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Yasuhiro Suzuki

Publications and source records attributed to Yasuhiro Suzuki.

At least 73 records · Page 4Linked to original sources
PubMed2004

Mechanism of photoacid generation for an arylcycloalkylsulfonium salt by ring opening and aryl cleavage.

The photochemistry of 1-(4-tert-butylphenyl)-tetrahydro-thiopyranium triflate (1), an arylcycloalkylsulfonium salt, was investigated in acetonitrile and methanol at low conversion in order to understand the reaction mechanism and its efficiency as photoacid generator. Both types of C-S bond in 1 are cleaved from the excited state. The heterolytic cleavage of the methylene C-S bond produces 4-t-BuC(6)H(4)S(CH(2))(4)CH(2)(+) by ring opening. The carbocation generates acid and arylalkenylsufides by elimination or 1,2 hydride shift and elimination. The predominantly homolytic cleavage of the aryl C-S bond yields 4-t-BuC(6)H(4)* and c-C(5)H(10)S(+)* as the fragmentation products. The radicals react with the solvent forming acid, pentamethylene sulfide and tert-butylbenzene. In methanol, the formation of 4-tert-butylanisole indicates a contribution of solvolysis in the excited state of 1 or a competing formation of free aryl cation by heterolytic fragmentation. The acid generation efficiency of 1 in solution (acetonitrile or methanol) is lower than that corresponding to triphenylsulfonium triflate (TPS OTf) under the same conditions. This suggests a pathway for the regeneration of 1 after photocleavage. The photochemistry of 1 is discussed in terms of the contribution of fragmentation and ring opening reaction paths to its overall acid generation efficiency, a key property in terms of its applications in resist formulations.

Journal Article↗
PubMed2004

Microplasmin reduces ischemic brain damage and improves neurological function in a rat stroke model monitored with MRI.

BACKGROUND AND PURPOSE: Microplasmin (microPli), a derivative of plasmin lacking the 5 "kringle" domains, was studied in a rat thrombotic stroke model with MRI monitoring. METHODS: Brain ischemia was induced by middle cerebral artery (MCA) occlusion with photochemically induced thrombosis. Brain tissue damage was assessed at 1 hour and 24 hours after MCA occlusion by MRI and 2,3,5-triphenyl tetrazolium chloride (TTC) staining. Neurological symptoms were scored at 24 hours. Animals with insufficient evidence of significant jeopardized brain tissue on perfusion-weighted imaging (PWI) at 1 hour were excluded before randomization. Included animals were randomized (blinded) to controls (solvent), 7.5 or 10 mg/kg microPli, administered as an intravenous bolus 90 minutes after MCA occlusion (n=8 per dose group). RESULTS: microPli treatment reduced cerebral damage measured by TTC staining at 24 hours, from 250+/-69 mm3 (mean+/-SD) in controls to 150+/-30 and 170+/-62 mm3 with 7.5 and 10 mg/kg microPli, respectively; it reduced the expansion of the PWI positive area between 1 and 24 hours, and it reduced neurological deficits from a Bederson score of 7 (6 to 9) in controls to 4.5 (3 to 8) and 4 (3 to 6), with 7.5 and 10 mg/kg microPli, respectively (median and rangeP<0.05 for each dose versus controls for all parameters). CONCLUSIONS: Bolus intravenous microPli given 90 minutes after thrombotic MCA occlusion in rats reduces cerebral ischemic damage and improves neurological dysfunction, suggesting that microPli could be beneficial in ischemic stroke patients.

Animals↗
PubMed2004

Retinoic acid controls blood vessel formation by modulating endothelial and mural cell interaction via suppression of Tie2 signaling in vascular progenitor cells.

Inhibition by all-trans retinoic acid (atRA) of the microvasculature formation in chicken chorioallantoic membrane (CAM) accompanied remarkably reduced numbers of endothelial cells (ECs) and increased numbers of mural cells (MCs) under the chorionic epithelial layer. Ro41-5253 (retinoid antagonist) exerted the opposite effect. Although atRA did not affect the differentiation of murine embryonic stem cell-derived vascular progenitor cells (VPCs) into ECs or MCs, atRA suppressed EC-MC interaction, leading to impaired branching. In both atRA-treated VPC cultures and CAM tissues underneath the chorionic epithelial layer, the expression of angiopoietin-2 (Ang-2; competitor for Ang-1) was enhanced, whereas that of Tie2 (a receptor for Angs) was reduced. Simultaneous treatment with Ang-1 partially blocked RA induction of EC-MC malinteraction and reduction in blood vessel formation. These results suggest that retinoid(s) may reduce EC-MC interaction by down-regulating Tie2 signaling as well as decreased EC numbers, which lead to impaired vascular remodeling.

Allantois↗
PubMed2004

Prompt chemoenzymatic synthesis of diverse complex-type oligosaccharides and its application to the solid-phase synthesis of a glycopeptide with Asn-linked sialyl-undeca- and asialo-nonasaccharides.

We describe herein the preparation of 24 pure asparagine-linked oligosaccharides (Asn-oligosaccharides) from asparagine-linked biantennary complex-type sialylundecasaccharide [(NeuAc-alpha-2,6-Gal-beta-1,4-GlcNAc-beta-1,2-Man-alpha-1,6/1,3-)(2)-Man-beta-1,4-GlcNAc-beta-1,4-GlcNAc-beta-1-asparagine, 2] obtained from egg yolk. Our synthetic strategy aimed at adapting branch specific exo-glycosidases digestion (beta-D-galactosidase, N-acetyl-beta-D-glucosaminidase and alpha-D-mannosidase) of the individual asialo-branch after preparation of monosialyloligosaccharides obtained from 2 by acid hydrolysis of NeuAc. In order to perform branch specific exo-glycosidase digestion, isolation of pure monosialyloligosaccharides obtained was essential. However, isolation of two kinds of monosialyloligosaccharides are difficult by HPLC due to their highly hydrophilic nature. Therefore, we examined chemical protection with hydrophobic protecting (Fmoc and benzyl) groups. These chemical protection enabled us to separate the monosialyloligosaccharides by use of a HPLC column (ODS) on synthetic scales. Using these pure monosialiloligosaccharides enable us to obtain 24 Asn-linked oligosaccharides (100 mg scale) within a few weeks by branch specific exo-glycosidase digestions (alpha-D-neuraminidase, beta-D-galactosidase, N-acetyl-beta-D-glucosaminidase and alpha-D-mannosidase). In addition, solid-phase synthesis of glycopeptide having Asn-linked sialyl-undeca- and asialo-nonasaccharides thus obtained, was also performed on an acid labile HMPA-PEGA resin.

Animals↗
PubMed2004

Vesicular acetylcholine transporter can be a morphological marker for the reinnervation to muscle of regenerating motor axons.

This study was designed to evaluate whether the vesicular acetylcholine transporter (VAChT), which packages acetylcholine into synaptic vesicles, can be used as a marker for regenerating motor axon terminal. We examined motor axon regeneration in the tongue after hypoglossal nerve axotomy, using an anterograde tracer biotin-dextran (BD), retrograde tracer Fluoro-Gold (FG), electron microscopic (EM) observation, and VAChT immunocytochemistry. BD study demonstrated that outgrowth of thin regenerating axons into the frontal area of the tongue was firstly observed at 14 post-operative days, and presynaptic formation of neuromuscular junction (NMJ) was observed from 21 post-operative days. Under electron microscopic observation, reconstruction of new NMJs was observed within the interval between 21 and 28 days. VAChT-immunoreactive nerve terminals disappeared by 3 days after axotomy, slightly appeared at 14 post-operative days, and thereafter gradually increased in number from 21 to 28 post-operative days. The re-expression of VAChT positive presynaptic terminal was almost the same as those obtained in BD, FG and EM studies. Regenerating axons tip in the crush model of the hypoglossal nerve exhibited prominent VAChT immunoreactivity in growing tip of regenerating axons. These indicate that VAChT is an excellent morphological indicator for regenerating nerve terminals of motor neurons.

Animals↗
PubMed2004

Preoperative evaluation of the venous system for potential interference in the clipping of cerebral aneurysm.

BACKGROUND: Variations of the venous system affecting the surgical treatment of cerebral aneurysm were evaluated using three-dimensional computed tomography angiography (3D-CTA) to evaluate the essential aspects of preoperative diagnosis. METHODS: This study included 50 patients who underwent clipping of cerebral aneurysm through the pterional and trans-sylvan approaches. The 3D-CTA and operative findings were compared to assess the characteristics of cases in which the veins restrict brain retraction, hinder operative manipulations or require sacrifice because of the position in the operative field. RESULTS: Superficial sylvian veins that restricted brain retraction were identified in 8 cases. The veins entered the cavernous sinus in a relatively high position just below either the sphenoid ridge (superior lateral type) or the anterior clinoid process (superior medial type), and the veins entering at a more medial position were closer to the spatula and tended to be compressed or directly excluded (superior medial type). The inferior medial type did not tend to become tense and so did not restrict brain retraction. The inferior lateral type hardly affected the operative manipulation. The first segment of the basal vein of Rosenthal, the uncal vein entering the cavernous sinus, or the sphenoparietal sinus were located in the operative field in six cases, and affected the manipulation of dissecting arteries, and exposure and clipping of the aneurysm. CONCLUSIONS: 3D-CTA provides essential information for operative planning to protect the venous system during the pterional and trans-sylvian approaches.

Brain↗
PubMed2004

Immunohistochemical evaluation of hormone receptors in breast cancer: which scoring system is suitable for highly sensitive procedures?

To evaluate hormone receptors immunohistochemically, standardized staining procedures and scoring systems are required. The authors previously reported that highly sensitive procedures affected basic factors for technical validation. The aim of the present study was to show the characteristics of scoring systems for highly sensitive procedures. To examine how highly sensitive procedures enhance the staining intensity and increase the positive cell population, two different staining methods were compared. To evaluate scoring systems, three systems--cell counting score, modified immunoreactive score, and H score--were compared using the same samples stained by an autostaining system. It was found that the highly sensitive procedure increased the positive cell population, especially in breast cancers with a low enzyme immunoassay (EIA) level of less than 100 fmol/mg, and strengthened the staining intensity. This enhancement led to a correlation in a logarithmic curve rather than a linear correlation by all three scoring systems. The results showed that scoring systems including a factor of staining intensity did not have an absolute advantage because boosted staining intensity by highly sensitive procedure did not reflect EIA value or protein contents accurately. To the authors' knowledge, there is no report discussing the nonlinear correlation between biochemical and immunohistochemical assay by highly sensitive procedures; however, it is important to select a scoring system and threshold based on nonlinear correlation.

Breast Neoplasms↗
PubMed2004

A case of fatal systemic toxoplasmosis in a cat being treated with cyclosporin A for feline atopy.

Acute systemic toxoplasmosis was diagnosed in a 4-5-year-old, male, Domestic Short Hair cat, which had been on cyclosporine A immunomodulatory therapy for feline atopy, over an 8-month period. Cyclosporin A (CsA) has shown promising results as a immunosuppressive agent in the cat for the treatment of eosinophilic plaque and granulomas, allergic cervico-facial pruritus, feline atopy and other immune-mediated dermatoses. However, inhibition of T-lymphocyte function by CsA is believed to have predisposed this cat to the development of a newly acquired, acute Toxoplasma gondii infection, as characterized by severe hepatic and pancreatic pathology in conjunction with the heavy parasite load demonstrated on immunohistochemical (IHC) stains for T. gondii. Cats on CsA therapy appear to be at risk of developing fatal systemic toxoplasmosis.

Animals↗
PubMed2004

Gamma interferon production, but not perforin-mediated cytolytic activity, of T cells is required for prevention of toxoplasmic encephalitis in BALB/c mice genetically resistant to the disease.

We previously showed the requirement of both T cells and gamma interferon (IFN-gamma)-producing non-T cells for the genetic resistance of BALB/c mice to the development of toxoplasmic encephalitis (TE). In order to define the role of IFN-gamma production and the perforin-mediated cytotoxicity of T cells in this resistance, we obtained immune T cells from spleens of infected IFN-gamma knockout (IFN-gamma(-/-)), perforin knockout (PO), and wild-type BALB/c mice and transferred them into infected and sulfadiazine-treated athymic nude mice, which lack T cells but have IFN-gamma-producing non-T cells. Control nude mice that had not received any T cells developed severe TE and died after discontinuation of sulfadiazine treatment due to the reactivation of infection. Animals that had received immune T cells from either wild-type or PO mice did not develop TE and survived. In contrast, nude mice that had received immune T cells from IFN-gamma(-/-) mice developed severe TE and died as early as control nude mice. T cells obtained from the spleens of animals that had received either PO or wild-type T cells produced large amounts of IFN-gamma after stimulation with Toxoplasma gondii antigens in vitro. In addition, the amounts of IFN-gamma mRNA expressed in the brains of PO T-cell recipients did not differ from those in wild-type T-cell recipients. Furthermore, PO mice did not develop TE after infection, and their IFN-gamma production was equivalent to or higher than that of wild-type animals. These results indicate that IFN-gamma production, but not perforin-mediated cytotoxic activity, by T cells is required for the prevention of TE in genetically resistant BALB/c mice.

Adoptive Transfer↗
PubMed2004

Simultaneous injection of bone marrow cells and stromal cells into bone marrow accelerates hematopoiesis in vivo.

We have previously demonstrated that stromal cells can support the proliferation and differentiation of hematopoietic cells in vitro and in vivo and that a major histocompatibility complex restriction exists between hematopoietic stem cells and stromal cells. We have also found that intra-bone marrow (IBM) injection of allogeneic bone marrow cells (BMCs) leads to more rapid reconstitution of hematopoietic cells than intravenous injection. In the present study, we examine the effect of simultaneous injection of stromal cells and BMCs into the same bone marrow on the recovery of donor hematopoietic cells and demonstrate that simultaneous IBM injection of BMCs plus stromal cells is more effective in reconstituting recipients with donor hematopoietic cells than intravenous injection of BMCs plus stromal cells or IBM injection of BMCs alone.

Bone Marrow Cells↗
PubMed2004

[Endovascular treatment of a ruptured aneurysm associated with unilateral moyamoya disease].

We report a case presenting with subarachnoid hemorrhage due to a ruptured aneurysm associated with unilateral moyamoya disease. The patient was a 29-year-old woman exhibiting sudden onset headache. Computed tomography revealed subarachnoid hemorrhage around the brain stem. Cerebral angiography showed a saccular aneurysm at the junction of the left P1 portion of the posterior cerebral artery and its perforator. The right internal carotid artery was occluded at the terminal portion, and the right middle cerebral artery territory was perfused anterogradely via abnormal moyamoya vessels in the basal ganglia. The aneurysm was completely embolized with preservation of the perforator. We suggest that as compared to surgical clipping by craniotomy, endovascular therapy is safe and effective for treatment of intracranial aneurysms associated with moyamoya disease.

Adult↗
PubMed2004

Evaluation of 5-(4-nitrophenyl)-2,4-pentadien-1-al (NPPD) as a tracer for shadowing pursuits.

The chemical compound 5-(4-nitrophenyl)-2,4-pentadien-1-al (NPPD), called "spy dust," was used in the Soviet Union as a shadowing pursuit, the act of following someone secretly, for investigating the activities of diplomatic personnel. It is also useful for counter-terrorism, and some criminal cases in the forensic science field. In this paper, it was synthesized and evaluated as a tracer for shadowing pursuits. The method for utilizing this reagent was very simple: it was dissolved in methanol (1 mg/mL) and sprayed on the restricted area. If the suspect was to enter this area or touched the sprayed material, NPPD was attached to the suspect's shoe surface or hands. The color examination was a two-steps process: first was the addition of 1 mL of a 0.1% naphthoresorcinol methanol solution to the methanol extracts of a methanol-contained cotton swab used to smear some surfaces of the suspect, and second, the addition of 1 mL of concentrated hydrochloric acid, which turned the solution dark red. The gamma max of the colored solution was 510 nm, measured by ultraviolet-vis spectroscopy. Detection limits for three methods were determined: a visual method (detection limit 100 ng/3 mL), an ultraviolet-visible spectrometric method (detection limit 10 ng/3 mL), and a selected-ion-monitoring gas chromatographic/mass spectrometric method (detection limit 300 pg/injection). The forensic utility of NPPD was demonstrated for two simulated cases: a theft case and a case where NPPD was used as a tracer to prove that an automobile had entered a restricted area. These examinations prove NPPD is a useful shadowing pursuit (spy dust) for the forensic science field.

Chromatography, Gas↗
PubMed2004

[A case of young adult presenting with cerebral infarction caused by homocystinuria].

Homocystinuria is a congenital metabolic disorder, and has been known as life-threatening risk factor of vascular disease including ischemic stroke. We report a case of cerebral infarction due to homocystinuria. The patient was a 21-year-old woman exhibiting left hemiparesis and a previous history of ectopia lentis. Magnetic resonance imaging showed multiple fresh infarctions in the right frontal and temporal lobes, basal ganglia, corona radiata, and internal capsule. The right common carotid angiogram demonstrated complete occlusion at the origin of the right internal carotid artery. Further investigation clarified increased level of serum methionine and homocysteine and urinary homocystin due to cystathionine beta-synthase deficiency. Homocystinuria was diagnosed as the cause of cerebral infarction. The patient was treated by low methionine diet and administration of folic acid, cobalamin, and aspirin. It should be recognized that some patients with homocystinuria are missed in the neonatal screening for congenital metabolic disorders. Recent studies indicated that the homocysteinemia is one of risk factors of ischemic stroke in the general population as well as in the patients of homocystinuria. We recommend metabolic screening for homocystinuria, when treating a juvenile patient with ischemic stroke of unknown etiology.

Adult↗
PubMed2003

Na+/H+ exchanger inhibitor, SM-20220, is protective against excitotoxicity in cultured cortical neurons.

BACKGROUND AND PURPOSE: Recently, it has been reported that Na+/H+ exchanger (NHE) inhibitors demonstrated protective effects on ischemia/reperfusion brain injury in animal models. However, the mechanisms by which the neurons were protected against ischemic insult remain unclear. To reveal the cellular mechanism of the NHE inhibitor on the neuronal death, we examined the effects of a selective NHE inhibitor, SM-20220 (N-[aminoiminomethyl]-1-methyl-1H-indole-2-carboxamide methanesulfonate), on glutamate-induced neuronal death in rat cortical culture. METHODS: Cortical neurons were prepared from 1-day old rats, and cultured on the glass-based dishes. Glutamate-induced neuronal death was assessed by staining the cells with propidium iodide. Morphological changes in the neurons were observed with a video-enhanced contrast-differential interference contrast microscope. The intracellular calcium concentration ([Ca2+]i) and the intracellular pH (pHi) were measured by fluorescence imaging with a confocal laser microscope using fluo-3/acetoxymethylester (AM) and 2', 7'-bis-2-carboxy-ethyl-5(6)-carboxyfluorescein (BCECF)/AM as a fluorescent dye, respectively. RESULTS: SM-20220 (0.3 to 30 nmol/L) dose-dependently attenuated glutamate (300 micromol/L)-induced neuronal death over a period of 6 hours, and inhibited the acute cellular swelling following glutamate (500 micromol/L) exposure. Dual peaks of [Ca2+]i rise were observed at 5 and 12 minutes after glutamate (500 micromol/L) exposure, followed by a persistent rise. SM-20220 suppressed the persistent [Ca2+]i increase. SM-20220 inhibited intracellular acidification following glutamate (500 micromol/L) exposure. All of the events induced by glutamate were also inhibited by the N-methyl-d-aspartate receptor antagonist, MK-801, indicating the death process was excitotoxicity. CONCLUSIONS: NHE inhibitor is neuroprotective through inhibition of both persistent [Ca2+]i increase and acidification in excitotoxicity.

Amides↗
PubMed2003

Essential role of endogenous tissue plasminogen activator through matrix metalloproteinase 9 induction and expression on heparin-produced cerebral hemorrhage after cerebral ischemia in mice.

Cerebral hemorrhage associated with antithrombotic and thrombolytic therapy in acute stroke continues to present a major clinical problem. Rupture of the cerebral microvasculature involves the degradation and remodeling of extracellular matrix. Here we demonstrated that the delayed administration of heparin 3 hours after photothrombotic middle cerebral artery occlusion (MCAO) caused cerebral hemorrhage in wild-type (WT) mice but not in tissue plasminogen activator (tPA)-deficient knockout (KO) mice. Heparin administration increased tPA activity and its mRNA expression at 6 and 12 hours after MCAO in the ischemic hemispheres of WT mice. The expression of tPA was enhanced in microglial cells in the ischemic border zone. We also observed an exacerbation of matrix metalloproteinase (MMP) 9 expression at the mRNA level and its conversion to an active form after heparin administration in the ischemic hemisphere in WT mice but not in tPA KO mice. The increased MMP 9 expression was localized in microglial cells and endothelial cells. These findings suggest that endogenous tPA, through the enhancement of MMP 9 expression and proteolytic activation, plays an essential role in the pathogenesis of heparin-produced cerebral hemorrhage. Targeting tPA, MMP 9, or both may provide a new approach for preventing cerebral hemorrhage associated with antithrombotic therapy for stroke in humans.

Animals↗
PubMed2003

Surfactant protein B in type II pneumocytes and intra-alveolar surfactant forms of human lungs.

Surfactant protein B (SP-B) is synthesized by type II pneumocytes as a proprotein (proSP-B) that is proteolytically processed to an 8-kD protein. In human type II pneumocytes, we identified not only proSP-B, processing intermediates of proSP-B, and mature SP-B, but also fragments of the N-terminal propeptide. By means of immunoelectron microscopy, proSP-B and processing intermediates were localized in the endoplasmic reticulum, Golgi vesicles, and few multivesicular bodies in type II pneumocytes in human lungs. A colocalization of fragments of the N-terminal propeptide and mature SP-B was found in multivesicular, composite, and some lamellar bodies. Mature SP-B was localized over the projection core of lamellar bodies and core-like structures in tubular myelin figures. In line with immunoelectron microscopy and Western blot analysis of human type II pneumocytes, a fragment of the N-terminal propeptide was also detected in isolated rat lamellar bodies. In conclusion, our data indicate that the processing of proSP-B occurs between the Golgi complex and multivesicular bodies and provide evidence that a fragment of the N-terminal propeptide and mature SP-B are transported together to the lamellar bodies. In human lungs, mature SP-B is involved in the structural organization of lamellar bodies and tubular myelin by the formation of core particles.

Adult↗
PubMed2003

Dietary supplementation of fermented soybean, natto, suppresses intimal thickening and modulates the lysis of mural thrombi after endothelial injury in rat femoral artery.

We have previously demonstrated that natto-extracts containing nattokinase (NK) inactivates plasminogen activator inhibitor type 1 and then potentiates fibrinolytic activity. In the present study, we investigated the effects of dietary supplementation with natto-extracts on neointima formation and on thrombolysis at the site of endothelial injury. Endothelial damage in the rat femoral artery was induced by intravenous injection of rose bengal followed by focal irradiation by transluminal green light. Dietary natto-extracts supplementation containing NK of 50 or 100 CU/body was started 3 weeks before endothelial injury and then continued for another 3 weeks. Intimal thickening in animals given supplementation was significantly (P<0.01) suppressed compared with controls and the intima/media ratio in animals with 50 and 100 CU/body NK and control group was 0.09 +/- 0.03, 0.09 +/- 0.06 and 0.16 +/- 0.12, respectively. Although femoral arteries were reopened both in control animals and those treated with NK within 8 hours after endothelial injury, mural thrombi were histologically observed at the site of endothelial injury. In the control group, the center of vessel lumen was reopened and mural thrombi were attached on the surface of vessel walls. In contrast, in NK-treated groups, thrombi near the vessel wall showed lysis and most of them detached from the surface of vessel walls. In conclusion, dietary natto-extracts supplementation suppressed intimal thickening produced by endothelial injury in rat femoral artery. These effects may partially be attributable to NK, which showed enhanced thrombolysis near the vessel wall.

Animals↗