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Biomedical subjects

Masaya Oda

Publications and source records attributed to Masaya Oda.

At least 19 recordsLinked to original sources
PubMed2005

Expression of adhesion molecules on mature cholangiocytes in canal of Hering and bile ductules in wedge biopsy samples of primary biliary cirrhosis.

AIM: To examine the expression of intercellular adhesion molecule-1 (ICAM-1) and lymphocyte function-associated antigen-1 (LFA-1) expression on canals of Hering (CoH) and bile ductules associated with the autoimmune process of bile duct destruction in primary biliary cirrhosis (PBC). METHODS: Ten wedged liver biopsies of PBC (five cases each of stages 2 and 3) were studied. The liver specimens were processed for transmission electron microscopy. Immunohistochemistry was performed using anti-ICAM-1 and anti-LFA-1 mouse mAbs. In situ hybridization was done to examine the messenger RNA expression of ICAM-1 in formalin-fixed, paraffin-embedded sections using peptide nucleic acid probes and the catalyzed signal amplification (CSA) technique. Immunogold-silver staining for electron microscopy was performed using anti-ICAM and anti-LFA-1 mouse mAbs. The immunogold particles on epithelial cells of bile ductules and cholangiocytes of CoH cells were counted and analyzed semi-quantitatively. Western blotting was performed to confirm ICAM-1 protein expression. RESULTS: In liver tissues of PBC patients, immunohistochemistry showed aberrant ICAM-1 expression on the plasma membrane of epithelial cells lining bile ductules, and also on mature cholangiocytes but not on hepatocytes in CoH. LFA-1-positive lymphocytes were closely associated with epithelial cells in bile ductules. ICAM-1 expression at protein level was confirmed by Western blot. In situ hybridization demonstrated ICAM-1 mRNA expression in bile ductules and LFA-1 mRNA in lymphocytes infiltrating the bile ductules. By immunoelectron microscopy, ICAM-1 was demonstrated on the basal surface of epithelial cells in bile ductules and on the luminal surfaces of cholangiocytes in damaged CoH. Cells with intermediate morphology resembling progenitor cells in CoH were not labeled with ICAM-1 and LFA-1. CONCLUSION: De novo expression of ICAM-1 both on mature cholangiocytes in CoH and epithelial cells in bile ductules in PBC implies that lymphocyte-induced destruction through adhesion by ICAM-1 and binding of LFA-1-expressing activated lymphocytes takes place not only in bile ductules but also in the CoH.

Aged↗
PubMed2005

High expressions of caveolins on the proliferating bile ductules in primary biliary cirrhosis.

AIM: An increase in bile ductular structures is observed in diverse human liver diseases, especially in primary biliary cirrhosis (PBC). These structures harbor the progenitor cell component of the liver. Caveolins are cholesterol-binding proteins involved in the regulation of several intracellular processes including cholesterol transport. This study aims to examine the role of caveolin in PBC. METHODS: Immunohistochemical and Western blotting studies were performed on human liver specimens obtained from patients with PBC and normal liver samples. The expression of caveolin (CAV)-1 and -2 was determined using specific antibodies. RESULTS: In normal liver, scanty immunostaining for CAV-1 and -2 was observed in bile ductules. In PBC liver samples, the expression levels of CAV-1 and -2 were increased on proliferating bile ductules especially in stage 3 cases, but was sparse on interlobular bile duct in stage 1 specimens. Especially, the regenerating bile ductules at the interface of portal tracts and necrotic areas were immunostained intensely for CAV-1 and -2. These phenomena were confirmed by Western blot. CONCLUSION: The present results demonstrate increased expression of caveolins in proliferating bile ductules in PBC, which may be related to the homeostasis of cholesterol transport in regenerating bile ductules in PBC liver.

Adult↗
PubMed2005

Metaiodobenzylguanidine (MIBG) scintigraphy at various parts of the body in Parkinson's disease and multiple system atrophy.

We compared MIBG uptake at various parts of the body in controls and patients with Parkinson's disease and multiple system atrophy. In the heart, MIBG uptake in Parkinson's disease (early H/M: 1.668+/-0.325, late H/M: 1.500+/-0.402) was less than that in multiple system atrophy (early H/M: 2.395+/-0.186, late H/M: 2.530+/-0.391) and controls (early H/M: 2.635+/-0.508, late H/M: 2.575+/-0.635) (early: P<0.0001, late: P<0.0001). There were no significant differences in uptake by the lung, thyroid, or liver in the three groups. Only on early images, uptake in the shoulder in multiple system atrophy (early S/M: 0.473+/-0.78) and Parkinson's disease (early S/M: 0.470+/-0.710) was decreased compared to that in controls (early S/M: 0.560+/-0.118) (P=0.0252). MIBG is reported to be taken up in the terminal part of sympathetic nerves and demonstrates sympathetic nerve activity, especially on late images. The cause of differences between the heart and other parts of the body remains unknown. We consider the following possibilities: (a) differences in the sympathetic nervous system between Parkinson's disease and multiple system atrophy are more subtle in organs other than the heart; (b) the cause of MIBG uptake reduction by the heart in Parkinson's disease involves factors in addition to sympathetic nervous system damage; and (c) MIBG uptake by organs other than the heart involves not only the sympathetic nervous system but also non-neuronal components. In conclusion, MIBG uptake by organs other than the heart cannot differentiate Parkinson's disease from multiple system atrophy at present.

3-Iodobenzylguanidine↗
PubMed2005

Candesartan reduces superoxide production after global cerebral ischemia.

Excessive superoxide production after cerebral ischemia is known to mediate neuronal injury. Angiotensin II type 1 receptor activation results in production of superoxide, but whether angiotensin II type 1 receptor blockade prevents production of superoxide and subsequent neuronal injury after ischemia remains unclear. Normotensive rats received the angiotensin II type 1 receptor blocker, candesartan or only vehicle before induction of global cerebral ischemia. Approximately 30% of the hippocampal CA1 neurons survived in candesartan-treated animals, whereas only 2% of neurons survived in vehicle-treated animals. Superoxide production was significantly less in these vulnerable neurons in candesartan-treated animals than in vehicle-treated animals. Angiotensin II type 1 receptor may have an essential role in superoxide production and subsequent injury in vulnerable neurons after global cerebral ischemia.

Animals↗
PubMed2005

Three-dimensional stereotactic surface projection study of freezing of gait and brain perfusion image in Parkinson's disease.

Gait disturbance is a cardinal symptom in patients with Parkinson's disease. Among the gait disturbances, freezing of gait is a unique and troublesome symptom, but its mechanism is unclear. We compared brain perfusion images using three-dimensional stereotactic surface projection analysis of N-isopropyl-p-123I iodoamphetamine single photon emission computed tomography between Parkinson's disease patients with freezing of gait and those without. Twenty-four cases (freezing of gait group) with Parkinson's disease with freezing of gait, and 31 Hoehn and Yahr stage-matched cases (no freezing of gait group) with Parkinson's disease without freezing of gait were studied. Bilateral Brodmann area 11 perfusion of the freezing of gait group decreased significantly compared to that of the no freezing of gait group. The Brodmann area 11 may play important roles in gait, and impairment in this region may have a close relationship with freezing of gait in Parkinson's disease.

Aged↗
PubMed2005

Metaiodobenzylguanidine (MIBG) uptake in Parkinson's disease also decreases at thyroid.

BACKGROUND: Decreased cardiac metaiodobenzylguanidine (MIBG) uptake was reported in Parkinson's disease and this contributes to the differential diagnosis between Parkinson's disease and other forms of parkinsonism such as multiple system atrophy. However, decreased MIBG uptake of the thyroid has not been demonstrated. OBJECTIVE: To compare MIBG uptake of the thyroid among Parkinson's disease, multiple system atrophy and controls. METHODS: Twenty-six patients with Parkinson's disease, 11 patients with multiple system atrophy and 14 controls were examined in this study. Planar images were taken 15 minutes (early images) and 3 hours (late images) after intravenous injection of 111 MBq 123I-MIBG. RESULTS: MIBG uptake of the thyroid on early images decreased significantly in Parkinson's disease compared to controls (p < 0.0001) and multiple system atrophy (p = 0.018). MIBG uptake of the thyroid on early images decreased significantly also in multiple system atrophy compared to controls (p = 0.027). On late images, thyroid uptake differed significantly only between Parkinson's disease and controls (p = 0.010). CONCLUSIONS: Our study is the first to demonstrate decreased MIBG uptake of the thyroid in Parkinson's disease. Sympathetic nervous denervation of Parkinson's disease occurred not only in the heart but also in the thyroid.

3-Iodobenzylguanidine↗
PubMed2005

Brain perfusion differences between Parkinson's disease and multiple system atrophy with predominant parkinsonian features.

BACKGROUND: The patterns of regional cerebral blood flow in Parkinson's disease and multiple system atrophy remain inconsistent. OBJECTIVES: To compare brain perfusion images of 123I-IMP SPECT between Parkinson's disease, multiple system atrophy with predominant parkinsonian features (MSA-P) and controls. METHODS: Eighty-two patients with Parkinson's disease, 10 patients with MSA-P and 14 controls were studied. We performed 3D-SSP and volume of interest analysis using 123I-IMP scintigraphy. RESULTS: Occipital perfusion of MSA-P increased compared to that of Parkinson's disease and perfusion in the cerebellum and primary sensorimotor cortex of Parkinson's disease increased compared to that of MSA-P. Perfusion in the putamen of MSA-P decreased compared to that of Parkinson's disease. CONCLUSION: Our study demonstrated perfusion differences in 123I-IMP SPECT between the two diseases.

Aged↗
PubMed2005

Multiple sclerosis following splenectomy as a treatment for idiopathic thrombocytopenic purpura.

A 27-year-old woman was admitted to our hospital with tetraparesis, dysesthesia and hypoesthesia of all regions below the breasts, urinary disturbance, and difficulty in breathing. Since age 21 idiopathic thrombocytopenic purpura (ITP) was diagnosed and steroid therapy was continued. At age 26, she had splenectomy for her ITP. On admission, steroid pulse therapy was administered with a tentative diagnosis of transverse myelitis. Symptoms gradually ameliorated. At age 29, she gradually lost her left vision, and multiple sclerosis was diagnosed and steroid therapy was administered, and her left vision gradually ameliorated. There are several reports describing other autoimmune disorders that arise after splenectomy. Since the spleen acts as a major pool of type 2 helper T cells, it is plausible that peripheral type 1 helper T cell activity may increase after splenectomy, promoting the development of autoimmune disorders. We considered there would be a close relation between splenectomy for ITP and multiple sclerosis in this case.

Adult↗
PubMed2005

[Significance of shunt efficacy decision of SPECT on idiopathic normal pressure hydrocephalus].

PURPOSE: The purpose of this study was to investigate the significance of the shunt-effect evaluation of SPECT in idiopathic normal pressure hydrocephalus (iNPH). SUBJECTS AND METHODS: The subjects were 15 patients with possible iNPH, aged 62-83 (mean 75.3, the ratio of males to females to 6:9), who were treated at our department during the period from June to September, 2004. All patients received the lumbar tap test (LTT) at the outpatient section before surgery. An L-P shunt was conducted on patients whose the LTT positive or negative with cerebrospinal fluid outflow resistance value (Ro) was 10 mmHg/ml/min. or higher patients. As for SPECT, a 3D-SSP Z-score, as well as an mCBF, was conducted before and after the LTT and within one month after surgery. Comparisons were made for (1) the shunt effect, (2) mCBF before and after the LTT and after surgery, (3) mean cerebral blood flow increase rate (mIR) after the LTT, and (4) 3D-SSP before and after surgery. RESULTS: (1) The shunt was effective for all the patients. (2) The mCBF levels was 30.8 +/- 4.02 ml/100 g/min. before the LTT, 37.1 +/- 100 g/min. after the LTT, and 38.6 +/- 3.4 ml/100 g/min. after surgery. A significant increase in mCBF was observed both after the LTT and after surgery (p < 0.05). (3) The mean mIR after the LTT was 21.2 +/- 8.01%, with all the patients showing 10% or higher. (4) The ischemic patterns in the SD-SSP Z-score before surgery were the frontal type (F: 10 cases, 66.7%), the occipitotemporal type (OT: 3 cases, 20%), and the mixed type (M: 2 cases, 13.3%), but not the parietal localized type. The post-operative course showed no-change in 4 cases, disappearance-reduction in 9 cases, and shift to OT in 2 cases. CONCLUSION: The evaluation factors in the measurement of the cerebral blood flow for evaluation of the shunt effect were the following two items. (1) The mIR of mCBF after the LIT was 10% or higher. (2) As for the preoperative cerebral ischemic patterns, there were many F cases and no parietial localized types found.

Aged↗
PubMed2005

[Reinvestigation of CSF outflow resistance value in idiopathic normal pressure hydrocephalus--comparing epidural pressure monitoring with lumbar subarachnoid cerebrospinal fluid pressure monitoring].

PURPOSE: To compare the cerebrospinal fluid (CSF) outflow resistance values (Ro) with epidural pressure (EDP) monitoring and lumbar subarachnoid CSF pressure (L-CSFP) monitoring. SUBJECTS AND METHODS: The subjects were 14 patients with possible iNPH (age: 59-74 years old, ratio of male and female 8:6). All the patients were subjected to an infusion test by a single bolus injection method (1 ml/sec., deltaV: 5 ml, t2: 2 min) as prescribed in the Standard of SINPHONI. EDP was monitored by continuous monitoring and the L-CSFP values By intermittent simple glass tube method (SINPHONI) were measured simultaneously. The Ro (RoEDP, RoL-CSFP) calculated from both methods, (1) the correlation of Ro and (2) the Ro threshold in a shunt effective group (E: nine cases) and a non effective group (NE, five cases) were compared. RESULTS: (1) Although a favorable correlation was found between both Ro measurements (r=0.784), the RoEDP was always higher than the RoL-CSFP. (2) The mean Ro values in the E and NE groups were 36.8 +/- 15.7 mmHg/ml/min, and 10 +/- 2.05 mmHg/ml/min for Ro-EDP, 22.1 +/- 13.95 mmg/ml/min and 6.4 +/- 1.7 mmHg/ml/min for RoL-CSFP, respectively. The approximate thresholds in the E and NE groups were 15 mmHg/ml/min for RoEDP and 10 mmHg/ml/min for RoL-CSFP. CONCLUSION: (1) Although the RoEDP is always higher than the RoL-CSFP, a favorable correlation is found between the RoEDP and RoL-CSFP, (2) The Ro thresholds of the E and NE groups in the infusion test are about 15 mmHg/ml/min for RoEDP and 10 mmHg/ml/min for RoL-CSFP. (3) After this, Ro calculation ought to execute by standard of SINPHONI and the Ro threshold of the E and NE groups is about 10 mmHg/ml/min.

Aged↗
PubMed2004

A novel haplotype of spinocerebellar ataxia type 6 contributes to the highest prevalence in western Japan.

The highest prevalence rate of spinocerebellar ataxia type 6 (SCA6) in the worldwide population is in the Chugoku and Kansai areas of Western Japan, but the reason of this geographic characteristics is unclear. We investigated the predisposing haplotypes and their geographic distribution. Genotyping of five microsatellite markers and three single nucleotide polymorphisms linked to the CACNA1A gene in 150 Japanese SCA6 patients from unrelated 118 families revealed three major haplotypes, carrying a pool of one common haplotype core. A founder chromosome was thought to have historically diverged into at least three types. One of the major haplotypes newly identified showed a strong geographical cluster around the Seto Inland Sea in the Chugoku and Kansai areas of Western Japan, whereas the others were widely distributed throughout Japan. The distribution of predisposing haplotypes contributes to the geographical differences in prevalence of SCA6.

Adult↗
PubMed2004

Dinucleotide repeat polymorphism in interferon-gamma gene is not associated with sporadic Alzheimer's disease.

Various factors have been suggested to participate in Alzheimer's disease (AD) pathology, and some inflammatory cytokines may play an important role in the development of AD. Interferon-gamma (IFNG), an important pro-inflammatory cytokine, is encoded by a single gene mapped to chromosome 12, one of the candidate locus of AD. The first intron in the IFNG gene represents a CA repeat polymorphism that is possible to affect the IFNG secretion dose. We speculate that the polymorphism may have some roles on the inflammatory process and the pathologic change in AD, so we analyzed the IFNG gene polymorphism in 199 Japanese AD patients and 225 Japanese controls. There were no significant differences in allele frequency between the AD and control groups. We conclude that IFNG gene polymorphism is not associated with development of AD.

Aged↗
PubMed2004

Possible reduced penetrance of expansion of 44 to 47 CAG/CAA repeats in the TATA-binding protein gene in spinocerebellar ataxia type 17.

BACKGROUND: Spinocerebellar ataxia type 17 (SCA17) is an autosomal dominant cerebellar ataxia caused by expansion of CAG/CAA trinucleotide repeats in the TATA-binding protein (TBP) gene. Because the number of triplets in patients with SCA17 in previous studies ranged from 43 to 63, the normal number of trinucleotide units has been considered to be 42 or less. However, some healthy subjects in SCA17 pedigrees carry alleles with the same number of expanded repeats as patients with SCA17. OBJECTIVE: To investigate the minimum number of CAG/CAA repeats in the TBP gene that causes SCA17. DESIGN: We amplified the region of the TBP gene containing the CAG/CAA repeat by means of polymerase chain reaction and performed fragment and sequence analyses. PATIENTS: The subjects included 734 patients with SCA (480 patients with sporadic SCA and 254 patients with familial SCA) without CAG repeat expansions at the SCA1, SCA2, Machado-Joseph disease, SCA6, SCA7, or dentatorubral-pallidolluysian atrophy loci, with 162 healthy subjects, 216 patients with Parkinson disease, and 195 with Alzheimer disease as control subjects. RESULTS: Eight patients with SCA possessed an allele with more than 43 CAG/CAA repeats. Among the non-SCA groups, alleles with 43 to 45 repeats were seen in 3 healthy subjects and 2 with Parkinson disease. In 1 SCA pedigree, a patient with possible SCA17 and her healthy sister had alleles with 45 repeats. A 34-year-old man carrying alleles with 47 and 44 repeats (47/44) had developed progressive cerebellar ataxia and myoclonus at 25 years of age, and he exhibited dementia and pyramidal signs. He was the only affected person in his pedigree, although his father and mother carried alleles with mildly expanded repeats (44/36 and 47/36, respectively). In another pedigree, 1 patient carried a 43-repeat allele, whereas another patient had 2 normal alleles, indicating that the 43-repeat allele may not be pathologic in this family. CONCLUSIONS: We estimate that 44 CAG/CAA repeats is the minimum number required to cause SCA17. However, the existence of unaffected subjects with mildly expanded triplets suggests that the TBP gene mutation may not penetrate fully. Homozygosity of alleles with mildly expanded triplet repeats in the TBP gene might contribute to the pathologic phenotype.

Adult↗
PubMed2004

Actin filaments around endothelial fenestrae in rat hepatic sinusoidal endothelial cells.

The presence of microfilaments in the vicinity of sinusoidal endothelial fenestrae (SEF) suggests that the cytoskeleton of liver sinusoidal endothelial cells (LSEC) plays an important role in the modulation of SEF. In this study, we investigated actin filaments around SEF in LSECs. Monolayers of LSEC culture were established by infusing a rat liver with collagenase for 30 min and then culturing in RMPI medium for 24 h. Cells were reacted with 0.1% Triton X for 5 s and 15% glycerinated PHEM buffer (60 mM PIPES, 25 mM HEPES, 10 mM EGTA, 2 mM MgCl, pH 6.9) containing heavy meromyosin for 10 min and observed under a transmission electron microscope. By electron microscopy with the modified heavy meromyosin decorated reaction, actin filaments were clearly demonstrated around SEF in LSEC.

Actins↗
PubMed2004

Sinusoidal endothelial fenestrae organization regulated by myosin light chain kinase and Rho-kinase in cultured rat sinusoidal endothelial cells.

The presence of actin filaments in the neighborhood of sinusoidal endothelial fenestrae (SEF) indicates that the cytoskeleton of sinusoidal endothelial cells (SEC) plays an important role in the modulation of SEF. We examined the roles of Rho-kinase and myosin light chain kinase (MLCK) in the organization of SEF. Cultured SEC were treated with MLCK inhibitor (ML-7) and Rho-kinase inhibitor (Y-27632). SEF morphology was observed by scanning electron microscopy. F-actin stress fibers were observed by confocal microscopy and heavy meromyosin-decorated reaction under transmission electron microscopy. Y-27632 caused disassembly of stress fibers in the center of the cell, while SEF clustered and dilated. However, stress fibers located in the periphery of the cell were not severely affected by Y-27632. ML-7 caused disruption and/or shortening of peripheral stress fibers, leaving the central stress fibers relatively intact. ML-7, but not Y-27632, caused cells to lose the spreading morphology, indicating that the peripheral fibers play a major role in keeping the flattened state of the cell. Thus, there are at least two different stress fiber systems in SEC. The central stress fiber system and SEF microfilaments depend more on the activity of Rho-kinase, while the peripheral stress fiber system depends on MLCK. These results indicate that Rho modulates fenestral changes in SEC via regulation of the actin cytoskeleton.

Journal Article↗
PubMed2004

Rho modulates hepatic sinusoidal endothelial fenestrae via regulation of the actin cytoskeleton in rat endothelial cells.

The presence of actin-like microfilaments in the vicinity of sinusoidal endothelial fenestrae (SEF) indicates that the cytoskeleton of sinusoidal endothelial cells (SEC) plays an important role in the modulation of SEF. Rho has emerged as an important regulator of the actin cytoskeleton, and consequently cell morphology. The present study aimed to examine how a Rho stimulator; lysophosphatidic acid (LPA), and a Rho inhibitor; bacterial toxin C3 transferase (C3-transferase), affect the morphology of SEF. Monolayers of SEC culture were established by infusing a rat liver with collagenase for 30 min and then culturing in RMPI medium for 24 h. The cells were separated into three groups; control, LPA-treated (15 microM), and C3-transferase-treated (15 microg/ml) groups. SEF morphology was observed by scanning electron microscopy. Formation of F-actin stress fibers was observed by confocal microscopy. Rho A and phosphorylated myosin light-chain kinase were analyzed by Western blotting. Active Rho was measured by Ren's modification. Treatment of SECs with LPA contracted the SEF, concomitant with increases in F-actin stress fiber and actin microfilament, and high expression of phosphorylated myosin light-chain kinase. Following treatment with C3-transferase, SEF dilated and fused, concomitant with a loss of F-actin and microfilament, and low expression of phosphorylated myosin light chain. Rho A expression does not change by both treatments. In conclusion, these results indicate that Rho modulates fenestral changes in SEC via regulation of the actin cytoskeleton.

Actins↗