Realization path and connotation of the Healthy China strategy: macroscopic perspective of dietary structure and the entry of individual health consciousness.

BACKGROUND: Dietary rationality and health concept have certain influence on individual health level. This study aims to explore the characteristics and existing problems of Chinese residents' health behaviors from both macro and micro perspectives, and explore the feasibility and realization path of Healthy China strategy. METHODS: We utilized regression models to evaluate the correlation between diet and the risk of disease causes of death. By use of the linear regression analysis model, we distinguished the impact of each dimension on health literacy index at the individual level. Then, we explored the influential factors of the diet health index using the binary logit regression model. RESULTS: Increased consumption of animal-derived foods in China has contributed to the burden of non-communicable diseases. The individuals' health awareness is still weak, and the health literacy index is greatly affected by the diet, while the individual gender and age are positively correlated with the diet health index, and the individual body mass index (BMI) level is negatively correlated with the diet health index. CONCLUSIONS: This study provided a comprehensive understanding of existing problems of Chinese residents' health behaviors. We have proposed a path model for the implementation of the Healthy China strategy from the perspectives of "diet health, physical health, conceptual health and environmental health," which is also a great contribution to the world.

Inhibition of miR-146a-5p and miR-8114 in Insulin-Secreting Cells Contributes to the Protection of Melatonin against Stearic Acid-Induced Cellular Senescence by Targeting Mafa.

BACKGRUOUND: Chronic exposure to elevated levels of saturated fatty acids results in pancreatic ß-cell senescence. However, targets and effective agents for preventing stearic acid-induced ß-cell senescence are still lacking. Although melatonin administration can protect ß-cells against lipotoxicity through anti-senescence processes, the precise underlying mechanisms still need to be explored. Therefore, we investigated the anti-senescence effect of melatonin on stearic acid-treated mouse ß-cells and elucidated the possible role of microRNAs in this process. METHODS: ß-Cell senescence was identified by measuring the expression of senescence-related genes and senescence-associated ß-galactosidase staining. Gain- and loss-of-function approaches were used to investigate the involvement of microRNAs in stearic acid-evoked ß-cell senescence and dysfunction. Bioinformatics analyses and luciferase reporter activity assays were applied to predict the direct targets of microRNAs. RESULTS: Long-term exposure to a high concentration of stearic acid-induced senescence and upregulated miR-146a-5p and miR- 8114 expression in both mouse islets and ß-TC6 cell lines. Melatonin effectively suppressed this process and reduced the levels of these two miRNAs. A remarkable reversibility of stearic acid-induced ß-cell senescence and dysfunction was observed after silencing miR-146a-5p and miR-8114. Moreover, V-maf musculoaponeurotic fibrosarcoma oncogene homolog A (Mafa) was verified as a direct target of miR-146a-5p and miR-8114. Melatonin also significantly ameliorated senescence and dysfunction in miR-146a-5pand miR-8114-transfected ß-cells. CONCLUSION: These data demonstrate that melatonin protects against stearic acid-induced ß-cell senescence by inhibiting miR-146a- 5p and miR-8114 and upregulating Mafa expression. This not only provides novel targets for preventing stearic acid-induced ß-cell dysfunction, but also points to melatonin as a promising drug to combat type 2 diabetes progression.

Pickering Emulsions Stabilized by Mesoporous Nanoparticles with Different Morphologies in Combination with DTAB.

The morphology of nanoparticles plays a significant role in the properties and applications of Pickering emulsions. Oil-in-water (O/W) Pickering emulsions were prepared using spherical, rod-like, and thread-like mesoporous silica nanoparticles (MSNPs) in combination with the cationic surfactant dodecyltrimethylammonium bromide (DTAB) as a stabilizer. The effects of nanoparticle morphology on the stability and stimuli-responsive properties of Pickering emulsions were investigated. For spherical and rod-like MSNP systems, stable Pickering emulsions were obtained at DTAB concentrations above 0.2 mmol·L-1. Stable Pickering emulsions containing thread-like MSNPs were produced at lower DTAB concentrations of approximately 0.1 mmol·L-1. The droplets with thread-like MSNPs were extremely large with an average diameter around 700 µm at DTAB concentrations of 0.1-0.3 mmol·L-1, which were approximately 20 times larger than those of conventional droplets. Scanning electron microscopy (SEM) images showed that all three types of MSNPs were located at the O/W interfaces. Irrespective of the morphology of the MSNPs, all the stable Pickering emulsions retained their original appearance for more than 6 months. By adding NaOH and HCl alternatively, the Pickering emulsions containing spherical and rod-like MSNPs could be switched between unstable and stable states more than 60 times. The Pickering emulsions containing thread-like MSNPs, by contrast, could have their droplet size switched between large and small more than 10 times without any obvious phase separation. The high anisotropy of thread-like MSNPs contributed to the low interface curvature of the droplets. This study revealed the relationship between the morphology of MSNPs and the characteristics of Pickering emulsions. These results enrich our knowledge about the formulation of Pickering emulsions and expand their applications.

Color Contrast Enhanced Rendering for Optical See-Through Head-Mounted Displays.

Most commercially available optical see-through head-mounted displays (OST-HMDs) utilize optical combiners to simultaneously visualize the physical background and virtual objects. The displayed images perceived by users are a blend of rendered pixels and background colors. Enabling high fidelity color perception in mixed reality (MR) scenarios using OST-HMDs is an important but challenging task. We propose a real-time rendering scheme to enhance the color contrast between virtual objects and the surrounding background for OST-HMDs. Inspired by the discovery of color perception in psychophysics, we first formulate the color contrast enhancement as a constrained optimization problem. We then design an end-to-end algorithm to search the optimal complementary shift in both chromaticity and luminance of the displayed color. This aims at enhancing the contrast between virtual objects and the real background as well as keeping the consistency with the original displayed color. We assess the performance of our approach using a simulated OST-HMD environment and an off-the-shelf OST-HMD. Experimental results from objective evaluations and subjective user studies demonstrate that the proposed approach makes rendered virtual objects more distinguishable from the surrounding background, thereby bringing a better visual experience.

PowerNet: Learning-Based Real-Time Power-Budget Rendering.

With the prevalence of embedded GPUs on mobile devices, power-efficient rendering has become a widespread concern for graphics applications. Reducing the power consumption of rendering applications is critical for extending battery life. In this paper, we present a new real-time power-budget rendering system to meet this need by selecting the optimal rendering settings that maximize visual quality for each frame under a given power budget. Our method utilizes two independent neural networks trained entirely by synthesized datasets to predict power consumption and image quality under various workloads. This approach spares time-consuming precomputation or runtime periodic refitting and additional error computation. We evaluate the performance of the proposed framework on different platforms, two desktop PCs and two smartphones. Results show that compared to the previous state of the art, our system has less overhead and better flexibility. Existing rendering engines can integrate our system with negligible costs.

Comparative analysis of circRNA expression profile and circRNA-miRNA-mRNA regulatory network between palmitic and stearic acid-induced lipotoxicity to pancreatic ß cells.

Chronic exposure to high concentrations of circulating palmitic acid and stearic acid leads to impaired ß cell function, which accelerates the development of type 2 diabetes. However, differences in the mechanisms underlying this process between these two saturated fatty acids remain largely unknown. In this study, we screened for potential circular RNAs (circRNAs) and their associated regulatory pathways in palmitic acid- and stearic acid-induced mouse ß-TC6 cell dysfunction. CircRNA high-throughput sequencing, gene ontology enrichment and Kyoto Encyclopedia of Genes and Genomes analysis were performed and co-expression and competing endogenous RNAs (ceRNA) networks were constructed. We identified that four circRNAs that were differentially expressed specifically in ß cells exposed to palmitic acid, whereas four circRNAs were differentially expressed specifically in ß cells exposed to stearic acid. Seven circRNAs were differentially co-expressed in palmitic acid- and stearic acid-treated ß cells. In pathway exploration, we identified the core protein Solute carrier family 2 member 2 (SLc2a2), which is mainly involved in insulin resistance, maturity onset diabetes of the young and type 2 diabetes. The expressions of key circRNAs in ß-TC6 cells were validated by Real time quantitative PCR, with a consistent result in high-throughput sequencing. The findings aid our understanding of the mechanisms governing the difference between palmitic acid- and stearic acid-induced ß cell dysfunction and provide potential therapeutic targets for developing treatments against long-term high fat diet-induced ß cell injury.Abbreviations: Acvr1c: Activin A receptor, type 1C; CeRNA, Competing endogenous RNAs; circRNA, circular RNA; DEcircRNA: Differentially Expressed circular RNA; DEmiRNA: Differentially Expressed microRNA; DEmRNA: Differentially Expressed mRNA; GO: Gene Ontology; HPDHigh Palmitic acid Diet; HSD: High Stearic acid Diet; KEGG: Kyoto Encyclopedia of Genes and Genomes; miRNA: microRNA; ncRNAs: non-coding RNAs; qPCR: Real time quantitative PCRS; FAs: Saturated Fatty Acids; SLc2a2: Solute carrier family 2 member 2; T2D: Type 2 Diabetes.

Inhibition of lncRNA TCONS_00077866 Ameliorates the High Stearic Acid Diet-Induced Mouse Pancreatic ß-Cell Inflammatory Response by Increasing miR-297b-5p to Downregulate SAA3 Expression.

Long-term consumption of a high-fat diet increases the circulating concentration of stearic acid (SA), which has a potent toxic effect on ß-cells, but the underlying molecular mechanisms of this action have not been fully elucidated. Here, we evaluated the role of long noncoding (lnc)RNA TCONS_00077866 (lnc866) in SA-induced ß-cell inflammation. lnc866 was selected for study because lncRNA high-throughput sequencing analysis demonstrated it to have the largest fold-difference in expression of five lncRNAs that were affected by SA treatment. Knockdown of lnc866 by virus-mediated shRNA expression in mice or by Smart Silencer in mouse pancreatic ß-TC6 cells significantly inhibited the SA-induced reduction in insulin secretion and ß-cell inflammation. According to lncRNA-miRNAs-mRNA coexpression network analysis and luciferase reporter assays, lnc866 directly bound to miR-297b-5p, thereby preventing it from reducing the expression of its target serum amyloid A3 (SAA3). Furthermore, overexpression of miR-297b-5p or inhibition of SAA3 also had marked protective effects against the deleterious effects of SA in ß-TC6 cells and mouse islets. In conclusion, lnc866 silencing ameliorates SA-induced ß-cell inflammation by targeting the miR-297b-5p/SAA3 axis. lnc866 inhibition may represent a new strategy to protect ß-cells against the effects of SA during the development of type 2 diabetes.

TCONS_00230836 silencing restores stearic acid-induced ß cell dysfunction through alleviating endoplasmic reticulum stress rather than apoptosis.

BACKGROUND: Chronic exposure of pancreatic ß cells to high levels of stearic acid (C18:0) leads to impaired insulin secretion, which accelerates the progression of type 2 diabetes mellitus (T2DM). Recently, long noncoding RNAs (lncRNAs) were found to participate in saturated fatty acid-induced metabolism dysfunction. However, their contribution to stearic acid-induced ß-cell dysfunction remains largely unknown. This study evaluated the possible role of the lncRNA TCONS_00230836 in stearic acid-stimulated lipotoxicity to ß cells. METHOD: Using high-throughput RNA-sequencing, TCONS_00230836 was screened out as being exclusively differentially expressed in stearic acid-treated mouse ß-TC6 cells. Co-expression network was constructed to reveal the potential mRNAs targeted for lncRNA TCONS_00230836. Changes in this lncRNA's and candidate mRNAs' levels were further assessed by real-time PCR in stearic acid-treated ß-TC6 cells and islets of mice fed a high-stearic-acid diet (HSD). The localization of TCONS_00230836 was detected by fluorescent in situ hybridization. The endogenous lncRNA TCONS_00230836 in ß-TC6 cells was abrogated by its Smart Silencer. RESULTS: TCONS_00230836 was enriched in mouse islets and mainly localized in the cytoplasm. Its expression was significantly increased in stearic acid-treated ß-TC6 cells and HSD-fed mouse islets. Knockdown of TCONS_00230836 significantly restored stearic acid-impaired glucose-stimulated insulin secretion through alleviating endoplasmic reticulum stress. However, stearic acid-induced ß cell apoptosis was not obviously recovered. CONCLUSION: Our findings suggest the involvement of TCONS_00230836 in stearic acid-induced ß-cell dysfunction, which provides novel insight into stearic acid-induced lipotoxicity to ß cells. Anti-lncRNA TCONS_00230836 might be a new therapeutic strategy for alleviating stearic acid-induced ß-cell dysfunction in the progression of T2DM.

Salt-Resistant Switchable Pickering Emulsions Stabilized by Mesoporous Nanosilica Hydrophobized In Situ by pH-Insensitive Surfactants.

Novel oil-in-water (O/W) Pickering emulsions (PEs) were prepared using mesoporous nanosilica in combination with a pH-insensitive cationic surfactant as a stabilizer and show an interesting sensitivity to acids and bases. Adding a suitable amount of NaOH (nNaOH/ncationic surfactant ≥ 1) led to prompt demulsification within 10 s. Upon further adding HCl solutions (nHCl/nNaOH = 1), stable PEs re-formed after homogenization. These emulsions remained stable for over 30 days after 60 cycles, switching from stable to unstable and back to stable states, and showed a high salt tolerance. A mechanism for the switching of the Pickering emulsion (PE) to unstable and back to stable states was derived and involved anionic and neutral forms of hydroxyl groups at the mesopores of the mesoporous silica nanoparticles (MSNPs). This work reveals a switchable PE system involving a pH-insensitive surfactant, in which the species of oils and cationic surfactants can be arbitrarily selected, a feature that greatly expands the applicability of PEs.

miRNA-mRNA profile and regulatory network in stearic acid-treated ß-cell dysfunction.

Chronic exposure of pancreatic ß-cells to saturated fatty acid (palmitic or stearic acid) is a leading cause of impaired insulin secretion. However, the molecular mechanisms underlying stearic-acid-induced ß-cell dysfunction remain poorly understood. Emerging evidence indicates that miRNAs are involved in various biological functions. The aim of this study was to explore the differential expression of miRNAs and mRNAs, specifically in stearic-acid-treated- relative to palmitic-acid-treated ß-cells, and to establish their co-expression networks. ß-TC-6 cells were treated with stearic acid, palmitic acid or normal medium for 24 h. Differentially expressed miRNAs and mRNAs were identified by high-throughput sequencing and bioinformatic analysis. Co-expression network, gene ontology (GO) and pathway analyses were then conducted. Changes in the expression of selected miRNAs and mRNAs were verified in ß-TC-6 cells and mouse islets. Sequencing analysis detected 656 known and 1729 novel miRNAs. miRNA-mRNA network and Venn-diagram analysis yielded two differentially expressed miRNAs and 63 mRNAs exclusively in the stearic-acid group. miR-374c-5p was up-regulated by a 1.801 log2(fold-change) and miR-297b-5p was down-regulated by a -4.669 log2(fold-change). We found that miR-297b-5p and miR-374c-5p were involved in stearic-acid-induced lipotoxicity to ß-TC-6 cells. Moreover, the effects of miR-297b-5p and miR-374c-5p on the alterations of candidate mRNAs expressions were verified. This study indicates that expression changes of specific miRNAs and mRNAs may contribute to stearic-acid-induced ß-cell dysfunction, which provides a preliminary basis for further functional and molecular mechanism studies of stearic-acid-induced ß-cell dysfunction in the development of type 2 diabetes.

Overexpression of miR-297b-5p protects against stearic acid-induced pancreatic ß-cell apoptosis by targeting LATS2.

Chronic exposure to high concentrations of stearic acid (C18:0) can result in ß-cell dysfunction, leading to development of type 2 diabetes. However, the molecular mechanisms underlying the destructive effects of stearic acid on ß-cells remain largely unknown. In this study, we aimed to investigate the role of miR-297b-5p on stearic acid-induced ß-cell apoptosis. Differential expression of microRNAs (miRNAs) was assessed in a ß-TC6 cell line exposed to stearic acid, palmitic acid, or a normal culture medium by high-throughput sequencing. The apoptosis rate was measured by flow cytometry after miR-297b-5p mimic/inhibitor transfection, and large-tumor suppressor kinase 2 (LATS2) was identified as a target of miR-297b-5p using a luciferase activity assay. In vivo, C57BL/6 mice were fed with normal and high-stearic-acid diet, respectively. Mouse islets were used for similar identification of miR-297b-5p and Lats2 in ß-TC6 cell. We selected two differentially expressed miRNAs in stearic acid compared with those in the palmitic acid and control groups. miR-297b-5p expression was significantly lower in ß-TC6 cells and mouse islets in stearic acid than in control group. Upregulation of miR-297b-5p alleviated the stearic acid-induced cell apoptosis and reduction in insulin secretion by inhibiting Lats2 expression in vitro. Meanwhile, silencing Lats2 significantly reversed the stearic acid-stimulated ß-cell dysfunction in both ß-TC6 cells and islets. Our findings indicate a suppressive role for miR-297b-5p in stearic acid-induced ß-cell apoptosis, which may reveal a potential target for the treatment of ß-cell dysfunction in the pathogenesis of type 2 diabetes.