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As the most prevalent subtype of aortic aneurysm, abdominal aortic aneurysm (AAA) features the apoptosis, extracellular matrix (ECM) disruption, and inflammation response of vascular smooth muscle cells (VSMCs). Noncoding RNAs (ncRNAs) are crucial factors in AAA progression, while the investigations have not been fully explained. miR-191-5p upregulation is found in aortic aneurysm. However, its role in AAA has not been addressed. This research purposed to excavate the possible and associated molecular axis of miR-191-5p in AAA. In our study, miR-191-5p level was detected to be high in the tissues from AAA patients in comparison with the control group. After miR-191-5p expression was enhanced, cell viability was repressed, cell apoptosis was boosted, and ECM disruption and the inflammation response were fortified. Furthermore, the relationship among MIR503HG, miR-191-5p, and phospholipase C delta 1 (PLCD1) in VSMCs was disclosed via mechanism assays. Decreased MIR503HG lacked the inhibition on miR-191-5p targeting PLCD1, resulting in downregulation of PLCD1, which facilitated the progression of AAA. Thus, targeting MIR503HG/miR-191-5p/PLCD1 pathway will provide an additional method for the cure of AAA patients.

The current mainstay therapeutic strategy for advanced prostate cancer is to suppress androgen receptor (AR) signaling. However, castration-resistant prostate cancer (CRPC) invariably arises with restored AR signaling activity. To date, the AR ligand-binding domain (LBD) is the only targeted region for all clinically available AR signaling antagonists, such as enzalutamide (ENZ). Major resistance mechanisms have been uncovered to sustain the AR signaling in CRPC despite these treatments, including AR amplification, AR LBD mutants, and the emergence of AR splice variants (AR-Vs) such as AR-V7. AR-V7 is a constitutively active truncated form of AR that lacks the LBD; thus, it can not be inhibited by AR LBD-targeting drugs. Therefore, an approach to inhibit AR through the regions outside of LBD is urgently needed. In this study, we have discovered a novel small molecule SC428, which directly binds to the AR N-terminal domain (NTD) and exhibits pan-AR inhibitory effect. SC428 potently decreased the transactivation of AR-V7, ARv567es, as well as full-length AR (AR-FL) and its LBD mutants. SC428 substantially suppressed androgen-stimulated AR-FL nuclear translocation, chromatin binding, and AR-regulated gene transcription. Moreover, SC428 also significantly attenuated AR-V7–mediated AR signaling that does not rely on androgen, hampered AR-V7 nuclear localization, and disrupted AR-V7 homodimerization. SC428 inhibited in vitro proliferation and in vivo tumor growth of cells that expressed a high level of AR-V7 and were unresponsive to ENZ treatment. Together, these results indicated the potential therapeutic benefits of AR-NTD targeting for overcoming drug resistance in CRPC.

To well extract the early fault characteristics of rotating machines, a new fast sparsity-enabled feature-energy-ratio method is investigated in this paper. This method includes two stages. In the first stage, the spectrum is adaptively segmented through a coarse-to-fine strategy based on the ordered local maximums. Thus, the fault characteristic band can be divided automatically. A novel index based on sparsity, energy ratio, and kurtosis, is constructed to evaluate periodic impulses in each sub-signal, and it can evaluate the periodic impulses from the globality and locality. In the second stage, the Fourier spectrum from the first stage are refined by an improved sparse coding shrinkage denoising (SCSD) method whose parameters can be dynamically determined for each point. Within the improved SCSD approach, the differential result of the amplitude spectrum is used as input to improve the sparsity. Moreover, the ratios between the SCSD output and its input are applied to weigh the Fourier spectrum and maintain the phase information. Finally, the inverse fast Fourier transform and squared envelope spectra are applied to detect the fault characteristics. Bearing and gearbox vibration signals are used to validate the proposed methodology. The experimental results show that the proposed method is superior to some typical methods and the proposed index are robust to the interferences from aperiodic impulses. Therefore, the proposed method has great potential in the fault diagnosis of rotating machine.

Nonalcoholic fatty liver disease and its progressive form, nonalcoholic steatohepatitis (NASH), are rapidly becoming the top causes of hepatocellular carcinoma (HCC). Currently, there are no approved therapies for the treatment of NASH. DEAD-box protein 5 (DDX5) plays important roles in different cellular processes. However, the precise role of DDX5 in NASH remains unclear.DDX5 expression was downregulated in patients with NASH, mouse models with diet-induced NASH (high-fat diet [HFD], methionine- and choline-deficient diet, and choline-deficient HFD), mouse models with NASH-HCC (diethylnitrosamine with HFD), and palmitic acid-stimulated hepatocytes. Adeno-associated virus-mediated DDX5 overexpression ameliorates hepatic steatosis and inflammation, whereas its deletion worsens such pathology. The untargeted metabolomics analysis was carried out to investigate the mechanism of DDX5 in NASH and NASH-HCC, which suggested the regulatory effect of DDX5 on lipid metabolism. DDX5 inhibits mechanistic target of rapamycin complex 1 (mTORC1) activation by recruiting the tuberous sclerosis complex (TSC)1/2 complex to mTORC1, thus improving lipid metabolism and attenuating the NACHT-, leucine-rich-repeat (LRR)-, and pyrin domain (PYD)-containing protein 3 inflammasome activation. We further identified that the phytochemical compound hyperforcinol K directly interacted with DDX5 and prevented its ubiquitinated degradation mediated by ubiquitin ligase (E3) tripartite motif protein 5, thereby significantly reducing lipid accumulation and inflammation in a NASH mouse model.These findings provide mechanistic insight into the role of DDX5 in mTORC1 regulation and NASH progression, as well as suggest a number of targets and a promising lead compound for therapeutic interventions against NASH.

Background: Irritable bowel syndrome needs long-term neuroscience detection after medical engineering modeling, during which time, computer engineering is needed to complete database collection. Research methods: The research team designed this model after constructing the illusion of intervention on different sweeteners and sugars. At the same time, the artificial intelligence neural system combined with data to predict which combination of sweeteners and sugars is likely to cause disease, which combination of sugar and glycogen may lead to irritable bowel syndrome in patients, and elaborate the neural network mechanism from the perspective of calculation. Results: Through experimental data processing and analysis, the research team completed the design of the model and established a complete computer network path. Conclusion: The model can be popularized in Europe, Russia, Belarus, China, Malaysia and other regions. After cooperation with Chifeng University, supported by the Autonomous University of Barcelona in Spain and the National University of Belarus, a more in-depth comparative experiment will be carried out to find a more accurate molecular mechanism.

Background: According to the data from the Autonomous University of Barcelona, Spain, at present, 20% of people in the world may suffer from irritable bowel syndrome. Research methods: The research group has carried out computational engineering modeling for music therapy of irritable bowel syndrome, which uses virtual reality technology that can interfere with human biological neural network, and has also carried out the process design of biological neural network working mechanism, using computer engineering to complete necessary stimulation, and using neural network algorithm model to complete in-depth learning, After the algorithm modeling is successful, it can complete the prediction of the improvement of patients by music chords of different emotional colors, and provide clinicians with new ideas for treatment and health economic intelligent products. The first author looks forward to the cooperation between Chifeng University and Barcelona Autonomous University in the research of irritable bowel syndrome, expounds the advantages of both sides, and expresses a strong willingness to communicate. At the same time, the advantages of the Sakharov Institute in Belarus are discussed. Results: The research team carried out research in combination with biological neural network experiment and social experiment, and completed the market demand survey. Conclusion: The chord trend in this model can complete the intervention for patients. Patients have better subjective feelings, and the algorithm model is highly popularized. Virtual reality technology can be used as an important medium to complete this work, which is suitable for promotion.

Chemical spraying is one of the most important and frequently performed intercultural agricultural operations. It is imperative to select the appropriate spraying technology as a selection of ineffective one leads to the wastage of a considerable volume of applied chemicals to the non-target area. Many precision technologies have been developed in the past few decades, such as image processing based on real-time variable-rate chemical spraying systems, autonomous chemical sprayers using machine vision and nozzle control, and use of unmanned aerial and ground vehicles. Cotton defoliation is a natural physiological process, but untimely and inadequate leaf defoliation by natural process hinders the mechanical cotton harvest. Induced defoliation is practiced by applying defoliants to address the issue with the natural process of defoliation. This paper covers spraying technologies in agriculture, cotton plants, cotton defoliation, new defoliant spraying systems, and the recent field test. The new spraying system attached to an autonomous mobile robot aims to improve the delivery of defoliant chemicals by adding a spray unit on the side of the plant. Preliminary results of the water-sensitive paper test at the field showed adequate penetration with low flow rates. This is a huge development as there is a huge potential to save on the cost of applying defoliant chemicals.

Objective. Ischemia–reperfusion injury (IRI) is an important cause of delayed functional recovery after transplantation. This study is aimed at investigating the molecular mechanism of ALDH2 in a kidney ischemia–reperfusion model based on RNA-seq. Methods. We performed kidney ischemia–reperfusion in ALDH2-/- and WT mice and evaluated kidney function and morphology using SCr, HE staining, TUNEL staining, and TEM. We used RNA-seq to compare mRNA expression in ALDH2-/- and WT mice after IR, and then, we verified the related molecular pathways by PCR and western blotting. In addition, activators and inhibitors of ALDH2 were used to alter the activity of ALDH2. Finally, we established a model of hypoxia and reoxygenation in HK-2 cells and clarified the role of ALDH2 in IR by interfering with ALDH2 and using an NF-κB inhibitor. Results. After kidney ischemia–reperfusion, the SCr value increased significantly, kidney tubular epithelial cells were damaged, and the apoptosis rate increased. In the microstructure, mitochondria were swollen and deformed, and ALDH2 deficiency aggravated these changes. The NF-κB pathway and IL-17 pathway were significantly enriched in ALDH2-/- mice compared with WT mice according to KEGG enrichment analysis of the RNA-seq data. The PCR results showed that the mRNA expression levels of IκBα and IL-17B, C, D, E, and F were significantly higher than those in the WT-IR group. Western blot verification results showed that ALHD2 knockdown resulted in increased phosphorylation of IκBα, increased phosphorylation of NF-κB, and increased expression of IL-17C. When we used ALDH2 agonists, the number of lesions and the expression levels of the corresponding proteins were reduced. Knockdown of ALDH2 in HK-2 cells resulted in a higher proportion of apoptotic cells after hypoxia and reoxygenation, but inhibiting the phosphorylation of NF-κB prevented the increase in apoptosis and reduced the protein expression level of IL-17C. Conclusion. ALDH2 deficiency can lead to the aggravation of kidney ischemia–reperfusion injury. RNA-seq analysis and validation by PCR and western blotting revealed that this effect may be due to the promotion of IκBα/NF-κB p65 phosphorylation during ischemia–reperfusion caused by ALDH2 deficiency, which then leads to an increase in inflammatory factors, including IL-17C. Thus, cell death is promoted, and kidney IRI is eventually aggravated. We link ALDH2 deficiency with inflammation, revealing a new idea for ALDH2-related research.

The bolt loosening detection method has been paid attention by engineering and academic scholars. The presented methods only focus on the identification of the bolt based on deep learning, and the problem of bolt localization and the influence of shadow on distortion correction is seldom studied. In this paper, a bolt self-localization method based on YOLOv4 deep learning algorithm is proposed. A bolt numbering rule is established and the deep learning is introduced to identify the number and locate the bolt. A new square bolt gasket is proposed and four corner points are used for distortion correction. In order to reduce the influence of shadows, a grayscale enhancement strategy is proposed to improve the correction stability. Finally, a laboratory flange joint is used to verify the proposed method. The results show that the bolt self-localization method is feasible and the new bolt gasket can effectively improve the stability of distortion correction and bolt loosening detection.