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Biomedical subjects

N Yamazaki

Publications and source records attributed to N Yamazaki.

At least 73 records · Page 4Linked to original sources
PubMed1997

Essentially minimal sequence for substrate recognition by tRNA (guanosine-2')-methyltransferase from Thermus thermophilus HB27.

Transfer RNA (guanosine-2'-)-methyltransferase (Gm-methylase, EC.2.1.1.32) from extreme thermophile, Thermus thermophilus HB27 is one of the tRNA-ribose modification enzymes; this enzyme specifically catalyze the transfer of a methyl group from S-adenosyl-L-methionine to 2'-OH of the ribose of the guanosine at position 18 in tRNA. A broad substrate specificity of Gm-methylase was observed using natural tRNAs as methyl group acceptors, which suggests that some local stractures common in tRNAs are recognized by the enzyme. By using yeast tRNA(Phe) variants obtained by transcription of their genes with T7 RNA polymerase, it was revealed that the residues G18 and G19, as well as the D-stem structure were primarily required for the methylation reaction and that the essentially minimal sequence for the substrate was Pyrimidine17-G18-G19. The other conserved sequences and the tertiary base-pairs were not essential, but G15, G46, U55 and C56 strongly affected the methylation efficiency.

Base Composition↗
PubMed1996

Genomic structure and transcription of a murine odorant receptor gene: differential initiation of transcription in the olfactory and testicular cells.

We have characterized genomic structure and transcription of a murine odorant receptor (OR) gene, MOR23. This gene has two distinct transcriptional initiation regions, which are differentially utilized in the olfactory and testicular cells. We have found that the MOR23 gene has an intron within the 5'-untranslated region upstream of the coding sequence. In olfactory cells, transcription of the gene is initiated in the region upstream of this intron, while in testicular cells, transcription starts within the intron. Differential initiation of transcription is discussed in the context of tissue-specific expression of the OR genes.

Animals↗
PubMed1996

Substitution of glycine for arginine-213 in extracellular-superoxide dismutase impairs affinity for heparin and endothelial cell surface.

Extracellular-superoxide dismutase (EC-SOD) levels in sera divide into two discontinuous groups: a low-level group below 400 ng/ml and a high-level group above 400 ng/ml [Adachi, Nakamura, Yamada, Futenma, Kato and Hirano (1994) Clin. Chim. Acta 229, 123-131]. Molecular genetic studies have shown that the donors in the high-level group have a single base substitution generating the exchange of glycine for arginine-213 (R213G) in the heparin-binding domain of EC-SOD [Sandström, Nilsson, Karlsson and Marklund (1994) J. Biol. Chem. 269, 19163-19166; Yamada, Yamada, Adachi, Goto, Ogasawara, Futenma, Kitano, Hirano and Kato (1995) Jpn. J. Hum. Genet. 40, 177-184]. The serum EC-SOD level in homozygote subjects was significantly higher than that in heterozygotes and in normal subjects. Serum EC-SOD from heterozygotes and homozygotes had equally decreased affinity for heparin, as judged by heparin-HPLC, as compared with that from normal donors. This result suggests that the serum EC-SOD in heterozygotes was mainly composed of the mutant form which has reduced heparin affinity. On the other hand, fibroblast cells derived from heterozygote subjects generated mRNA of both normal and mutant EC-SOD (m-EC-SOD), and expressed the corresponding proteins. EC-SOD is a tetrameric enzyme, and in heterozygote donors would be heterogeneous with regard to the constitution of normal and mutant subunits. The enzyme form consisting of only mutant subunits, the form with the weakest heparin affinity, can be preferentially driven out to the plasma phase, because EC-SOD in the vasculature exists in equilibrium between plasma and the endothelial cell surface. The binding of m-EC-SOD to bovine aortic endothelial cells was about 50-fold less than that of normal EC-SOD. This result suggests that the binding of m-EC-SOD to vascular endothelial cells is much decreased in vivo, which causes a high level of serum EC-SOD.

Animals↗
PubMed1996

Antinociceptive effects of repeated systemic injections of calcitonin in formalin-induced hyperalgesic rats.

Calcitonin (CT) produces long-lasting analgesia in patients suffering from painful diseases following repeated systemic injections, but there have been only a few contradictory reports on the antinociceptive action of systemic injections of CTs in animal experiments. This study was conducted to elucidate an antinociceptive action of systemic CT in rats. An injection of dilute formalin induced hyperalgesia for about 2 h. Single topical injections of 0.12 and 1.2 U, but not 0.012 U, of [Asu1.7] eel CT (eCT) into the same site of formalin injection inhibited the hyperalgesia. Repeated systemic injections of eCT (4 and 40, but not 0.4, U kg-1 day-1) for 7 days inhibited the hyperalgesia, while the single injection was without effects at doses tested. Although the highest dose of eCT (40 U kg-1 day-1) inhibited an increase in body weight following repeated injections, lower doses (0.4 and 4 U kg-1 day-1) were without effects. The suppression of hyperalgesia following repeated systemic injections of eCT (4 U kg-1 day-1) lasted for at least 24 h, and subsided by 3 days following the last eCT injection. These results indicate that the repeated systemic injections of eCT produce a long-lasting inhibition of formalin-induced hyperalgesia in rats. This inhibitory effect is similar to CT analgesia in human subjects in terms of a necessity for repeated administration, effective dose and long-lasting effects.

Analgesics↗
PubMed1996

An arginine-213 to glycine mutation in human extracellular-superoxide dismutase reduces susceptibility to trypsin-like proteinases.

Molecular genetic studies of extracellular-superoxide dismutase (EC-SOD) have shown that individuals with high serum EC-SOD content have a single base substitution generating the exchange of glycine for arginine-213 (R213G) in the heparin-binding domain of this enzyme [Sandström, J. et al. (1994) J. Biol. Chem. 269, 19163-19166], which causes the impairment of its binding ability to endothelial cell surface [Adachi, T. et al. (1996) Biochem. J. 313, 235-239]. Serum EC-SOD in healthy individuals without the above mutation is heterogeneous with regard to heparin affinity and consists of five fractions, forms (I) to (V), of which (IV) and (V) are the main fractions with high affinity for heparin [Adachi, T. et al. (1995) J. Biochem. 117, 586-590], whereas the major fraction in hemodialysis patients was serum EC-SOD form (I), which is thought to be the proteolytic truncated form. On the other hand, serum EC-SOD in both healthy individuals and hemodialysis patients with the R213G mutation consisted mainly of the high heparin-affinity type. This observation suggests that the susceptibility of EC-SOD to proteinases is reduced by the R213G mutation. The affinity of normal EC-SOD (n-EC-SOD) for heparin decreased by the treatment with trypsin, accompanied by a reduction in the molecular mass. The IC50 of trypsin for the heparin affinity of R213G mutant EC-SOD (m-EC-SOD) was 0.15 microgram/ml, fivefold that for n-EC-SOD. Heparin affinity of n-EC-SOD was again more susceptible to neutrophils than that of m-EC-SOD. These results suggested that m-EC-SOD is more resistant to trypsin and neutrophil-release trypsin-like proteinases than n-EC-SOD, which causes the heparin affinity of serum EC-SOD to differ in individuals with and without the R213G mutation.

Animals↗
PubMed1996

Clinical and pathological features of cutaneous malignant melanoma: a retrospective analysis of 124 Japanese patients.

A review of mainly histopathologic factors associated with the survival of patients with malignant melanoma was carried out in a retrospective study of 124 Japanese patients treated at the National Cancer Center Hospital between July 1962 and December 1992. There were 60 females and 64 males, and the median follow-up period was 52.7 months (range, 1.1 to 235.3 months). The histologic features included tumor thickness, level of invasion, histologic subtype, ulceration, pigmentation, and cell type. Melanomas thicker than 1.5 mm (P<0.01) and with ulceration (P<0.001) had a significantly worse prognosis. With regard to histologic type, ten-year survival was 65.1% for acral lentiginous melanoma, 50.7% for nodular melanoma, and 47.0% for superficial spreading melanoma (SSM), there being no significant differences among them. We suggest that the prognosis was affected not by histologic type but by the large radial or vertical growth component. With regard to clinical features, the clinicopathological stage, patient age, and year when the disease was diagnosed were reflected in the prognosis (P<0.001). Multifactorial analysis showed that the most significant prognostic variables were histopathologic type (SSM or other), stage (I and II or III and IV), and patient age (<70 or > or = 70 yr).

Adolescent↗
PubMed1996

Effects of Mg2+ on Ca2+ waves and Ca2+ transients of rat ventricular myocytes.

It has been shown that the occurrence of the transient inward current, which is responsible for triggered activity, was often associated with propagating regions of increased intracellular Ca2+ concentration ([Ca2+]i), i.e., the "Ca2+ wave." To investigate the mechanism of antiarrhythmic action of Mg2+, we have studied effects of high concentrations of Mg2+ on Ca2+ waves in isolated rat ventricular myocytes. [Ca2+]i was estimated using the Ca(2+)-indicating probe indo 1. Ca2+ waves in myocytes, stimulated at 0.2 Hz, were induced by perfusion of isoproterenol (10(-7) M). High Mg2+ concentration suppressed Ca2+ waves in a concentration-dependent manner (36% at 4 mM, 70% at 8 mM, and 82% at 12 mM). The Ca2+ channel blocker verapamil also suppressed Ca2+ waves in a similar way. In contrast with marked depression of Ca2+ transients by verapamil, Ca2+ transients were not affected by high Mg2+ concentration (8 mM). High Mg2+ concentration also reduced frequencies of Ca2+ waves in the absence of electrical stimulation, whereas verapamil failed to reduce frequencies of Ca2+ waves. Reduction in frequency of Ca2+ waves by high Mg2+ concentration was associated with slowing of propagation velocity of Ca2+ waves. To examine whether suppressive effects of high Mg2+ concentration on Ca2+ waves were related to an increase in intracellular Mg2+ concentration ([Mg2+]i), the effect of high-Mg2+ solution on [Mg2+]i was examined in myocytes loaded with mag-fura 2. An increase in extracellular Mg2+ concentration from 1 to 12 mM increased [Mg2+]i from 1.06 +/- 0.16 to 1.87 +/- 0.22 mM (P < 0.01) in 30 min. To examine the effect of high Mg2+ concentration on amount of releasable Ca2+ in the sarcoplasmic reticulum, the effect of high Mg2+ concentration on the Ca2+ transient induced by a rapid application of caffeine was examined. High-Mg2+ solution increased the peak of the caffeine-induced Ca2+ transient. These results suggest that the inhibitory effect of Mg2+ on Ca2+ waves was not due to inhibition of the sarcolemmal Ca2+ channel but could be due to a decreased propensity for the sarcoplasmic reticulum to divest itself of excess Ca2+.

Animals↗
PubMed1996

Biomechanical analysis of the development of human bipedal walking by a neuro-musculo-skeletal model.

A new computer simulation method, using a neuro-musculo-skeletal model, is used to clarify the process of acquisition of erect bipedal walking during human ontogeny. Walking was autonomously generated as a dynamic interaction called 'mutual entrainment' between the neural oscillation and the pendular movement of differently proportioned bodies. Walking patterns of humans with 8 different sets of alternative body proportions, varying from those of 8-month-old children to those of 22 years old adults, were simulated. The development of bipedal walking is characterized as the change from a forced oscillation controlled by the nervous system to the natural oscillation of pendular motion, determined by body proportions. Body proportions are the fundamental factor in the development of bipedal walking.

Adult↗
PubMed1995

High expression of a novel carnitine palmitoyltransferase I like protein in rat brown adipose tissue and heart: isolation and characterization of its cDNA clone.

To characterize energy metabolism in rat brown adipose tissue (BAT), we carried out differential screening of a cDNA library of BAT with a cDNA probe of white adipose tissue (WAT) and isolated one cDNA clone. It contained a single open reading frame of 2,316 bases which encodes a protein of 88.2 kDa. The predicted amino acid sequence showed the highest homology (62.6%) with that of rat carnitine palmitoyltransferase I (CPTI). The transcript corresponding to this cDNA was found to be abundantly expressed in BAT and heart. Therefore, the isolated clone is concluded to encode a CPTI like protein expressed in BAT and heart.

Adipose Tissue, Brown↗
PubMed1995

New method for evaluating left ventricular wall motion by color-coded tissue Doppler imaging: in vitro and in vivo studies.

OBJECTIVES: The aim of this study was to examine the accuracy and validity of a newly developed tissue Doppler imaging system in in vitro and in vivo studies. BACKGROUND: Because quantitative measurement of wall motion velocity in real time is still difficult by conventional echocardiography, we developed a new system for evaluating ventricular wall motion by analyzing Doppler signals from cardiac tissue. METHODS: We used a modified Doppler color imaging system, omitting the high pass filter to allow Doppler signals from cardiac tissue to enter the auto-correlator. Ultrasound carrier and pulse repetition frequencies were 3.75 MHz and 3.0 to 6.0 kHz, respectively. Under these conditions, the lowest measurable velocity was 0.2 cm/s. RESULTS: In the rotating sponge model, the measured velocity correlated well with the actual velocity (y = 0.97x + 2.17, r = 0.99). In clinical settings, the mid-ejection mean velocity at either endocardial or epicardial sites of the left ventricular posterior wall measured by M-mode tissue Doppler imaging correlated well with that measured by conventional M-mode echocardiography (y = 0.94x + 0.64, r = 0.99). During systole, in healthy subjects, the anterior left ventricular wall was color-coded blue and the posterior wall was color-coded red, whereas the akinetic regions associated with myocardial infarction showed no color throughout the cardiac cycle. The ventricular posterior wall excursion velocity, defined as the difference between velocities at the endocardial and epicardial sites, was significantly slower in patients with dilated cardiomyopathy (0.4 +/- 0.3 cm/s) than in normal subjects (2.0 +/- 0.6 cm/s). CONCLUSIONS: These results indicate that the present system accurately represents tissue velocity and can create two-dimensional color images that facilitate visual assessment of ventricular wall motion.

Adult↗
PubMed1995

Myocardial velocity gradient as a new indicator of regional left ventricular contraction: detection by a two-dimensional tissue Doppler imaging technique.

OBJECTIVES: This study was performed to assess a new indicator of regional left ventricular contraction determined by a two-dimensional tissue Doppler imaging technique. BACKGROUND: Recent studies have demonstrated that instantaneous tissue motion velocity can be noninvasively assessed by tissue Doppler imaging. However, quantitative assessment of regional left ventricular contraction is still difficult because of the effects of the Doppler angle of incidence and parallel motion of the whole heart. METHODS: We assessed left ventricular wall motion in 11 normal subjects, 14 patients with an old myocardial infarction (anteroseptal in 7, posterior in 7) and 8 patients with dilated cardiomyopathy. Tissue Doppler velocity was corrected by the Doppler angle of incidence after the hypothetical center of contraction was set. Subsequently, the myocardial velocity gradient between the endocardium and epicardium was determined from the velocity profile along each radial line from the center of contraction by using least squares linear regression. RESULTS: In normal subjects, peak myocardial velocity gradient was lower in the anteroseptal wall (mean [+/- SD] 1.69 +/- 0.53 s-1) than in the posterior wall (3.28 +/- 0.67 s-1, p < 0.01). Myocardial velocity gradient in the infarct regions was significantly lower (anteroseptal 0.58 +/- 0.41 s-1, p < 0.05; posterior 0.17 +/- 0.27 s-1, p < 0.01) than that in normal subjects as well as that in the corresponding noninfarct regions (2.84 +/- 0.37 s-1 and 1.48 +/- 0.25 s-1, p < 0.01, respectively). In patients with dilated cardiomyopathy, myocardial velocity gradient was generally lower (anteroseptal 0.72 +/- 0.59 s-1; posterior 0.93 +/- 0.67 s-1) than that in normal subjects (p < 0.01). CONCLUSIONS: These results demonstrate that regional left ventricular contraction can be quantitatively assessed by the myocardial velocity gradient derived from two-dimensional tissue Doppler imaging. We suggest that myocardial velocity gradient has potential for the quantitative assessment of regional left ventricular contraction abnormalities in patients.

Adult↗
PubMed1995

A cellular form of prion protein (PrPC) exists in many non-neuronal tissues of sheep.

A cellular form of the prion protein (PrPC) is thought to be a substrate for an abnormal isoform of th eprion protein (PrPSc) in scrapie. PrPC is abundant in tissues of the central nervous system, but little is known about the distribution of PrPC in non-neuronal tissues of sheep, the natural host of scrapie. This study investigated the tissue distribution of PrPC in sheep. Although PrPC was abundant in neuronal tissues, it was detected in non-neuronal tissues such as spleen, lymph node, lung, heart, kidney, skeletal muscle, uterus, adrenal gland, parotid gland, intestine, proventriculus, abomasum and mammary gland. Neither PrPC nor PrP mRNA was detected in the liver. The tissue distribution of PrPC appears to be inconsistent with the tissues which possess scrapie infectivity, suggesting that factor(s) specific to certain cell types may be required to support multiplication of the scrapie agent.

Amino Acid Sequence↗
PubMed1995

Role of an endogenous monoamine oxidase inhibitor, isatin, in SHRSP brain.

1. The acute effects of isatin, an endogenous monoamine oxidase (MAO) inhibitor, on norepinephrine (NE) and serotonin (5-HT) concentrations in the brain of stroke-prone spontaneously hypertensive rats (SHRSP) and Wistar-Kyoto rats (WKY) were determined in order to elucidate its pathophysiological role. 2. Isatin was identified in purified extracts of SHRSP brain. 3. A single dose of isatin significantly increased NE concentration in the cerebral cortex of WKY. Isatin also significantly increased 5-HT concentration in WKY brains. 4. After isatin administration NE and 5-HT levels in the SHRSP brain did not differ from those in WKY. 5. These data suggest that isatin, an endogenous MAO inhibitor, presents in the SHRSP brain and maintains high blood pressure.

Animals↗
PubMed1995

Creatine kinase kinetics in diabetic cardiomyopathy.

One feature of the diabetic cardiomyopathy is the appearance of contractile dysfunction as the workload increases. We hypothesized that this resulted from an impaired creatine kinase/phosphocreatine system and therefore examined the creatine kinase kinetics at both low and high workloads. Creatine kinase flux (by 31P nuclear magnetic resonance saturation transfer method), cardiac performance, and oxygen consumption were measured in control and streptozotocin-induced diabetic rat hearts. Creatine kinase flux was inhibited by iodoacetamide in control hearts to confirm the role of the creatine kinase/phosphocreatine system in cardiac performance. In diabetic hearts, 1) the contractile dysfunction became apparent only at high workloads, 2) the ATP synthesis rate was not significantly different from control hearts, 3) the creatine kinase flux was reduced by 30.8% (257.5 +/- 7.7 mumol.g wet wt-1.min-1 in control vs. 178.3 +/- 9.4 in diabetes, P < 0.001), and 4) the creatine kinase flux did not increase as the workload increased. In control hearts, 5) iodoacetamide inhibited the creatine kinase flux to the same degree as that in diabetic hearts, and 6) the contractile dysfunction was not as severe as that observed in diabetic hearts. These results suggest that the impaired creatine kinase/phosphocreatine system is, at least in part, responsible for the contractile dysfunction in the diabetic cardiomyopathy.

Adenosine Triphosphate↗
PubMed1995

Restriction endonuclease analysis of bovine herpesvirus type 1 isolates from calves with fatal encephalitis: comparison with vaccine virus.

Meningo-encephalitis in feedlot cattle sporadically occurred in the Tokachi area in northern Japan. The calves had been vaccinated intranasally with a mixed live-vaccine (infectious bovine rhinotracheitis virus, bovine viral diarrhea-mucosal disease virus, and parainfluenza 3 virus) for which intramuscular inoculation was indicated. Two additional live vaccines, bovine adenovirus type 7 and bovine respiratory syncytical virus, had been inoculated simultaneously. Eleven isolates of bovine herpesvirus type 1 were plaque-purified from two brains with fatal encephalitis; their viral DNAs were examined by restriction endonuclease analysis (REA) using PstI and HindIII. The REA patterns of the virus clones were almost identical to those of the vaccine strains 758-43, suggesting that the isolates from this outbreak of fatal encephalitis originated in the abnormally administered vaccine.

Administration, Intranasal↗
PubMed1995

Intracellular sodium concentration in diabetic rat ventricular myocytes.

We measured intracellular NA+ concentration ([Na+]i) of diabetic rat ventricular myocytes using sodium-binding benzofuran isophthalate (SBFI). We used diabetic rats at 8 weeks after the injection of streptozotocin (45 mg/kg i.v.). The level of [Na+]i during the control perfusion was significantly lower in diabetic myocytes than that in normal myocytes (9.2 +/- 0.4 mM v.s. 12.0 +/- 0.3 mM, p < 0.01). After the 40 min perfusion of 1 microM hexamethylene amiloride (HMA), [Na+]i decreased significantly in both groups. However, there was no difference in [Na+]i between the two groups after the perfusion of HMA. It was suggested that the lower [Na+]i in diabetic myocytes could be due to the decreased activity of Na+/H+ exchange system.

Amiloride↗