Sensors and process control systems are essential for process automation and optimization. Many sectors have adapted to the Industry 4.0 paradigm, but copper smelters remain hesitant to implement these technologies without appropriate justification, as many critical functions remain subject to ground operator experience. Recent experiments and industrial trials using radiometric optoelectronic data acquisition, coupled with advanced quantitative methods and expert systems, have successfully distinguished between mineral species in reactive vessels with high classification rates. These experiments demonstrate the increasing potential for the online monitoring of the state of a charge in pyrometallurgical furnaces, allowing data-driven adjustments to critical operational parameters. However, the justification to implement an innovative control system requires a quantitative framework that is conducive to multiphase engineering projects. This paper presents a unified quantitative framework for copper and nickel-copper smelters, which integrates thermochemical modeling into discrete event simulation and is, indeed, able to simulate smelters, with and without a proposed set of sensors, thus quantifying the benefit of these sensors. Sample computations are presented, which are based on the authors’ experiences in smelter reengineering projects.
Dietary intake of eicosapentaenoic/docosahexaenoic acid (EPA/DHA) reduces insulin resistance and hepatic manifestations through the regulation of metabolism in the liver. Obese mice present insulin resistance and lipid accumulation in intracellular lipid droplets (LDs). LD-associated proteins perilipin (Plin) have an essential role in both adipogenesis and lipolysis; Plin5 regulates lipolysis and thus contributes to fat oxidation. The purpose of this study was to compare the effects of deodorized refined salmon oil (DSO) and its polyunsaturated fatty acids concentrate (CPUFA) containing EPA and DHA, obtained by complexing with urea, on obesity-induced metabolic alteration. CPUFA maximum content was determined using the Box–Behnken experimental design based on Surface Response Methodology. The optimized CPUFA was administered to high-fat diet (HFD)-fed mice (200 mg/kg/day of EPA + DHA) for 8 weeks. No significant differences (p > 0.05) in cholesterol, glycemia, LDs or transaminase content were found. Fasting insulin and hepatic Plin5 protein level increased in the group supplemented with the EPA + DHA optimized product (38.35 g/100 g total fatty acids) compared to obese mice without fish oil supplementation. The results suggest that processing salmon oil by urea concentration can generate an EPA+DHA dose useful to prevent the increase of fasting insulin and the decrease of Plin5 in the liver of insulin-resistant mice.
A two‐hit hypothesis has been proposed for the etiology of NAFLD: first, increased lipogenesis results in triacylglycerol (TG) accumulation, then inflammatory stimuli, e.g., saturated fatty acids (SFA)‐induced lipotoxicity and inflammation, cause disease progression. Previously, we showed that NAFLD‐like symptoms developed in mice fed a liquid high carbohydrate diet (76% en‐%, HCD) for 5‐wk, while mice fed HCD containing 13.5% (en‐%) of lipid emulsion (LE, Intralipid®) exhibited less hepatic TG accumulation and inflammation. However, it is unknown whether LE can cease the first hit of NAFLD once TG accumulation has begun. To test this, male C57BL/6 mice (6 wk; n=8/group) were fed either HCD for 5 wk (HCD) or HCD for 2.5 wk followed by HCD with LE for 2.5 wk (HCD/LE). At this time, liver TG in mice fed HCD/LE was 60% lower (P<0.001) as compared to mice fed HCD. Hepatic mRNAs of PNPLA3, associated with NAFLD,and several lipogenic genes, e.g., acetyl‐CoA carboxylase 1, fatty acid synthase, and stearoyl‐CoA desaturase 1, assayed by qRT‐PCR, were decreased by 42‐93% in HCD/LE vs. HCD mice (all P<0.001). We further analyzed liver total fatty acid composition, determined as fatty acid methyl esters by GC‐MS, and found that HCD/LE mice had lower levels of C14:0, C16:0 and C18:1 (n‐9) as compared to HCD mice (all P<0.001). In conclusion, in the presence of a HCD, LE can halt the first hit of NAFLD and lower the levels of saturated FA, reducing lipotoxicity and lipogenesis.
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