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Byline: Yuh-Yih Wu, Bo-Chiuan Chen, Jen-Jyh Hwang, Chung-Ying Chen This article studied water-gasoline emulsions for reducing the NOx emissions of a motorcycle engine. Emulsified gasoline fuels of 0, 5, 10 and 15% water by volume were used in a four-stroke, 125 cc, port injection, spark-ignition engine. Both full throttle speed ranging from 2,000 to 7,000 rpm and low load were tested. The engine torque, fuel consumption, exhaust emissions and combustion characteristics were investigated. The experimental results show that the engine torque and fuel consumption are improved for 5 and 10% water emulsions. However, at 15%, the engine torque and fuel consumption deteriorate and the exhaust temperature is increased owing to slow burn rate. The exhaust emissions of NOx and CO decrease as the water percentage in the emulsion increases. A higher oxygen concentration in exhaust gas of emulsified fuel was found, which results in lower CO emission. The HC emission is increased with increasing water content, which might be caused by the thicker quench layer of emulsified fuel combustion. An appropriate concentration of water in the emulsified gasoline fuel for a 125 cc motorcycle engine is found to be 10%.

Phosphate (Pi) deficiency induces a multitude of responses aimed at improving the acquisition of Pi, including an increased density of root hairs. To understand the mechanisms involved in Pi deficiency-induced alterations of the root hair phenotype in Arabidopsis (Arabidopsis thaliana), we analyzed the patterning and length of root epidermal cells under control and Pi-deficient conditions in wild-type plants and in four mutants defective in the expression of master regulators of cell fate, CAPRICE (CPC), ENHANCER OF TRY AND CPC 1 (ETC1), WEREWOLF (WER) and SCRAMBLED (SCM). From this analysis we deduced that the longitudinal cell length of root epidermal cells is dependent on the correct perception of a positional signal (‘cortical bias’) in both control and Pi-deficient plants; mutants defective in the receptor of the signal, SCM, produced short cells characteristic of root hair-forming cells (trichoblasts). Simulating the effect of cortical bias on the time-evolving probability of cell fate supports a scenario in which a compromised positional signal delays the time point at which non-hair cells opt out the default trichoblast pathway, resulting in short, trichoblast-like non-hair cells. Collectively, our data show that Pi-deficient plants increase root hair density by the formation of shorter cells, resulting in a higher frequency of hairs per unit root length, and additional trichoblast cell fate assignment via increased expression of ETC1. [ABSTRACT FROM AUTHOR]

Phosphate (Pi) deficiency induces a multitude of responses aimed at improving the acquisition of Pi, including an increased density of root hairs. To understand the mechanisms involved in Pi deficiency-induced alterations of the root hair phenotype in Arabidopsis (Arabidopsis thaliana), we analyzed the patterning and length of root epidermal cells under control and Pi-deficient conditions in wild-type plants and in four mutants defective in the expression of master regulators of cell fate, CAPRICE (CPC), ENHANCER OF TRY AND CPC 1 (ETC1), WEREWOLF (WER) and SCRAMBLED (SCM). From this analysis we deduced that the longitudinal cell length of root epidermal cells is dependent on the correct perception of a positional signal (‘cortical bias’) in both control and Pi-deficient plants; mutants defective in the receptor of the signal, SCM, produced short cells characteristic of root hair-forming cells (trichoblasts). Simulating the effect of cortical bias on the time-evolving probability of cell fate supports a scenario in which a compromised positional signal delays the time point at which non-hair cells opt out the default trichoblast pathway, resulting in short, trichoblast-like non-hair cells. Collectively, our data show that Pi-deficient plants increase root hair density by the formation of shorter cells, resulting in a higher frequency of hairs per unit root length, and additional trichoblast cell fate assignment via increased expression of ETC1. [ABSTRACT FROM AUTHOR]