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As a common air pollutant, formaldehyde is widely present in nature, industrial production and consumer products. Endogenous formaldehyde is mainly produced through the oxidative deamination of methylamine catalysed by semicarbazide‐sensitive amine oxidase (SSAO) and is ubiquitous in human body fluids, tissues and cells. Vascular endothelial cells and smooth muscle cells are rich in this formaldehyde‐producing enzyme and are easily damaged owing to consequent cytotoxicity. Consistent with this, increasing evidence suggests that the cardiovascular system and stages of heart development are also susceptible to the harmful effects of formaldehyde. Exposure to formaldehyde from different sources can induce heart disease such as arrhythmia, myocardial infarction (MI), heart failure (HF) and atherosclerosis (AS). In particular, long‐term exposure to high concentrations of formaldehyde in pregnant women is more likely to affect embryonic development and cause heart malformations than long‐term exposure to low concentrations of formaldehyde. Specifically, the ability of mouse embryos to effect formaldehyde clearance is far lower than that of the rat embryos, more readily allowing its accumulation. Formaldehyde may also exert toxic effects on heart development by inducing oxidative stress and cardiomyocyte apoptosis. This review focuses on the current progress in understanding the influence and underlying mechanisms of formaldehyde on cardiovascular disease and heart development.

In this paper, we first construct ontology and entity learning to construct a knowledge graph by matching the knowledge to the schema layer. Then, we obtain users’ learning styles, extract interest keywords from user behavioral data, map them into the vector space encoded based on the KgTransH algorithm, and compare them with the original algorithm on multiple datasets. Then, the business English learning path is planned based on learning path length, learning time and achievement ranking. Finally, the effect of the knowledge graph-based business English learning path planning method is analyzed through comparative experiments. Through 50 iterations, the satisfaction of the knowledge graph method, GA method and ACO method are between 4.3-4.8, 4-4.7 and 4.05-4.7, respectively, which indicates that the method of this paper is better than the other methods. This study is important for improving the learning effect of Business English.

Inflammation and endothelial dysfunction are important participants and drivers in atherosclerosis. NOD‐, LRR‐ and pyrin domain‐containing protein 3 (NLRP3) inflammasome activation and the resulting pyroptosis are involved in the initiation and vicious circle of chronic inflammation, thus playing an indispensable role in atherosclerosis. Accordingly, blocking the activation of NLRP3 inflammasome may be a promising treatment strategy to blunt the progression of atherosclerosis. In this study, it was demonstrated that miR‐302c‐3p exerted anti‐pyroptosis effects by directly targeting NLRP3 in vivo and in vitro. In brief, the expression of miR‐302c‐3p was down‐regulated whereas the expression of NLRP3 was up‐regulated in human plaques and in vitro pyroptosis model of endothelial cells. Overexpression of miR‐302c‐3p suppressed endothelial cell pyroptosis by targeting specific sites of NLRP3. By comparison, down‐regulation of endogenous miR‐302c‐3p led to the opposite results, which were reversed by silencing the expression of NLRP3. Finally, the up‐regulation of miR‐302c‐3p inhibited the inflammation and pyroptosis of atherosclerosis mouse model. In conclusion, miR‐302c‐3p may be a powerful and attractive target for suppressing endothelial inflammation and pyroptosis, providing a novel strategy for preventing or alleviating the progression of atherosclerosis.

Osteoblast apoptosis plays an important role in age-related bone loss and osteoporosis. Our previous study revealed that advanced oxidation protein products (AOPPs) could induce nicotinamide adenine dinucleotide phosphate oxidase (NOX)-derived reactive oxygen species (ROS) production, cause mitochondrial membrane potential (ΔΨm) depolarization, trigger the mitochondria-dependent intrinsic apoptosis pathway, and lead to osteoblast apoptosis and ultimately osteopenia and bone microstructural destruction. In this study, we found that AOPPs also induced mitochondrial ROS (mtROS) generation in osteoblastic MC3T3-E1 cells, which was closely related to NOX-derived ROS, and aggravated the oxidative stress condition, thereby further promoting apoptosis. Removing excessive ROS and damaged mitochondria is the key factor in reversing AOPP-induced apoptosis. Here, by in vitro studies, we showed that rapamycin further activated PINK1/Parkin-mediated mitophagy in AOPP-stimulated MC3T3-E1 cells and significantly alleviated AOPP-induced cell apoptosis by eliminating ROS and damaged mitochondria. Our in vivo studies revealed that PINK1/Parkin-mediated mitophagy could decrease the plasma AOPP concentration and inhibit AOPP-induced osteoblast apoptosis, thus ameliorating AOPP accumulation-related bone loss, bone microstructural destruction and bone mineral density (BMD) loss. Together, our study indicated that therapeutic strategies aimed at upregulating osteoblast mitophagy and preserving mitochondrial function might have potential for treating age-related osteoporosis.

Doxorubicin (DOX) is a kind of representative anthracyclines. It has greatly prolonged lifespan of cancer patients. However, a long course of DOX chemotherapy could induce various forms of deaths of cardiomyocytes, such as apoptosis, pyroptosis and ferroptosis, contributing to varieties of cardiac complications called cardiotoxicity. It has become a major concern considering the large number of cancer patients' worldwide and increased survival rates after chemotherapy. Exosomes, a subgroup of extracellular vesicles (EVs), are secreted by nearly all cells and consist of lipid bilayers, nucleic acids and proteins. They can serve as mediators between intercellular communication via the transfer of bioactive molecules from secretory to recipient cells, modulating multiple pathophysiological processes. It has been proven that exosomes in body fluids can serve as biomarkers for doxorubicin-induced cardiotoxicity (DIC). Moreover, exosomes have attracted considerable attention because of their capacity as carriers of certain proteins, genetic materials (miRNA and lncRNA), and chemotherapeutic drugs to decrease the dosage of DOX and alleviate cardiotoxicity. This review briefly describes the characteristics of exosomes and highlights their clinical application potential as diagnostic biomarkers and drug delivery vehicles for DIC, thus providing a strategy for addressing it based on exosomes.

This article discusses the relationship between language and society, introduces the definition and scope of sociolinguistics, demonstrates the social variation of language, regional variation, as well as the relationship between language and ethnicity and culture, and ultimately proposes how to apply sociolinguistic theories to college English teaching activities.

Background and Purpose Curcumin, a natural antioxidant isolated from Curcuma longa, has been reported to exert neuroprotective effect in animal models of ischemic stroke. However, the underlying mechanism is still not fully understood. The purpose of this study was to investigate the effect of curcumin treatment on neuronal apoptosis in the periinfarct cortex after cerebral ischemia/reperfusion (I/R) injury and in mouse N2a cells after oxygen‐glucose deprivation/reoxygenation (OGD/R) injury and its underlying mechanism. Methods The cerebral I/R injury was established by 1‐hr middle cerebral artery occlusion (MCAO) and reperfusion in mice. Infarct volume was determined by TTC staining, and neurological score was evaluated by mNSS. Cell morphology in the ischemic boundary zone were detected by HE staining. The number and apoptotic rate of neurons in ischemic boundary zone were assayed by immunohistochemistry and TUNEL, respectively. Mouse neuroblastoma N2a cells were subjected to OGD/R. Cell viability was assessed with CCK‐8. The mitochondrial membrane potential was measured using JC‐1 staining. The expression of Bax, Bcl‐2, and caspase‐3 was detected using Western blotting. Besides, cellular distribution of Bax was determined by immunofluorescence assays. Results Curcumin treatment reduced infarct volume, improved neurological function, alleviated the morphological damage of neurons, and increased neuronal survival rate after I/R injury in vivo. Moreover, curcumin treatment improved cell viability, reduced cell apoptosis, increased Bcl‐2 protein levels while decreased Bax and caspase‐3 expressions in mouse N2a cells after OGD/R injury. Besides, curcumin treatment inhibited Bax activation and maintained mitochondrial membrane integrity. Conclusion Curcumin promotes neuron survival in vivo and in vitro to exert neuroprotective effects against ischemia injury. Moreover, our results for the first time demonstrated curcumin inhibited ischemia‐induced mitochondrial apoptosis via restricting Bax activation, which may be one of the possible mechanisms underlying the neuroprotective effects of curcumin. Curcumin promotes neuron survival in vivo and in vitro to exert neuroprotective effects against ischemia injury. Moreover, our results for the first time demonstrated curcumin inhibited ischemia‐induced mitochondrial apoptosis via restricting Bax activation, which may be one of the possible mechanisms underlying the neuroprotective effects of curcumin.

High-speed cutting technology has become a development trend in the material processing industry. However, high-intensity noise generated during high-speed cutting exerts a potential effect on the processing efficiency, processing accuracy, and product quality of the workpiece; it may even cause hidden safety hazards. To conduct an in-depth study of noise in high-speed cutting machining, this work reviews noise sources, noise collection and numerical recognition, noise control, and condition monitoring based on acoustic signals. First, this article introduces noise sources, noise signal acquisition equipment, and analysis software. It is pointed out that how to accurately classify and recognize the target signal in the complex high-speed machining environment is one of the focuses of scholars’ research. Then, it points out that a computer achieves high accuracy and practicability in signal analysis, processing, and result display. Second, in the aspect of noise signal processing, the characteristics of noise signals are analyzed. It is pointed out that accurately analyzing the characteristics of different noise source signals and adopting appropriate methods for identification and processing are the necessary conditions for effectively controlling and reducing the noise in the process of high-speed cutting. The advantages and applicable fields of artificial intelligence algorithms in processing mixed noise source signals with different frequency characteristics are compared, providing ideas for studying the mechanism of noise generation and the identification of noise sources. Third, in terms of noise control, a detailed overview is provided from the aspects of the treatment of the noise source that contributes the most to the overall noise, the improvement of the tool structure, the optimization of cutting parameters, and the analysis of contact factors between the tool and the workpiece. It provides an effective way for noise control in the process of high-speed cutting. In addition, the application of acoustic signals to condition monitoring is also thoroughly analyzed. The practical application value of condition monitoring based on acoustic signals in high-speed machining is highlighted. Finally, this paper summarizes the positive significance of noise research in high-speed machining and identifies key problems and possible research methods that require further study in the future.

Summary Osteoblast apoptosis contributes to age‐related bone loss. Advanced oxidation protein products (AOPPs) are recognized as the markers of oxidative stress and potent inducers of apoptosis. We have demonstrated that AOPP accumulation was correlated with age‐related bone loss. However, the effect of AOPPs on the osteoblast apoptosis still remains unknown. Exposure of osteoblastic MC3T3‐E1 cells to AOPPs caused the excessive generation of reactive oxygen species (ROS) by activating nicotinamide adenine dinucleotide phosphate (NADPH) oxidases. Increased ROS induced phosphorylation of mitogen‐activated protein kinases (MAPKs), which subsequently triggered intrinsic apoptosis pathway by inducing mitochondrial dysfunction, endoplasmic reticulum stress, and Ca2+ overload and eventually leads to apoptosis. Chronic AOPP loading in aged Sprague‐Dawley rats induced osteoblast apoptosis and activated NADPH oxidase signaling cascade, in combination with accelerated bone loss and deteriorated bone microstructure. Our study suggests that AOPPs induce osteoblast apoptosis by the NADPH oxidase‐dependent, MAPK‐mediated intrinsic apoptosis pathway.

A new species in Gesneriaceae, Petrocosmea miechangensis , is described from southeastern Yunnan, China. This species bears a resemblance to P. sericea in the shape of the adaxial corolla lip and in having very densely appressed hairs on the abaxial leaf blade. However, it can be distinguished by its flowering period, the hairs on the leaf blade, calyx, and filaments, as well as the shape of the filaments. An identification key to P. miechangensis and its related species is presented.