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H Kanoh

Publications and source records attributed to H Kanoh.

At least 19 recordsLinked to original sources

Synthesis of nanoporous graphite-derived carbon-silica composites by a mechanochemical intercalation approach.

A mechanochemical intercalation approach which applies a simple mechanical milling to induce intercalation reaction was applied to introduce controlled amount of tetraethoxylsilane (TEOS) into surfactant-preexpanded graphite oxide, and the relationships between the intercalation structure, the porosities of the calcined products, and the Si addition were examined. It was found that a small added amount of TEOS produced a more expanded ordered layer structure with the interlayer distance and silicon content increasing with the amount of TEOS added, although a large amount of added TEOS easily induces layer delamination, resulting in a less ordered structure. The silica structure in the composite is changed from a disordered structure having enhanced bond strain to a condensed silica network when the amount of TEOS added increases. The porosities of the final calcined samples increase with the increase of silicon content but then decrease slightly after reaching a maximum where silicon content starts to become constant, indicating that both silicon content and the composition state of silica particles and carbon layers play important roles in porosity formation.

Journal Article↗

Changes in microporosity and CH4 adsorptivity of preoxidized pitch-based activated carbon fibers by Mg deposition.

Magnesium oxide/hydroxide was deposited on pitch-based activated carbon fibers which were previously oxidized in air at different temperatures, and the changes in carbon oxidation activity, microporosity, and CH4 adsorptivity of the parent carbons due to Mg deposition were examined. DTA results, chemical analysis, and DRIFT spectra indicate that Mg species are mainly supported on the -COOH groups of the parent carbons, which serve as the catalysts to improve the oxidation activity of carbon. Mg deposition either increases or decreases the specific surface area, pore volume, and average micropore width of the parent carbon depending on the preoxidation temperatures. Mg deposition does not simply enhance CH4 adsorptivity: the complex changes are due to the differences in the supporting states of Mg species and slight modifications in micropore structure.

Journal Article↗

Air oxidation effects on microporosity, surface property, and CH4 adsorptivity of pitch-based activated carbon fibers.

The changes in microporous structure and surface properties of pitch-based activated carbon fibers upon air oxidation were examined by high-resolution N2 adsorption and various physicochemical methods such as DTA, DRIFT, XPS, and chemical titration/analysis. It was found that air oxidation below 673 K slightly modifies the microporous structure together with a minor replacement of surface -C=O groups by -C-O groups. However, oxidation above 773 K gradually increases the specific surface area and the average width of micropores by producing micropores with larger widths and greatly induces the formation of surface functional groups, especially the -COOH group. A slight change in microporosities has an evident effect on CH4 storage property.

Journal Article↗

Adsorption energy distribution from the Aranovich-Donohue lattice density functional theory.

We propose a new methodology projected for the estimation of the adsorption energy distribution from the monolayer part of a single nitrogen adsorption isotherm determined at 77 K based on the lattice density functional theory (DFT) via the Aranovich-Donohue formalism. At first sight, the presented approach is computationally more difficult than a classical one. However, it is more flexible and comprehensible. Next, we developed a numerical program and used it for the estimation of the adsorption energy distribution from the experimental data on carbon black samples. The main nitrogen molecule-carbon black surface interaction energy can be estimated as approximately 7-8 kJ/mol, but the heterogeneity of the investigated materials differs significantly. Furthermore, we compare the results obtained from the lattice DFT via the Aranovich-Donohue formalism with the solution of the integral equation with the kernel represented by the classical monolayer localized Fowler-Guggenheim isotherm equation. The similarity between these two independent approaches is observed. The proposed methodology can be used for the investigation of the energetic heterogeneity of not only the carbonaceous materials but also the other "flat-surfaced" solids.

Journal Article↗

Gaseous adsorption properties of a silica-pillared layered manganese oxide.

Adsorptions of N(2), H(2)O, and organic vapors including CH(2)Cl(2), CCl(4), c-C(6)H(12), C(6)H(6), n-C(6)H(14), and n-C(9)H(20) on a silica-pillared layered manganese oxide (SiHMnO) and nonane-preadsorbed SiHMnO were examined. It is found that SiHMnO has a microporosity with a wide pore width distribution showing different pore wall affinities. Micropores with smaller width preferentially accommodate the nonane preadsorbate while the surface hydrophilicity of pore wall leads to an easier detachment of the adsorbed nonane molecules. H(2)O adsorption influences both the porosity and the surface properties by accelerating a sufficient hydrolysis of the remained TEOS molecules in SiHMnO. Examinations using Dubinin-Radeshkevich (DR) equation and isosteric heat of adsorption of organic molecules provide evidences that the wall surface of micropores with smaller and larger width have less affinity toward nonpolar and polar organic vapors, respectively.

Journal Article↗

Antiasthmatic effect of YM976, a novel PDE4 inhibitor, in guinea pigs.

YM976 is a novel and specific phosphodiesterase 4 inhibitor. In our previous report, we indicated that YM976 has less emetogenicity, a major adverse effect of PDE4 inhibitors, than rolipram. In the present study, we examined the antiasthmatic effects of YM976 in guinea pigs. YM976 orally administered exhibited inhibition of antigen-induced bronchoconstriction, airway plasma leakage, airway eosinophil infiltration, and airway hyperreactivity (AHR), with ED(50) values of 7.3, 5.7, 1.0, and 0.52 mg/kg, respectively. Rolipram also dose dependently suppressed these responses. Prednisolone suppressed eosinophil infiltration and AHR, whereas it failed to inhibit bronchoconstriction and plasma leakage. Theophylline moderately suppressed bronchoconstriction and edema, but neither eosinophil infiltration nor AHR. YM976 suppressed the peroxidase activity in the bronchoalveolar lavage fluid, and elevated the intracellular peroxidase activity and cAMP contents of infiltrated cells, suggesting that YM976 inhibited not only the infiltration but also the activation of leukocytes. In vitro studies revealed that YM976 potently suppressed eosinophil activation (EC(30) = 83 nM), and exerted a little relaxation on LTD(4)-precontracted tracheal smooth muscle (EC(50) = 370 nM). Rolipram exhibited a potent tracheal relaxation activity (EC(50) = 50 nM). In vivo studies indicated that the inhibitory effect of YM976 on LTD(4)-induced bronchospasm was marginal even at 30 mg/kg p.o., although rolipram significantly inhibited the bronchospasm at the same dose. These results suggested that YM976, unlike rolipram, showed the inhibition of antigen-induced airway responses due to anti-inflammatory effects, but not to direct tracheal relaxation. In conclusion, YM976 may have potential therapeutic value in the treatment of asthma through its anti-inflammatory activities.

Animals↗

Selectivity of the diacylglycerol kinase inhibitor 3-[2-(4-[bis-(4-fluorophenyl)methylene]-1-piperidinyl)ethyl]-2, 3-dihydro-2-thioxo-4(1H)quinazolinone (R59949) among diacylglycerol kinase subtypes.

Diacylglycerol kinases (DGKs) attenuate diacylglycerol-induced protein kinase C activation during stimulated phosphatidylinositol turnover. This reaction also initiates phosphatidylinositol resynthesis. Two agents, 3-(2-(4-[bis-(4-fluorophenyl)methylene]-1-piperidinyl)ethyl)-2,3-dihydro -2-thioxo-4(1H)quinazolinone (R59949) and 6-(2-(4-[(4-fluorophenyl)phenylmethylene]-1-piperidinyl)ethyl)-7-m ethyl-5H-thiazolo(3,2-a)pyrimidin-5-one (R59022), inhibit diacylglycerol phosphorylation in several systems. To examine the mechanism of this effect, we developed a mixed micelle method suitable for in vitro study of DGK inhibition. Animal cells express multiple DGK isoforms. In a survey of DGK isotypes, these agents selectively inhibited Ca2+-activated DGKs. R59949 was the more selective of the two. To map the site of interaction with the enzyme, a series of DGKalpha deletion mutants were prepared and examined. Deletion of the Ca2+-binding EF hand motif, which is shared by Ca2+-activated DGKs, had no effect on inhibition. Consistent with this observation, inhibition kinetics were noncompetitive with Ca2+. A construct expressing only the catalytic domain was also inhibited by R59949. Studies of substrate kinetics demonstrated that MgATP potentiated R59949 inhibition, indicating synergy of inhibitor and MgATP binding. These results indicate that R59949 inhibits DGKalpha by binding to its catalytic domain.

3T3 Cells↗

A refractory case of secondary erythermalgia successfully treated with lumbar sympathetic ganglion block.

A 59-year-old Japanese man with myasthenia gravis, who had a 10-year history of temperature-sensitive pain in the lower extremities, i.e. improved by cooling and worsened by warming, consulted us because the pain had become intolerable during the previous 4 months. Bilateral erythema, swelling and large ulcers were noted on the calves, dorsal aspects of the feet, and soles. Laboratory data showed thrombocythaemia and a positive antibody to the acetylcholine receptor, but were negative for antinuclear and antiphospholipid antibodies. A diagnosis of secondary erythermalgia was made because of the clinical features, the laboratory data, and the lack of family history of this disease. Although steroid pulse therapy, oral aspirin and antiserotonin drugs were ineffective, bilateral lumbar sympathetic ganglion block succeeded in relieving the severe pain and curing the ulcers. The clinical course in our patient suggests that sympathetic ganglion block may be one of the most effective treatments for secondary erythermalgia. Although the mechanism of this effect is uncertain, microcirculation disturbance in secondary erythermalgia, if any, may be improved by this block.

Erythromelalgia↗

Cell surface activities of the human type 2b phosphatidic acid phosphatase.

Several isozymes of mammalian type 2, Mg(2+)-independent phosphatidic acid phosphatase (PAP-2) have recently been cloned, and they are predicted to have their catalytic sites exposed at the cell surface membranes. We investigated the mode of utilization of extracellular lipid substrates by the human PAP-2b expressed in HEK293 cells as a green fluorescent fusion protein. We first confirmed the plasma membrane localization of the expressed PAP-2b. PAP-2b actively hydrolyzed exogenously added lysophosphatidic acid and short-chain phosphatidic acid. In the case of dephosphorylation of lysophosphatidic acid, the reaction products, including inorganic phosphate and monoacylglycerol, were recovered exclusively in the extracellular medium. Interestingly, PAP-2b exhibited negligible activities toward long-chain phosphatidic acid either exogenously when added or generated within the membranes by treating the cells with bacterial phospholipase D. These findings indicate that PAP-2b acts at the outer leaflet of cell surface bilayers and can account for the ecto-PAP activities previously described for various types of cells.

Cell Line↗

Molecular characterization of the type 2 phosphatidic acid phosphatase.

Phosphatidic acid phosphatase (PAP) converts phosphatidic acid to diacylglycerol, thus regulating the de novo synthesis of glycerolipids and also signal transduction mediated by phospholipase D. We initially succeeded in the cDNA cloning of the mouse 35 kDa PAP bound to plasma membranes (type 2 enzyme). This work subsequently led us to the identification of two human PAP isozymes designated 2a and 2b. A third human PAP isozyme (2c) has also been described. The cloned enzymes are, in common, N-glycosylated and possess six transmembrane domains. The transmembrane dispositions of these enzymes are predicted and the catalytic sites are tentatively located in the 2nd and 3rd extracellular loops, thus suggesting that the type 2 PAPs may act as ecto-enzymes dephosphorylating exogenous substrates. Furthermore, the type 2 PAPs have been proposed to belong to a novel phosphatase superfamily consisting of a number of soluble and membrane-bound enzymes. In vitro enzyme assays show that the type 2 PAPs can dephosphorylate lyso-phosphatidate, ceramide-1-phosphate, sphingosine-1-phosphate and diacylglycerol pyrophosphate. Although the physiological implications of such a broad substrate specificity need to be further investigated, the type 2 PAPs appear to metabolize a wide range of lipid mediators derived from both glycero- and sphingolipids.

Amino Acid Sequence↗

d-Alpha-tocopherol prevents the hyperglycemia induced activation of diacylglycerol (DAG)-protein kinase C (PKC) pathway in vascular smooth muscle cell by an increase of DAG kinase activity.

We have reported that d-alpha-tocopherol can prevent hyperglycemia-induced activation of DAG and PKC levels in vascular tissues as well as normalizing retinal blood flow and renal hyperfiltration. The mechanism of this effect, however, is not clear. Aside from alpha-tocopherol's principal role as an antioxidant agent, it has also been shown to act as a membrane stabilizer. Another possibility is that the effect of alpha-tocopherol is focused on the activation of DAG kinase, which is a key enzyme in the metabolism of DAG. Therefore, in this study, we examined the effect of alpha-tocopherol on the DAG kinase activity in vascular smooth muscle cell. We have also examined the effect of alpha-tocopherol, its analogues, and probucol on DAG kinase activities and expression. The present study showed that d-alpha-tocopherol's inhibitory effect on DAG-PKC pathway is by increasing DAG kinase activity in rat and human vascular smooth muscle cell (VSMC). Total DAG level was increased by 40 +/- 10% (mean +/- S.E.) (P < 0.05) in human VSMC, after exposure to 22 vs 5 mM glucose. This increase was normalized by d-alpha-tocopherol treatment in a concentration-dependent manner. In parallel, DAG kinase activation by d-alpha-tocopherol was also induced in a time- and dose-dependent manner. DAG kinase activity was increased by 57 +/- 19% (P < 0.05) in human VSMC and 112 +/- 35% (P < 0.05) in rat VSMC after 24 h of incubation with d-alpha-tocopherol (100 microg/ml). Another lipophilic antioxidant, probucol, also increased DAG kinase activity by 124 +/- 34%, but other vitamin E analogues with much less antioxidant potencies were ineffective. Western blots of various DAG kinase isoforms were not changed by d-alpha-tocopherol treatment. These results provide strong and detailed evidence that d-alpha-tocopherol can prevent hyperglycemia induced DAG-PKC activation by enhancing DAG kinase activity, probably through an antioxidant effect.

Animals↗

A case of dermatomyositis that developed after delivery: the involvement of pregnancy in the induction of dermatomyositis.

A relationship between dermatomyositis (DM) and pregnancy has rarely been documented, and most cases have been reported from the viewpoint of the management of high-risk pregnancy. We report a patient with DM which developed after the delivery of a healthy infant. This case, with support from a literature review, suggests that pregnancy could be a trigger for the development of DM. Furthermore, it is suggested that there are at least two types of pregnancy related DM: in one type, the disease activity is provoked during pregnancy and tends to improve after delivery, while the other type (including the present case) has onset in the postpartum period.

Adult↗

Molecular cloning of a second phospholipase B gene, caPLB2 from Candida albicans.

Accumulating evidence suggests that phospholipase B, secreted by pathogenic fungi such as Candida albicans, Cryptococcus neoformans and Aspergillus fumigatus, functions as one of the virulence factors. In the present study, we have attempted to clone phospholipase B gene from C. albicans. By RT-PCR analysis with degenerate primers based on conserved regions of phospholipase B from Saccharomyces cerevisiae, Penicillium notatum and Torulaspora delbrueckii two similar but different cDNA fragments were obtained. One corresponded to the partial sequence of caPLB1, recently cloned phospholipase B gene from C. albicans by a different approach (Leidich et al.: J Biol Chem 1998; 273: 26078-86). The other fragments contained sequences similar to the corresponding sequences of phospholipase B from other fungi. The presence of two related genes was confirmed by Southern and Northern blot analyses. The full length of the second C. albicans phospholipase B gene (caPLB2) encoded a putative protein with 608 amino acids and contained a potential signal peptide sequence and a putative catalytic region, which are found in phospholipase B from other fungi. Consistent with the findings of caPLB1, caPLB2 also lacks a cluster of hydrophobic amino acids at the COOH-terminal, which may function as a signal of glycosylphosphatidylinositol anchor.

Amino Acid Sequence↗

Effects of arfaptin 1 on guanine nucleotide-dependent activation of phospholipase D and cholera toxin by ADP-ribosylation factor.

Arfaptin 1, a approximately 39-kDa protein based on the deduced amino acid sequence, had been initially identified in a yeast two-hybrid screen using dominant active ARF3 (Q71L) as bait with an HL-60 cDNA library. It was suggested that arfaptin 1 may be involved in Golgi functions, since the FLAG-tagged protein was associated with Golgi membranes when expressed in COS-7 cells and could be bound to Golgi in vitro in an ADP-ribosylation factor (ARF)- and GTPgammaS-dependent, brefeldin A-inhibited fashion. Arfaptin 2, found in the same two-hybrid screen as arfaptin 1, is 60% identical in amino acid sequence and may or may not have an analogous function. We now report some effects of arfaptin 1 on ARF activation of phospholipase D and cholera toxin ADP-ribosyltransferase. Arfaptin 1 inhibited activation of both enzymes in a concentration-dependent manner and was without effect in the absence of ARF. Two ARF1 mutants that activated the toxin, one lacking 13 N-terminal amino acids and the other, in which 73 residues at the N terminus were replaced with the analogous sequence from ARL1, were not inhibited by arfaptin, consistent with the conclusion that arfaptin interaction requires the N terminus of ARF. This region has also been implicated in phospholipase D activation, but whether the two proteins interact with the same structural elements in ARF remains to be determined. Arfaptin inhibition of the action of ARF5 and ARF6 was less than that of ARF1 and ARF3; its effects were less on nonmyristoylated than myristoylated ARFs. Arfaptin effects on guanine nucleotide binding by ARFs were minimal whether or not a purified ARF guanine nucleotide-exchange protein was present. These findings indicate that arfaptin acts as an inhibitor of ARF actions in vitro, raising the possibility that it has a similar role in vivo.

ADP-Ribosylation Factor 1↗

Molecular cloning of a gene encoding phospholipase D from the pathogenic and dimorphic fungus, Candida albicans.

A phospholipase D gene (CaPLD) has been cloned from the Candida albicans genomic DNA library. The CaPLD is a member of a highly conserved gene family of PLD and has the highest homology to Saccharomyces cerevisiae PLD (SPO14) with an overall homology of 42%. Phylogenetic analysis indicated that fungus PLDs including CaPLD composed one of the three clusters of PLD genes.

Amino Acid Sequence↗