Biomedical subjects

M Yamazaki

Publications and source records attributed to M Yamazaki.

At least 289 records · Page 16Linked to original sources

PubMed1998

Effect of ease-of-acquisition on naming latency for Japanese kanji: a reanalysis of Yamazaki, et al.'s (1997) data.

Yamazaki, Ellis, Morrison, and Lambon Ralph in 1997 found two age-of-acquisition measures exerted greater independent effects on the naming latency of kanji than well-established variables such as word frequency. The current study is a sequel to that study but has reached a different conclusion. To find a better predictor than the two age-of-acquisition measures, Yamazaki, et al.'s data were reanalyzed with the new variable, ease-of-acquisition. The main finding was that the correlation between ease-of-acquisition at age 13 and naming latency was high .67 (df = 145, p < .001). The status of ease-of-acquisition and its possible role in psycholinguistic research are briefly discussed.

Adolescent↗

PubMed1998

Increased plasma levels of free tissue factor pathway inhibitor in patients with Graves' disease.

Tissue factor pathway inhibitor (TFPI) is present in a free-form and in lipoprotein-associated forms in plasma. In this study, the plasma concentrations of total TFPI (tTFPI) and free-form TFPI (fTFPI) were measured in 25 patients with Graves' disease and 25 age-matched healthy subjects, and the relationship between thyroid state and plasma TFPI was examined. Plasma concentrations (median) of tTFPI and fTFPI in Graves' patients who were hyperthyroid were significantly increased compared with Graves' patients who were euthyroid (152 ng/ml versus 124 ng/ml, p < 0.01 and 41.3 ng/ml versus 20.2 ng/ml, p < 0.0001, respectively), and control subjects (152 ng/ml versus 96 ng/ml, p < 0.0001 and 41.3 ng/ml versus 18.7 ng/ml, p < 0.0001, respectively). There was no significant difference in plasma fTFPI concentrations between the euthyroid group and the control group. Plasma fTFPI concentrations correlated closely with thyroid hormone (T3) levels in the patients (r = 0.559, p < 0.005). Serial measurement of individual patients revealed that plasma concentrations of fTFPI and tTFPI were significantly decreased, reaching normal control values upon attainment of euthyroidism. In conclusion, the close correlation between plasma fTFPI and serum thyroid hormone levels suggests that thyroid hormones might influence the synthesis or metabolism of TFPI on the surface of endothelial cells in patients with Graves' disease. This is the first report concerning high concentrations of plasma tTFPI in patients with hyperthyroidism.

Adult↗

PubMed1998

[A case of dural arteriovenous malformation associated with progressive dementia showing marked improvement with endovascular treatment].

An 81-year-old man was admitted with a 3-month history of progressive dementia. Neurological examination revealed marked dementia, parkinsonism and myoclonus in his extremities. His cerebrospinal fluid examination was normal. An electroencephalogram showed a mildly slowed background. Computed tomography (CT) disclosed diffuse low-density areas in bilateral cerebral white matter. Contrast-enhanced CT demonstrated vermiform enhancement of engorged cortical veins, suggesting increased pressure of the venous system. Magnetic resonance imaging (MRI) disclosed diffuse high-intensity areas in bilateral cerebral white manner on T2-weighted images, and abnormal flow-voids presenting venous congestion on proton-density images. Cerebral angiography revealed arteriovenous malformation (AVM) fed by four branches of the right external carotid artery with retrograde drainage into the right transverse sinus, superior sagittal sinus, and dilated cortical veins. The ipsilateral sigmoid sinus was not visualized. After transarterial embolization, transvenous embolization of the right transverse sinus was performed. These treatments resulted in a marked clinical improvement. We emphasize the role of AVM as a cause of progressive dementia.

Aged↗

PubMed1998

[A case of chronic inflammatory demyelinating polyradiculoneuropathy complicated by phrenic nerve palsy].

We report on a patient with chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) complicated by phrenic nerve palsy. A 50-year-old man was admitted to our hospital due to dyspnea and numbness in his limbs. On admission, severe muscle atrophy, weakness, and sensory disturbance were seen in the distal part of his extremities. Deep tendon reflexes were absent in all the limbs. Routine blood examinations showed no abnormal findings except for mild hyperglycemia (fasting blood sugar 145 mg/dl). Right phrenic nerve palsy was observed on a chest roentgenogram and % vital capacity (%VC) was 56%. Cerebrospinal fluid showed elevated levels of total protein (116 mg/dl) and IgG (16.9 mg/dl). Sural nerve biopsy revealed severe loss of myelinated fibers with demyelination and onion-bulb formation. After immunoadsorption plasmapheresis, the phrenic nerve palsy improved rapidly and %VC recovered to 76%. Although phrenic nerve palsy is rare in patients with CIDP, it is important to take notice of this condition, because phrenic nerve palsy is critical when it occurs bilaterally or when it develops in patients who have suffered from respiratory diseases. Immunoadsorption plasmapheresis is one of the effective treatments for CIDP, especially in patients with serious complications such as phrenic nerve palsy.

Chronic Disease↗

PubMed1998

[Comprehensive medicine and 17-KS-S].

In order to evaluate QOL from the perspective of comprehensive medicine, a self-rated QOL Questionnaire and urine 17-KS-S (abbreviated S), 17-OHCS (OH), S/OH were examined in 268 patients (including 11 terminally ill cancer patients) and 31 nurses. Lower S and S/OH were observed in both groups, but OH was higher in patients' group and lower in the nurses' group. Total QOL score was lower in patients' group, but higher in nurses' group. The correlation of each parameter, S, OH and S/OH was related to QOL items. Among terminally ill cancer patients, supplementary treatments were performed. During the course, the elevation of S were observed. In conclusion, S, OH and S/OH were related to QOL and they were considered an objective method of evaluating QOL.

17-Hydroxycorticosteroids↗

PubMed1998

[A study of soluble form of selectin family in the sera of patients with neuroimmunological disorders].

Members of the selectin family mediate the first step of leukocyte-endothelial cell interaction in inflammatory lesions. Soluble(s) L-selectin, sE-selectin and sP-selectin were examined by monoclonal antibody-based enzyme linked immunosorbent assay on serum samples taken from patients with neuroimmunological disorders, namely, 35 cases of multiple sclerosis (MS), 18 of Guillain-Barré syndrome (GBS), 7 of Miller-Fisher syndrome (MFS), 8 of chronic inflammatory demyelinating polyneuropathy (CIDP), and 25 of human T-lymphotropic virus type-1 associated myelopathy (HAM). The levels of sL-selectin in active phase of MS (2.20 +/- 0.6 mg/ml: p < 0.05) were increased rather than in inactive phase (0.6 +/- 0.25 mg/ml) and control (1.47 +/- 0.24 mg/ml), the levels of sE-selectin in HAM (37.6 +/- 25.7 ng/ml: p < 0.05) were increased, and the levels of sP-selectin were increased in active phase of MS (179.5 +/- 103.8 ng/ml), GBS (151.2 +/- 81.6 ng/ml), CIDP (198.6 +/- 81.9 ng/ml), and HAM (115.3 +/- 73.5 ng/ml). Moreover, the levels of all soluble selectin family are more increased in active phase of MS (sL-selectin 2.20 +/- 0.6 mg/ml: p < 0.05, sE-selectin 44.2 +/- 32.8 ng/ml: p < 0.05, sP-selectin 179.5 +/- 103.8 ng/ml: p < 0.05) than in inactive phase of MS(sL-selectin 0.6 +/- 0.25 mg/ml, sE-selectin 9.8 +/- 2.6 ng/ml, sP-selectin 63.7 +/- 26.6 ng/ml). In conclusion, we have here first demonstrated that levels of all soluble selectin family were increased in the bloods of patients with MS in active phase. In GBS only the levels of sP-selectin were increased. Thus, these findings suggest that soluble selectin family may reflect the disease activity of multiple sclerosis.

Adult↗

PubMed1998

Clinical study of refractory apical periodontitis treated by apicectomy. Part 1. Root canal morphology of resected apex.

The morphology of the root apex was analysed by observation of the anatomy of specimens obtained by apicoectomy in cases of refractory apical periodontitis that did not respond to nonsurgical root canal treatment. Apical ramifications were present in 19 (70%) of the roots, while one were found in the remaining eight (3%) roots. This frequency is far higher than that reported by other investigators, suggesting that there is a close relationship between the anatomical complexity of the root canal and the occurrence of refractory apical periodontitis.

Apicoectomy↗

PubMed1998

[An autopsy case of poisoning by neuropsychopharmaceuticals including zopiclone].

We report here a suicide case involving neuropsychopharmaceuticals. The deceased was a 30-year-old housewife, 151 cm in height and 46.0 kg in weight. Macroscopically, slight lung congestion and edema and slight brain edema were noted. The stomach contained approximately 200 ml of a greenish-brown material with many solid granules. Toxicological analysis demonstrated 44.9 micrograms/ml of zopiclone (ZP), 12.8 micrograms/ml of phenobarbital (PB), 10.9 micrograms/ml of chlorpromazine (CPZ), and 4.8 micrograms/ml of promethazine (PM) in the gastric contents; 0.5 microgram/ml of ZP, 8.6 micrograms/ml of PB, 0.2 microgram/ml of CPZ, and 0.3 microgram/ml of PM in the serum; and 43.0 micrograms/ml of ZP, 8.1 micrograms/ml of PB, 1.3 micrograms/ml of CPZ, and 1.3 micrograms/ml of PM in the urine. On the basis of these findings, the cause of death was considered to be neuropsychopharmaceutical poisoning; ZP was most probably responsible for her death.

Adult↗

PubMed1997

Phase transition between hexagonal II (H[II]) and liquid-crystalline phase induced by interaction between solvents and segments of the membrane surface of dioleoylphosphatidylethanolamine.

We have investigated effects of several water-soluble organic solvents such as acetone, acetonitrile, and ethanol, which also have high solubility in alkane, on the structure and phase behavior of dioleoylphosphatidylethanolamine (DOPE) dispersion. X-ray diffraction data indicated that a phase transition from hexagonal II (H[II]) to liquid-crystalline (L alpha) phase in DOPE dispersion, occurred at 13% (v/v) acetone in H2O at 20 degrees C. The temperature of the L alpha-H(II) phase transition of DOPE dispersion increased with an increase in acetone concentration, and it was 37 degrees C at 20% (v/v) acetone. These results indicated that acetone stabilized L alpha phase relative to H(II) phase. Similar results were obtained in interactions of DOPE dispersions in H2O with acetonitrile or ethanol. X-ray diffraction data indicated that the H(II)-L alpha phase transition occurred at 9.0% (v/v) acetonitrile or at 9.8% (v/v) ethanol in water at 20 degrees C. The L alpha-H(II) phase transition temperature of DOPE dispersion increased with an increase in acetonitrile or ethanol concentration, and it was 66 degrees C at 20% (v/v) acetonitrile. Substitution of H2O by D2O (deuterium oxide) increased their threshold concentrations of the H(II)-L alpha phase transition induced by these organic solvents. A mechanism of these phase transitions and the effect of the substitution of H2O by D2O is proposed and discussed; an interaction free energy between solvents and the hydrophobic segments of the alkyl chains in the membrane surface, and also a packing parameter of the phospholipid may be main factors to explain these phenomena reasonably.

Acetone↗

PubMed1997

Regulation of sulfur assimilation in higher plants: a sulfate transporter induced in sulfate-starved roots plays a central role in Arabidopsis thaliana.

Proton/sulfate cotransporters in the plasma membranes are responsible for uptake of the environmental sulfate used in the sulfate assimilation pathway in plants. Here we report the cloning and characterization of an Arabidopsis thaliana gene, AST68, a new member of the sulfate transporter gene family in higher plants. Sequence analysis of cDNA and genomic clones of AST68 revealed that the AST68 gene is composed of 10 exons encoding a 677-aa polypeptide (74.1 kDa) that is able to functionally complement a Saccharomyces cerevisiae mutant lacking a sulfate transporter gene. Southern hybridization and restriction fragment length polymorphism mapping confirmed that AST68 is a single-copy gene that maps to the top arm of chromosome 5. Northern hybridization analysis of sulfate-starved plants indicated that the steady-state mRNA abundance of AST68 increased specifically in roots up to 9-fold by sulfate starvation. In situ hybridization experiments revealed that AST68 transcripts were accumulated in the central cylinder of sulfate-starved roots, but not in the xylem, endodermis, cortex, and epidermis. Among all the structural genes for sulfate assimilation, sulfate transporter (AST68), APS reductase (APR1), and serine acetyltransferase (SAT1) were inducible by sulfate starvation in A. thaliana. The sulfate transporter (AST68) exhibited the most intensive and specific response in roots, indicating that AST68 plays a central role in the regulation of sulfate assimilation in plants.

Amino Acid Sequence↗

PubMed1997

Methotrexate is excreted into the bile by canalicular multispecific organic anion transporter in rats.

Methotrexate [(+) amethopterin, L-MTX] has two carboxyl groups in its structure and is eliminated mainly by excretion into urine and bile. To investigate the biliary excretion mechanism of L-MTX, we performed in vivo and in vitro studies using mutant rats, Eisai hyperbilirubinemic rats (EHBRs), whose canalicular multispecific organic anion transporter (cMOAT) is defective as a consequence of heredity. After i.v. administration of L-MTX to EHBRs, its plasma disappearance and biliary excretion was slower than in normal Sprague Dawley rat (SDR). ATP-dependence and overshoot phenomena were observed in the uptake of [3H]L-MTX by canalicular membrane vesicles (CMV) prepared from SDR, whereas no ATP-dependence was observed in CMV from EHBRs. The ATP-dependent uptake of L-MTX by SDR CMV exhibited saturable kinetics with a Km of 295 microM. L-MTX competitively inhibited the ATP-dependent uptake of [3H]2,4-dinitrophenyl-S-glutathione, a typical substrate for cMOAT, and the inhibition constant (Ki) of L-MTX was comparable with its own Km. These results suggest that L-MTX is excreted into bile by cMOAT. The inhibitory effects of L-MTX and its optical isomer, (-) amethopterin (D-MTX), on the uptake of [3H]L-MTX differed with Kis of 326 and 93 microM, respectively, indicating that the biologically inactive D form has a higher affinity for cMOAT than L-MTX.

Adenosine Triphosphate↗

PubMed1997

Cytoplasmic processing of human profilaggrin by active mu-calpain.

The differentiation of keratinocytes involves numerous steps including the formation of the cornified envelope and the aggregation of keratin filaments by filaggrin monomer molecules. In this study, we investigated whether mu-calpain is involved in the processing of profilaggrin to filaggrin monomers by using both an active mu-calpain specific antibody and a 27-mer synthetic calpastatin peptide, a cell-permeable calpain-specific inhibitor. Upon incubation of cultured keratinocytes with Ca2+ for 96 hours, active mu-calpain with a molecular mass of 76 kDa appeared preceded by an increase in mu-calpain mRNA. In synchrony with the appearance of active mu-calpain, the processing of profilaggrin occurred. Furthermore, the Ca2+-induced activation of mu-calpain and the processing of profilaggrin were affected by the addition of the synthetic calpastatin inhibitor. These results indicate that the activation of mu-calpain plays a major role in the profilaggrin processing.

Amino Acid Sequence↗

PubMed1997

Residues within the polycationic region of cGMP phosphodiesterase gamma subunit crucial for the interaction with transducin alpha subunit. Identification by endogenous ADP-ribosylation and site-directed mutagenesis.

Interaction between the gamma subunit (Pgamma) of cGMP phosphodiesterase and the alpha subunit (Talpha) of transducin is a key step for the regulation of cGMP phosphodiesterase in retinal rod outer segments. Here we have utilized a combination of specific modification by an endogenous enzyme and site-directed mutagenesis of the Pgamma polycationic region to identify residues required for the interaction with Talpha. Pgamma, free or complexed with the alphabeta subunit (Palphabeta) of cGMP phosphodiesterase, was specifically radiolabeled by prewashed rod membranes in the presence of [adenylate-32P]NAD. Identification of ADP-ribose in the radiolabeled Pgamma and radiolabeling of arginine-replaced mutant forms of Pgamma indicate that both arginine 33 and arginine 36 are similarly ADP-ribosylated by endogenous ADP-ribosyltransferase, but only one arginine is modified at a time. Pgamma complexed with Talpha (both GTP- and GDP-bound forms) was not ADP-ribosylated; however, agmatine, which cannot interact with Talpha, was ADP-ribosylated in the presence of Talpha, suggesting that a Pgamma domain containing these arginines is masked by Talpha. A Pgamma mutant (R33,36K), as well as wild type Pgamma, inhibited both GTP hydrolysis of Talpha and GTP binding to Talpha. Moreover, GTP-bound Talpha activated Palphabeta that had been inhibited by R33,36K. However, another Pgamma mutant (R33,36L) could not inhibit these Talpha functions. In addition, GTP-bound Talpha could not activate Palphabeta inhibited by R33,36L. These results indicate that a Pgamma domain containing these arginines is required for its interaction with Talpha, but not with Palphabeta, and that positive charges in these arginines are crucial for the interaction.

3',5'-Cyclic-GMP Phosphodiesterases↗

PubMed1997

Nucleotide sequence analysis of the HLA class I region spanning the 237-kb segment around the HLA-B and -C genes.

To elucidate the detailed gene organization of the human leukocyte antigen (HLA) class I region on chromosome 6, seven contiguous cosmid genomic clones covering the 237-kb segment around the HLA-B and -C loci were subjected to DNA sequencing by the shotgun strategy to give a single contig of 236,822 bp from the MICA gene (58.2 kb centromeric of HLA-B) to 90.8 kb telomeric of HLA-C. This region was confirmed to contain four known genes, MICA, HLA-17, HLA-B, and HLA-C, from centromere to telomere. Further, a new member of the P5 multicopy genes was found to be about 1.3 kb upstream of the HLA-17 gene and designated P5.8. Five novel genes designated NOB1-5 were identified by RT-PCR and Northern blot hybridization. In addition, two pseudogenes, dihydrofolate reductase pseudogene (DHFRP) and ribosomal protein L3 homologous gene (RPL3-Hom), were also found in the vicinity of the HLA-B and -C genes, respectively. The two segments (about 40 kb) downstream of the HLA-B and HLA-C genes showed high sequence homology to each other, suggesting that segmental genome duplication including the major histocompatibility complex (MHC) class I gene must have occurred during the evolution of the MHC.

Blotting, Northern↗

PubMed1997

Osmotic stress induces a phase transition from interdigitated gel phase to bilayer gel phase in multilamellar vesicles of dihexadecylphosphatidylcholine.

We have investigated the effects of poly(ethylene glycol) (PEG) on the structure and phase behavior of multilamellar vesicles of dihexadecylphosphatidylcholine (DHPC-MLVs) using an X-ray diffraction method. At low concentrations of PEG-6K (MW = 7500), DHPC-MLVs were in an interdigitated gel (L(beta)I) phase, a gel phase with interdigitated hydrocarbon chains. At around 24% (w/v) PEG 6K, a phase transition from the L(beta)I phase to a bilayer gel phase occurred in the DHPC-MLVs, and above this concentration, they were in a bilayer gel phase. On the other hand, ethylene glycol (EG), the monomer of PEG, did not induce this phase transition in the DHPC-MLVs. A mechanism of this phase transition is proposed and discussed; a decrease in the repulsive interaction between the head groups of the phospholipids in the bilayer gel phase with an increase in PEG concentration, which is due to a decrease in the cross-sectional area of the head group region by osmotic stress, may be the main reason for this phase transition.

Journal Article↗

PubMed1997

Triplet repeat polymorphism in the transmembrane region of the MICA gene: a strong association of six GCT repetitions with Behçet disease.

A member of a novel family of the human major histocompatibility complex (MHC) class I genes termed MIC (MHC class I chain-related genes), MICA, has been recently identified near the HLA-B gene on the short arm of human chromosome 6. The predicted amino acid sequence of the MICA chain suggests that it folds similarly to typical class I chains and may have the capacity to bind peptides or other short ligands. Therefore, MICA is predicted to have a specialized function in antigen presentation or T cell recognition. During nucleotide sequence analyses of the MICA genomic clone, we found a triplet repeat microsatellite polymorphism of (GCT/AGC)n in the transmembrane (TM) region of the MICA gene. In 68 HLA homozygous B cell lines, 5 distinct alleles of this microsatellite sequence were detected. One of them contained an additional one base insertion that created a frameshift mutation resulting in a premature termination codon in the TM region. This particular allele may encode a soluble, secreted form of the MICA molecule. In addition, we have investigated this microsatellite polymorphism in 77 Japanese patients with Behcet disease, which is known to be associated with HLA-B51. The microsatellite allele consisting of 6 repetitions of GCT/AGC was present at significantly higher frequency in the patient group (Pc = 0.00055) than in a control population. Furthermore, the (GCT/AGC)6 allele was present in all B51 positive patients and in an additional 13 B51 negative patients. These results suggest the possibility of a primary association of Behcet disease with MICA rather than HLA-B.

Asian People↗

PubMed1997

Spatial and temporal expression of fibril-forming minor collagen genes (types V and XI) during fracture healing.

Skeletal development involves the coordinated participation of several types of collagen, including both major and minor fibrillar collagens. Although much is known about the major fibrillar collagens, such as types I and II, less is known about the minor fibrillar collagens, and their role in the repair and regeneration of bone has not been extensively studied. To clarify the role of minor fibrillar collagens in fracture repair, we examined the spatial and temporal expression of mRNAs for pro-alpha 2(V) collagen and pro-alpha 1(XI) collagen in healing fractures in the rat by in situ hybridization and compared their patterns of expression with those of mRNAs for pro-alpha 1(I) collagen, pro-alpha 1(II) collagen, and osteocalcin. A strong signal for pro-alpha 2(V) was detected in the periosteal osteoprogenitor cells, whereas osteocalcin mRNA was strongly expressed only in the deep layers of the hard callus. The distribution of the pro-alpha 2(V) signal was correlated with that of pro-alpha 1(I) but was mutually exclusive of that of pro-alpha 1(II). The expression of pro-alpha 1(XI) mRNA was synchronously regulated with that of pro-alpha 1(II) during chondrogenesis in the soft callus. In the hard callus, pro-alpha 1(XI) signal was found in osteoblastic cells at the site of intramembranous and endochondral ossification. These cells simultaneously expressed pro-alpha 2(V), although they were negative for pro-alpha 1(II). These findings suggest that the alpha 2(V) collagen chain participates in the formation of the noncartilaginous fibrillar network in the hard callus and preferentially contributes to the initial stage of the intramembranous bone formation. Recent reports have revealed that type-XI collagen, which had been classified as a cartilage-type collagen, is not necessarily specific for cartilage. The present results advanced this recognition and demonstrated a coexpression of alpha 1(XI) mRNA and alpha 2(V) mRNA in the noncartilaginous tissues in the fracture callus; this suggests the presence of tissue-specific and stage-specific heterotrimers consisting of alpha 1(XI) and alpha 2(V) collagen chains and the association of such hybrid trimers with the major fibrillar collagens in the process of fracture healing.

Animals↗

PubMed1997

Bone morphogenetic protein-2 stimulates differentiation of cultured spinal ligament cells from patients with ossification of the posterior longitudinal ligament.

Ossification of the posterior longitudinal ligament (OPLL) of the spine is characterized by heterotopic bone formation occurring in spinal ligament, causing severe compression myelopathy. In order to investigate the mechanism of OPLL development, we isolated spinal ligament cells from OPLL patients as well as non-OPLL patients, and established 10 OPLL cell lines and 7 non-OPLL cell lines, respectively. We analyzed the effects of bone morphogenetic protein-2 (BMP-2) on these cells with respect to alkaline phosphatase (AP) activity, DNA synthesis, and collagen production. BMP-2 caused a significant increase of AP activity in 4 OPLL cell lines, whereas the activity did not change in any non-OPLL cells. Among OPLL cells, BMP-2 stimulated DNA synthesis in four cell lines and procollagen type I carboxyl-terminal peptide (PICP) synthesis in five cell lines. Some non-OPLL cells also responded to BMP-2, as there was an increase of DNA synthesis in three cell lines and PICP synthesis in one cell line. These data collectively indicate that BMP-2 preferentially induces osteogenic differentiation in OPLL cells rather than in non-OPLL cells. OPLL cells, therefore, exhibit a different response to BMP-2 than non-OPLL cells, suggesting that the expression of BMP receptor(s) and/or the signal transduction initiated by BMP-2 in the spinal ligament cells of OPLL patients somewhat deviate from those in normal spinal ligament cells. Such abnormal characteristics of OPLL cells as described here provide some clues to the clarification of the pathogenesis of OPLL.

Alkaline Phosphatase↗