Pulsed combustion process for black liquor gasification

The objective of this project is to test an energy efficient, innovative black liquor recovery system on an industrial scale. In the MTCI recovery process, black liquor is sprayed directly onto a bed of sodium carbonate solids which is fluidized by steam. Direct contact of the black liquor with hot bed solids promotes high rates of heating and pyrolysis. Residual carbon, which forms as a deposit on the particle surface, is then gasified by reaction with steam. Heat is supplied from pulse combustor resonance tubes which are immersed within the fluid bed. A portion of the gasifier product gas is returned to the pulse combustors to provide the energy requirements of the reactor. Oxidized sulfur species are partially reduced by reaction with the gasifier products, principally carbon monoxide and hydrogen. The reduced sulfur decomposed to solid sodium carbonate and gaseous hydrogen sulfide (H{sub 2}S). Sodium values are recovered by discharging a dry sodium carbonate product from the gasifier. MTCI's indirectly heated gasification technology for black liquor recovery also relies on the scrubbing of H{sub 2}S for product gases to regenerate green liquor for reuse in the mill circuit. Due to concerns relative to the efficiency of sulfur recovery in the MTCI integrated process, an experimental investigation was undertaken to establish performance and design data for this portion of the system

High flux ceramic membrane for hydrogen separation. Final technical progress report

Fuel cells that convert hydrogen to electricity will play an increasingly important role in the generation of future electric power for stationary and transportation sector applications. However, more economic methods to produce hydrogen from fossil fuels are needed. This project addresses the need to develop low cost ceramic membranes for hydrogen separation from reformed fuels

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Not AvailableThe present investigation aimed to assess the nature and magnitude of genetic divergence available in the Hybridization Block (E1) and National Hybridization Garden (E2) of ICAR-Sugarcane Breeding Institute, Coimbatore and to select the suitable diverse genotypes as parents for further utilization. Principal component and hierarchical cluster analyses were carried out in sixty eight genotypes with nine traits. In E1, the first three principal components explained about 73.45 per cent of the total variability and remaining six components accounted 26.55 per cent of variability. The PC 1 explained a maximum variability of 44.85 per cent followed by PC 2 and PC3. In E2, the first three principal components explained about 76.71 per cent of the total variability among the genotypes and the remaining six components described 23.29 per cent towards the total diversity. Nineteen clones viz., Co 0314, Co 8371, Co 85019, Co 86010, Co 94008, Co 98010, Co 11015, Co 12014, Co 14002, CoSnk 05103, CoV 89101, CoV 92103, CoC 671, CoT 8201 Co 1148, CoH 119, SP 80-185, ISH 100 and ISH 2 were found promising in both the environments indicating their potential to perform under varied ecological situations. Twenty clones in E1 and 38 clones in E2 can be further exploited as trait specific donors and the traits cane height, cane diameter, cane weight should be given more emphasis for further selection.Not Availabl

Aldose reductase deficiency in mice prevents azoxymethane-induced colonic preneoplastic aberrant crypt foci formation

Aldose reductase (AR; EC 1.1.1.21), an nicotinamide adenine dinucleotide phosphate-dependent aldo–keto reductase, has been shown to be involved in oxidative stress signaling initiated by inflammatory cytokines, chemokines and growth factors. Recently, we have shown that inhibition of this enzyme prevents the growth of colon cancer cells in vitro as well as in nude mice xenografts. Herein, we investigated the mediation of AR in the formation of colonic preneoplastic aberrant crypt foci (ACF) using azoxymethane (AOM)-induced colon cancer mice model. Male BALB/c mice were administrated with AOM without or with AR inhibitor, sorbinil and at the end of the protocol, all the mice were euthanized and colons were evaluated for ACF formation. Administration of sorbinil significantly lowered the number of AOM-induced ACF. Similarly, AR-null mice administered with AOM demonstrated significant resistance to ACF formation. Furthermore, inhibition of AR or knockout of AR gene in the mice significantly prevented AOM-induced expression of inducible nitric oxide synthase and cyclooxygenase-2 proteins as well as their messenger RNA. AR inhibition or knockdown also significantly decreased the phosphorylation of protein kinase C (PKC) β2 and nuclear factor kappa binding protein as well as expression of preneoplastic marker proteins such as cyclin D1 and β-catenin in mice colons. Our results suggest that AR mediates the formation of ACF in AOM-treated mice and thereby inhibition of AR could provide an effective chemopreventive approach for the treatment of colon cancer