A comparative evaluation of recarbonated CaCO3 derived from limestone under oxy-fuel circulating fluidized bed conditions.

SO2 emissions from coal-fired boilers are air pollutants and a source of acid rain, causing extensive environmental pollution. Limestone (CaCO3) is a Ca-based sorbent which is injected into circulating fluidized bed (CFB) boilers, where it combines with SO2 to produce calcium sulfate (CaSO4). As a result, SO2 emissions from a power plant are reduced. In this study, CaCO3 addition was proposed and the desulfurization efficiency improved. The direct desulfurization reaction is dominant in a commercial CFB boiler due to the high CO2 partial pressure, but CaO is formed at a fast reaction rate by calcination in the high temperature or in the low CO2 partial pressure region. When CaO remains in the loop seal, it is exposed to a high CO2 partial pressure condition moving through the recirculation section for an extended period and re-injected into the furnace as recarbonated CaCO3. To analyze the direct desulfurization reaction kinetics, a shrink core model in which the reaction proceeds inside the particle was adopted. Surface observations through FE-SEM of CaSO4 produced by the 180 minute long desulfurization experiment using TGA suggest that the CaSO4 crystal growth rate increased after the pre-treatment (recarbonation) of limestone. Recarbonation lowered the limestone crystallinity, causing a faster reaction. The CaCO3 recarbonation increased the Ca utilization by more than 20% when the direct desulfurization reaction occurred. The TGA experiments show that recarbonation contributes to CaSO4 conversion. Increasing the desulfurization efficiency using recarbonation can reduce the fixed investment and operating costs of oxy-fuel CFB plants because only desulfurization in the furnace is able to meet SO2 emission regulations or lower the flue gas desulfurization (FGD) dependence. Accordingly, the desulfurization conversions of recarbonated CaCO3 and limestone were compared in this study. Morphological changes in the limestone were also evaluated using XRD, FE-SEM, and other analysis methods.

Protective effects of peroxiredoxin 6 overexpression on amyloid ß-induced apoptosis in PC12 cells.

Oxidative stress triggered by amyloid beta (Aß) accumulation contributes substantially to the pathogenesis of Alzheimer's disease (AD). In the present study, we examined the involvement of the antioxidant activity of peroxiredoxin 6 (Prdx 6) in protecting against Aß25-35-induced neurotoxicity in rat PC12 cells. Treatment of PC12 cells with Aß25-35 resulted in a dose- and time-dependent cytotoxicity that was associated with increased accumulation of intracellular reactive oxygen species (ROS) and mitochondria-mediated apoptotic cell death, including activation of Caspase 3 and 9, inactivation of poly ADP-ribosyl polymerse (PARP), and dysregulation of Bcl-2 and Bax. This apoptotic signaling machinery was markedly attenuated in PC12 cells that overexpress wild-type Prdx 6, but not in cells that overexpress the C47S catalytic mutant of Prdx 6. This indicates that the peroxidase activity of Prdx 6 protects PC12 cells from Aß25-35-induced neurotoxicity. The neuroprotective role of the antioxidant Prdx 6 suggests its therapeutic and/or prophylactic potential to slow the progression of AD and limit the extent of neuronal cell death caused by AD.

Ret finger protein inhibits muscle differentiation by modulating serum response factor and enhancer of polycomb1.

Skeletal myogenesis is precisely regulated by multiple transcription factors. Previously, we demonstrated that enhancer of polycomb 1 (Epc1) induces skeletal muscle differentiation by potentiating serum response factor (SRF)-dependent muscle gene activation. Here, we report that an interacting partner of Epc1, ret finger protein (RFP), blocks skeletal muscle differentiation. Our findings show that RFP was highly expressed in skeletal muscles and was downregulated during myoblast differentiation. Forced expression of RFP delayed myoblast differentiation, whereas knockdown enhanced it. Epc1-induced enhancements of SRF-dependent multinucleation, transactivation of the skeletal α-actin promoter, binding of SRF to the serum response element, and muscle-specific gene induction were blocked by RFP. RFP interfered with the physical interaction between Epc1 and SRF. Muscles from rfp knockout mice (Rfp(-/-)) mice were bigger than those from wild-type mice, and the expression of SRF-dependent muscle-specific genes was upregulated. Myotube formation and myoblast differentiation were enhanced in Rfp(-/-) mice. Taken together, our findings highlight RFP as a novel regulator of muscle differentiation that acts by modulating the expression of SRF-dependent skeletal muscle-specific genes.

Development of a natural preservative system using the mixture of chitosan-Inula helenium L. extract.

The aim of this study was to develop a new natural preservative system making up for the weak points of chitosan as a preservative. As reported in a previous manuscript (20th IFSCC Congress, Cannes, France, 1998), the minimum inhibitory concentrations (MICs) of water-soluble chitosan against bacteria and yeast were 0.9-3.0 mg mL(-1), whereas MICs of chitosan against Aspergillus niger were over 5.0 mg mL(-1). However, the result of recent study showed that the MICs of Inula helenium L. extract against A. niger were below 1.0 mg mL(-1). Thus, we could develop a new preservative system containing both chitosan and I. helenium L. extract named CI-mixture. MICs of CI-mixture against bacteria and fungi (yeast and mould) were 2.0-4.0 mg mL(-1). When 10.0% of the mixture (the ratio of chitosan to I. helenium L. extract = 7.5% : 2.5%) was applied to cosmetic formulae such as skin lotion, milk lotion, cream and pack, it revealed appropriate preservative efficacy. Our result of the patch test also showed that this preservative system reduced skin irritation by about 30-50%, as compared to the organic preservative system. Therefore, the good natural preservative system including chitosan and Inula helenium L. extract could be incorporated in cosmetic formulations.

Regulation of CLOCK and MOP4 by nuclear hormone receptors in the vasculature: a humoral mechanism to reset a peripheral clock.

Circadian clock genes are expressed in the suprachiasmatic nucleus and in peripheral tissues to regulate cyclically physiological processes. Synchronization of peripheral oscillators is thought to involve humoral signals, but the mechanisms by which these are mediated and integrated are poorly understood. We report a hormone-dependent interaction of the nuclear receptors, RAR alpha and RXR alpha, with CLOCK and MOP4. These interactions negatively regulate CLOCK/MOP4:BMAL1-mediated transcriptional activation of clock gene expression in vascular cells. MOP4 exhibits a robust rhythm in the vasculature, and retinoic acid can phase shift Per2 mRNA rhythmicity in vivo and in serum-induced smooth muscle cells in vitro, providing a molecular mechanism for hormonal control of clock gene expression. We propose that circadian or periodic availability of nuclear hormones may play a critical role in resetting a peripheral vascular clock.

Novel findings in inhibition of mast cell-dependent immediate-type cutaneous reactions by Gahmi-Shini-San.

This report describes an inhibitory effect of Gahmi-Shini-San (GSS) on mast cell-mediated immediate-type allergic reactions. GSS is an Oriental herbal medication, which has been successfully used in Korea for the treatment of allergic disorders, mainly skin anaphylactic diseases. GSS inhibited the ear swelling response induced by intradermal injection of compound 48/80 in a mouse model on a concentration-dependent basis. The mast cells in mouse ear tissue were stained by alcian blue/nuclear fast red. GSS significantly inhibited the compound 48/80-induced degranulation from mast cells in ear tissue. GSS dose-dependently inhibited the histamine release from the rat peritoneal mast cells by compound 48/80. We also studied the effect of GSS on mast cell-dependent passive cutaneous anaphylaxis activated by dinitrophenyl IgE antibody. GSS showed inhibition of passive cutaneous anaphylaxis following oral administration. These results indicated that GSS has inhibitory effect on mast cell-dependent immediate type cutaneous reactions.

Kunbi-Boshin-Hangam-Tang stimulates nitic oxide production through activation of nuclear factor-kappaB.

The objective of the currently study was to determine the effect of Kunbi-Boshin-Hangam-Tang (KBH-Tang) on the production of nitric oxide (NO). Stimulation of RAW 264.7 cells with KBH-Tang after the treatment of recombinant interferon-gamma (rIFN-gamma) resulted in increased NO synthesis. KBH-Tang partially increased NO synthesis by itself. When KBH-Tang was used in combination with rIFN-gamma, there was a marked cooperative induction of NO synthesis in a dose-dependent manner. This increase in NO synthesis was reflected as increased amount of inducible NO synthase (iNOS) protein. NO production was inhibited by NG-monomethyl-L-arginine (NGMMA). Furthermore, activation of nuclear factor (NF)-kappaB was increased by KBH-Tang. These results suggest that KBH-Tang may stimulate the NO production through the activation of the NF-kappaB.

Disodium cromoglycate inhibits production of immunoglobulin E.

Disodium cromoglycate (DSCG) has been shown to inhibit the release of mediators from mast cells. In the present study, the effect of DSCG on active anaphylactic reaction was studied in mice. DSCG dose-dependently inhibited the active systemic anaphylactic reaction and serum immunoglobulin (Ig)E production induced by immunization with ovalbumin, Bordetella pertussis toxin and aluminum hydroxide gel. DSCG strongly inhibited IL-4-dependent IgE production by lipopolysaccharide-stimulated murine whole spleen cells. In the case of U266 human IgE-bearing B cells, DSCG also showed an inhibitory effect on the IgE production. These results suggest that DSCG has an anti-anaphylactic activity by inhibition of IgE production from B cells.

Mutation in PMR1, a Ca(2+)-ATPase in Golgi, confers salt tolerance in Saccharomyces cerevisiae by inducing expression of PMR2, an Na(+)-ATPase in plasma membrane.

Sodium tolerance in yeast is enhanced by continuous activation of calcineurin, a Ca(2+)/calmodulin-dependent protein phosphatase that is required for modulation of the Na(+) efflux mechanism. We isolated several salt-tolerant mutations with the treatment of ethylmethane sulfonate under high salt stress. One of the mutations was mapped in the PMR1 gene. Pmr1p, the P-type Ca(2+)-ATPase in the Golgi apparatus, regulates a cytosolic Ca(2+) level in various responses. Cytosolic Ca(2+) concentration in the pmr1 mutant is highly maintained, and thus calcineurin is activated continuously. The treatment of FK506, a specific inhibitor of calcineurin, abolishes the salt-tolerant phenotype of the pmr1 mutant. Activated calcineurin induces the expression of PMR2, encoding the P-type Na(+)-ATPase, through the specific transcription factor, Tcn1p/Crz1p. Also, expression of the PMR2::lacZ reporter gene in the pmr1 mutant was higher than that in wild type. We propose that the pmr1 mutation confers salt tolerance through continuous activation of calcineurin and that Pmr1p might act as a major Ca(2+)-ATPase under high salt stress.

Regulation of histone acetylation and transcription by INHAT, a human cellular complex containing the set oncoprotein.

Acetylation of histones by p300/CBP and PCAF is considered to be a critical step in transcriptional regulation. In order to understand the role of cellular activities that modulate histone acetylation and transcription, we have purified and characterized a multiprotein cellular complex that potently inhibits the histone acetyltransferase activity of p300/CBP and PCAF. We have mapped a novel acetyltransferase-inhibitory domain of this INHAT (inhibitor of acetyltransferases) complex that binds to histones and masks them from being acetyltransferase substrates. Endogenous INHAT subunits, which include the Set/TAF-Ibeta oncoprotein, associate with chromatin in vivo and can block coactivatormediated transcription when transfected in cells. We propose that histone masking by INHAT plays a regulatory role in chromatin modification and serves as a novel mechanism of transcriptional regulation.

Analysis of expressed sequence tags of Porphyra yezoensis.

Single direct partial sequencing of anonymous cDNA clones was performed to obtain genetic information on red algae Porphyra yezoensis of which genetic information is not available. This expressed sequence tags (EST) analysis revealed 81 clones (42%) had significant homologies to known genes in GenBank. Of these clones, eight are related to known algal genes, whereas above 90% of the EST clones were newly identified in algae. Putative functional categories of these clones showed that the most abundant genes were involved in stress and defense mechanisms and that the next abundant genes were associated with protein synthetic pathways.