Showing papers by "Hiroshima University published in 2005"

Biomass gasification in near- and super-critical water: Status and prospects

Abstract: The current status of biomass gasification in near- and supercritical water (SCWG) is reviewed. There are two approaches to biomass gasification in supercritical water. The first: low-temperature catalytic gasification, employs reaction temperature ranging from 350 to 600 °C, and gasifies the feedstock with the aid of metal catalysts. The second: high-temperature supercritical water gasification, employs reaction temperatures ranging from 500 to 750 °C, without catalyst or with non-metallic catalysts. Reviews are made on reaction mechanism, catalyst, and experimental results for these two approaches. Engineering technologies for SCWG gasification, and an example of process analysis are also introduced. Finally, the authors’ prognostications on the future prospects of this technology are offered.

Catalytic effect of nanoparticle 3d-transition metals on hydrogen storage properties in magnesium hydride MgH2 prepared by mechanical milling.

Abstract: We examined the catalytic effect of nanoparticle 3d-transition metals on hydrogen desorption (HD) properties of MgH(2) prepared by mechanical ball milling method. All the MgH(2) composites prepared by adding a small amount of nanoparticle Fe(nano), Co(nano), Ni(nano), and Cu(nano) metals and by ball milling for 2 h showed much better HD properties than the pure ball-milled MgH(2) itself. In particular, the 2 mol % Ni(nano)-doped MgH(2) composite prepared by soft milling for a short milling time of 15 min under a slow milling revolution speed of 200 rpm shows the most superior hydrogen storage properties: A large amount of hydrogen ( approximately 6.5 wt %) is desorbed in the temperature range from 150 to 250 degrees C at a heating rate of 5 degrees C/min under He gas flow with no partial pressure of hydrogen. The EDX micrographs corresponding to Mg and Ni elemental profiles indicated that nanoparticle Ni metals as catalyst homogeneously dispersed on the surface of MgH(2). In addition, it was confirmed that the product revealed good reversible hydriding/dehydriding cycles even at 150 degrees C. The hydrogen desorption kinetics of catalyzed and noncatalyzed MgH(2) could be understood by a modified first-order reaction model, in which the surface condition was taken into account.

Apparent diffusion coefficient of human brain tumors at MR imaging.

Abstract: PURPOSE: To determine if apparent diffusion coefficient (ADC) can be used to differentiate brain tumors at magnetic resonance (MR) imaging. MATERIALS AND METHODS: Institutional review board approval or informed patient consent was not required. MR images were reviewed retrospectively in 275 patients with brain tumors: 147 males and 128 females 1–81 years old, treated between September 1997 and July 2003. Regions of interest were placed manually in tumor regions on MR images, and ADC was calculated with a five-point regression method at b values of 0, 250, 500, 750, and 1000 sec/mm2. ADC values were average values in tumor. All brain tumor subgroups were analyzed. Logistic discriminant analysis was performed by using ADC, age, and patient sex as independent variables to discriminate among tumor groups. RESULTS: A significant negative correlation existed between ADC and astrocytic tumors of World Health Organization grades 2–4 (grade 2 vs grades 3 and 4, accuracy of 91.3% [P < .01]; grade 3 vs 4, accuracy o...

The attentional blink: resource depletion or temporary loss of control?

Abstract: Identification of the second of two targets is impaired if it is presented less than about 500 ms after the first. Theoretical accounts of this second-target deficit, known as attentional blink (AB), have relied on some form of limited attentional resource that is allocated to the leading target at the expense of the trailing target. Three experiments in the present study reveal a failure of resource-limitation accounts to explain why the AB is absent when the targets consist of a stream of three items belonging to the same category (e.g., letters or digits). The AB is reinstated, however, if an item from a different category is inserted in the target string. This result, and all major results in the AB literature, is explained by the hypothesis that the AB arises from a temporary loss of control over the prevailing attentional set. This lapse in control renders the observer vulnerable to an exogenously-triggered switch in attentional set.

Antimicrobial Peptides in the Oral Environment: Expression and Function in Health and Disease

Abstract: The oral cavity is a unique environment in which antimicrobial peptides play a key role in maintaining health and may have future therapeutic applications. Present evidence suggests that α-defensins, β-defensins, LL-37, histatin, and other antimicrobial peptides and proteins have distinct but overlapping roles in maintaining oral health and preventing bacterial, fungal, and viral adherence and infection. The expression of the inducible hBD-2 in normal oral epithelium, in contrast to other epithelia, and the apparent differential signaling in response to commensal and pathogenic organisms, provides new insights into innate immunity in this body site. Commensal bacteria are excellent inducers of hBD-2 in oral epithelial cells, suggesting that the commensal bacterial community acts in a manner to benefit the overall innate immune readiness of oral epithelia. This may have major significance for understanding host defense in the complex oral environment.

Evidence for Muon Neutrino Oscillation in an Accelerator-Based Experiment

Abstract: We present results for nu(mu) oscillation in the KEK to Kamioka (K2K) long-baseline neutrino oscillation experiment. K2K uses an accelerator-produced nu(mu) beam with a mean energy of 1.3 GeV directed at the Super-Kamiokande detector. We observed the energy-dependent disappearance of nu(mu), which we presume have oscillated to nu(tau). The probability that we would observe these results if there is no neutrino oscillation is 0.0050% (4.0 sigma).

Measurement of the J/ψ meson and b-hadron production cross sections in pp̄ collisions at √s = 1960 GeV

Abstract: The authors present a new measurement of the inclusive and differential production cross sections of J/{psi} mesons and b-hadrons in proton-antiproton collisions at {radical}s = 1960 GeV The data correspond to an integrated luminosity of 397 pb{sup -1} collected by the CDF Run II detector They find the integrated cross section for inclusive J/{psi} production for all transverse momenta from 0 to 20 GeV/c in the rapidity range |y| 125 GeV/c They find the total cross section for b-hadrons, including both hadrons and anti-hadrons, decaying to J/{psi} with transverse momenta greater than 125 GeV/c in the rapidity range |y(J/{psi})| < 06, is 0330 {+-} 0005(stat){sub -0033}{sup +0036}(syst) {mu}b Using a Monte Carlo simulation of the decay kinematics of b-hadrons to all final states containing a J/{psi}, they extract the first measurement of the total single b-hadron cross section down to zero transverse momentum at {radical}s = 1960 GeV They find the total single b-hadron cross section integrated over all transverse momenta for b-hadrons in themore » rapidity range |y| < 06 to be 176 {+-} 04(stat){sub -23}{sup +25}(syst) {mu}b« less

Phosphorylation of β-Catenin by Cyclic AMP-Dependent Protein Kinase Stabilizes β-Catenin through Inhibition of Its Ubiquitination

Abstract: β-Catenin not only regulates cell-to-cell adhesion by interacting with cadherin but also functions as a component of the Wnt signaling pathway (34). The Wnt signaling pathway is conserved evolutionally and regulates cellular proliferation and differentiation by stabilizing β-catenin (2, 37). The β-catenin gene is often mutated in human cancer, and in such cases the protein level of β-catenin increases (17, 35). Therefore, clarifying the regulation of β-catenin stabilization is important for understanding the molecular mechanism of tumor formation. According to the most widely accepted current model, casein kinase Iα (CKIα) and glycogen synthase kinase 3β (GSK-3β) target cytoplasmic β-catenin for degradation in the absence of Wnt (13, 26, 42). Axin has been shown to form a complex with GSK-3β, CKIα, β-catenin, and adenomatous polyposis coli gene product (APC) (13, 16, 21, 26). In the Axin complex CKIα serves as a priming kinase that phosphorylates Ser45 of β-catenin and enhances the phosphorylation at Ser33, Ser37, and Thr41 of β-catenin by GSK-3β (26, 43). Phosphorylated β-catenin is ubiquitinated and degraded by the proteasome pathway (22). When Wnt acts on its cell surface receptor consisting of Frizzled and lipoprotein receptor-related protein (LRP) 5/6 (9), Dvl induces the accumulation of β-catenin in the cytoplasm by inhibiting the GSK-3β-dependent phosphorylation of β-catenin (10, 20, 41). Accumulated β-catenin is translocated into the nucleus, where it binds to the transcription factors T-cell factor (Tcf) and lymphoid enhancer factor (Lef) and thereby stimulates the expression of various genes, including c-myc, cyclin D1, and Axin2 (2, 28, 37). Thus, Wnt stabilizes β-catenin and activates Tcf and Lef. Although CKIα- and GSK-3β-dependent phosphorylation is essential for the degradation of β-catenin in the Wnt pathway, a phosphorylation-independent pathway through Siah-1 has been found (27, 30). It has also been shown that release of Ca2+ from internal stores by the Gq pathway results in calpain-mediated degradation of β-catenin (25). Therefore, it is likely that there are multiple pathways to regulate the stability of β-catenin. The Alzheimer's disease-linked gene presenilin1 forms a complex with GSK-3β, β-catenin, and the catalytic subunit of cyclic AMP (cAMP)-dependent protein kinase (PKA) (15). In the presenilin1 complex, PKA phosphorylates Ser45 of β-catenin and enhances the GSK-3β-dependent phosphorylation of β-catenin, suggesting that PKA and presenilin1 induce the downregulation of β-catenin independently of the Wnt-controlled Axin complex. Indeed, nuclear accumulation of β-catenin is observed in the epidermis of presenilin1-deficient mice (15). However, in contrast to the finding that PKA might function as a negative regulator of β-catenin stability, it has been shown that stimulation with prostaglandin E2 (PGE2), which activates PKA, increases the transcriptional activity of Tcf in HEK-293 cells, probably through phosphorylation and inhibition of GSK-3β (8). Thus, the molecular mechanism of the cross talk between the Wnt and PKA signaling pathways is largely unknown. In this study, we examined the effects of PKA on the ubiquitin-dependent degradation of β-catenin. We here show that phosphorylation of β-catenin at Ser675 by PKA stabilizes β-catenin by inhibiting its ubiquitination.

Induction of Keratinocyte Migration via Transactivation of the Epidermal Growth Factor Receptor by the Antimicrobial Peptide LL-37

Abstract: The closure of skin wounds is essential for resistance against microbial pathogens, and keratinocyte migration is an important step in skin wound healing. Cathelicidin hCAP18/LL-37 is an innate antimicrobial peptide that is expressed in the skin and acts to eliminate microbial pathogens. Because hCAP18/LL-37 is up-regulated at skin wound sites, we hypothesized that LL-37 induces keratinocyte migration. In this study, we found that 1 μg/ml LL-37 induced the maximum level of keratinocyte migration in the Boyden chamber assay. In addition, LL-37 phosphorylated the epidermal growth factor receptor (EGFR) after 10 min, which suggests that LL-37-induced keratinocyte migration occurs via EGFR transactivation. To test this assumption, we used inhibitors that block the sequential steps of EGFR transactivation, such as OSU8-1, CRM197, anti-EGFR no. 225 Ab, and AG1478. All of these inhibitors completely blocked LL-37-induced keratinocyte migration, which indicates that migration occurs via HB-EGF-mediated EGFR transactivation. Furthermore, CRM197, anti-EGFR no. 225, and AG1478 blocked the LL-37-induced phosphorylation of STAT3, and transfection with a dominant-negative mutant of STAT3 abolished LL-37-induced keratinocyte migration, indicating the involvement of the STAT3 pathway downstream of EGFR transactivation. Finally, we tested whether the suppressor of cytokine signaling (SOCS)/cytokine-inducible Src homology 2-containing protein (CIS) family of negative regulators of STAT3 regulates LL-37-induced keratinocyte migration. Transfection with SOCS1/Jak2 binding protein or SOCS3/CIS3 almost completely abolished LL-37-induced keratinocyte migration. In conclusion, LL-37 induces keratinocyte migration via heparin-binding-EGF-mediated transactivation of EGFR, and SOCS1/Jak 2 binding and SOCS3/CIS3 negatively regulate this migration. The results of this study suggest that LL-37 closes skin wounds by the induction of keratinocyte migration.

Orbital-Assisted Metal-Insulator Transition in VO2

Abstract: We found direct experimental evidence for an orbital switching in the V $3d$ states across the metal-insulator transition in ${\mathrm{VO}}_{2}$. We have used soft-x-ray absorption spectroscopy at the V ${L}_{2,3}$ edges as a sensitive local probe and have determined quantitatively the orbital polarizations. These results strongly suggest that, in going from the metallic to the insulating state, the orbital occupation changes in a manner that charge fluctuations and effective bandwidths are reduced, that the system becomes more one dimensional and more susceptible to a Peierls-like transition, and that the required massive orbital switching can only be made if the system is close to a Mott insulating regime.

Recent advances in understanding the cell death pathways activated by anticancer therapy.

Abstract: Over the past two decades, the role of apoptosis in the cytotoxicity of anticancer drugs has become clear. Apoptosis may occur via a death receptor-dependent (extrinsic) or independent (intrinsic or mitochondrial) pathway. Mitochondria play a central role in cell death in response to DNA damage, and mediate the interaction(s) of various cytoplasmic organelles, including the endoplasmic reticulum, Golgi apparatus, and lysosomes. The mitochondrial pathway of cell death is mediated by Bcl-2 family proteins, a group of antiapoptotic and proapoptotic proteins that regulate the passage of small molecules, such as cytochrome c, Smac/Diablo, and apoptosis-inducing factor, which activates caspase cascades, through the mitochondrial transition pore. In addition, apoptosis can induce autophagic cell death via crosstalk between the two pathways upon treatment with anticancer drugs. The current review focused on recent advances surrounding the mechanism(s) of cell death induced by anticancer agents and discussed potential molecular targets for enhancing the chemotherapeutic effect(s) of anticancer agents.

Melatonin induces the expression of gonadotropin-inhibitory hormone in the avian brain

Abstract: We recently identified a novel hypothalamic neuropeptide inhibiting gonadotropin release in quail and termed it gonadotropin-inhibitory hormone (GnIH). Cell bodies and terminals containing the dodecapeptide GnIH are localized in the paraventricular nucleus (PVN) and median eminence, respectively. To understand the physiological role of GnIH, we investigated the mechanisms that regulate GnIH expression. In this study, we show that melatonin originating from the pineal gland and eyes induces GnIH expression in the quail brain. Pinealectomy (Px) combined with orbital enucleation (Ex) (Px plus Ex) decreased the expression of GnIH precursor mRNA and content of mature GnIH peptide in the diencephalon, which includes the PVN and median eminence. Melatonin administration to Px plus Ex birds caused a dosedependent increase in expression of GnIH precursor mRNA and production of mature peptide. The expression of GnIH was photoperiodically controlled and increased under short-day photoperiods, when the duration of melatonin secretion increases. To identify the mode of melatonin action on GnIH induction, we investigated the expression of Mel1c, a melatonin receptor subtype, in GnIH neurons. In situ hybridization of Mel1c mRNA combined with immunocytochemistry for GnIH revealed that Mel1c mRNA was expressed in GnIH-immunoreactive neurons in the PVN. Melatonin receptor autoradiography further revealed specific binding of melatonin in the PVN. These results indicate that melatonin is a key factor for GnIH induction. Melatonin appears to act directly on GnIH neurons through its receptor to induce GnIH expression. This is the first demonstration, to our knowledge, of a direct action of melatonin on neuropeptide induction in any vertebrate class.

Aqueous humor levels of cytokines are related to vitreous levels and progression of diabetic retinopathy in diabetic patients

Abstract: Cytokine levels are elevated in the ocular fluid of diabetic patients. It is unclear whether aqueous humor levels of vascular endothelial growth factor (VEGF) and interleukin-6 (IL-6) are related to the vitreous fluid levels of these substances and to the progression of diabetic retinopathy. Aqueous humor and vitreous fluid samples were obtained during cataract and vitreous surgery from ten eyes of ten patients with diabetic macular edema and 26 eyes of 26 patients with proliferative diabetic retinopathy (PDR). The VEGF and IL-6 levels in aqueous humor, vitreous fluid, and plasma were measured by enzyme-linked immunosorbent assay. VEGF and IL-6 levels in aqueous humor were significantly correlated with those in vitreous fluid (ρ=0.793 and ρ=0.737, respectively). VEGF levels in aqueous humor and vitreous fluid were significantly correlated with the corresponding IL-6 levels (ρ=0.631 and ρ=0.687, respectively). The aqueous and vitreous levels of VEGF were significantly correlated with the severity of diabetic retinopathy (ρ=0.659 and ρ=0.771, respectively). Aqueous and vitreous levels of IL-6 were also significantly correlated with the severity of diabetic retinopathy (ρ=0.742 and ρ=0.746, respectively). Aqueous and vitreous levels of both VEGF and IL-6 were significantly higher in the patients with active PDR than those in quiescent PDR. Our results suggest that there is a significant relationship between VEGF and IL-6 levels in aqueous humor and in vitreous fluid. Measurement of the aqueous levels of VEGF and IL-6 may be useful to analyze the pathogenesis of diabetic retinopathy and to predict disease activity.

Molecular-pathological prognostic factors of gastric cancer: a review.

Abstract: Invasion and metastasis are critical determinants of cancer morbidity. Genes and molecules participating in these steps must be regarded as potential prognostic factors. Growth factors and their receptors, cell-cycle regulators, cell-adhesion molecules and matrix-degrading enzymes are those to be used as prognostic factors, including epidermal growth factor (EGF), EGF receptor, K-sam, HER-2, interleukin (IL)-8, vascular endothelial growth factor (VEGF), cyclin E, p27, E-cadherin, CD44v6, matrix metalloproteinase-1 (MMP-1), and tissue inhibitor of matrix metalloproteinase-1 (TIMP-1). Alterations in epigenetics, such as aberrant DNA methylation and histone modification that are, in part, associated with the tumor progression of gastric cancer, can be candidate prognostic factors. The number of methylated genes may serve as a marker of tumor progression. Genetic polymorphism not only affects cancer susceptibility but also influences malignant phenotype; examples include single-nucleotide polymorphism in the HER-2 and MMP-9 genes. Comprehensive gene expression analyses are useful to search for novel genes related to invasion and metastasis and potential prognostic factors. Serial analysis of gene expression (SAGE) has identified several these genes, such as CDH17, APOE, FUS, COL1A1, COL1A2, GW112, and MIA. Overexpression of MIA is found to be associated with poor prognosis. Microarray analysis has great potential for identifying the characteristics of individual cancers, from the view point of gene expression profiles. A combination of these examinations can not only foretell a patient’s prognosis but can also give information directly connected with personalized cancer medicine and prevention.

The superoxide-producing NAD(P)H oxidase Nox4 in the nucleus of human vascular endothelial cells

Abstract: The superoxide-producing NAD(P)H oxidase Nox4 was initially identified as an enzyme that is highly expressed in the kidney and is possibly involved in oxygen sensing and cellular senescence. Although the oxidase is also abundant in vascular endothelial cells, its role remains to be elucidated. Here we show that Nox4 preferentially localizes to the nucleus of human umbilical vein endothelial cells (HUVECs), by immunocytochemistry and immunoelectron microscopy using three kinds of affinity-purified antibodies raised against distinct immunogens from human Nox4. Silencing of Nox4 by RNA interference (RNAi) abrogates nuclear signals given with the antibodies, confirming the nuclear localization of Nox4. The nuclear fraction of HUVECs exhibits an NAD(P)H-dependent superoxide-producing activity in a manner dependent on Nox4, which activity can be enhanced upon cell stimulation with phorbol 12-myristate 13-acetate. This stimulant also facilitates gene expression as estimated in the present transfection assay of HUVECs using a reporter regulated by the Maf-recognition element MARE, a DNA sequence that constitutes a part of oxidative stress response. Both basal and stimulated transcriptional activities are impaired by RNAi-mediated Nox4 silencing. Thus Nox4 appears to produce superoxide in the nucleus of HUVECs, thereby regulating gene expression via a mechanism for oxidative stress response.

Chow groups are finite dimensional, in some sense

Abstract: When S is a surface with p g (S)>0, Mumford proved that its Chow group A*S is not “finite dimensional” in some sense. In this paper, we propose another definition of “finite dimensionality” for the Chow groups. Using this new definition, at least the Chow group of some surface S with p g (S)>0 (for example, the product of two curves) becomes finite dimensional. The finite dimensionality of the Chow groups follows from the finite dimensionality of the Chow motives. It turns out that the finite dimensionality of the Chow motives is a very strong property. For example, we can prove Bloch’s conjecture (representability of the Chow groups of surfaces with p g (S)=0) under the assumption that the Chow motive of S is finite dimensional.

The effect of cooperative hydrogen bonding on the OH stretching-band shift for water clusters studied by matrix-isolation infrared spectroscopy and density functional theory.

Abstract: Infrared spectra of the water clusters have been measured in the N2 + O2 matrix. The aggregation process of water in the matrix has been monitored by annealing the deposited samples up to 40 K and UV irradiation. The monomer, dimer, cyclic trimer and cyclic pentamer are found as water clusters in the matrix. For the hexamer, several structures such as chair, cage, prism, bag 1 and/or book 1 are likely to exist. By UV irradiation, the cyclic pentamer is predominantly formed from the monomer and dimer. On the other hand, by annealing the deposited sample, several hexamers are formed. The theoretical calculation for water clusters has revealed that the formation of one hydrogen bonding in a hydrogen-bonded chain cooperatively enhances or diminishes the strength of another hydrogen bond. Both proton donor (D) and acceptor (A) participating in a hydrogen-bonding pair DA are capable of forming hydrogen bonding with the other water molecules; D can additionally accept two protons and donate one proton, and A can additionally donate two protons and accept one proton. We have proposed the classification of hydrogen-bonding patterns considering the cooperativity, denoting as d′a′DAd″a″, where d and a are integers indicating the number of proton donors and acceptors to D (the single prime) and A (the double prime), respectively. Then, a magnitude given by MOH = −d′ + a′ + d″ − a″ has been introduced, which is very useful for connecting the hydrogen-bonding patterns to their OH wavenumbers. As a result, it is revealed that the OH stretching bands of water clusters are characterized by eight indicators (free and MOH = −2, −1, 0, 1, 2, 3 and 4). The classification proposed here is applicable to the OH band analysis for the hydrogen-bonded water and alcohols in a condensed phase.

Origin of the metallic properties of heavily boron-doped superconducting diamond

Abstract: The recent discovery that heavily boron-doped diamond is a superconductor with a transition temperature of 7.4 K raises the prospect of superconducting devices with the unique properties of diamond. A study of the electronic structure responsible for superconductivity in heavily boron-doped diamond supports the idea that superconductivity is phonon-mediated, and provides information on the electronic structure that must be retained in order to harness this effect in practical devices. The physical properties of lightly doped semiconductors are well described by electronic band-structure calculations and impurity energy levels1. Such properties form the basis of present-day semiconductor technology. If the doping concentration n exceeds a critical value nc, the system passes through an insulator-to-metal transition and exhibits metallic behaviour; this is widely accepted to occur as a consequence of the impurity levels merging to form energy bands2. However, the electronic structure of semiconductors doped beyond nc have not been explored in detail. Therefore, the recent observation of superconductivity emerging near the insulator-to-metal transition3 in heavily boron-doped diamond4,5 has stimulated a discussion on the fundamental origin of the metallic states responsible for the superconductivity. Two approaches have been adopted for describing this metallic state: the introduction of charge carriers into either the impurity bands6 or the intrinsic diamond bands7,8,9. Here we show experimentally that the doping-dependent occupied electronic structures are consistent with the diamond bands, indicating that holes in the diamond bands play an essential part in determining the metallic nature of the heavily boron-doped diamond superconductor. This supports the diamond band approach and related predictions, including the possibility of achieving dopant-induced superconductivity in silicon and germanium7. It should also provide a foundation for the possible development of diamond-based devices10.

Demonstration of an Optical Quantum Controlled-NOT Gate without Path Interference

Abstract: We report the first experimental demonstration of an optical quantum controlled-NOT gate without any path interference, where the two interacting path interferometers of the original proposals have been replaced by three partially polarizing beam splitters with suitable polarization dependent transmittance and reflectance. The performance of the device is evaluated using a recently proposed method, by which the quantum process fidelity and the entanglement capability can be estimated from the 32 measurement results of two classical truth tables, significantly less than the 256 measurement results required for full quantum tomography.