland in a dose-related manner. The inhibitory effect of TRH on corticosterone release from the adrenal gland was prevented by the addition of anti-TRH-receptor antibody. The present findings suggest that TRH inhibits corticosterone release from the adrenal gland in vitro and its effect is mediated via TRH receptor.

Journal Article↗
PubMed1996

[A case of erythroleukemia found after multiple cerebral hemorrhage].

A 61-year-old man without hypertension was admitted for unconsciousness. Brain CT showed multiple cerebral hemorrhage of the left frontal lobe and right occipital lobe. The hemoglobin was 7.0 g/dl, the platelet count 7,000, the white-cell count 7,600 with erythroblasts, and the fibrinogen 327 mg/dl. No disseminated intravascular coagulation was found. Bone marrow examination demonstrated 69.2% erythroblasts including abnormal types of nucleus, 12.8% myeloblasts, 12.8% neutrophils, 0.8% monocytes, 4% lymphocytes, and 0.4% reticulocytes. Chromosomal examination showed 7 of 20 bone marrow cells were variously abnormal. A diagnosis of erythroleukemia with major karyotype aberrations (MAKA) was made. The patient died 5 days after admission. Histologically, cerebral hemorrhagic lesions showed complete necrosis, but neither invasion of leukemic cells nor amyloid angiopathy. We suspected that the cause of cerebral hemorrhage was severe loss of platelets. This is a rare case of erythroleukemia found after multiple cerebral hemorrhage. As a cause of cerebral hemorrhage in an old man without hypertension, one should consider not only cerebral amyloid angiopathy but also leukemia.

Cerebral Hemorrhage↗
PubMed1996

[Immunostaining of mitochondrial heat shock proteins (mtHSPs) in skeletal muscle fibers of mitochondrial cytopathy].

Expression of the mtHSPs (HSP60 and mtHSP70) was immunohistochemicall observed in biopsied limb muscles of genetically determined mitochondrial cytopathies (chronic progressive ophthalmoplegia 14, MELAS 4, limb girdle syndrome with the A-to-G transition at nt.3243 of tRNALeu(UUR), exertional myoglobinuria with multiple deletions of mtDNA 2, and Leber's hereditary optic neuropathy 2). mtHSP 70 and HSP 60 were strongly localized at ragged-red fibers. In strongly succinate dehydrogenase-reactive vessels of MELAS, mtHSP70 was expressed. GRP78 was expressed in the cytoplasmic body, which is often observed in this disorder. The present data suggest that expression of mtHSPs may reflect increased numbers of mitochondria, an impairment of assembly of mitochondrial proteins encoded by the genomic DNA and abnormal mitochondrial DNA, and/or an impaired mitochondrial function due to recurrent oxygen radical attacks against mitochondria.

Chaperonin 60↗
PubMed1996

[Favorable prognosis in a case of recurrent cerebral infarctions caused by chronic disseminated intravascular coagulation due to ovarian carcinoma].

We report a 53-year-old woman who developed a cerebral infarction in the left middle cerebral artery area. Although she did not have a hemorrhagic tendency, the results of her examination showed a chronic disseminated intravascular coagulation (DIC) and a left ovarian carcinoma. Gabexate mesilate (FOY) and nafamostat mesilate (FUT) were not effective for her DIC. One month after admission, she had another cerebral infarction in the right posterior cerebral artery area. She was treated by heparin sodium and her chronic DIC improved. Then, she was operated on for ovarian carcinoma; the histologic finding was clear cell adenocarcinoma. No recurrence of DIC nor cerebral infarction was observed postoperatively. Patients with cerebral infarctions caused by chronic DIC due to ovarian carcinoma have been reported in the literature, but few patients had a favorable prognosis such as the present case. Heparin therapy appears to be the treatment of choice for chronic DIC rather than FOY or FUT, if there is no hemorrhagic tendency. When a patient with DIC develops cerebral infarction, one should always investigate for possible malignant tumors.

Adenocarcinoma, Clear Cell↗