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In this paper, we study the non-fragile (Here, the term “non-fragile” refers to robustness against controller perturbations) robust stabilization problem for discrete time-delay switched systems with memory feedback and actuator saturation. Our objective is to design a switching law and a non-fragile state feedback control law with memory such that the closed-loop system is asymptotically stable at the origin with a large domain of attraction. Via the switched Lyapunov functional approach, sufficient conditions for non-fragile robust stabilization are derived. If some scalars parameters are selected in advance, we present the non-fragile state feedback control law with memory and maximizing the estimated region of attraction by solving a convex optimization problem with LMI constraints. Furthermore, the numerical example is given to verify the effectiveness of the proposed method by comparing the state response or the size of estimation of domain of attraction under the action of the state feedback control law with memory and the memoryless controller.

Abstract Context Iron overload is a known risk factor for type 2 diabetes (T2D); however, iron overload and iron deficiency have both been associated with metabolic disorders in observational studies. Objective Using mendelian randomization (MR), we assessed how genetically predicted systemic iron status affected T2D risk. Methods A 2-sample MR analysis was used to obtain a causal estimate. We selected genetic variants strongly associated (P < 5 × 10−8) with 4 biomarkers of systemic iron status from a study involving 48 972 individuals performed by the Genetics of Iron Status consortium and applied these biomarkers to the T2D case-control study (74 124 cases and 824 006 controls) performed by the Diabetes Genetics Replication and Meta-analysis consortium. The simple median, weighted median, MR-Egger, MR analysis using mixture-model, weighted allele scores, and MR based on a Bayesian model averaging approaches were used for the sensitivity analysis. Results Genetically instrumented serum iron (odds ratio [OR]: 1.07; 95% CI, 1.02-1.12), ferritin (OR: 1.19; 95% CI, 1.08-1.32), and transferrin saturation (OR: 1.06; 95% CI, 1.02-1.09) were positively associated with T2D. In contrast, genetically instrumented transferrin, a marker of reduced iron status, was inversely associated with T2D (OR: 0.91; 95% CI, 0.87-0.96). Conclusion Genetic evidence supports a causal link between increased systemic iron status and increased T2D risk. Further studies involving various ethnic backgrounds based on individual-level data and studies regarding the underlying mechanism are warranted for reducing the risk of T2D.

Background Acute spinal cord injury (SCI) could cause mainly two types of pathological sequelae, the primary mechanical injury, and the secondary injury. The macrophage in SCI are skewed toward the M1 phenotype that might cause the failure to post-SCI repair. Methods SCI model was established in Balb/c mice, and the changes in macrophage phenotypes after SCI were monitored. Bioinformatic analyses were performed to select factors that might regulate macrophage polarization after SCI. Mouse bone marrow-derived macrophages (BMDMs) were isolated, identified, and induced for M1 or M2 polarization; the effects of lncRNA guanylate binding protein-9 (lncGBP9) and suppressor of cytokine signaling 3 (SOCS3) on macrophages polarization were examined in vitro and in vivo. The predicted miR-34a binding to lncGBP9 and SOCS3 was validated; the dynamic effects of lncGBP9 and miR-34a on SOCS3, signal transducer and activator of transcription 1 (STAT1)/STAT6 signaling, and macrophage polarization were examined. Finally, we investigated whether STAT6 could bind the miR-34a promoter to activate its transcription. Results In SCI Balb/c mice, macrophage skewing toward M1 phenotypes was observed after SCI. In M1 macrophages, lncGBP9 silencing significantly decreased p-STAT1 and SOCS3 expression and protein levels, as well as the production of Interleukin (IL)-6 and IL-12; in M2 macrophages, lncGBP9 overexpression increased SOCS3 mRNA expression and protein levels while suppressed p-STAT6 levels and the production of IL-10 and transforming growth factor-beta 1 (TGF-β1), indicating that lncGBP9 overexpression promotes the M1 polarization of macrophages. In lncGBP9-silenced SCI mice, the M2 polarization was promoted on day 28 after the operation, further indicating that lncGBP9 silencing revised the predominance of M1 phenotype at the late stage of secondary injury after SCI, therefore improving the repair after SCI. IncGBP9 competed with SOCS3 for miR-34a binding to counteract miR-34a-mediated suppression on SOCS3 and then modulated STAT1/STAT6 signaling and the polarization of macrophages. STAT6 bound the promoter of miR-34a to activate its transcription. Conclusions In macrophages, lncGBP9 sponges miR-34a to rescue SOCS3 expression, therefore modulating macrophage polarization through STAT1/STAT6 signaling. STAT6 bound the promoter of miR-34a to activate its transcription, thus forming two different regulatory loops to modulate the phenotype of macrophages after SCI.

Zirconia (ZrO2) is a ceramic material with high-temperature resistance and good insulating properties. Herein, for the first time, the surface of ZrO2 was modified with docosanoic acid (DCA) to improve its self-cleaning and hydrophobic properties. This surface modification transformed the surface of ZrO2 from hydrophilic to superhydrophobic. A two-step spraying method was used to prepare the superhydrophobic surface of ZrO2 by sequentially applying a primer and a topcoat. The primer was a solution configured using an epoxy resin as the adhesive and polyamide as the curing agent, while the topcoat was a modified ZrO2 solution. The superhydrophobic surface of ZrO2 exhibited a contact angle of 154° and a sliding angle of 4°. Scanning electron microscopy, X-ray diffraction, energy-dispersive X-ray spectroscopy, thermogravimetric analysis, and other analytical techniques were used to characterize the prepared zirconia particles and their surfaces. Moreover, results from surface self-cleaning and droplet freezing tests showed that DCA-modified ZrO2 can be well combined, and its coatings show good self-cleaning and anti-icing properties on TA2 bases.

Background N 4 -acetylcytidine (ac 4 C) as a significant RNA modification has been reported to maintain the stability of mRNA and to regulate the translation process. However, the roles of both ac 4 C and its ‘writer’ protein N-acetyltransferase 10 (NAT10) played in the disease especially colorectal cancer (CRC) are unclear. At this point, we discover the underlying mechanism of NAT10 modulating the progression of CRC via mRNA ac 4 C modification. Methods The clinical significance of NAT10 was explored based on the TCGA and GEO data sets and the 80 CRC patients cohort of our hospital. qRT-PCR, dot blot, WB, and IHC were performed to detect the level of NAT10 and ac 4 C modification in CRC tissues and matched adjacent tissues. CCK-8, colony formation, transwell assay, mouse xenograft, and other in vivo and in vitro experiments were conducted to probe the biological functions of NAT10. The potential mechanisms of NAT10 in CRC were clarified by RNA-seq, RIP-seq, acRIP-seq, luciferase reporter assays, etc. Results The levels of NAT10 and ac 4 C modification were significantly upregulated. Also, the high expression of NAT10 had important clinical values like poor prognosis, lymph node metastasis, distant metastasis, etc. Furthermore, the in vitro experiments showed that NAT10 could inhibit apoptosis and enhance the proliferation, migration, and invasion of CRC cells and also arrest them in the G2/M phase. The in vivo experiments discovered that NAT10 could promote tumor growth and liver/lung metastasis. In terms of mechanism, NAT10 could mediate the stability of KIF23 mRNA by binding to its mRNA 3’UTR region and up-regulating its mRNA ac 4 c modification. And then the protein level of KIF23 was elevated to activate the Wnt/β-catenin pathway and more β-catenin was transported into the nucleus which led to the CRC progression. Besides, the inhibitor of NAT10, remodelin, was applied in vitro and vivo which showed an inhibitory effect on the CRC cells. Conclusions NAT10 promotes the CRC progression through the NAT10/KIF23/GSK-3β/β-catenin axis and its expression is mediated by GSK-3β which forms a feedback loop. Our findings provide a potential prognosis or therapeutic target for CRC and remodelin deserves more attention. Graphical Abstract

Background Pulmonary mucous gland adenoma (MGA) is an exceptionally rare benign tumor. Even with the assistance of 18 F-FDG PET/CT, the accurate diagnosis of MGA as lung cancer remains challenging. Only one case of fluorodeoxyglucose(FDG)-avid pulmonary mucous gland adenoma and two case of low FDG uptake pulmonary mucous gland adenoma have been reported in English literature, while a single case of moderately increased FDG uptake pulmonary mucous gland adenoma has been documented in French literature. To minimize misdiagnosis and select appropriate treatment strategies, it is crucial to comprehensively analyze its 18 F-FDG PET/CT manifestations in conjunction with clinical symptoms and pathological findings. Case presentation In our study, we present a case involving a 70-year-old woman with clinical manifestations of persistent cough and sputum with an FDG-avid mucous gland adenoma mimicking lung cancer on 18 F-FDG PET/CT imaging. Ultimately, the patient underwent a potentially unnecessary video-assisted thoracoscopic lobectomy, and the pathological diagnosis was determined to be MGA. The patient was discharged and remained clinically well without any complaints for a period of 6 months. Conclusions The use of 18 F-FDG PET/CT lacks specificity in detecting MGA and may lead to misdiagnosis as a lung malignancy. A comprehensive analysis combining clinical manifestations, bronchoscopy findings, imaging results, and pathological findings is essential for accurate identification of pulmonary mucus gland adenoma.

Myocardial ischemia is a high-risk disease among middle-aged and senior individuals. After thrombolytic therapy, heart tissue can potentially suffer further damage, which is called myocardial ischemia-reperfusion injury (MIRI). At present, the treatment methods and drugs for MIRI are scarce and cannot meet the current clinical needs. The mechanism of MIRI involves the interaction of multiple factors, and the current research hotspots mainly include oxidative stress, inflammation, calcium overload, energy metabolism disorders, pyroptosis, and ferroptosis. Traditional Chinese medicine (TCM) has multiple targets and few toxic side effects; clinical preparations containing Panax ginseng C. A. Mey., Panax notoginseng (Burk.) F. H. Chen, Aralia chinensis L., cardioprotection, and other Chinese herbal medicines have been used to treat patients with coronary heart disease, angina pectoris, and other cardiovascular diseases. Studies have shown that saponins are the main active substances in TCMs containing Panax ginseng C. A. Mey., Panax notoginseng (Burk.) F. H. Chen, Aralia chinensis L., and Radix astragali . In the present review, we sorted the saponin components with anti-MIRI effects and their regulatory mechanisms. Each saponin can play a cardioprotective role via multiple mechanisms, and the signaling pathways involved in different saponins are not the same. We found that more active saponins in Panax ginseng C. A. Mey. are mainly dammar-type structures and have a strong regulatory effect on energy metabolism. The highly active saponin components of Aralia chinensis L. are oleanolic acid structures, which have significant regulatory effects on calcium homeostasis. Therefore, saponins in Chinese herbal medicine provide a broad application prospect for the development of highly effective and low-toxicity anti-MIRI drugs.

Triboelectric nanogenerators (TENGs) are an emerging technology capable of converting the ambient mechanical energy into electricity, promising for complete utilization of the distributed energy to improve the quality of human life. However, realizing material innovation for good trade‐off between the high triboelectric output and environment friendliness remains huge challenge, but it is of great importance for sustainable development of TENGs. Cellulose is a typical natural polymer that promises to address the challenge. Herein, the sustainable TENGs that originate from cellulose and potentially back to the natural world are focused on, realizing on‐spot TENGs. First, the sources, forms, morphologies, structures, and modifications of cellulose are systematically summarized, indicating the commercial and noncommercial cellulose materials’ potential for TENGs’ application. Second, the dominating additive properties of cellulose such as hydrophobicity, self‐cleaning, corrosion resistance, optical transparency, electrical conductivity, and degradability are introduced, which can effectively steer the development of TENGs. Thereafter, the TENGs with tailorable functions enabled by less‐refined cellulose and various physical/chemical modified cellulose are reviewed, as well as plants‐supported on‐spot TENGs with environment adaptivity and transient property, embracing a sustainable future of versatile cellulose to adapt the distributed network of multiscenario TENGs for energy management and information communication. A recyclable concept of cellulose‐based triboelectric nanogenerators (TENGs) that originates from plants and returns to the plants is proposed for sustainable development of TENGs. The importance of the one‐to‐one correspondence between property requirement of TENGs and matchable performance of cellulose derivatives are indicated, inspiring researchers to exploit cellulose with diversity and ingenuity for future on‐spot and on‐demand TENGs with environment‐adaptivity.

Background Chemotherapy resistance is a major challenge in the treatment of intermediate and advanced gastric cancer (GC). This study aimed to recognize oxaliplatin resistance-related genes (OXARGs) in GC and to explore their role and mechanism in oxaliplatin resistance of GC. Methods OXARGs with prognostic value in GC were analyzed using GC oxaliplatin resistance data from the GEO and TCGA databases. RT-qPCR and WB assay were applied to verify the expression of MT2A, NOTCH1 and SLC7A5 in oxaliplatin-resistant GC cells (HGC27R and MKN45R). The effect of SLC7A5 on the malignant phenotype of oxaliplatin-resistant GC cells was verified by CCK-8, EDU, TUNEL, colony formation, wound healing, transwell assay, tumor bearing experiments and WB assay. Results Bioinformatics analysis and experimental validation indicate that SLC7A5 was a target for oxaliplatin-resistance in GC. Knockdown of SLC7A5 obviously decreased the viability, migration, and invasion of oxaliplatin-resistant GC cells in vitro and tumor growth in vivo. It also increased the apoptosis levels and BAX expression, and reduced the expression of BCL2, MMP 2 and MMP9. Additionally, the knockdown of SLC7A5 enhanced the sensitivity of oxaliplatin-resistant GC cells to oxaliplatin both in vitro and in vivo. Furthermore, knockdown of SLC7A5 downregulated the expression of HK2, LDHA, Glut1, and PDK1 both in vivo and in vitro, leading to increased extracellular glucose levels and decreased lactate levels. However, glutathione significantly attenuated the regulatory effect of SLC7A5 knockdown on the malignant phenotype of oxaliplatin-resistant GC cells. Trial registration Not Applicable. Conclusion Knockdown of SLC7A5 inhibits malignant progression and attenuates oxaliplatin resistance in GC by suppressing glycolysis.

Aiming at the fault diagnosis accuracy of rolling bearings is not high enough, and unknown faults cannot be correctly identified. A priority elimination (PE) method is proposed in this paper. First, the priority diagnosis sequence of faults was determined by comparing the ratios of the inter-class distance to the intra-class distance for all faults. Then, the model training and fault diagnosis were carried out in order of the priority sequence, and the samples of the fault that had been identified were eliminated from the data set until all faults were diagnosed. For the diagnosis model, the stacked sparse auto-encoder network (SSAE) was selected to extract the features of the vibration signal. The extreme gradient boosting algorithm (XGBoost) was chosen to identify the fault type. Finally, the method was tested and verified by experimental data and compared with classical algorithms. Research results indicate the following: (1) with the addition of PE based on SSAE-XGBoost, the fault diagnosis accuracy can be improved from 96.3% to 99.27%, which is higher than other methods; (2) for the test set with the samples of unknown faults, the diagnosis accuracy of SSAE-XGBoost with PE can reach 92.34%, which is nearly 6% higher than that without PE and is also obviously higher than other classical fault diagnosis methods with or without PE. The PE method can not only improve the diagnosis accuracy of faults but also identify unknown faults, which provides a new method and way for fault diagnosis.