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In order to develop a high stability slow-release solid chlorine dioxide preservative for fresh-cut broccoli preservation, sodium chlorite was used as the main material, tartaric acid was used as activator, sodium carboxymethyl cellulose, polyacrylamide and sodium bicarbonate were used as slow-release agents, sodium chloride and calcium chloride were used as stabilizers. And the formula of preservative were optimized by single factors combined with orthogonal test. The results showed that the optimal mass ratio of chlorine dioxide slow-release preservative was sodium chlorite:tartaric acid:sodium bicarbonate:sodium chloride:calcium chloride:sodium carboxymethyl cellulose:polyacrylamide=2:3:1:1:0.6:2.5:0.4, and the slow-release time of chlorine dioxide gas was up to 15 d. The preservative effectively delayed the yellowing of fresh-cut broccoli, maintained higher hardness, soluble solids and chlorophyll content, significantly (P

Abstract Lung adenocarcinoma is the main type of lung cancer in women. Our previous findings have evidenced that 25-hydroxycholesterol (25-HC) promotes migration and invasion of lung adenocarcinoma cells (LAC), during which LXR as a 25-HC receptor plays an important role. Estrogen receptor beta (ERβ) is a receptor of 27-hydroxycholesterol that is structurally analogous to 25-HC, but its role in the functional actions of 25-HC remained largely unknown. In this study, we demonstrated that 25-HC treatment triggered ERβ expression in LAC. Knockdown of ERβ inhibited 25-HC-mediated proliferation, migration and invasion, and reduced 25-HC-induced LAC metastasis in vivo. Further investigation revealed that ERβ knockdown restrained the expression of TNFRSF17 (BCMA). In vivo experiments also confirmed that ERβ knockdown blocked 25-HC-induced TNFRSF17 expression. TNFRSF17 knockdown also restrained 25-HC-induced proliferation, migration and invasion. Bioinformatic analysis showed that the levels of ERβ and TNFRSF17 were elevated in lung adenocarcinoma, and were closely related to tumor stages and nodal metastasis status. These results suggested that 25-HC promoted the proliferation and metastasis of LAC by regulating ERβ/TNFRSF17 axis.

Mountain bridges and highways frequently implement shed structures to guard against rolling stone disasters. Due to the random and variable nature of the angle at which stones impact sheds, bedding material is often easily displaced, leading to a wider range of potential damages. In this paper, we analyze the effectiveness of varying grades of shed bedding material when struck by rolling stones at different angles. We also examine the mechanism of the microscopic force chains involved in this process through the use of numerical simulations and physical testing.In this paper, numerical simulation and physical tests are carried out to analyze the shovel scraping effect and plowing effect of rolling stone on bedding layer, the energy dissipation effect of bedding material ，and the internal force chain dispersion transfer law, so as to provide a reference for the design of bedding layer of shanty holes. The results show that: (1) with the increase of impact angle, the impact force of the bedding layer under the same level of proportion increases, but the kinetic energy of the rolling stone is smaller, the fine particle group can reduce the kinetic energy of the rolling stone to the minimum at the earliest time, and the medium particle group can buffer the kinetic energy of the rolling stone to the minimum after the end of the impact process so that we can consider mixing the ratio of the fine particle group and the medium particle group to reach the optimal combination of energy dissipation. (2) 60° for the most unfavorable impact angle, impact angle on the depth of shovel scraping and plowing height of the influence of the trend line fitting formula for y = ax2 + bx + c, which coefficients a, b, c with the particle size; impact angle is larger, the bedding is shovel scraped the smaller the area, but the roof of the hole will be the greater the peak force. (3) Rolling stone initial impact bedding stage, the lower part of the force chain network rapid formation and stress, but the force chain network then quickly extends to the front end, the stress value becomes smaller; the smaller the particle size of the bedding layer, and the larger the coordination number, that is, the better the degree of contact, the larger the particle size of the bedding layer shoveling effect is not obvious, and the force chain is more solid and not easy to rupture.

To reduce the impact of mountain rockfall on the shed tunnel, cushion buffering materials were designed as protective measures. The optimized design can improve the impact energy of rockfall by effectively dissipating it. In the present study, numerical simulation of the impact dynamics of three granular materials (spherical, cylindrical, and square) was investigated by the discrete element method. Particularly, this article discussed how particle shape and V0 (initial impact velocity) affect impact pressure, kinetic energy, friction mobilization, force chain evolution, distribution, transmission efficiency, and anisotropy of granular materials. The results showed that among these three different shapes of granular materials, the spherical granular material had the best cushioning capacity. The sensitivity of impact pressure to particle shape depends on V0, whether or not above Vc (critical initial impact velocity). Besides, as V0 increases, the probability distribution function of the weak contact force is smaller, while the strong contact force is larger, and the decreases exponentially with the increase of force. Furthermore, the transmission capacity of the primary force chain is the best, while secondary force chain transmission is the largest force,Under low velocity impact, the sharper the particle surface, the stronger the spatial negative correlation of the force chain, which increases the spatial normal force and normal relationship of the force chain structure, and thus the stronger the force.

Polysaccharide is one of the most important active ingredients of edible fungi, which is composed of diverse monosaccharide. Polysaccharide has various biological activities such as antioxidant, antitumor and immune regulation. Therefore, it has been widely used as additive in functional foods. In recent years, more and more researches have been conducted on edible fungal polysaccharides, including the structure analysis, extraction process, conventional fermentation process, biosynthesis and biological activity. In this paper, the monosaccharide composition, molecular weight and glycosidic bond connection methods of several common edible fungal polysaccharides are reviewed, and the advantages and disadvantages of traditional and new extraction methods are discussed. Afterwards, the current status of edible fungal polysaccharides produced by fermentation in shake flasks and small bioreactor is summarized, and finally the biosynthetic mechanism of polysaccharides and its current research status are summarized. Sorting out, this review could provide a theoretical basis for the research and industrial utilization of fungal polysaccharides.

Abstract Numerous studies have reported the association of long non-coding RNAs (lncRNAs) in cancers, yet the function of lncRNA high expressed in hepatocellular carcinoma (HEIH) in esophageal carcinoma (EC) has seldom been explored. Here, we aimed to explore the mechanism of HEIH on EC via microRNA-185 (miR-185)/kallikrein-related peptidase 5 (KLK5) modulation. Cancer and non-tumoral tissues were collected, in which HEIH, miR-185 and KLK5 expression were detected, as well as their correlations. Also, the relation between the prognosis of EC patients and HEIH/miR-185/KLK5 expression was clarified. EC cells (KYSE-30 and TE-1) were screened for subsequent gain- and loss-of-function assays and their biological functions were further monitored. Tumor volume and weight in EC mice were also measured. Results from this study indicated that HEIH and KLK5 were elevated and miR-185 was declined in EC. The positive correlation was seen in HEIH and KLK5 expression, while the negative correlation was observed in HEIH or KLK5 and miR-185 expression. High HEIH and KLK5 indicated worse prognosis and high miR-185 suggested better prognosis of EC patients. Depleting HEIH or restoring miR-185 suppressed the malignant phenotypes of EC cells, and delayed tumor growth in EC mice. HEIH was found to bind with miR-185 to regulate KLK5 expression. Overexpressing KLK5 alone promoted EC cell progression while up-regulating miR-185 reversed such effects on EC cells. Collectively, we reveal that HEIH depletion dampens EC progression by upregulating miR-185 and downregulating KLK5, which provides novel treatments for EC.

Glycogen branching enzyme (GBE1) is a critical gene that participates in regulating glycogen metabolism. However, the correlations between GBE1 expression and the prognosis and tumor-associated macrophages in lung adenocarcinoma (LUAD) also remain unclear. Herein, we firstly analyzed the expression level of GBE1 in LUAD tissues and adjacent lung tissues via The Cancer Genome Atlas (TCGA) database. The effect of GBE1 on prognosis was estimated by utilizing TCGA database and the PrognoScan database. The relationships between the clinical characteristics and GBE1 expression were evaluated via TCGA database. We then investigated the relationships between GBE1 and infiltration of immune cells in LUAD by utilizing the CIBERSORT algorithm and Tumor Immune Estimation Resource (TIMER) database. In addition, we used a tissue microarray (TMA) containing 92 LUAD tissues and 88 adjacent lung tissues with immunohistochemistry staining to verify the association between GBE1 expression and clinical characteristics, as well as the immune cell infiltrations. We found the expression level of GBE1 was significantly higher in LUAD tissues. High expression of GBE1 was associated with poorer overall survival (OS) in LUAD. In addition, high expression of GBE1 was correlated with advanced T classification, N classification, M classification, TNM stage, and lower grade. Moreover, GBE1 was positively correlated with infiltrating levels of CD163+ tumor-associated macrophages in LUAD. In conclusion, the expression of GBE1 is associated with the prognosis and CD163+ tumor-associated macrophage infiltration in LUAD, suggesting that it has potential to be prognostic and immunological biomarkers in LUAD.

BackgroundCD8+ T cells are one of the central effector cells in the immune microenvironment. CD8+ T cells play a vital role in the development and progression of lung adenocarcinoma (LUAD). This study aimed to explore the key genes related to CD8+ T-cell infiltration in LUAD and to develop a novel prognosis model based on these genes.MethodsWith the use of the LUAD dataset from The Cancer Genome Atlas (TCGA), the differentially expressed genes (DEGs) were analyzed, and a co-expression network was constructed by weighted gene co-expression network analysis (WGCNA). Combined with the CIBERSORT algorithm, the gene module in WGCNA, which was the most significantly correlated with CD8+ T cells, was selected for the subsequent analyses. Key genes were then identified by co-expression network analysis, protein–protein interactions network analysis, and least absolute shrinkage and selection operator (Lasso)-penalized Cox regression analysis. A risk assessment model was built based on these key genes and then validated by the dataset from the Gene Expression Omnibus (GEO) database and multiple fluorescence in situ hybridization experiments of a tissue microarray.ResultsFive key genes (MZT2A, ALG3, ATIC, GPI, and GAPDH) related to prognosis and CD8+ T-cell infiltration were identified, and a risk assessment model was established based on them. We found that the risk score could well predict the prognosis of LUAD, and the risk score was negatively related to CD8+ T-cell infiltration and correlated with the advanced tumor stage. The results of the GEO database and tissue microarray were consistent with those of TCGA. Furthermore, the risk score was higher significantly in tumor tissues than in adjacent lung tissues and was correlated with the advanced tumor stage.ConclusionsThis study may provide a novel risk assessment model for prognosis prediction and a new perspective to explore the mechanism of tumor immune microenvironment related to CD8+ T-cell infiltration in LUAD.

ObjectivesThe study aims to investigate the state anxiety of parents of special needs children during the 2019 coronavirus disease (COVID-19) epidemic and the influence of parental stress, social support, and other related variables on the anxiety of parents.MethodsBespoke questionnaires of children’s and parent’s mental and behavioral problems during the epidemic were used in the study. We also used the State Anxiety Inventory (S-AI), the Parenting Stress Index—Short Form-15 (PSI-SF-15), the NEO Five-Factor Inventory (NEO-FFI), and the Multidimensional Scale of Perceived Social Support (MSPSS). The data used in the study were pooled from an online survey of parents of special needs children and analyzed by one-way analysis of variance (ANOVA) and multiple linear regression.ResultsOverall, 1,451 individuals were included, of which 402 were fathers (27.71%) and 1,049 were mothers (72.29%). ANOVA results showed that educational background, family monthly income, and type of their child’s disability made parents’ state anxiety significantly different. The results of multiple linear regression showed that during the epidemic, social support negatively predicted parents’ state anxiety (B = −0.15, p < 0.001), whereas parenting stress (B = 0.07, p = 0.001) and parental mental and behavioral problems (B = 0.37, p < 0.001) positively predicted parents’ state anxiety.ConclusionsDuring the outbreak of COVID-19, parents of special needs children suffered mental and behavioral problems, together with parenting stress and social support, which influenced their state anxiety. These findings can be used to develop relevant psychological interventions to improve the mental health of vulnerable groups during a pandemic like COVID-19.

Long noncoding RNAs (lncRNAs) have emerged as regulators of gene expression and play critical regulatory roles in diverse biological functions and diseases, including cancer. In this study, we report the downregulation of LINC01089 in non-small cell lung cancer (NSCLC) samples, relative to adjacent non-tumor tissues, and demonstrate its role in the inhibition of proliferation, migration, and epithelial–mesenchymal transition (EMT) of NSCLC cells. Mechanistic analysis indicates that LINC01089 acts as a sponge for miR-27a, regulating its expression in NSCLC. Interestingly, LINC01089 mediated the upregulation of SFRP1 expression by inhibiting the Wnt/β-catenin–EMT pathway and inhibiting the epithelial–mesenchymal transition of NSCLC via sponging miR-27a. Overall, our findings highlight LINC01089’s tumorigenic role and regulatory mechanism in NSCLC, thereby suggesting its potential as a therapeutic target for managing NSCLC.

The soy beverage is a healthy product rich in plant protein; however, its unpleasant flavor affects consumer acceptance. The aim of this study was to determine the feasibility of using Naematelia aurantialba as a strain for the preparation of fermented soybean beverages (FSB). Increases in Zeta potential, particle size, and viscosity make soy beverages more stable. We found that nutrient composition was increased by fermenting N. aurantialba, and the antioxidant activity of soybean beverages significantly increased after 5 days of fermentation. By reducing the content of beany substances such as hexanal and increasing the content of 1-octen-3-ol, the aroma of soybean beverages fermented by N. aurantialba changed from “beany, green, and fatty” to “mushroom and aromatic”. The resulting FSB had reduced bitterness but considerably increased sourness while maintaining the fresh and sweet taste of unfermented soybean beverages (UFSB). This study not only provides a theoretical basis for the market promotion of FSB but also provides a reference for basidiomycetes-fermented beverages.

Abstract Nonalcoholic fatty liver disease (NAFLD) is a serious threat to public health, but its underlying mechanism remains poorly understood. In screening important genes using Gene Importance Calculator (GIC) we developed previously, ribosomal modification protein rimK-like family member A (RIMKLA) was predicted as one essential gene but its functions remained largely unknown. The current study determined the roles of RIMKLA in regulating glucose and lipid metabolism. RIMKLA expression was reduced in livers of human and mouse with NAFLD. Hepatic RIMKLA overexpression ameliorated steatosis and hyperglycemia in obese mice. Hepatocyte-specific RIMKLA knockout aggravated high-fat diet (HFD)-induced dysregulated glucose/lipid metabolism in mice. Mechanistically, RIMKLA is a new protein kinase that phosphorylates betaine-homocysteine S-methyltransferase 1 (BHMT1) at threonine 45 (Thr45) site. Upon phosphorylation at Thr45 and activation, BHMT1 eliminated homocysteine (Hcy) to inhibit the activity of transcription factor activator protein 1 (AP1) and its induction on fatty acid synthase (FASn) and cluster of differentiation 36 (CD36) gene transcriptions, concurrently repressing lipid synthesis and uptake in hepatocytes. Thr45 to alanine (T45A) mutation inactivated BHMT1 to abolish RIMKLA’s repression on Hcy level, AP1 activity, FASn/CD36 expressions, and lipid deposition. BHMT1 overexpression rescued the dysregulated lipid metabolism in RIMKLA-deficient hepatocytes. In summary, RIMKLA is a novel protein kinase that phosphorylates BHMT1 at Thr45 to repress lipid synthesis and uptake. Under obese condition, inhibition of RIMKLA impairs BHMT1 activity to promote hepatic lipid deposition.

Non-small cell lung cancer (NSCLC) is a prevalent and aggressive global malignancy. Conventional surgical treatments, radiotherapy, chemotherapy, and targeted therapies often fall short in halting disease progression due to inherent limitations, resulting in suboptimal prognosis. Despite the advent of immunotherapy drugs offering new hope for NSCLC treatment, current efficacy remains insufficient to meet all patient needs. Therefore, actively exploring novel immunotherapeutic approaches to further reduce mortality rates in NSCLC patients has become a crucial focus of NSCLC research. This article aims to systematically review the anti-tumor effects of interleukin-21 and follicular helper T cells in NSCLC immunotherapy by summarizing and analyzing relevant literatures from both domestic and international sources, as well as exploring the potential for enhancing NSCLC treatment prospects through immune checkpoint regulation via immunotherapeutic means.

BackgroundPatients with low back pain (LBP) often suffer from sleep disorder, and insufficient sleep duration was recognized as a potential risk factor for LBP. Our aim was to explore the exact effect of sleep duration on LBP and the optimal sleep duration to reduce the risk of LBP.MethodsAnalyzing data from the Korean National Health and Nutrition Examination Survey (KNHANES), we investigated the association between sleep duration and LBP in individuals aged 50 years and older. We used logistic regression models, interaction stratification analysis, and threshold effect assessment to analyze the relationship between sleep duration and LBP.ResultsA total of 6,285 participants, comprising 3,056 males and 3,229 females with a median age of 63.1 years, were enrolled in the study. The association between sleep duration and LBP risk exhibited an L-shaped curve (p < 0.015) in RCS analysis. In the threshold analysis, the OR of developing risk of LBP was 0.864 (95% CI:0.78–0.957, p = 0.005) in participants with sleep duration

Trichostatin A (TSA), a histone deacetylase (HDAC) inhibitor, promotes the cytotoxicity of the genotoxic anticancer drug cisplatin, yet the underlying mechanism remains poorly understood. Herein, we revealed that TSA at a low concentration (1 μM) promoted the cisplatin-induced activation of caspase-3/6, which, in turn, increased the level of cleaved PARP1 and degraded lamin A&C, leading to more cisplatin-induced apoptosis and G2/M phase arrest of A549 cancer cells. Both ICP-MS and ToF-SIMS measurements demonstrated a significant increase in DNA-bound platinum in A549 cells in the presence of TSA, which was attributable to TSA-induced increase in the accessibility of genomic DNA to cisplatin attacking. The global quantitative proteomics results further showed that in the presence of TSA, cisplatin activated INF signaling to upregulate STAT1 and SAMHD1 to increase cisplatin sensitivity and downregulated ICAM1 and CD44 to reduce cell migration, synergistically promoting cisplatin cytotoxicity. Furthermore, in the presence of TSA, cisplatin downregulated TFAM and SLC3A2 to enhance cisplatin-induced ferroptosis, also contributing to the promotion of cisplatin cytotoxicity. Importantly, our posttranslational modification data indicated that acetylation at H4K8 played a dominant role in promoting cisplatin cytotoxicity. These findings provide novel insights into better understanding the principle of combining chemotherapy of genotoxic drugs and HDAC inhibitors for the treatment of cancers.

Strophanthidin (SPTD), one of the cardiac glycosides, is refined from traditional Chinese medicines such as Semen Lepidii and Antiaris toxicaria, and was initially used for the treatment of heart failure disease in clinic. Recently, SPTD has been shown to be a potential anticancer agent, but the underlying mechanism of action is poorly understood. Herein, we explored the molecular mechanism by which SPTD exerts anticancer effects in A549 human lung adenocarcinoma cells by means of mass spectrometry-based quantitative proteomics in combination with bioinformatics analysis. We revealed that SPTD promoted the expression of tumor necrosis factor (TNF)-related apoptosis-inducing ligand receptor 2 (TRAIL-R2, or DR5) in A549 cells to activate caspase 3/6/8, in particular caspase 3. Consequently, the activated caspases elevated the expression level of apoptotic chromatin condensation inducer in the nucleus (ACIN1) and prelamin-A/C (LMNA), ultimately inducing apoptosis via cooperation with the SPTD-induced overexpressed barrier-to-autointegration factor 1 (Banf1). Moreover, the SPTD-induced DEPs interacted with each other to downregulate the p38 MAPK/ERK signaling, contributing to the SPTD inhibition of the growth of A549 cells. Additionally, the downregulation of collagen COL1A5 by SPTD was another anticancer benefit of SPTD through the modulation of the cell microenvironment.

Abstract Bioactive lipid molecules have been proposed to play important roles linking obesity/metabolic syndrome and cancers. Studies reveal that aberrant lipid metabolic signaling can reprogram cancer cells and non-cancer cells in the tumor microenvironment, contributing to cancer initiation, progression, metastasis, recurrence, and poor therapeutic response. Existing evidence indicates that controlling lipid metabolism can be a potential strategy for cancer prevention and therapy. By reviewing the current literature on the lipid metabolism in various cancers, we summarized major lipid molecules including fatty acids and cholesterol as well as lipid droplets and discussed their critical roles in cancer cells and non-cancer in terms of either promoting- or anti-tumorigenesis. This review provides an overview of the lipid molecules in cellular entities and their tumor microenvironment, adding to the existing knowledge with lipid metabolic reprogramming in immune cells and cancer associated cells. Comprehensive understanding of the regulatory role of lipid metabolism in cellular entities and their tumor microenvironment will provide a new direction for further studies, in a shift away from conventional cancer research. Exploring the lipid-related signaling targets that drive or block cancer development may lead to development of novel anti-cancer strategies distinct from traditional approaches for cancer prevention and treatment.

Descurainia sophia seeds (DS), Astragalus mongholicus (AM), and their formulas are widely used to treat heart failure caused by various cardiac diseases in traditional Chinese medicine practice. However, the molecular mechanism of action of DS and AM has not been completely understood. Herein, we first used mass spectrometry coupled to UPLC to characterize the chemical components of DS and AM decoctions, then applied MS-based quantitative proteomic analysis to profile protein expression in the heart of rats with isoproterenol-induced cardiomyopathy (ISO-iCM) before and after treated with DS alone or combined with AM, astragaloside IV (AS4), calycosin-7-glucoside (C7G), and Astragalus polysaccharides (APS) from AM. We demonstrated for the first time that DS decoction alone could reverse the most of differentially expressed proteins in the heart of the rats with ISO-iCM, including the commonly recognized biomarkers natriuretic peptides (NPPA) of cardiomyopathy and sarcomeric myosin light chain 4 (MYL4), relieving ISO-iCM in rats, but AM did not pronouncedly improve the pharmacological efficiency of DS. Significantly, we revealed that AS4 remarkably promoted the pharmacological potency of DS by complementarily reversing myosin motor MYH6/7, and further downregulating NPPA and MYL4. In contrast, APS reduced the efficiency of DS due to upregulating NPPA and MYL4. These findings not only provide novel insights to better understanding in the combination principle of traditional Chinese medicine but also highlight the power of mass spectrometric proteomics strategy combined with conventional pathological approaches for the traditional medicine research.

The stimuli-responsive polymer-based platform for controlled drug delivery has gained increasing attention in treating hepatocellular carcinoma (HCC) owing to the fascinating biocompatibility and biodegradability, improved antitumor efficacy, and negligible side effects recently. Herein, a disulfide bond-contained polypeptide nanogel, methoxy poly(ethylene glycol)−poly(l-phenylalanine-co-l-cystine) [mPEG−P(LP-co-LC)] nanogel, which could be responsive to the intracellular reduction microenvironments, was developed to deliver lenvatinib (LEN), an inhibitor of multiple receptor tyrosine kinases, for HCC therapy. The lenvatinib-loaded nanogel (NG/LEN) displayed concise drug delivery under the stimulus of glutathione in the cancer cells. Furthermore, the intracellular reduction-responsive nanomedicine NG/LEN showed excellent antitumor effect and almost no side effects toward both subcutaneous and orthotopic HCC tumor-allografted mice in comparison to free drug. The excellent tumor-inhibition efficacy with negligible side effects demonstrated the potential of NG/LEN for clinical molecular targeted therapy of gastrointestinal carcinoma in the future.