Effect of TiO2-ZnO/GAC on by-product distribution of CVOCs decomposition in a NTP-assisted catalysis system

In this study, the catalytic effect of TiO2-ZnO/GAC coupled with non-thermal plasma was investigated on the byproducts distribution of decomposition of chlorinated VOCs in gas streams. The effect of specific input energy, and initial gas composition was examined in a corona discharge reactor energized by a high frequency pulsed power supply. Detected by-products for catalytic NTP at 750 J L-1 included CO, CO2, Cl2, trichloroacetaldehyde, as well as trichlorobenzaldehyde with chloroform feeding, while they were dominated by CO, CO2, and lower abundance of trichlorobenzaldehyde and Cl2 with chlorobenzene introduction. Some of the by-products such as O3, NO, NO2, and COCl2 disappeared totally over TiO2-ZnO/GAC. Furthermore, the amount of heavy products such as trichlorobenzaldehyde decreased significantly in favor of small molecules such as CO, CO2, and Cl2 with the hybrid process. The selectivity towards COx soared up to 77 over the catalyst at 750 J L-1 and 100 ppm of chlorobenzene. © by Farshid Ghorbani-Shahna 2015

Enhanced performance of non-thermal plasma coupled with TiO2/GAC for decomposition of chlorinated organic compounds: Influence of a hydrogen-rich substance

Background: No study was found in the literature on the combination of TiO 2 /GAC catalyst and non-thermal plasma for chlorinated volatile organic compounds abatement in air. This paper presents this hybrid process for the decomposition of chloroform (as a target compound) using a multi-pin to plate discharge reactor. The experiments were performed using a high frequency pulsed transformer as the power supply system to examine the effect of SIE, frequency, as well as initial concentration on the chloroform removal efficiency (RE). Toluene was added as a hydrogen-rich source to shift the reactions into the formation of environmentally desirable products. Results: RE of around 60% was observed with the NTP-alone process at the highest possible SIE (3000 J L -1 ), while it rocketed up to 100% (total oxidation) in the presence of TiO 2 /GAC at SIE of 1000 J L -1 . About 100% O 3 destruction over TiO 2 /GAC and both adsorption and catalytic activities of GAC may be considered as the reasons for better performance of the hybrid process. Toluene feeding diminished the chlorinated by-products such as Cl 2 and TCE significantly. The selectivity towards CO 2 was noticed to enhance noticeably, when both catalyst and toluene were introduced, regardless of the input concentration. Conclusions: Our findings suggest that the hybrid of NTP with TiO 2 /GAC will highly be effective in the abatement of chloroform, and the addition of toluene will successfully decline harmful chlorinated by-products. © 2014 Abedi et al., licensee BioMed Central Ltd

Oxygen-sensing neurons reciprocally regulate peripheral lipid metabolism via neuropeptide signaling in <i>Caenorhabditis elegans</i>

<div><p>The mechanisms by which the sensory environment influences metabolic homeostasis remains poorly understood. In this report, we show that oxygen, a potent environmental signal, is an important regulator of whole body lipid metabolism. <i>C</i>. <i>elegans</i> oxygen-sensing neurons reciprocally regulate peripheral lipid metabolism under normoxia in the following way: under high oxygen and food absence, URX sensory neurons are activated, and stimulate fat loss in the intestine, the major metabolic organ for <i>C</i>. <i>elegans</i>. Under lower oxygen conditions or when food is present, the BAG sensory neurons respond by repressing the resting properties of the URX neurons. A genetic screen to identify modulators of this effect led to the identification of a BAG-neuron-specific neuropeptide called FLP-17, whose cognate receptor EGL-6 functions in URX neurons. Thus, BAG sensory neurons counterbalance the metabolic effect of tonically active URX neurons via neuropeptide communication. The combined regulatory actions of these neurons serve to precisely tune the rate and extent of fat loss to the availability of food and oxygen, and provides an interesting example of the myriad mechanisms underlying homeostatic control.</p></div

Pheromone-sensing neurons regulate peripheral lipid metabolism in <i>Caenorhabditis elegans</i>

It is now established that the central nervous system plays an important role in regulating whole body metabolism and energy balance. However, the extent to which sensory systems relay environmental information to modulate metabolic events in peripheral tissues has remained poorly understood. In addition, it has been challenging to map the molecular mechanisms underlying discrete sensory modalities with respect to their role in lipid metabolism. In previous work our lab has identified instructive roles for serotonin signaling as a surrogate for food availability, as well as oxygen sensing, in the control of whole body metabolism. In this study, we now identify a role for a pair of pheromone-sensing neurons in regulating fat metabolism in C. elegans, which has emerged as a tractable and highly informative model to study the neurobiology of metabolism. A genetic screen revealed that GPA-3, a member of the Gα family of G proteins, regulates body fat content in the intestine, the major metabolic organ for C. elegans. Genetic and reconstitution studies revealed that the potent body fat phenotype of gpa-3 null mutants is controlled from a pair of neurons called ADL(L/R). We show that cAMP functions as the second messenger in the ADL neurons, and regulates body fat stores via the neurotransmitter acetylcholine, from downstream neurons. We find that the pheromone ascr#3, which is detected by the ADL neurons, regulates body fat stores in a GPA-3-dependent manner. We define here a third sensory modality, pheromone sensing, as a major regulator of body fat metabolism. The pheromone ascr#3 is an indicator of population density, thus we hypothesize that pheromone sensing provides a salient 'denominator' to evaluate the amount of food available within a population and to accordingly adjust metabolic rate and body fat levels