Effectiveness of grease interceptors in food service establishments for controlling fat, oil and grease deposition in the sewer system.

The water industry worldwide experiences numerous sewer blockages each year, partially attributed to the accumulation of fat, oil and grease (FOG). Managing this issue involves various strategies, including the requirement for installation of grease interceptors (GIs) installation. However, the claimed efficacy of commercial GIs of eliminating 99 % of FOG has been questioned for many years because FOG deposit formation occurs despite food service establishments (FSEs) using GIs, therefore detailed understanding of FOG wastewater compositions and its removal by GIs is required. This study provides an insight into the key FOG components such as FOG particle size, metals and fatty acid (FA) profile in GI influent and effluent, and within the GI, at three different FSEs. Analysis of FAs identified substantial proportions of extra-long-chain FAs in the effluents, including arachidic (C20:0), behenic (C22:0), mead (C20:3), lignoceric (C24:0), and nervonic (C24:1) acids. In contrast, the household kitchen released palmitic (C16:0), oleic (C18:1) and linoleic (C18:2) acids. It was further observed that scums effectively remove the larger FOG particles, leaving only 10 % below 75.4 µm. Notably, FSEs which employed automatic dishwashers produced up to 80.4 % of particles ≤45 µm, whereas FSEs and household kitchen which used handwash sinks generated only 36.9 % and 26.3 % of particles ≤45 µm, respectively. This study demonstrated that the commercial GIs do not remove FOG entirely but clearly demonstrated that they discharge high concentrations of FOG with extra-long FFAs which were attributed to the occurrence of microbial activity and hydrolysis of triglycerides within the GI, potentially contributing to FOG deposition.

Understanding the properties of fat, oil, and grease and their removal using grease interceptors.

Treatment of wastewater with high levels of fat, oil, and grease (FOG), produced by the growing number (annually 2%) of food service establishments (FSEs), is a major concern for water utilities. About 30-40% of sewer blockages are caused primarily by the formation of FOG deposits in sewer pipes, and an annual additional maintenance cost is required for sewer management. To manage FOG deposition, FSEs are required to recover the FOG at the point of generation by installing grease interceptors (GIs) before release to the sewer system. The successful control of FOG deposition is largely dependent on clear understanding of its complex properties, pre-treatment processes, deposition mechanism and public awareness. The objective of this study is to provide a comprehensive understanding of the physicochemical properties of FOG, including particle size distribution and their removal efficiencies by existing GIs. Nowadays, generation of FOG particles of ≤45 µm is increasing because of the increasing use of automatic dishwashers. Current hybrid processes which comprise pre-treatment prior to GI use are ineffective since they are unable to completely remove particle sizes of ≤45 µm. Hence, there is potential for these particles to be released into the sewer system and eventually cause blockages. This critical review discusses the characteristics of effluents, including the particle size distributions generated from automatic dishwashers and handwash sinks. It concludes by providing some case studies and a perspective of the future opportunities to develop a novel GI process integrated with pre-treatment to remove particles of all sizes, including colloidal particles.

GLAST (GLutamate and ASpartate Transporter) in human prefrontal cortex; interactome in healthy brains and the expression of GLAST in brains of chronic alcoholics.

We have analysed post-mortem samples of prefrontal cortex from control and alcoholic human brains by the technique of Western blotting to estimate and compare the expressions of glutamate transporter GLAST (Excitatory Amino Acid Transporter One; EAAT1). Furthermore, using the non-alcoholic prefrontal cortex and custom-made GLAST (EAAT1) antibody we determined GLAST (EAAT1) "interactome" i.e. the set of proteins selectively bound by GLAST (EAAT1). We found that GLAST (EAAT1) was significantly more abundant (about 1.6-fold) in the cortical tissue from alcoholic brains compared to that from non-alcoholic controls. The greatest increase in the level of GLAST (EAAT1) was found in plasma membrane fraction (2.2-fold). Additionally, using the prefrontal cortical tissue from control brains, we identified 38 proteins specifically interacting with GLAST (EAAT1). These can be classified as contributing to the cell structure (6 proteins; 16%), energy and general metabolism (18 proteins; 47%), neurotransmitter metabolism (three proteins; 8%), signalling (6 proteins: 16%), neurotransmitter storage/release at synapses (three proteins; 8%) and calcium buffering (two proteins; 5%). We discuss possible consequences of the increased expression of GLAST (EAAT1) in alcoholic brain tissue and whether or how this could disturb the function of the proteins potentially interacting with GLAST (EAAT1) in vivo. The data represent an extension of our previous proteomic and metabolomic studies of human alcoholism revealing another aspect of the complexity of changes imposed on brain by chronic long-term consumption of ethanol.

Exposure of Rat Neural Stem Cells to Ethanol Affects Cell Numbers and Alters Expression of 28 Proteins.

Developing brain cells express many proteins but little is known of how their protein composition responds to chronic exposure to alcohol and/or how such changes might relate to alcohol toxicity. We used cultures derived from embryonic rat brain (previously shown to contain mostly neural stem cells; rat NSC, rNSC), exposed them to ethanol (25-100 mM) for up to 96 h and studied how they reacted. Ethanol (50 and 100 mM) reduced cell numbers indicating either compromised cell proliferation, cytotoxicity or both. Increased lipid peroxidation was consistent with the presence of oxidative stress accompanying alcohol-induced cytotoxicity. Proteomics revealed 28 proteins as altered by ethanol (50 mM for 96 h). Some were constituents of cytoskeleton, others were involved in transcription/translation, signal transduction and oxidative stress. Nucleophosmin (NPM1) and dead-end protein homolog 1 (DND1) were further studied by immunological techniques in cultured neurons and astrocytes (derived from brain tissue at embryonic ages E15 and E20, respectively). In the case of DND1 (but not NPM1) ethanol induced similar pattern of changes in both types of cells. Given the critical role of the protein NPM1 in cell proliferation and differentiation, its reduced expression in the ethanol-exposed rNSC could, in part, explain the lower cells numbers. We conclude that chronic ethanol profoundly alters protein composition of rNSC to the extent that their functioning-including proliferation and survival-would be seriously compromised. Translated to humans, such changes could point the way towards mechanisms underlying the fetal alcohol spectrum disorder and/or alcoholism later in life.

Metabolomics of Neurotransmitters and Related Metabolites in Post-Mortem Tissue from the Dorsal and Ventral Striatum of Alcoholic Human Brain.

We report on changes in neurotransmitter metabolome and protein expression in the striatum of humans exposed to heavy long-term consumption of alcohol. Extracts from post mortem striatal tissue (dorsal striatum; DS comprising caudate nucleus; CN and putamen; P and ventral striatum; VS constituted by nucleus accumbens; NAc) were analysed by high performance liquid chromatography coupled with tandem mass spectrometry. Proteomics was studied in CN by two-dimensional gel electrophoresis followed by mass-spectrometry. Proteomics identified 25 unique molecules expressed differently by the alcohol-affected tissue. Two were dopamine-related proteins and one a GABA-synthesizing enzyme GAD65. Two proteins that are related to apoptosis and/or neuronal loss (BiD and amyloid-ß A4 precursor protein-binding family B member 3) were increased. There were no differences in the levels of dopamine (DA), 3,4-dihydrophenylacetic acid (DOPAC), serotonin (5HT), homovanillic acid (HVA), 5-hydroxyindoleacetic acid (HIAA), histamine, L-glutamate (Glu), γ-aminobutyric acid (GABA), tyrosine (Tyr) and tryptophan (Tryp) between the DS (CN and P) and VS (NAc) in control brains. Choline (Ch) and acetylcholine (Ach) were higher and norepinephrine (NE) lower, in the VS. Alcoholic striata had lower levels of neurotransmitters except for Glu (30 % higher in the alcoholic ventral striatum). Ratios of DOPAC/DA and HIAA/5HT were higher in alcoholic striatum indicating an increase in the DA and 5HT turnover. Glutathione was significantly reduced in all three regions of alcohol-affected striatum. We conclude that neurotransmitter systems in both the DS (CN and P) and the VS (NAc) were significantly influenced by long-term heavy alcohol intake associated with alcoholism.

GLAST But Not Least--Distribution, Function, Genetics and Epigenetics of L-Glutamate Transport in Brain--Focus on GLAST/EAAT1.

Synaptically released L-glutamate, the most important excitatory neurotransmitter in the CNS, is removed from extracellular space by fast and efficient transport mediated by several transporters; the most abundant ones are EAAT1/GLAST and EAAT2/GLT1. The review first summarizes their location, functions and basic characteristics. We then look at genetics and epigenetics of EAAT1/GLAST and EAAT2/GLT1 and perform in silico analyses of their promoter regions. There is one CpG island in SLC1A2 (EAAT2/GLT1) gene and none in SLC1A3 (EAAT1/GLAST) suggesting that DNA methylation is not the most important epigenetic mechanism regulating EAAT1/GLAST levels in brain. There are targets for specific miRNA in SLC1A2 (EAAT2/GLT1) gene. We also note that while defects in EAAT2/GLT1 have been associated with various pathological states including chronic neurodegenerative diseases, very little is known on possible contributions of defective or dysfunctional EAAT1/GLAST to any specific brain disease. Finally, we review evidence of EAAT1/GLAST involvement in mechanisms of brain response to alcoholism and present some preliminary data showing that ethanol, at concentrations which may be reached following heavy drinking, can have an effect on the distribution of EAAT1/GLAST in cultured astrocytes; the effect is blocked by baclofen, a GABA-B receptor agonist and a drug potentially useful in the treatment of alcoholism. We argue that more research effort should be focused on EAAT1/GLAST, particularly in relation to alcoholism and drug addiction.