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Biomedical subjects

Y Muramatsu

Publications and source records attributed to Y Muramatsu.

At least 19 recordsLinked to original sources
PubMed2004

Pitavastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, reduces hippocampal damage after transient cerebral ischemia in gerbils.

Pitavastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, is a potent cholesterol-lowering drug that reduces the risk of myocardial infarction and stoke. In this study, we examined its neuroprotective effects against hippocampal CA1 neuronal damage following transient cerebral ischemia in gerbils. Forebrain ischemia was induced by occlusion of bilateral common carotid arteries for 5 min. Pitavastatin, at a dose of 3, 10 or 30 mg/kg, was administered orally twice a day for 5 consecutive days and transient cerebral ischemia was induced in mice 1 h after the last treatment with pitavastatin. Histopathological observations showed that neuronal damage to the hippocampal CA1 neurons, which was observed 5 days after ischemia in animals, was prevented by pitavastatin treatment. Immunohistochemical staining for copper/zinc superoxide dismutase (SOD) and manganese SOD decreased in the hippocampal CA1 sector of gerbils 2 days after ischemia when histological neuronal destruction was not yet found, but was clearly observed in pitavastatin-treated animals. These results indicate that pitavastatin can protect dose-dependently against ischemia-induced neuronal damage and that the mechanism of the neuroprotection may be related to the preservation of SODs, especially copper/zinc-SOD. This in part explains how pitavastatin therapy, which targets free radicals, has beneficial effects against disorders including ischemic stroke.

Animals↗
PubMed2004

Equilibrium of radiocesium with stable cesium within the biological cycle of contaminated forest ecosystems.

Concentrations of (137)Cs and stable Cs were determined in plant, mushroom, lichen and soil samples collected at two forest sites with different contamination levels in Belarus in 1998. The concentration of (137)Cs in soil was the highest in near-surface organic layers (Of and Oh horizons) and decreased with depth in the mineral layers, whereas the concentrations of stable Cs were almost constant in the soil profile. The levels of (137)Cs and stable Cs in biological samples varied depending both on the species and the plant part sampled. Even though different species and parts of the same species were included, the concentration ratios of (137)Cs to stable Cs were fairly constant for samples collected at the same forest site, and were in the same order of magnitude as the (137)Cs to stable Cs ratios for the organic soil layers. This finding suggests that (137)Cs, mainly deposited on the forest ecosystems from the Chernobyl accident in 1986, was well mixed with stable Cs within the biological cycle in the forest ecosystems by 1998. The transfer factor for each biological sample of (137)Cs was almost the same as that of stable Cs, if they were calculated based on the concentrations in the Of + Oh layer. This suggests that the stable-Cs-based transfer factor could be used as equilibrium transfer factor of (137)Cs for different types of biological samples in the forest.

Agaricales↗
PubMed2004

Effect of pitavastatin against expression of S100beta protein in the gerbil hippocampus after transient cerebral ischaemia.

AIM AND METHODS: We investigated the immunohistochemical alterations of S100beta-, S100-, glial fibrillary acidic protein (GFAP)- and isolectin B4-positive cells in the hippocampus after 5 min of transient cerebral ischaemia in gerbils. We also examined the effect of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor pitavastatin against neuronal damage in the hippocampal CA1 sector after ischaemia. RESULTS: Severe neuronal damage was observed in the hippocampal CA1 pyramidal neurons from 5 days after ischaemia. GFAP-positive cells increased gradually in the hippocampus from 5 days after ischaemia. Five and 14 days after ischaemia, significant increases in the number of GFAP-positive cells and isolectin B4-positive cells were observed in the hippocampal CA1 and CA3 sector. Mild increases in the number of S100 and S100beta-positive cells were observed in the hippocampal CA1 sector from 1 h to 2 days after ischaemia. Thereafter, S100beta-positive cells increased in the hippocampal CA1 sector after ischaemia, whereas S100-positive cells decreased in this region. In our double-labelled immunostainings, S100 and S100beta immunoreactivity was found in GFAP-positive astrocytes, but not in isolectin B4-positive microglia. Pharmacological study showed that HMG-CoA reductase inhibitor, pitavastatin, can protect against the hippocampal CA1 neuronal damage after ischaemia. This drug also prevented increases in the number of GFAP-positive astrocytes, isolectin B4-positive microglia, S100-positive astrocytes and S100beta-positive astrocytes after ischaemia. CONCLUSION: The present study demonstrates that pitavastatin can decrease the neuronal damage of hippocampal CA1 sector after ischaemia. This beneficial effect may be, at least in part, mediated by inhibiting the expression of astrocytic activation in the hippocampus at the acute phase after ischaemia. Thus the modulation of astrocytic activation may offer a novel therapeutic strategy of ischaemic brain damage.

Animals↗
PubMed2004

Protective effect of pitavastatin, a 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor, on ischemia-induced neuronal damage.

We investigated the neuroprotective effects of a novel 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase inhibitor (pitavastatin) on ischemic neuronal damage in gerbils using immunohistochemistry. The animals were allowed to survive for 14 days after 5 min of ischemia induced by bilateral occlusion of the common carotid arteries. Five days after ischemia, severe neuronal cell loss was observed in the hippocampal CA1 sector. Prophylactic treatment with pitavastatin dose-dependently prevented the hippocampal CA1 neuronal cell loss 5 days after ischemia. Immunohistochemical study did not show the change of nNOS and iNOS expression in the hippocampus except for, in a few regions, up to 1 day after ischemia. Thereafter, the expression of iNOS was observed in the hippocampal CA1 sector 5 and 14 days after ischemia. In contrast, the expression of nNOS and eNOS gradually decreased in the hippocampal CA1 sector up to 14 days after ischemia. Prophylactic treatment with pitavastatin also prevented the expression of iNOS and the decrease of eNOS expression and the number of nNOS-positive cells in the hippocampal CA1 sector 5 days after ischemia. However, prophylactic treatment with pitavastatin at a dose of 10 mg kg(-1) did not change the immunoreactivity of iNOS and nNOS in the hippocampus at an early phase after ischemia. In contrast, this drug prevented the reduction of eNOS immunoreactivity in the hippocampal CA1 neurons at an early phase after ischemia. These findings demonstrate that the HMG-CoA reductase inhibitor pitavastatin can protect hippocampal CA1 neurons after transient forebrain ischemia through up-regulation of eNOS expression in this region. Thus pharmacological modulation of eNOS expression may offer a novel therapeutic strategy for cerebral ischemic stroke.

Animals↗
PubMed2004

Neuroprotective effect of the angiotensin-converting enzyme inhibitor perindopril in MPTP-treated mice.

The angiotensin -converting enzyme (ACE) inhibitor perindopril has been shown to exert beneficial effects on the dopaminergic system. Here, we investigated the effects of perindopril on the dopaminergic system in mice after 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) treatment, in comparison with a Ca(2+) antagonist, amlodipine. Administration of perindopril showed dose-dependent neuroprotective effects against MPTP-induced striatal dopamine and 3,4-dihydroxyphenylacetic acid (DOPAC) depletion. However, administration of amlodipine showed no significant effects on striatal dopamine depletion after MPTP treatment. In our immunohistochemical studies with antibodies against tyrosine hydroxylase (TH), microtubule-associated protein 2a, b (MAP2), dopamine transporter (DAT), parvalbumin (PV), glial fibrillary acidic protein (GFAP) and Cu/Zn-superoxide dismutase (Cu/Zn-SOD), the administration of perindopril significantly attenuated MPTP-induced substantia nigra and striatal damage. This drug also blocked the increases in GFAP-positive astrocytes in the striatum and substantia nigra after MPTP treatment. Furthermore, the administration of perindopril showed a protective effect against the intense Cu/Zn-SOD immunoreactivity in the neurons and glial cells in both the striatum and substantia nigra after MPTP treatment. These results indicated that the ACE inhibitor perindopril can protect against MPTP-induced striatal dopamine and DOPAC depletion in mice. The protective effect may be, at least in part, caused by the reduction of free radicals caused by MPTP. The present study also demonstrated that perindopril is effective against MPTP-induced neurodegeneration of the nigro-striatal dopaminergic pathway. Furthermore, our results provided further evidence that free radical scavengers may be effective in the treatment of neurodegenerative diseases such as Parkinson's disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2004

[Reusable imaging plate (IP) for swift and automatic measurement of X-ray CT dose profiles].

PURPOSE: In multi-slice CT, over beaming by penumbra effect has been reported, and measurements of X-ray CT beam profiles are very important for accurate performance assessment. This study was conducted in order to facilitate and economize on the measurement of CT dose profiles. METHODS: The imaging plate (IP: HR-V type, Fuji) was placed in its case, X-rayed, and then read with a digital IP reader, which then erased the data in preparation for reuse. The values were then compared with the values obtained with the standard one-use imaging film. The CT scanner used was a Toshiba Aquilion Multi (4 rows). RESULTS: The shape of the beam profile obtained using the IP method was for all practical purposes identical to that obtained using the film method. The FWHM values for 2.0, 4.0, 8.0, 12.0, 16.0, 20.0 and 32-mm beam were 4.88, 6.61, 10.2, 14.9, 18.2, 22.4 and 35.0 mm for the IP method and 4.81, 6.66, 10.2, 14.7, 18.1, 22.3 and 34.8 mm for the film method. In addition, in the IP method, the results obtained for the shape of the beam profile and the FWHM were found to be extremely similar irrespective of the X-ray tube used or individual differences between IPs. CONCLUSION: We have developed a new X-ray CT beam profile measurement system using an IP. This IP method permits data processing to be performed entirely in the digital domain, allowing high-precision measurements to be obtained with ease.

Equipment Reuse↗
PubMed2003

Cerebral alterations in a MPTP-mouse model of Parkinson's disease--an immunocytochemical study.

We investigated the immunohistochemical alterations of neuronal nitric oxide synthase (nNOS), endothelial NOS (eNOS), tyrosine hydroxylase (TH), microtubule-associated protein 2a,b (MAP 2), glial fibrillary acidic protein (GFAP), parvalbumin (PV), and dopamine transporter (DAT) in the striatum and substantia nigra following the application of 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) in mice. TH-, MAP 2- and DAT-immunoreactive cells were decreased gradually in the striatum and substantia nigra from 1 day up to 7 days after MPTP treatment, as well as the reduction of the striatal dopamine, DOPAC and HVA content. The number of GFAP-immunoreactive astrocytes increased gradually in the striatum and substantia nigra from 1 day up to 7 days after MPTP treatment. Striatal nNOS-immunoreactive cells were unchanged in MPTP-treated mice. In the substantia nigra, intense immunoreactivity of nNOS-positive cells increased 5 hr after MPTP treatment. Thereafter, the immunoreactivity of nNOS-positive cells decreased gradually from 1 day up to 7 days after MPTP treatment. eNOS-immunopositive cells were unchanged in the striatum and substantia nigra. These results demonstrate that nNOS may play a key role in the development of MPTP neurotoxicity. Our findings also indicate that MPTP can cause the functional damage of interneurons in the substantia nigra, but not in the striatum.

Animals↗
PubMed2003

Role of dopamine transporter against MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine) neurotoxicity in mice.

We investigated the alterations of dopamine transporter (DAT)-immunopositive cells against MPTP neurotoxicity, in comparison with tyrosine hydroxylase (TH)-immunopositive neurons and glial fibrillary acidic protein (GFAP)-immunopositive cells. This study showed that DAT and TH immunoreactivity was decreased gradually in the striatum and substantia nigra of mice after MPTP treatment. The patterns of the intense TH-immunoreactive fibers and cell bodies were similar to those of DAT-immunoreactive fibers and cell bodies in the striatum and substantia nigra of mice after MPTP treatment. In contrast, GFAP immunoreactivity was increased gradually in the striatum and substantia nigra after MPTP treatment. In our double-labeled immunostaining with anti-DAT and anti-GFAP antibodies, DAT immunoreactivity was observed only in the nigral dopaminergic neurons, but not in the reactive astrocytes. The present results provide further evidence that the functional damage of DAT may precede dopaminergic neuronal death after MPTP treatment, although the decrease in the number of TH-immunopositive neurons was more pronounced than that in the number of DAT-immunopositive neurons. Furthermore, our findings demonstrate that MPTP can selectively injure the dopaminergic neurons which DAT proteins are predominantly distributed on the striatum and substantia nigra. The results provide beneficial information for MPTP-induced neurodegeneration of the nigrostriatal dopaminergic neuronal pathway.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2003

Chromosomal mapping of HSPCB and MYL1 expressed abundantly in the bovine fetus.

Chromosomal mapping of expressed sequence tags for HSPCB and MYL1 expressed abundantly in the bovine fetus was performed by analyzing bovine/murine somatic cell hybrid DNAs with polymerase chain reaction (PCR) using primers specific for those 3'-untranslated regions. HSPCB and MYL1 were assigned to bovine chromosomes 23 and 2, respectively.

Animals↗
PubMed2003

Experimental transmission of abnormal prion protein (PrPsc) in the small intestinal epithelial cells of neonatal mice.

Using an immunohistochemical method, we attempted to detect the transmission of abnormal prion protein (PrPsc) to the enterocytes of the small intestine of neonatal mice by oral exposure with sheep brain affected by scrapie. Five 1-day-old neonatal mice were exposed by oral inoculation to the homogenized brain of a scrapie-affected sheep. In the small intestine of all mice 1 hour after inoculation, immunoreactivity with antinormal prion protein (PrPc) antibody was seen in the cytoplasm of villus enterocytes. This finding suggests transmission of abnormal PrPsc into the cytoplasm of enterocytes. In control mice treated with normal sheep brain, no PrPc signal was seen in enterocytes of the small intestine. Immunopositivity for neurofilament protein and glial fibrillary acidic protein was seen in the cytoplasm of enterocytes of mice inoculated with scrapie and normal sheep brain. This suggests that the enterocytes of neonatal mice can absorb PrPsc and other macromolecular proteins of the sheep brain affected by scrapie and may be more important than previously thought as a pathway for PrPsc transmission in neonatal animals.

Animals↗
PubMed2002

Direct probe of the bent and linear geometries of the core-excited Renner-Teller pair states by means of the triple-ion-coincidence momentum imaging technique.

The doubly degenerate core-excited Pi state of CO2 splits into two due to static Renner-Teller effect. Using the triple-ion-coincidence momentum imaging technique and focusing on the dependence of the measured quantities on the polarization of the incident light, we have probed, directly and separately, the linear and bent geometries for the B1 and A1 Renner-Teller pair states, as a direct proof of the static Renner-Teller effect.

Journal Article↗
PubMed2002

Transfer factors of radioactive Cs, Sr, Mn, Co and Zn from Japanese soils to root and leaf of radish.

Transfer factors (TFs) of some selected radionuclides from ten different Japanese soils to radish have been studied by radiotracer experiments. The geometric mean values of TFs (on a wet weight basis) of radioactive Cs, Sr, Co, Mn and Zn for edible parts of radish (tuber) were 0.0090. 0.029, 0.00094, 0.0034 and 0.067, respectively. TFs for leaf were higher than those for tuber. The geometric mean values of leaf/tuber ratios were 4.1 for Cs, 4.9 for Sr, 1.6 for Co, 11 for Mn and 1.9 for Zn. Most of the Cs TFs obtained for andosol, which is the most common arable soil in Japan, were higher than those for the other soils. This might be due to the high concentrations of organic matter and alophen in andosol. The obtained TFs were compared to reference values of IAEA Technical Report 364.

Japan↗
PubMed2002

Therapeutic effect of neuronal nitric oxide synthase inhibitor (7-nitroindazole) against MPTP neurotoxicity in mice.

Effects of neuronal nitric oxide synthase (nNOS) inhibitor (7-nitroindazole), nonselective NOS inhibitor (N(G)-nitro-L-arginine methyl ester; L-NAME), and monoamine oxidase inhibitor (pargyline) were studied on 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP)-treated mice. The mice received four intraperitoneal injections of MPTP at 1-h intervals. A significant depletion in dopamine and DOPAC concentration was observed in the striatum from 1 day after MPTP treatment. The pretreatment of 7-nitroindazole and pargyline, but not L-NAME, dose-dependently protected against MPTP-induced depletion in dopamine content 3 days after MPTP treatment. Our histochemical study also showed that 7-nitroindazole and pargyline can prevent a marked decrease in the nigral cells and a marked increase in astrocytes in striatum 7 days after MPTP treatment. The protective effect of 7-nitroindazole against MPTP-induced dopamine and DOPAC depletion in the striatum was not attenuated by intraperitoneal pretreatment with L-arginine. Furthermore, the posttreatment of 7-nitroindazole or pargyline protected against MPTP-induced depletion of dopamine content. These results demonstrate that the protective mechanism by which 7-nitroindazole counteracts MPTP neurotoxicity in mice may be due not only to inhibition of nNOS, but also to MAO-B inhibition. Furthermore, our study suggests that the posttreatment of 7-nitroindazole and pargyline can prevent a significant decrease in dopamine levels in the striatum of MPTP-treated mice. These findings have important implications for the therapeutic time window and choice of nNOS or MAO inhibitors in patients with Parkinson's disease.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2002

Role of nitric oxide synthase against MPTP neurotoxicity in mice.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) causes nigrostriatal dopaminergic pathway injury similar to that observed in Parkinson's disease. Many hypotheses have been proposed to explain the mechanisms underlying MPTP neurotoxicity. Previous work showed that the inhibitor of neuronal nitric oxide synthase (nNOS) might produce protection against MPTP-induced dopaminergic toxicity. To exactly test the role of NO in MPTP neurotoxicity, we examined the effect of nNOS inhibitor 7-nitroindazole, in comparison with that of nonselective NOS inhibitor (L-NAME), immunosuppressant (FK-506), monoamine oxidase (MAO) inhibitors (clorgyline and pargyline), N-methyl-D-aspartate receptor antagonist (MK-801) and Ca2+ antagonist (amlodipine). Among seven compounds, 7-nitroindazole produced dose-dependent protection against MPTP-induced depletion of striatal dopamine and its metabolite 3,4-dihydroxyphenyl acetic acid (DOPAC) in mice. Clorgyline and pargyline also showed a significant effect on MPTP-induced dopamine depletion in the mouse striatum. However, both compounds did not protect against MPTP-induced depletion of striatal DOPAC Our immunohistological study with tyrosine hydroxylase (TH) and microtuble-associated protein 2 (MAP 2) showed that 7-nitroindazole or pargyline can protect against MPTP-induced depletion of TH and MAP 2 immunostained neurons in the substantia nigra. Furthermore, these compounds reduced a marked increase in GFAP-positive astrocytes of the mouse striatum after MPTP treatments. The present study demonstrates that nNOS inhibitor 7-nitroindazole as well as MAO inhibitors clorgyline and pargyline can produce dose-dependent neuroprotection against the dopaminergic neurotoxicity of MPTP. However, nonselective NOS inhibitor L-NAME, immunosuppressant FK-506, NMDA receptor antagonist MK-801 and Ca2+ antagonist amlodipine did not show a beneficial effect on MPTP neurotoxicity.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine↗
PubMed2002

CT imaging of intrabiliary growth of colorectal liver metastases: a comparison of pathological findings of resected specimens.

The objective of this study was to assess the usefulness of CT in the pre-operative evaluation of macroscopic intrabiliary tumour growth of colorectal liver metastases. 25 metastatic nodules of 18 patients who underwent an initial hepatectomy for colorectal liver metastasis were retrospectively evaluated. The CT appearance and pathological findings of the resected specimens were correlated. A number of unusual peritumoral features associated with intrabiliary tumour growth were detected by pre-operative CT. These were classified into three patterns: (1) thickened portal tract; (2) intrahepatic bile duct dilatation; and (3) a wedge-shaped area with enhancement. In 8 (32%) of the 25 nodules the portal tract was depicted as thicker than usual and these features were found proximal to the tumour in three instances, distal to the tumour in four instances, and both proximal and distal in one instance. All of the three intrabiliary tumours larger than 30 mm resulted in thickening of the portal tract. Intrahepatic bile duct dilatation was detected in association with 10 (40%) of 25 nodules. Bile duct dilatation was observed in more than one segment when intrabiliary tumour reached the hepatic hilus from the tumour. The presence of bile duct dilatation was not related to either the size of the tumour or the extent of intrabiliary tumour growth. An abnormally high density wedge-shaped area on contrast enhanced CT was another feature indicating intrabiliary tumour growth and was seen in association with four nodules. Such areas were seen in the liver parenchyma distal to the tumour on three occasions, or encompassing the tumour on one accasion. This wedge-shaped area appeared as a well demarcated dark red-brown region in the cut surface of the resected specimen. CT was useful for detecting the presence of intrabiliary tumour growth with these three patterns of radiological findings in patients with liver metastases from colorectal cancer

Aged↗
PubMed2001

Determination of uranium isotopes in soil core samples collected on the JCO grounds after the criticality accident.

To evaluate the impact of the 1999 criticality accident in Tokai-mura on the U isotope composition in soils, U isotopes (235U and 238U) were determined with inductively coupled plasma-mass spectrometry (ICP-MS) for soil core samples collected on the JCO grounds after the accident. The 235U/238U ratios were higher than the natural ratio in most samples. The highest ratio observed was 0.0262. Although vertical profiles of the 235U/238U ratio differed among the soil cores, the ratios tended to be high at the surface and decreased with depth. The U concentration also changed with depth. The percentages of 235U in the excess U, estimated from the positive correlation between U concentration and the 235U/238U ratio in soil samples, were less than 4% by mass (mostly 1-3%) and were much lower than the enrichment of the U used in the uranium conversion building at the time of the criticality accident (18.8%). These findings indicate that enriched U had been released before the criticality accident during the U processing at JCO in connection with the reconversion of light water reactor fuel. Since the range of the U concentrations found was comparable to the range of uncontaminated Japanese surface soils, the amount of U added to the soil was judged negligible from a radiation protection viewpoint.

Japan↗
PubMed2001

Measurement of 240Pu/239Pu isotopic ratios in soils from the Marshall Islands using ICP-MS.

Nuclear weapons tests conducted by the United States in the Marshall Islands produced significant quantities of regional or tropospheric fallout contamination. Here we report on some preliminary inductively coupled plasma-mass spectrometry (ICP-MS) measurements of plutonium isolated from seven composite soil samples collected from Bikini, Enewetak and Rongelap Atolls in the northern Marshall Islands. These data show that 240Pu/239Pu isotopic signatures in surface soils from the Marshall Island vary significantly and could potentially be used to help quantify the range and extent of fallout deposition (and associated impacts) from specific weapons tests. 137Cs and 60Co were also determined on the same set of soil samples for comparative purposes.

Environmental Monitoring↗