A Fuzzy-Wavelet Neural Network Model for the Detection of Meat Spoilage using an Electronic Nose

Food product safety is one of the most promising areas for the application of electronic noses. The performance of a portable electronic nose has been evaluated in monitoring the spoilage of beef fillet stored aerobically at different storage temperatures (0, 4, 8, 12, 16 and 20°C). This paper proposes a fuzzy-wavelet neural network model which incorporates a clustering pre-processing stage for the definition of fuzzy rules. The dual purpose of the proposed modeling approach is not only to classify beef samples in the respective quality class (i.e. fresh, semi-fresh and spoiled), but also to predict their associated microbiological population directly from volatile compounds fingerprints. Comparison results indicated that the proposed modeling scheme could be considered as a valuable detection methodology in food microbiology

Neuro-Fuzzy based Identification of Meat Spoilage using an Electronic Nose

Freshness and safety of muscle foods are generally considered as the most important parameters for the food industry. The performance of a portable electronic nose has been evaluated in monitoring the spoilage of beef fillet stored aerobically at different storage temperatures (0, 4, 8, 12, 16 and 20°C). An adaptive fuzzy logic system model that utilizes a prototype defuzzification scheme has been developed to classify beef samples in their respective quality class and to predict their associated microbiological population directly from volatile compounds fingerprints. Results confirmed the superiority of the adopted methodology and indicated that volatile information in combination with an efficient choice of a modeling scheme could be considered as an alternative methodology for the accurate evaluation of meat spoilage

Effect of Short-Chain Fatty Acid Acetate on Colon Cancer

Acetate is a short chain fatty acid produced as a result of fermentation of ingested fibers by the gut microbiota. While it has been shown to reduce cell proliferation in some cancer cell lines1,2, more recent studies on liver3 and brain4 tumours suggest that acetate may actually promote tumour growth. Acetate in the cell is normally converted into acetyl-coA by two enzymes and metabolized; mitochondrial (ACSS1) and cytosolic (ACSS2) acetyl-coA synthetase. In the mitochondria acetyl-coA is utilized in the TCA cycle. In the cytosol it is utilized in lipid synthesis. In this study, the effect of acetate treatment on the growth of HT29 colon cancer cell line and its mechanism of action was assessed. HT29 human colorectal adenocarcinoma cells were treated with 10mM NaAc and cell viability, cellular bioenergetics and gene expression were investigated. Cell viability was assessed 24 hours after treatment using an MTT assay (Sigma, UK, n=8). Cellular oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) was measured by XFe Analyzer (Seahorse Bioscience, USA). After a baseline reading cells were treated and OCR and ECAR measurements were observed for 18 hours (n=4). Total mRNA was isolated 24 hours after treatment using RNeasy kit (Qiagen, USA). Quantitative PCR reactions were performed using Taqman gene expression assays and Taqman Universal PCR Master Mix (ThermoFisher Scientific, UK) on Applied Biosystems 7500 Fast Real-Time PCR System (Life Technologies, USA) and analysed using ΔΔCt method (n=3). Acetate treatment led to a significant reduction in cell viability (15.9%, Figure 1). OCR, an indicator of oxidative phosphorylation, was significantly increased (p<0.0001) while ECAR, an indicator of glycolysis, was significantly reduced (p<0.0001, Figure 2). Gene expression of ACSS1 was increased by 1.7 fold of control (p=0.07) and ACSS2 expression was reduced to 0.6 fold of control (p=0.06, Figure 3). In conclusion, in colon cancer cells acetate supplementation induces cell death and increases oxidative capacity. These changes together with the trending decrease in ACSS2 expression suggest suppression of lipid synthesis pathways. We hypothesize that the reduced tumor growth by acetate is a consequence of the suppression of ACSS2 and lipid synthesis, both effects reported previously to reduce tumor growth3–5. These effects clearly warrant further investigation.