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Abstract. Background:. Long non-coding RNAs (lncRNAs) plays an important role in the progression of gastric cancer (GC). Their involvement ranges from genetic regulation to cancer progression. However, the mechanistic roles of RP11-789C1.1 in GC are not fully understood. Methods:. We identified the expression of lncRNA RP11-789C1.1 in GC tissues and cell lines by real-time fluorescent quantitative polymerase chain reaction. A series of functional experiments revealed the effect of RP11-789C1.1 on the proliferation of GC cells. In vivo experiments verified the effect of RP11-789C1.1 on the biological behavior of a GC cell line. RNA pull-down unveiled RP11-789C1.1 interacting proteins. Western blot analysis indicated the downstream pathway changes of RP11-789C1.1, and an oxaliplatin dosing experiment disclosed the influence of RP11-789C1.1 on the drug sensitivity of oxaliplatin. Results:. Our results demonstrated that RP11-789C1.1 inhibited the proliferation of GC cells and promoted the apoptosis of GC cells. Mechanistically, RP11-789C1.1 inhibited checkpoint kinase 1 (CHK1) phosphorylation by binding ataxia-telangiectasia mutated and Rad3 related (ATR), a serine/threonine-specific protein kinase, promoted GC apoptosis, and mediated oxaliplatin sensitivity. Conclusion:. In general, we discovered a tumor suppressor molecule RP11-789C1.1 and confirmed its mechanism of action, providing a theoretical basis for targeted GC therapy.

Abstract Background Circular RNAs (circRNAs) have been proved to play crucial roles in the development of various cancers. However, the molecular mechanism of circGLIS3 involved in gastric cancer (GC) tumorigenesis has not been elucidated. Methods The higher expression level of circGLIS3 was identified in GC through RNA sequencing and subsequent tissue verification using Quantitative real-time PCR (qRT-PCR). A series of functional experiments in vitro and in vivo were performed to evaluated the effects of circGLIS3 on tumor growth and metastasis in GC. The interaction and regulation of circGLIS3/miR-1343-3p/PGK1 axis was confirmed by RNA pulldown, western blot, and rescue experiments. RIP and western blot were performed to demonstrate the role of circGLIS3 in regulating phosphorylation of VIMENTIN. We then used qRT-PCR and co culture system to trace circGLIS3 transmission via exosomal communication and identify the effect of exosomal circGLIS3 on gastric cancer and macrophages. Finally, RIP experiments were used to determine that EIF4A3 regulates circGLIS3 expression. Results CircGLIS3(hsa_circ_0002874) was significantly upregulated in GC tissues and high circGLIS3 expression was associated with advanced TNM stage and lymph node metastasis in GC patients. We discovered that overexpression of circGLIS3 promoted GC cell proliferation, migration, invasion in vitro and in vivo, while suppression of circGLIS3 exhibited the opposite effect. Mechanistically, circGLIS3 could sponge miR-1343-3p and up-regulate the expression of PGK1 to promote GC tumorigenesis. We also found that circGLIS3 reduced the phosphorylation of VIMENTIN at ser 83 site by binding with VIMENTIN. Moreover, it was proven that exosomal circGLIS3 could promote gastric cancer metastasis and the M2 type polarization of macrophages. In the final step, the mechanism of EIF4A3 regulating the generation of circGLIS3 was determined. Conclusion Our findings demonstrate that circGLIS3 promotes GC progression through sponging miR-1343-3p and regulating VIMENTIN phosphorylation. CircGLIS3 is a potential therapeutic target for GC patients.

To make news communication better adapt to the era of big data, it is necessary to innovate news communication. Accordingly, this paper constructs a big data analysis platform for news communication innovation methods based on the regression analysis model in big data analysis, determines the parameters and coefficients of the regression model with the help of the maximum likelihood estimation method, and determines the form of the regression model. Based on the platform, the main paths of news communication innovation are analyzed, standardized regression coefficients are calculated, and the main methods of news communication innovation are changing news communication forms and news communication media. To verify that the above methods can make news communication innovative, we designed a visualization information platform to change the news communication format and launched a simulation experiment to analyze the effect of news communication under different media. The results showed that after the visualization of the news communication format, the number of viewers of news programs increased from 2.45 million to 3.65 million, an increase of 1.2 million. The conversion rate of audience behavior of news programs increased from the original 63% to 87%, an increase of 24%. From the above results, it is clear that news communication under the big data approach has improved from a theoretical definition to an operational route.

Per‐ and polyfluoroalkyl substances (PFAS) pose significant environmental and health risks due to their ubiquitous presence and persistence in water systems. Herein, the efficacy of piezocatalysis using barium titanate nanoparticles under ultrasound irradiation for the degradation and defluorination of perfluorooctane sulfonate (PFOS) in water is investigated. The research demonstrates a substantial 90.5% degradation and 29% defluorination of PFOS after 6 h of treatment, highlighting the potential of piezocatalysis as a promising approach for PFAS degradation. Additionally, the quantification of degradation products elucidates the transformation pathways of PFOS, suggesting a stepwise chain‐shortening mechanism. The findings underscore the importance of continued research in optimizing piezocatalytic processes and exploring synergistic approaches with other advanced oxidation methods to effectively address PFAS contamination challenges. These efforts are essential for advancing sustainable water treatment strategies and mitigating the environmental and health hazards associated with PFAS contamination. [ABSTRACT FROM AUTHOR]

Covalent Organic Frameworks (COFs) emerged as versatile materials with promising potential in biomedicine. Their customizable functionalities and tunable pore structures make them valuable for various biomedical applications such as biosensing, bioimaging, antimicrobial activity, and targeted drug delivery. Despite efforts made to create nanoscale COFs (nCOFs) to enhance their interaction with biological systems, a comprehensive understanding of their inherent biological activities remains a significant challenge. In this study, a thorough investigation is conducted into the biocompatibility and anti‐neoplastic properties of two distinct imine‐based nCOFs. The approach involved an in‐depth analysis of these nCOFs through in vitro experiments with various cell types and in vivo assessments using murine models. These findings revealed significant cytotoxic effects on tumor cells. Moreover, the activation of multiple cellular death pathways, including apoptosis, necroptosis, and ferroptosis is determined, supported by evidence at the molecular level. In vivo evaluations exhibited marked inhibition of tumor growth, associated with the elevated spontaneous accumulation of nCOFs in tumor tissues and the modulation of cell death‐related protein expression. The research contributes to developing a roadmap for the characterization of the intricate interactions between nCOFs and biological systems and opens new avenues for exploiting their therapeutic potential in advanced biomedical applications. [ABSTRACT FROM AUTHOR]

The role of glial scars in the pathophysiology of spinal cord injury (SCI) is widely recognized, as they pose physical barriers against axonal regeneration and persistent chronic inflammation by releasing cytotoxic agents, thereby impeding nerve repair. Consequently, preventing glial scarring has emerged as an important therapeutic objective in SCI management. Following SCI, astrocytes undergo a phenotypic transition into scar‐forming astrocytes, which critically depends on the activation of inflammatory responses and the integrin‐N‐cadherin pathway. To explore improved SCI treatment, a nano‐antagonist hydrogel (Nano‐ant Gel), comprising N‐cadherin nano‐antagonists and a polyphenol hydrogel designed to inhibit glial scarring by mitigating inflammatory response and modulating astrocyte behavior, thereby facilitating spinal cord‐injury repair, is developed and characterized. The hydrogel exhibits notable anti‐inflammatory properties, specific calcium ion‐adsorption capabilities, and antagonistic effects against N‐cadherin, effectively impeding the formation and aggregation of scar‐forming astrocytes. Its efficacy is comprehensively assessed using a model of contusive SCI, with which it effectively inhibits glial scar formation and promotes axonal regeneration. Notably, the Nano‐ant Gel significantly improves the locomotor functions of mice with SCI, suggesting that it represents a promising approach for treating the condition. [ABSTRACT FROM AUTHOR]

Background Pregnant women with chronic hepatitis B (CHB) exhibit unique clinical features in terms of postpartum immune system reconstitution and recovery from pregnancy-related changes. However, current studies focus primarily on the outcomes of maternal–infant transmission and postpartum hepatitis flares. We aimed to evaluate the profiles of hepatitis B core-related antigen (HBcrAg) and pregenomic RNA (pgRNA) in pregnant women with CHB. Methods This retrospective analysis included treatment-naïve pregnant women with CHB who were followed up regularly in an outpatient clinic from 2014 to 2021. Baseline HBcrAg and pgRNA levels were compared in patients with different disease phases. Changes in these parameters were examined in a subset of patients receiving antiviral prophylaxis. HBcrAg and pgRNA levels were measured before treatment, at 32 weeks of gestation, and postpartum. Results The final analysis included a total of 121 patients, 100 of whom were hepatitis B e antigen (HBeAg)–positive (96 and 4 in the immune-tolerant and -indeterminate phases, respectively) and 21 of whom were HBeAg-negative (6 and 15 in the immune-active and -inactive carrier phases, respectively). The HBeAg-negative group vs the HBeAg-positive group had lower levels of baseline HBcrAg (median [interquartile range {IQR}], 3.7 [3.0–5.9] vs 8.6 [8.4–8.7] log10 U/mL; P <.01) and pgRNA (median [IQR], 0.0 [0.0–2.5] vs 7.8 [7.6–8.1] log10 copies/mL; P <.01). The serum levels of HBcrAg and pgRNA were highest in immune-tolerant carriers and lowest in immune-inactive carriers. In HBeAg-positive patients, the correlation coefficients of HBcrAg and pgRNA with hepatitis B virus (HBV) DNA were 0.40 and 0.43, respectively; in HBeAg-negative patients, they were 0.53 and 0.51, respectively (all P <.05). The correlation coefficients with hepatitis B surface antigen (HBsAg) were 0.55 and 0.52 (P <.05) in HBeAg-positive patients, respectively, while in HBeAg-negative patients they were 0.42 and 0.37, respectively (P >.05). Among 96 patients receiving antiviral prophylaxis, we detected a rapid decrease in HBV DNA to an undetectable level during treatment but relatively stable levels of pgRNA and HBcrAg. Conclusions HBcrAg and pgRNA levels are lower in HBeAg-negative patients than in HBeAg-positive patients. These 2 markers are significantly associated with HBV DNA irrespective of HBeAg status, while they are significantly associated with HBsAg only in HBeAg-positive patients. [ABSTRACT FROM AUTHOR]

Ensuring the solution feasibility and achieving an acceptable solution time for the non-deterministic polynomial-time hard (NP-hard) problem of heat exchanger network (HEN) synthesis is still challenging. In this study, we developed a novel optimization framework for efficiently solving large-scale HEN synthesis problems to obtain near global optimal solutions, simultaneously addressing the solution's infeasibility and time. The optimization framework consists of a multiple initial HEN design model (M-INI model), a new distance-based auto structure transformer (A-STR transformer), and a reduced non-linear programming model (R-NLP model). The M-INI model generates various HEN designs based on pinch analysis by varying the minimum approach temperature and the modes of stream splitting and mixing. The A-STR transformer is first proposed to automatically convert various HEN designs into associated superstructure-based topologies as multiple initial starting points for accelerating the solution of the R-NLP model. A strategy for approximating the temperature difference calculation is further applied to reduce the computational loads. Four case studies were conducted using the proposed method to minimize the total annual cost (TAC). The solutions of general cases 1 and 2 are almost equal to the best results in the literature, while the solution time is reduced by 98.7 % and 99.8 %, respectively, which demonstrates the performance of the proposed method. Especially, the method was applied to two practical industrial HEN cases: a large-scale low-grade heat recovery system and a crude distillation unit. The results of large-scale case 3 show that the optimal solution near the global optimal solution only requires 251.7 s. Case 4 includes pre-splitting in scenario A and free splitting in scenario B. Compared to scenario A, the TAC and solution time in scenario B were reduced by 33.9 % and 93.1 %, indicating that the pre-splitting strategy excludes the optimal from the search space. The proposed novel optimization framework demonstrates the efficiency and applicability of handling large-scale HEN synthesis problems. It can also guide engineers in the design of a large-scale HEN with lower costs and effort. [Display omitted] • A novel optimization framework is presented to accelerate complex HEN synthesis. • An R-NLP model is formulated to reduce the integer variables in HEN synthesis. • An approximation strategy is introduced for calculating temperature differences. • A transformer is proposed to convert initial HEN flowsheets into superstructures. • Two industrial HEN cases are fully investigated and solved less than 252 s. [ABSTRACT FROM AUTHOR]

Sleep disorders, a common concern in modern society, seriously affect people's physical and mental health. Reported findings suggest that both acute exercise intervention and long-term regular exercise intervention can improve the disrupted sleep structure and normalize the duration and proportion of the different phases of sleep. Moreover, exercise intervention has a positive effect on the endocrine functions, the metabolic functions, the immune response, the autonomic nervous system, and cardiac functions during sleep. It is a non-medicative therapeutic strategy for improving sleep disorders. The specific type of exercise intervention (aerobic exercise, resistance exercise, or meditative movement) adopted is one of the moderating variables of exercise intervention programs. Different types of exercise improve sleep disorders by way of different mechanisms. Exercise volume and intensity are another moderating variable of exercise intervention programs. The optimal amount and intensity of exercise for different individuals to improve sleep disorders may vary. Exercise interventions implemented at the different times throughout a day can also have varying degrees of impact on sleep disorders and there is no consensus on the optimal exercise time for improving sleep quality at present. Herein, we summarized the mechanisms by which exercise intervention improves sleep disorders from four perspectives, including epigenetics, hyperarousal, human circadian rhythm, and body temperature regulation. In addition, we discussed the current gaps and prospects of research in this field, aiming to provide a theoretical basis for the development of exercise prescriptions for sleep disorders., Competing Interests: 利益冲突　所有作者均声明不存在利益冲突, (© 2024《四川大学学报（医学版）》编辑部 版权所有Copyright ©2024 Editorial Board of Journal of Sichuan University (Medical Sciences).)

Objective: This study aimed to evaluate the expression of genes involved in cholesterol metabolism and establish their association with oxidative stress (OS)., Methods: We employed an in vitro experimental design and cells were divided into six groups: C (control), CH (HepG2 + H2O2), CHN (HepG2 + H2O2 + NAC), F (FFA-treated HepG2), FH (FFA-treated HepG2 + H2O2), and FHN (FFA-treated HepG2 + H2O2 + NAC). Cell viability was assessed using the MTT assay, while successful FFA model establishment was confirmed via Oil Red staining and absorbance. Oxidative stress injury was gauged by measuring ROS, SOD activity, and MDA content. RNA transcription and protein expression of cholesterol-related (DHCR24, DHCR7) and oxidative stress-related (NFE2L2, HMOX1) genes were also examined via RT-qPCR and WB., Results: The impact of H2O2 on cell viability exhibited a time-dose-dependent pattern, paralleling the changes in reactive oxygen species (ROS) levels. Compared to the C group, FFA treatment led to an increase in Oil Red absorption and MDA content and decreased SOD activity. However, it did not result in a significant reduction in cell viability. The FH group exhibited reduced cell viability and SOD activity, along with a further elevation in MDA content compared to the F group. Furthermore, the increased SOD activity and decreased MDA content observed in the CH group were effectively reversed following NAC treatment. Such a reversal was not evident between the FHN and FH groups. Compared to the control group, genes associated with cholesterol metabolism and oxidative stress (OS) displayed heightened expression levels in the other treatment groups, with the FHN group showing lower expression levels than the FH group. Notably, changes in the protein expressions of DHCR24, DHCR7, NFE2L2, and HMOX1 were consistent and exhibited correlations., Conclusions: Cholesterol metabolism emerges as a potential mechanism underlying H2O2-induced oxidative stress injury in HepG2 cells treated with FFA.