Exploring Prognostic and Diagnostic Techniques for Jet Engine Health Monitoring: A Review of Degradation Mechanisms and Advanced Prediction Strategies

Maintenance is crucial for aircraft engines because of the demanding conditions to which they are exposed during operation. A proper maintenance plan is essential for ensuring safe flights and prolonging the life of the engines. It also plays a major role in managing costs for aeronautical companies. Various forms of degradation can affect different engine components. To optimize cost management, modern maintenance plans utilize diagnostic and prognostic techniques, such as Engine Health Monitoring (EHM), which assesses the health of the engine based on monitored parameters. In recent years, various EHM systems have been developed utilizing computational techniques. These algorithms are often enhanced by utilizing data reduction and noise filtering tools, which help to minimize computational time and efforts, and to improve performance by reducing noise from sensor data. This paper discusses the various mechanisms that lead to the degradation of aircraft engine components and the impact on engine performance. Additionally, it provides an overview of the most commonly used data reduction and diagnostic and prognostic techniques

A key role of the mitochondrial citrate carrier (SLC25A1) in TNFα- and IFNγ-triggered inflammation

The chronic induction of inflammation underlies multiple pathological conditions, including metabolic, autoimmune disorders and cancer. The mitochondrial citrate carrier (CIC), encoded by the SLC25A1 gene, promotes the export of citrate from the mitochondria to the cytoplasm, a process that profoundly influences energy balance in the cells. We have previously shown that SLC25A1 is a target gene for lipopolysaccharide signaling and promotes the production of inflammatory mediators. We now demonstrate that SLC25A1 is induced at the transcriptional level by two key pro-inflammatory cytokines, tumor necrosis factor-α (TNFα) and interferon-γ (IFNγ), and such induction involves the activity of the nuclear factor kappa B and STAT1 transcription factors. By studying the down-stream events following SLC25A1 activation during signals that mimic inflammation, we demonstrate that CIC is required for regulating the levels of nitric oxide and of prostaglandins by TNFα or IFNγ. Importantly, we show that the citrate exported from mitochondria via CIC and its downstream metabolic intermediate, acetyl-coenzyme A, are necessary for TNFα or IFNγ to induce nitric oxide and prostaglandin production. These findings provide the first line of evidence that the citrate export pathway, via CIC, is central for cytokine-induced inflammatory signals and shed new light on the relationship between energy metabolism and inflammation