Biomedical subjects

Tsuyoshi Ando

Publications and source records attributed to Tsuyoshi Ando.

11 recordsLinked to original sources

PubMed2006

In situ hydrogenation of terminal halogen in poly(methyl methacrylate) by ruthenium-catalyzed living radical polymerization: direct transformation of "polymerization catalyst" into "hydrogenation catalyst".

An in situ, selective, and quantitative hydrogenation of the terminal chlorine (alpha-haloester) in living PMMA-Cl into PMMA-H was achieved via direct transformation of a "polymerization catalyst" into a "hydrogenation catalyst" in the Ru(II)-catalyzed living radical polymerization, where the polymerization mixture of MMA was directly treated in situ with K2CO3 as a base and 2-propanol as a hydrogen donor. The reaction terminated the polymerization and, more importantly, the terminal chlorine was quantitatively hydrogenated, as confirmed by SEC, 1H NMR, and MALDI-TOF MS.

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PubMed2005

Opacity effect on extreme ultraviolet radiation from laser-produced tin plasmas.

Opacity effects on extreme ultraviolet (EUV) emission from laser-produced tin (Sn) plasma have been experimentally investigated. An absorption spectrum of a uniform Sn plasma generated by thermal x rays has been measured in the EUV range (9-19 nm wavelength) for the first time. Experimental results indicate that control of the optical depth of the laser-produced Sn plasma is essential for obtaining high conversion to 13.5 nm-wavelength EUV radiation; 1.8% of the conversion efficiency was attained with the use of 2.2 ns laser pulses.

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PubMed2004

Effects of nefiracetam on the levels of brain-derived neurotrophic factor and synapsin I mRNA and protein in the hippocampus of microsphere-embolized rats.

Our recent study demonstrated that nefiracetam, N-(2,6-dimethylphenyl)-2-(2-oxo-1-pyrrolidinyl) acetamide, prevented impairment of the cyclic AMP (cAMP)/cAMP-responsive element binding (CREB) protein signaling pathway in sustained cerebral ischemia. The purpose of the present study was to determine whether nefiracetam has an effect on the expression of brain-derived neurotrophic factor (BDNF) and synapsin I mRNAs that are believed to be produced via CREB, and the alteration in their protein contents in the hippocampus after cerebral ischemia. Sustained cerebral ischemia was induced by injection of 700 microspheres into the right hemisphere of each rat. The rats were treated once daily with 10 mg/kg nefiracetam, p.o., from 15 h after the operation. Treatment with nefiracetam reduced the prolongation of the escape latency in the water maze test on days 7-9 after microsphere embolism-induced sustained cerebral ischemia, suggesting an improvement in the spatial learning function. Microsphere-embolized rats on day 5 showed decreases in BDNF and synapsin I mRNA levels and their protein contents in the ipsilateral hippocampus. Treatment with nefiracetam partially attenuated the decreases. These results suggest that enhancement of BDNF and synapsin I expression by nefiracetam treatment may be, at least in part, due to the improvement in the CREB binding activity, contributing to the prevention of learning and memory dysfunction after sustained cerebral ischemia.

Animals↗

PubMed2004

Cation pool-initiated controlled/living polymerization using microsystems.

The "cation pool" of an N-acyliminium ion was found to serve as an effective initiator of cationic polymerization of vinyl ethers in a microsystem consisting of two micromixers and a microtube reactor. The polymerization led to very narrow molecular weight distribution (Mw/Mn = 1.14). The molecular weight (Mn) increased linearly with an increase in the amount of the monomer. The carbocationic polymer end was effectively trapped by allyltrimethylsilane. The present observations illustrate the potential of microsystems, in conjunction with the cation pool, to effect polymerization in a highly controlled manner without the deceleration inherent in the dynamic equilibrium between active and dormant species.

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PubMed2004

Metal-catalyzed living radical polymerization: discovery and developments.

Control of radical polymerization has been one of the most challenging frontiers in polymerization chemistry. This review presents the discovery of metal-catalyzed living radical polymerization and recent developments in the evolution of catalysts in terms of versatility and activity, scope of monomers, controlled polymerization in water, catalyst removal, and precision synthesis of well-controlled polymers such as random, block, end-functionalized, and star polymers.

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PubMed2003

Polymer catalysts from polymerization catalysts: direct encapsulation of metal catalyst into star polymer core during metal-catalyzed living radical polymerization.

Star polymers containing ruthenium complex in the core were prepared by ruthenium-catalyzed living radical polymerization, where the metal catalysts were directly encapsulated on linking reactions of living poly(MMA) in the presence of ethylene glycol dimethacrylate as a linker and diphenyl-4-styrylphosphine as a ligand incorporated in the core. The products were characterized by SEC/MALLS, UV-vis, NMR, AFM, TEM, and ICP-AES and were employed as polymer catalysts for the oxidation reaction of alcohol.

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PubMed2003

A possible mechanism for improvement by a cognition-enhancer nefiracetam of spatial memory function and cAMP-mediated signal transduction system in sustained cerebral ischaemia in rats.

1. Accumulated evidence indicates that the adenylyl cyclase (AC)/cyclic adenosine monophosphate (cAMP)/protein kinase A (PKA)/cAMP-responsive element binding protein (CREB) signal transduction system may be linked to learning and memory function. 2. The effects of nefiracetam, which has been developed as a cognition enhancer, on spatial memory function and the AC/cAMP/PKA/CREB signal transduction system in rats with sustained cerebral ischaemia were examined. 3. Microsphere embolism (ME)-induced sustained cerebral ischaemia was produced by injection of 700 microspheres (48 micro m in diameter) into the right hemisphere of rats. Daily oral administration of nefiracetam (10 mg kg(-1) day(-1)) was started from 15 h after the operation. 4. The delayed treatment with nefiracetam attenuated the ME-induced prolongation of the escape latency in the water maze task that was examined on day 7 to 9 after ME, but it did not reduce the infarct size. 5. ME decreased Ca(2+)/calmodulin (CaM)-stimulated AC (AC-I) activity, cAMP content, cytosolic PKA Cbeta level, nuclear PKA Calpha and Cbeta levels, and reduced the phosphorylation and DNA-binding activity of CREB in the nucleus in the right parietal cortex and hippocampus on day 3 after ME. The ME-induced changes in these variables did not occur by the delayed treatment with nefiracetam. 6. These results suggest that nefiracetam preserved cognitive function, or prevented cognitive dysfunction, after sustained cerebral ischaemia and that the effect is, in part, attributable to the prevention of the ischaemia-induced impairment of the AC/cAMP/PKA/CREB signal transduction pathway.

Animals↗

PubMed2003

Persistent effects of delayed treatment with nefiracetam on the water maze task in rats with sustained cerebral ischemia.

The present study was aimed at determining whether nefiracetam might have a persistent cognition-enhancing effect in animals with sustained cerebral ischemia. Sustained cerebral ischemia was induced by injecting 700 microspheres into the right internal carotid artery of rats [microsphere-embolized (ME) rats]. The ME and sham-operated rats were treated with 10 mg/kg/day nefiracetam p.o. from the first to the 9th day after the operation. The escape latency of the ME rat in the water maze test, when performed on days 7 to 9 after the operation, was lengthened. This effect was attenuated by the delayed treatment with nefiracetam. The nefiracetam-treated ME rat showed a shortened escape latency in the retention test on day 17 as well as in the contraposition test on day 18. These results indicate that a persistent improvement of the spatial memory function impaired by sustained cerebral ischemia was achieved even after cessation of treatment with nefiracetam. The functional damage to learning and memory was associated with decreases in the membranous adenylyl cyclase I and cytosolic protein kinase A (PKA) catalytic subunit and regulatory subunit proteins in the right hippocampus and cerebral cortex. The delayed treatment with nefiracetam appreciably prevented the decreases in these proteins. The present study suggests that nefiracetam may have an ability to cause persistent improvement of learning and memory function, possibly through protection against the ischemia-induced impairment to the adenylyl cyclase/cAMP/PKA signal transduction pathway.

Animals↗

PubMed2003

Effects of nefiracetam on cerebral adenylyl cyclase activity in rats with microsphere embolism-induced memory dysfunction.

The effects of nefiracetam on the cerebral adenylyl cyclase (AC) activity of animals with microsphere embolism-induced memory dysfunction were examined. Sustained cerebral ischemia in the right cerebral hemisphere was induced by an injection of microspheres into the right internal carotid artery of rats. To examine learning and memory function, the water maze test was performed from day 7 to day 10 after the operation. The escape latency of the microsphere-embolized (ME) rat in the water maze task was longer than that of the sham-operated (Sham) rat, suggesting that spatial memory dysfunction occurred in the ME rat. Gsalpha and Gi(1/2)alpha protein levels in the cerebral cortex, striatum and hippocampus of the ME rat, when determined on day 11, were similar to those of the Sham rats. The basal AC activity in the striatum, but not in the other two regions, of the ME rat decreased. The AC activity in the presence of 10 microM colforsin daropate (Col), a direct stimulator of AC, was increased by approximately 20-fold in sham animals and 7- to 10-fold in the ME rat. Treatment of the ME rat with 10 mg/kg/d nefiracetam p.o. from day 1 to day 10 after the operation shortened the escape latency, restored the basal AC activity in the striatum, and reversed the Col-induced increases in AC in these three regions without any changes in the cerebral Gsalpha and Gi(1/2)alpha protein levels. These results suggest that nefiracetam-mediated activation of AC activity may contribute to the improvement of memory and learning function in sustained cerebral ischemia.

Animals↗

PubMed2002

Effects of nefiracetam on spatial memory function and acetylcholine and GABA metabolism in microsphere-embolized rats.

The present study aimed to determine whether nefiracetam, N-(2,6-dimethylphenyl)-2-(2-oxo-1-pyrrolidinyl) acetamide, a cognition enhancer, has an effect on learning and memory function in sustained cerebral ischemia, and whether the effect, if any, may accompany modification of the cholinergic or gamma-aminobutyric acid (GABA)ergic system, which are conceived to be involved in the learning and memory function, in the ischemic brain. Sustained cerebral ischemia was induced by the injection of 700 microspheres into the right hemisphere of the rat. The animals were treated once daily with 10 mg/kg nefiracetam p.o. from 15 h after the operation to either 10 days for the water maze study, or 3 or 5 days after the operation for neurochemical examination. Microsphere-embolized rats showed stroke-like symptoms 15 h after the operation and lengthened the escape latency in the water maze task on days 7-10, suggesting a spatial learning dysfunction. The delayed treatment did not reduce the stroke-like symptoms, but effectively shortened the escape latency. The animals at days 3 and 5 after the operation showed decreases in acetylcholine content and choline acetyltransferase activity, which were not prevented by nefiracetam. The microsphere-embolized rats showed decreases in GABA content and glutamic acid decarboxylase activity. The delayed treatment appreciably restored GABA content in the hippocampus on day 5 and reversed glutamic acid decarboxylase activity in both brain regions on day 5. These results suggest that the GABAergic activity rather than the cholinergic activity may be, at least in part, involved in the pharmacological effects of nefiracetam in the ischemic brain.

Acetylcholine↗

PubMed2002

A new ruthenium complex with an electron-donating aminoindenyl ligand for fast metal-mediated living radical polymerizations.

A new ruthenium complex with an electron-donating aminoindenyl ligand induces a fast living radical polymerization of methyl methacrylate (MMA) in the presence of a chloride initiator to give polymers with controlled and variable molecular weights (Mn = 103-105) and very narrow molecular weight distributions (Mw/Mn < 1.1). The structure and high activity of the catalyst were analyzed by X-ray crystallography and cyclic voltammetry in comparison to those of a similar complex with an indenyl ligand.

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