Fault Detection of Wind Turbine Gearboxes Based on IBOA-ERF.

As one of the key components of wind turbines, gearboxes are under complex alternating loads for a long time, and the safety and reliability of the whole machine are often affected by the failure of internal gears and bearings. Aiming at the difficulty of optimizing the parameters of wind turbine gearbox fault detection models based on extreme random forest, a fault detection model with extreme random forest optimized by the improved butterfly optimization algorithm (IBOA-ERF) is proposed. The algebraic sum of the false alarm rate and the missing alarm rate of the fault detection model is constructed as the fitness function, and the initial position and position update strategy of the individual are improved.

Fault Detection for Wind Turbine Blade Bolts Based on GSG Combined with CS-LightGBM.

Aiming at the problem of class imbalance in the wind turbine blade bolts operation-monitoring dataset, a fault detection method for wind turbine blade bolts based on Gaussian Mixture Model-Synthetic Minority Oversampling Technique-Gaussian Mixture Model (GSG) combined with Cost-Sensitive LightGBM (CS-LightGBM) was proposed. Since it is difficult to obtain the fault samples of blade bolts, the GSG oversampling method was constructed to increase the fault samples in the blade bolt dataset. The method obtains the optimal number of clusters through the BIC criterion, and uses the GMM based on the optimal number of clusters to optimally cluster the fault samples in the blade bolt dataset.

A velocity-guided Harris hawks optimizer for function optimization and fault diagnosis of wind turbine.

Harris hawks optimizer (HHO) is a relatively novel meta-heuristic approach that mimics the behavior of Harris hawk over the process of predating the rabbits. The simplicity and easy implementation of HHO have attracted extensive attention of many researchers. However, owing to its capability to balance between exploration and exploitation is weak, HHO suffers from low precision and premature convergence.

Clean Process to Utilize the Potassium-Containing Phosphorous Rock with Simultaneous HCl and KCl Production via the Steam-Mediated Reactions.

In this paper, a clean process based on the steam-mediated reactions for simultaneous HCl and KCl production using the potassium (K)-containing phosphorous rock as a precursor is proposed. Through hydrochloric acid (HCl) leaching, not only the generation of HPO and CaCl (via further precipitation) were realized but also the acid-insoluble residue [phosphorous-rock slag (PS)] rich in elements, that is, K, Al, Si, and so on, in the form of microcline (KAlSiO) and quartz (SiO) was obtained and became readily available for further HCl and KCl generation. Over 95% of the elements, that is, K, Al, and Si, come into the final products, and the overall acid consumption (based on HCl) is significantly reduced (90%) due to recovery of acids.

MCU-dependent mitochondrial calcium uptake-induced mitophagy contributes to apelin-13-stimulated VSMCs proliferation.

Apelin is an endogenous ligand of the G protein-coupled receptor APJ. Both apelin and APJ receptors, which are expressed in vascular smooth muscle cells (VSMCs), play important roles in the cardiovascular system. Our previous studies researches indicated that mitophagy mediated apelin-13-induced VSMCs proliferation.

Fault Detection of Wind Turbine Electric Pitch System Based on IGWO-ERF.

It is difficult to optimize the fault model parameters when Extreme Random Forest is used to detect the electric pitch system fault model of the double-fed wind turbine generator set. Therefore, Extreme Random Forest which was optimized by improved grey wolf algorithm (IGWO-ERF) was proposed to solve the problems mentioned above. First, IGWO-ERF imports the Cosine model to nonlinearize the linearly changing convergence factor α to balance the global exploration and local exploitation capabilities of the algorithm.

Apelin/APJ signaling activates autophagy to promote human lung adenocarcinoma cell migration.

Aims: Beclin1(BECN1) is known as an autophagy-related protein and the expression is promoted by apelin in lung adenocarcinoma cells, suggesting that apelin activates autophagy in lung adenocarcinoma. However, the functions of apelin-induced autophagy in lung adenocarcinoma tumorigenesis and deterioration are still unknown. Thus, this study aims to investigate the effects of apelin-induced autophagy on lung adenocarcinoma tumorigenesis and deterioration.

Oxidative stress-mediated AMPK inactivation determines the high susceptibility of LKB1-mutant NSCLC cells to glucose starvation.

The liver kinase B1 (LKB1) is an important tumor suppressor and its loss-of-function mutations are observed in around 16% of non-small cell lung cancer (NSCLC) cases. One of the main functions of LKB1 is to activate AMP-activated protein kinase (AMPK) via direct phosphorylation. Under metabolic or energy stress conditions, the LKB1-AMPK axis inhibits the anabolic pathways and activates the catabolic pathways to maintain metabolic homeostasis for cell survival.

Regulation of the Golgi apparatus via GOLPH3-mediated new selective autophagy.

Aims: Although previous studies elaborated that selective autophagy was involved in quality control of some organelles, including nucleus, mitochondria, the endoplasmic reticulum and peroxisomes, it remained unclear whether the selective autophagy of the Golgi apparatus (Golgiphagy) existed or not.

Main Methods: In this study, H9c2 cells, HUVECs, HA-VSMCs and HEK293T cells were treated with autophagy inducers, Golgi stress inducers and cardiomyocytes hypertrophy stimulators. The Golgiphagy was evaluated by analysing the co-localization of Golgi markers and LC3B.

Junctophilins emerge as novel therapeutic targets.

Junctophilins (JPs) emerge to play key role in human pathophysiology. This family includes four subtypes (JP1-4), which are differentially detected in excitable cells. Previous work demonstrated the knockout of JPs that seriously damage physiological functions in skeletal muscle, cardiac, and neurons.

Ferritinophagy activation and sideroflexin1-dependent mitochondria iron overload is involved in apelin-13-induced cardiomyocytes hypertrophy.

Excess iron accumulation and cardiac oxidative stress have been shown as important mediators of cardiac hypertrophy, whereas it remains largely elusive about the occurrence of mitochondrial iron overload and its significance during cardiac hypertrophy. In the present study, we aim to investigate the role of NCOA4-mediated ferritinophagy and SFXN1-dependent mitochondria iron overload in apelin-13-induced cardiomyocytes hypertrophy. Apelin-13 significantly promotes ferric citrate (FAC)-induced total cellular and mitochondria ion production, as well as mitochondria ROS contents.

Warburg effect is involved in apelin-13-induced human aortic vascular smooth muscle cells proliferation.

Apelin is the endogenous ligand for the G protein-coupled receptor APJ. Both apelin and APJ receptor are distributed in vascular smooth muscle cells (VSMCs) and play important roles in the cardiovascular system. Our previous reports have indicated that apelin-13 promoted the proliferation of VSMCs, but its exact mechanism remains to be further explored.

PINK1/Parkin-mediated mitophagy promotes apelin-13-induced vascular smooth muscle cell proliferation by AMPKα and exacerbates atherosclerotic lesions.

Aberrant proliferation of vascular smooth muscle cells (VSMC) is a critical contributor to the pathogenesis of atherosclerosis (AS). Our previous studies have demonstrated that apelin-13/APJ confers a proliferative response in VSMC, however, its underlying mechanism remains elusive. In this study, we aimed to investigate the role of mitophagy in apelin-13-induced VSMC proliferation and atherosclerotic lesions in apolipoprotein E knockout (ApoE-/-) mice.

Apelin/APJ system: A novel promising target for anti-aging intervention.

Apelin, an endogenous ligand for the G protein-coupled receptor APJ, is widely expressed in various organs. Recent research has indicated that the Apelin/APJ system plays an important role in aging. Apelin and APJ receptor expression are down-regulated with increasing age.

Ferritinophagy/ferroptosis: Iron-related newcomers in human diseases.

Nuclear receptor coactivator 4 mediated ferritinophagy is an autophagic phenomenon that specifically involves ferritin to release intracellular free iron. Ferritinophagy is implicated in maintaining efficient erythropoiesis. Notably, ferritinophagy also plays a central role in driving some pathological processes, including Parkinson's disease (PD) and urinary tract infections.

Glycophagy: An emerging target in pathology.

Autophagy, a highly conserved self-digestion process, is initially regarded as non-selectively sequestering and degradation cytoplasmic contents. Nowadays, many kinds of selective autophagy have been found in response to various physiological cues such as mitophagy, reticulophagy and glycophagy. Glycophagy, as a selective autophagy, plays a crucial role in maintaining glucose homeostasis in many tissues including heart, liver and skeletal muscles.

ROS-Autophagy pathway mediates monocytes-human umbilical vein endothelial cells adhesion induced by apelin-13.

Apelin is the endogenous ligand of APJ receptor. Both monocytes (MCs) and human umbilical vein endothelial cells (HUVECs) express apelin and APJ, which play important roles in the physiological processes of atherosclerosis. Our previous research indicated that apelin-13 promoted MCs-HUVECs adhesion.

Physicochemical Evidence on Sublethal Neonicotinoid Imidacloprid Interacting with an Odorant-Binding Protein from the Tea Geometrid Moth, Ectropis obliqua.

Nowadays the excessive usage of neonicotinoid insecticides always results in residues in Chinese tea fields. It is not clear whether the insecticide residue at the sublethal level influences the physiological processes of tea pests. Here, we provide evidence of interaction between the neonicotinoid imidacloprid and a general odorant-binding protein, EoblGOBP2, from the tea geometrid moth, Ectropis obliqua.

Sublethal doses of neonicotinoid imidacloprid can interact with honey bee chemosensory protein 1 (CSP1) and inhibit its function.

As a frequently used neonicotinoid insecticide, imidacloprid can impair the chemoreceptive behavior of honey bees even at sublethal doses, while the physiochemical mechanism has not been further revealed. Here, multiple fluorescence spectra, thermodynamic method, and molecular docking were used to study the interaction and the functional inhibition of imidacloprid to the recombinant CSP1 protein in Asian honey bee, Apis cerana. The results showed that the fluorescence intensity (λ = 332 nm) of CSP1 could be significantly quenched by imidacloprid in a dynamic mode.