Proactive Fault Diagnosis of a Radiator: A Combination of Gaussian Mixture Model and LSTM Autoencoder.

Radiator reliability is crucial in environments characterized by high temperatures and friction, where prompt interventions are often required to prevent system failures. This study introduces a proactive approach to radiator fault diagnosis, leveraging the integration of the Gaussian Mixture Model and Long-Short Term Memory autoencoders. Vibration signals from radiators were systematically collected through randomized durability vibration bench tests, resulting in four operating states-two normal, one unknown, and one faulty. Time-domain statistical features of these signals were extracted and subjected to Principal Component Analysis to facilitate efficient data interpretation. Subsequently, this study discusses the comparative effectiveness of the Gaussian Mixture Model and Long Short-Term Memory in fault detection. Gaussian Mixture Models are deployed for initial fault classification, leveraging their clustering capabilities, while Long-Short Term Memory autoencoders excel in capturing time-dependent sequences, facilitating advanced anomaly detection for previously unencountered faults. This alignment offers a potent and adaptable solution for radiator fault diagnosis, particularly in challenging high-temperature or high-friction environments. Consequently, the proposed methodology not only provides a robust framework for early-stage fault diagnosis but also effectively balances diagnostic capabilities during operation. Additionally, this study presents the foundation for advancing reliability life assessment in accelerated life testing, achieved through dynamic threshold adjustments using both the absolute log-likelihood distribution of the Gaussian Mixture Model and the reconstruction error distribution of the Long-Short Term Memory autoencoder model.

Preventing Forklift Front-End Failures: Predicting the Weight Centers of Heavy Objects, Remaining Useful Life Prediction under Abnormal Conditions, and Failure Diagnosis Based on Alarm Rules.

This paper addresses the critical challenge of preventing front-end failures in forklifts by addressing the center of gravity, accurate prediction of the remaining useful life (RUL), and efficient fault diagnosis through alarm rules. The study's significance lies in offering a comprehensive approach to enhancing forklift operational reliability. To achieve this goal, acceleration signals from the forklift's front-end were collected and processed. Time-domain statistical features were extracted from one-second windows, subsequently refined through an exponentially weighted moving average to mitigate noise. Data augmentation techniques, including AWGN and LSTM autoencoders, were employed. Based on the augmented data, random forest and lightGBM models were used to develop classification models for the weight centers of heavy objects carried by a forklift. Additionally, contextual diagnosis was performed by applying exponentially weighted moving averages to the classification probabilities of the machine learning models. The results indicated that the random forest achieved an accuracy of 0.9563, while lightGBM achieved an accuracy of 0.9566. The acceleration data were collected through experiments to predict forklift failure and RUL, particularly due to repeated forklift use when the centers of heavy objects carried by the forklift were skewed to the right. Time-domain statistical features of the acceleration signals were extracted and used as variables by applying a 20 s window. Subsequently, logistic regression and random forest models were employed to classify the failure stages of the forklifts. The F1 scores (macro) obtained were 0.9790 and 0.9220 for logistic regression and random forest, respectively. Moreover, random forest probabilities for each stage were combined and averaged to generate a degradation curve and determine the failure threshold. The coefficient of the exponential function was calculated using the least squares method on the degradation curve, and an RUL prediction model was developed to predict the failure point. Furthermore, the SHAP algorithm was utilized to identify significant features for classifying the stages. Fault diagnosis using alarm rules was conducted by establishing a threshold derived from the significant features within the normal stage.

Korean Red Ginseng attenuates Di-(2-ethylhexyl) phthalate-induced inflammatory response in endometrial cancer cells and an endometriosis mouse model.

Background: Di-(2-ethylhexyl) phthalate (DEHP) is the most common endocrine disrupting chemical used as a plasticizer. DEHP is associated with the development of endometrium-related diseases through the induction of inflammation. The major therapeutic approaches against endometrial cancer and endometriosis involve the suppression of inflammatory response. Korean Red Ginseng (KRG) is a natural product with anti-inflammatory and anti-carcinogenic properties. Thus, the purpose of this study is to investigate the effects of KRG on DEHP-induced inflammatory response in endometrial cancer Ishikawa cells and a mouse model of endometriosis. Methods: RNA-sequencing was performed and analyzed on DEHP-treated Ishikawa cells in the presence and absence of KRG. The effects of KRG on DEHP-induced cyclooxygenase-2 (COX-2) mRNA levels in Ishikawa cells were determined by RT-qPCR. Furthermore, the effects of KRG on the extracellular signal-regulated kinases (ERKs) pathway, COX-2, and nuclear factor-kappa B (NF-κB) p65 after DEHP treatment of Ishikawa cells were evaluated by western blotting. In the mouse model, the severity of endometriosis induced by DEHP and changes in immunohistochemistry were used to assess the protective effect of KRG. Results: According to the RNA-sequencing data, DEHP-induced inflammatory response-related gene expression was downregulated by KRG. Moreover, KRG significantly inhibited DEHP-induced ERK1/2/NF-κB/COX-2 levels in Ishikawa cells. In the mouse model, KRG administration significantly inhibited ectopic endometriosis growth after DEHP-induced endometriosis. Conclusions: Overall, these results suggest that KRG may be a promising lead for the treatment of endometrial cancer and endometriosis via suppression of the inflammatory response.

Hypoxic induction of apoptosis occurs through HIF-1α and accompanies mammalian sterile 20-like kinase 2 cleavage in human endometrial adenocarcinoma Ishikawa cells.

The incidence of endometrial cancer is increasing worldwide. One of the main causes of this cancer is a hormone imbalance; progesterone derivatives have been used for treatment. However, reports have shown that hypoxia plays important and possibly beneficial roles in endometrial function. Here, we show the effect of hypoxia on the proliferation of human endometrial adenocarcinoma Ishikawa cells. Hypoxia induced caspase-dependent apoptosis in Ishikawa cells. Overexpression and siRNA-mediated knockdown of hypoxia-inducible factor-1α (HIF-1α) confirmed that HIF-1α accelerates hypoxia-induced cell death. Treatment with dimethyloxalglycine, which stabilizes HIF-1α, suppressed cell proliferation. Kaplan-Meier analysis showed that the expression level of HIF-1α has a significant positive effect on the survival rate of endometrial cancer patients. In our search for cellular targets involved in hypoxic apoptosis, we noticed that mammalian sterile 20-like kinase 2 (MST2), a member of the Hippo pathway, was positively correlated with HIF-1α expression in 176 endometrial cancer patients extracted from the TCGA database. Hypoxia induced caspase-dependent MST2 cleavage. In addition, a MST2 inhibitor suppressed HIF-1α-mediated reporter activity. These results suggest HIF-1α and the Hippo signaling pathway are involved in endometrial cancer.

The Effect of Korean Red Ginseng on Bisphenol A-Induced Fatty Acid Composition and Lipid Metabolism-Related Gene Expression Changes.

Bisphenol A (BPA), which is known to be an endocrine-disrupting chemical (EDC), is associated not only with estrogen activity and reproductive toxicity but also with a variety of metabolic disorders. BPA affects glucose tolerance, cholesterol biosynthesis, and fatty acid synthesis. Ginseng is a traditional medicinal plant that has been widely used in East Asia for more than 2000 years, and a number of health effects have been reported. Korean Red Ginseng (KRG) has also been shown to have effects on lipid metabolism and body weight reduction in vivo in obese mice. In this study, we administered BPA and KRG to ovariectomized (OVX) ICR mice. BPA (800 mg/kg/day) and KRG (1.2 g/kg/day) were orally administered to OVX mice for 3 days. KRG inhibited the increase in total fatty acid level by BPA as determined by lipid profiling in the liver of OVX mice. In addition, transcriptome analysis showed that KRG inhibited BPA-induced changes in lipid metabolic process-related genes. Our findings suggest that KRG can regulate BPA-induced changes in lipid metabolism.

MST2 silencing induces apoptosis and inhibits tumor growth for estrogen receptor alpha-positive MCF-7 breast cancer.

Mammalian sterile 20-like kinase 1/2 (MST1/2) plays an important role in cell growth and apoptosis and functions as a tumor suppressor. Previously, we showed that MST2 overexpression activates Estrogen receptor alpha (ERα) in human breast cancer MCF-7 cells in the absence of a ligand. Here, we examined the role of MST2 in the growth of ER-positive MCF-7 cells. Cell cycle, apoptosis, and mammosphere formation assay method were implemented to detect the biological effects of MST2 ablation on the growth of MCF-7 cells in vitro. The effect of MST2-siRNA on MCF-7 cells tumor growth in vivo was studied in tumor-bearing mouse model. Kaplan-Meier plotter analysis was used to determine the effect of MST2 on overall survival in breast cancer patients. MST2 overexpression increased cell viability marginally. The ablation of MST2 using siRNA dramatically suppressed the viability of the MCF-7 cells, but not ER-negative MDA-MB-231 breast cancer cells. Furthermore, MST2 knockdown increased caspase-dependent apoptosis and led to decreased mammosphere formation. Treatment of MCF-7 tumor-bearing mice with MST2 siRNA significantly inhibited tumor growth. The tumor weight was reduced further when tamoxifen was added. Patients with ER-positive breast cancer with low MST2 expression had better overall survival than did those with high MST2 expression in Kaplan-Meier survival analyses using public datasets. Our results provide new insight into the role of MST2, a key component of the Hippo signaling pathway, in mediating breast cancer progression.

Comparative transcriptome analysis of the protective effects of Korean Red Ginseng against the influence of bisphenol A in the liver and uterus of ovariectomized mice.

BACKGROUND: Bisphenol A (BPA), known as an endocrine disruptor, is widely used in the world. BPA is reported to cause inflammation-related diseases. Korean Red Ginseng (KRG) has been used safely in human for a long time for the treatment of diverse diseases. KRG has been reported of its mitigating effect on menopausal symptoms and suppress adipose inflammation. Here, we investigate the protective effect of orally administered KRG on the impacts of BPA in the liver and uterus of menopausal mice model. METHODS: The transcriptome analysis for the effects of BPA on mice liver was evaluated by Gene Expression Omnibus (GEO) database-based data (GSE26728). In vivo assay to evaluate the protective effect of KRG on BPA impact in ovariectomized (OVX) mice were designed and analyzed by RNA sequencing. RESULTS: We first demonstrated that BPA induced 12 kinds of gene set in the liver of normal mice. The administration of BPA and KRG did not change body, liver, and uterine weight in OVX mice. KRG downregulated BPA-induced inflammatory response and chemotaxis-related gene expression. Several gene set enrichment analysis (GSEA)-derived inflammatory response genes increased by BPA were inhibited by KRG in OVX mice. CONCLUSION: Our data suggest that BPA has commonly influenced inflammatory response effects on both normal and OVX mice. KRG protects against BPA impact of inflammatory response and chemotaxis in OVX mouse models. Our comparative analysis will provide new insight into the efficacy of KRG on endocrine disrupting chemicals and OVX mouse.

Ginsenoside Rf inhibits cyclooxygenase-2 induction via peroxisome proliferator-activated receptor gamma in A549 cells.

BACKGROUND: Ginsenoside Rf is a ginseng saponin found only in Panax ginseng that affects lipid metabolism. It also has neuroprotective and antiinflammatory properties. We previously showed that Korean Red Ginseng (KRG) inhibited the expression of cyclooxygenase-2 (COX-2) by hypoxia via peroxisome proliferator-activated receptor gamma (PPARγ). The aim of the current study was to evaluate the possibility of ginsenoside Rf as an active ingredient of KRG in the inhibition of hypoxia-induced COX-2 via PPARγ. METHODS: The effects of ginsenoside Rf on the upregulation of COX-2 by hypoxia and its antimigration effects were evaluated in A549 cells. Docking of ginsenoside Rf was performed with the PPARγ structure using Surflex-Dock in Sybyl-X 2.1.1. RESULTS: PPARγ protein levels and peroxisome proliferator response element promoter activities were promoted by ginsenoside Rf. Inhibition of COX-2 expression by ginsenoside Rf was blocked by the PPARγ-specific inhibitor, T0070907. The PPARγ inhibitor also blocked the ability of ginsenoside Rf to suppress cell migration under hypoxia. The docking simulation results indicate that ginsenoside Rf binds to the active site of PPARγ. CONCLUSIONS: Our results demonstrate that ginsenoside Rf inhibits hypoxia induced-COX-2 expression and cellular migration, which are dependent on PPARγ activation. These results suggest that ginsenoside Rf has an antiinflammatory effect under hypoxic conditions. Moreover, docking analysis of ginsenoside Rf into the active site of PPARγ suggests that the compound binds to PPARγ in a position similar to that of known agonists.

The effects of bisphenol A, benzyl butyl phthalate, and di(2-ethylhexyl) phthalate on estrogen receptor alpha in estrogen receptor-positive cells under hypoxia.

Endocrine-disrupting chemicals (EDCs) are widely used in various consumer goods. Consequently, humans are constantly exposed to EDCs, which is associated with a variety of endocrine-related diseases. In this study, we demonstrated the effects of bisphenol A (BPA), benzyl butyl phthalate (BBP), and di(2-ethylhexyl) phthalate (DEHP) on estrogen receptor alpha (ERα) expression under normoxia and hypoxia. First, we confirmed the effects of EDCs on ER activity using OECD Test Guideline 455. Compared to the 100% activity induced by 1 nM 17-ß-estradiol (positive control), BPA and BBP exhibited 50% ERα activation at concentrations of 1.31 µM and 4.8 µM, respectively. In contrast, and consistent with previous reports, DEHP did not activate ERα. ERα is activated and degraded by hypoxia in breast cancer cells. BPA, BBP, and DEHP enhanced ERα-mediated transcriptional activity under hypoxia. All three EDCs decreased ERα protein levels under hypoxia in MCF-7 cells. The transcriptional activity of hypoxia-inducible factor-1 was decreased and secretion of vascular endothelial growth factor (VEGF) was increased by BPA and BBP under hypoxia in MCF-7 cells, but not by DEHP. All three EDCs decreased the ERα protein expression level in Ishikawa human endometrial adenocarcinoma cells, and DEHP caused a weak decrease in VEGF secretion under hypoxia. These results demonstrate down-regulation of ERα by EDCs may influence the pathological state associated with hypoxia.

Increased expression of MIP-3alpha/CCL20 in peripheral blood mononuclear cells from patients with ulcerative colitis and its down-regulation by sulfasalazine and glucocorticoid treatment.

UNLABELLED: CCL20 expression is known to increase in the mucosal tissues of inflammatory bowel diseases (IBDs). Moreover, the discovery of Nod2 as the IBD1 susceptibility gene has underscored the significance of blood mononuclear cells in IBD pathogenesis. METHODS: This study addresses whether CCL20 expression is similarly altered in peripheral blood mononuclear cells (PBMCs) of patients with ulcerative colitis (UC), a major type of IBD in Korea. RESULTS: Expression of CCL20 was significantly up-regulated in the PBMCs of patients with UC compared with those of normal healthy controls. Interestingly, untreated UC groups expressed higher levels of CCL20 mRNA than either treated UC or normal control groups, suggesting that CCL20 could be modulated by anti-inflammatory drugs. Accordingly, a strong association between CCL20 levels and disease activity index was observed. Supporting these findings, results from a 3-month follow-up study revealed that the UC groups treated with 5-aminosalicylic acid and glucocorticoid exhibited dramatic decreases of CCL20 mRNA in PBMCs, accompanied by ameliorated disease states. Moreover, tumor necrosis factor-alpha- or interleukin-1beta-induced CCL20 secretion was greatly diminished by 5-aminosalicylic acid and/or glucocorticoid treatment of human intestinal epithelial HT-29 cells. Of note, CCR6 cell populations were significantly reduced in the blood of severe patients with UC compared with normal controls, whereas no significant changes in CCR6 cell populations were observed in the blood of patients with mild UC or acute colitis. CONCLUSIONS: Collectively, these findings suggest that CCL20 expression in blood mononuclear cells is associated with altered immune and inflammatory responses in patients with UC.