The Emulsification and Stabilization Mechanism of an Oil-in-Water Emulsion Constructed from Tremella Polysaccharide and Citrus Pectin.

The objective of this study was to investigate the feasibility of the mixture of tremella polysaccharide (TP) and citrus pectin (CP) as an emulsifier by evaluating its emulsifying ability/stability. The results showed that the TP:CP ratio of 5:5 (w/w) could effectively act as an emulsifier. CP, owing its lower molecular weight and highly methyl esterification, facilitated the emulsification of oil droplets, thereby promoting the dispersion of droplets. Meanwhile, the presence of TP enhanced the viscosity of emulsion system and increased the electrostatic interactions and steric hindrance, therefore hindering the migration of emulsion droplets, reducing emulsion droplets coalesce, and enhancing emulsion stability. The emulsification and stabilization performances were influenced by the molecular weight, esterified carboxyl groups content, and electric charge of TP and CP, and the potential mechanism involved their impact on the buoyant force of droplet size, viscosity, and steric hindrance of emulsion system. The emulsions stabilized by TP-CP exhibited robust environmental tolerance, but demonstrated sensitivity to Ca2+. Conclusively, the study demonstrated the potential application of the mixture of TP and CP as a natural polysaccharide emulsifier.

Development of soy protein isolate gels added with Tremella polysaccharides and psyllium husk powder as 3D printing inks for people with dysphagia.

The aim of this study was to investigate the feasibility of soy protein isolate (SPI) gels added with Tremella polysaccharides (TPs) and psyllium husk powder (PHP) as 3D printing inks for developing dysphagia-friendly food and elucidate the potential mechanism of TPs and PHP in enhancing the printing and swallowing performance of SPI gels. The results indicated that the SPI gels with a TP : PHP ratio of 3 : 7 could be effectively used as printing inks to manufacture dysphagia-friendly food. The addition of TPs increased the free water content, resulting in a decrease in the viscosity of the SPI gels, which, in turn, reduced the line width of the 3D-printed product and structural strength of the gel system. The addition of PHP increased disulfide bond interactions and excluded volume interactions, which determined the mechanical strength of SPI gels and increased the line width of the printed product. The synergistic effects between TPs and PHP improved the printing precision and structural stability. This study presents meaningful insights for the utilization of 3D printing in the creation of dysphagia-friendly food using protein-polysaccharide complexes.

lncRNA Profiling of Exosomes and Its Communication Role in Regulating Silica-Stimulated Macrophage Apoptosis and Fibroblast Activation.

Long-term silica particle exposure leads to interstitial pulmonary inflammation and fibrosis, called silicosis. Silica-activated macrophages secrete a wide range of cytokines resulting in persistent inflammation. In addition, silica-stimulated activation of fibroblast is another checkpoint in the progression of silicosis. The pathogenesis after silica exposure is complex, involving intercellular communication and intracellular signaling pathway transduction, which was ignored previously. Exosomes are noteworthy because of their crucial role in intercellular communication by delivering bioactive substances, such as lncRNA. However, the expression profile of exosomal lncRNA in silicosis has not been reported yet. In this study, exosomes were isolated from the peripheral serum of silicosis patients or healthy donors. The exosomal lncRNAs were profiled using high-throughput sequencing technology. Target genes were predicted, and functional annotation was performed using differentially expressed lncRNAs. Eight aberrant expressed exosomal lncRNAs were considered to play a key role in the process of silicosis according to the OPLS-DA. Furthermore, the increased expression of lncRNA MSTRG.43085.16 was testified in vitro. Its target gene PARP1 was critical in regulating apoptosis based on bioinformatics analysis. In addition, the effects of exosomes on macrophage apoptosis and fibroblast activation were checked based on a co-cultured system. Our findings suggested that upregulation of lncRNA MSTRG.43085.16 could regulate silica-induced macrophage apoptosis through elevating PARP1 expression, and promote fibroblast activation, implying that the exosomal lncRNA MSTRG.43085.16 might have potential as a biomarker for the early diagnosis of silicosis.

3-D real-time ultrasound tracking of acoustically actuated swimming microdrone.

Maneuverable microswimmers/microdrones that navigate in hard-to-reach spaces inside human bodies hold a great potential for various biomedical applications. Acoustically actuated microswimmers have already demonstrated feasibility. However, for eventual translation of this technology, a robust 3-D tracking strategy for the microswimmer is particularly required. This paper presents our lab-designed 3-D ultrasound tracking system for real-time tracking of an acoustically actuated 3-D swimming microdrone. The ultrasound tracking system utilizing two ultrasound probes, a step motor and a host controller, was built to track the 3-D arbitrary motion of the microdrone in real-time. The performance of tracking was evaluated in the benchtop experiments by comparing the reconstructed trajectories with synchronized camera recordings. The ultrasound tracking system showed high reliability, with an average error of less than 0.3 mm across six different trials when compared to camera tracking. The results demonstrated the capability of our lab-designed 3-D ultrasound tracking system in accurately tracking the undetermined motion of the acoustic actuated 3-D swimming microdrone in real-time. The developed tracking system holds promise as a potential approach for biomedical applications and could pave the way for future clinical translation of the microswimmer technology.

Lilium Gray Mold Suppression Conferred by the Host Antimicrobial Protein LsGRP1 Involves Main Pathogen-Targeted Manipulation of the Nonantimicrobial Region LsGRP1N.

Antimicrobial protein LsGRP1 protects Lilium from gray mold mainly caused by the destructive pathogen Botrytis elliptica; however, its nonantimicrobial region LsGRP1N conversely promotes spore germination of this fungus. By assaying the effects of LsGRP1N, LsGRP1, and the combination of LsGRP1N and the antimicrobial region LsGRP1C on fungal spore germination, hyphal growth, and Lilium gray mold development, LsGRP1N was found to improve the LsGRP1C sensitivity of B. elliptica and disease suppression by LsGRP1C. B. elliptica cell vitality assays indicated that LsGRP1N pretreatment uniquely enhanced the lethal efficiency of LsGRP1C compared to the control peptides. In addition, LsGRP1N-treated B. elliptica was demonstrated to lower infection-related gene expression and increase host-defense-eliciting activity, as indicated by reverse transcription quantitative polymerase chain reaction and histochemical-staining-based callose detection results, respectively. Therefore, LsGRP1N showed a novel mode of action for antimicrobial proteins by manipulating the main pathogen, which facilitated the development of target-specific and dormant microbe-eradicating antimicrobial agents.

The therapeutic effect of exosomal lncRNA MSTRG.91634.7 on mitochondrial dysfunction during SiO2-induced lung fibrosis.

Long-term silica (SiO2) exposure led to irreversible lung fibrosis, in which epithelial-mesenchymal transition (EMT) played an essential role. A novel lncRNA MSTRG.91634.7 in the peripheral exosomes of silicosis patients was reported in our previous study, which could remold the pathological process of silicosis. However, whether its regulatory role on the development of silicosis was related to EMT process is unclear, and its mechanism remains to be further studied. In this study, up-regulating lncRNA MSTRG91634.7 restricted SiO2-activated EMT and restored mitochondrial homeostasis binding to PINK1 in vitro. Moreover, overexpressing PINK1 could inhibit SiO2-activated EMT in pulmonary inflammation and fibrosis in mice. Meanwhile, PINK1 contributed to restoring the SiO2-induced mitochondrial dysfunction in mice lung. Our results revealed that exosomal lncRNA MSTRG.91634.7 from macrophages could restore mitochondrial homeostasis to restrict the SiO2-activated EMT by binding to PINK1 during pulmonary inflammation and fibrosis due to SiO2 exposure.

Effects of Drying Treatments on Nutritional Compositions, Volatile Flavor Compounds, and Bioactive Substances of Broad Beans.

In this study, different drying methods, including hot air drying, sun drying, and freeze drying were employed to dry fresh broad beans. The nutritional composition, volatile organic components and bioactive substances of the dried broad beans were systematically compared. The results indicated significant differences (p < 0.05) in nutritional composition, such as protein and soluble sugar content. Among the 66 identified volatile organic compounds, freeze drying and hot air drying significantly promote the production of alcohols and aldehydes, while sun drying effectively preserves esters. In terms of bioactive substances, broad beans dried by freeze drying exhibit the highest total phenol content as well as the strongest antioxidant capacity and gallic acid, followed by sun drying. The chemometric analysis revealed that the bioactive compounds in broad beans dried by three different methods were primarily composed of flavonoids, organic acids, and amino acids with significant differentiation. Notably, freeze-dried and sun-dried broad beans exhibited a higher concentration of differential substances.

Effects of xanthan gum, konjac glucomannan, and arabinogalactan on the in vitro digestion and fermentation characteristics of biscuits.

Background: Diabetes and its complications have a significant economic impact on individuals and their families. A diet with a low glycemic index (GI) and high fiber content is considered to be associated with the control of blood glucose. Scope and approach: This study explored the effect of polysaccharides, i.e., xanthan gum (BXG), konjac glucomannan (BKG), and arabinogalactan (BAG), on the digestive and prebiotic characteristics of biscuits using a simulated digestion and fermentation model in vitro. Also, the rheological property and structural properties of the polysaccharides were measured to clarify their structure-activity relationships. Key findings and conclusions: During simulated gastrointestinal digestion, the results showed that three types of biscuits containing polysaccharides were low GI foods (estimated GI < 55), in which BAG had the lowest estimated GI value. During in vitro fermentation with diabetic or healthy subjects' fecal microbiota, the three types of biscuits containing polysaccharides (after digestion) decreased the fermentation pH, increased the level of short-chain fatty acids, and modulated the microbiota composition over time. Among the three types of biscuits, BAG increased the abundance of Bifidobacterium and Lactobacillus during fermentation in diabetic and healthy subjects' fecal microbiota. These results showed that the addition of a lower-viscosity polysaccharide (arabinogalactan) may be more beneficial for the blood glucose control of biscuits.

The protective role of HMGB1 in affecting the balance between autophagy and pyroptosis to maintain neutrophils homeostasis during ß-glucan-induced mice lung inflammation.

Fungal contamination is omnipresent, and inhalation of fungi-contaminated organic dust leads to hypersensitivity pneumonitis (HP), in which neutrophils played a pivotal role. Existing studies have suggested that cell homeostasis is crucial for the pathogenesis of the inflammatory disease. Although HMGB1 has been shown to contribute to suppressing HP, there is a lack of studies on its mechanisms, especially the regulation of neutrophil homeostasis. This study aims to investigate how HMGB1 regulates neutrophil function by affecting neutrophil homeostasis, and then affects lung inflammation induced by ß-glucan, the exposure marker of fungi. Our results showed that deficient HMGB1 led to neutrophil death by disrupting the balance between autophagy and pyroptosis after ß-glucan treatment. And HMGB1 deficiency exacerbated the ß-glucan-induced lung inflammation and neutrophil dysfunction both in vivo and in vitro. Furthermore, HMGB1 contributed to remodeling neutrophil function by restricting autophagy and aggravating pyroptosis ß-glucan exposure. Our funding suggested that HMGB1 deficiency could break the balance between autophagy and pyroptosis towards pyroptosis to cause neutrophil dysfunction during the exacerbated inflammatory response, which provides insights into the pathogenesis of HP and the potential biological targets for its treatment. DATA AVAILABILITY: The datasets used during the current study are available from the corresponding author on reasonable request.

The aggravate role of exosomal circRNA11:120406118|12040782 on macrophage pyroptosis through miR-30b-5p/NLRP3 axis in silica-induced lung fibrosis.

Silica dust inhalation could lead to silicosis, and there is no specific biomarker for its early diagnosis and no effective treatment due to the lack of research on its pathogenesis. The homeostasis of macrophages was considered to be crucial during the development of silicosis from persistent chronic inflammation to irreversible fibrosis. However, its regulatory mechanism and the communication between macrophages and others are still not clear. Exosomal circRNAs emerge as favorable candidates for cellular communication. Therefore, our study aimed to illustrate the regulatory mechanism of silicosis from the view of exosomal circRNAs. Our study identified a novel exosomal circRNA, circRNA11:120406118|12040782, in the peripheral serum of silicosis patients. Furthermore, the detailed role of circRNA11:120406118|12040782 was investigated both in silicosis mouse model and in silica-stimulated macrophages and fibroblasts. On the one hand, circRNA11:120406118|12040782 was shown to regulate silica-stimulated macrophage pyroptosis through circRNA11:120406118|12040782/miR-30b-5p/NLRP3 network. And this macrophage-derived cirRNA could promote the activation of fibroblasts. On the other hand, overexpressing miR-30b-5p, the crucial component of circRNA11:120406118|12040782/miR-30b-5p/NLRP3 regulatory network, could inhibit pyroptosis and attenuate silica-induced lung inflammation and fibrosis in mice. Our findings suggested that exosomal circRNA11:120406118|12040782 could aggravate NLRP3-mediated macrophages pyroptosis through sponging miR-30b-5p in silicosis development, which provide an experimental basis and shed light on the early diagnosis and treatment of silicosis.

Macrophage-derived exosomal lncRNA MSTRG.91634.7 inhibits fibroblasts activation by targeting PINK1 in silica-induced lung fibrosis.

Silicosis is a fibrotic lung disease caused by the inhalation of free crystalline silica. Its pathogenesis is extremely complex and involves a variety of cells. Exosomes emerge as a favorable candidate for communication between cells. LncRNA is a major component transported by exosomes in many inflammatory diseases. However, the role of exosomal lncRNA in the pathogenesis of silicosis is still unclear. In this study, the decreased expression of a novel exosomal lncRNA MSTRG.91634.7 in silicosis patients was identified according to high-throughput sequencing. Then, this macrophage-derived exosomal lncRNA MSTRG.91634.7 could regulate the fibroblast's activation by targeting PINK1 in a co-culture system of THP-1 and MRC-5. Finally, the mouse was exposed to 3 mg/50 µL silica to set up the silicosis model. AAV-ov-Pink1 was intratracheally injected to overexpress PINK1 in mice lungs. Our results suggested that PINK1, the target protein of lncRNA MSTRG.91634.7, participated in restricting the silica-induced lung inflammation and fibrosis in mice.

Food for the elderly based on sensory perception: A review.

Background: The impairments of physiological functions caused by aging are common problems in the elderly, especially the impairments of sensory perception. Besides, close relationship between food sensory perception and nutritional status also suggests the importance of dietary management for the elderly population. The foods taking sensory perception into account are urgently needed by the elderly. Scope and approach: This review analyzed sensory perception changes and their effects on food behaviors and nutritional status. Besides, sensory properties essential for aged-foods and acquisition methods, as well as current status of such foods were summarized. Key findings and conclusions: Soft, smooth and moisty foods were more suitable for the elderly with chewing and swallowing dysfunction, which can be prepared by gelation, enzyme treatment, blade tenderization and other non-thermal technologies. Flavor enhancement/enrichment, irritant addition and packet sauces were recommended to compensate the impairment of chemical sensory. Molds, piping bag and 3D printing were suggested for refining appearance of pureed foods, and improving appetite of the elderly.

In vitro digestion of eight types of wholegrains and their dietary recommendations for different populations.

Wholegrains have been promoted for human consumption due to their various health benefits. However, different wholegrains vary in nutritional composition and their beneficial impact on health. In this study, we compared the in vitro starch and protein digestibility, as well as dietary fiber content of eight different wholegrains including barley, buckwheat, coix seed, foxtail millet, oat, proso millet, quinoa, and sorghum and their porridges. We found that boiling improved starch digestibility of all grains, and protein digestibility except proso millet and sorghum. Porridges made from oats, quinoa, or buckwheat are considered healthier than others due to their lower glycemic index and glycemic load, higher digestible protein content and amino acid bioaccessibility, and higher dietary fiber content (>12%). This study could provide a comprehensive nutritional composition and digestibility of the eight types of wholegrains and their porridges. Dietary recommendations were also given for different populations based on factor analysis.

HMGB1 could restrict 1,3-ß-glucan induced mice lung inflammation by affecting Beclin1 and Bcl2 interaction and promoting the autophagy of epithelial cells.

Fungi were microorganisms that are ubiquitous in a variety of environments. Inhalation of fungi-contaminated organic dust led to hypersensitivity pneumonitis and might eventually cause irreversible pulmonary fibrosis. Studies showed that maintaining the homeostasis of epithelial cells was vital for defending the exogenous fungi invasion. HMGB1-dependent autophagy played a critical role in maintaining cell homeostasis in multiple inflammatory diseases. However, the actual role of HMGB1-dependent autophagy in hypersensitivity pneumonitis was unclear. In our study, mice were exposed to 0.3 mg/50 µL 1,3-ß-glucan solution by intratracheal instillation to set up the lung inflammation model. To investigate the role of HMGB1-dependent autophagy in 1,3-ß-glucan induced lung inflammation, AAV-sh-HMGB1 was intratracheally injected to silence HMGB1 in the lung. Our finding suggested that silencing HMGB1 could aggravate the 1,3-ß-glucan induced lung inflammation by inhibiting the autophagy of epithelial cells. And ubiquitination of Beclin1 contributed to decreasing the interaction of Beclin1 and Bcl2, which might be a key regulatory mechanism of HMGB1 on 1,3-ß-glucan induced autophagy.

Occupational noise exposure and the prevalence of dyslipidemia in a cross-sectional study.

BACKGROUND: Occupational noise exposure was related to cardiovascular disease, of which dyslipidemia was an important inducement. This study investigated the relationship between occupational noise exposure and dyslipidemia. METHODS: Four hundred ninety-two occupational noise-exposed workers and 664 non-exposed workers were recruited to conduct environmental noise tests and personal occupational physical examinations. A lasso-logistic regression model was used to estimate the relative risk of dyslipidemia. A restricted cubic spline was used to estimate the association between noise exposure years and dyslipidemia after adjusting for potential confounding factors. RESULTS: A crude association was observed between the occupational noise exposure (75-85 dB(A)) and dyslipidemia. After adjusting for confounding factors, there was a non-linear relationship between noise exposure years and dyslipidemia (P for non-linearity =0.01). Workers exposed to 75-85 dB(A) for 11 to 24.5 years had a higher risk of dyslipidemia than non-exposed workers. CONCLUSIONS: A positive and non-linear exposure-response relationship was found in workers exposed to 75-85 dB(A) whose exposure years were between 11 and 24.5. Workers had the highest risk of dyslipidemia when exposed for 13.5 years.

IL-10 producing B cells regulated 1,3-ß-glucan induced Th responses in coordinated with Treg.

Repeated exposure to fungi-contaminated dust can lead to multiple adverse effects on the lung, such as hypersensitivity pneumonitis, granuloma even irreversible fibrosis. 1,3-ß-glucan, a major cell wall component of fungi, is considered as its exposure biomarker. Existing studies showed that a series of Th responses were involved in 1,3-ß-glucan induced hypersensitivity pneumonitis, in which macrophages, Treg, and IL-10 producing B cells were reported to participate. The reciprocal interaction among those critical immune cells in 1,3-ß-glucan induced inflammation was not investigated yet. To clarify the regulatory mechanism of IL-10 producing B cells on Th and Treg, the current study set up a primary cell co-culture system. The anti-CD22 antibody was injected intraperitoneally to generate IL-10 producing B cells deficiency mouse model. Cells were isolated and purified from C57BL∖6 mice in different groups. Flow cytometry was used to check the phenotype of different cell subtypes. CBA assay and real-time PCR were used to examine the levels of multiple cytokines. Our results indicated that IL-10 producing B cells could modulate the 1,3-ß-glucan induced inflammatory response. The modulation of IL-10 producing B cells on Th response after 1,3-ß-glucan treatment was cell contact independent. What's more, the modulation pattern of IL-10 producing B cells might be impaired without Treg response. IL-10-producing B cells regulated 1,3-ß-glucan induced Th responses in co-ordination with Treg cells.

3-D swimming microdrone powered by acoustic bubbles.

Mobile microrobots that maneuver in liquid environments and navigate inside the human body have drawn a great interest due to their possibility for medical uses serving as an in vivo cargo. For this system, the effective self-propelling method, which should be powered wirelessly and controllable in 3-D space, is of paramount importance. This article describes a bubble-powered swimming microdrone that can navigate in 3-D space in a controlled manner. To enable 3-D propulsion with steering capability, air bubbles of three lengths are trapped in microtubes that are embedded and three-dimensionally aligned inside the drone body using two-photon polymerization. These bubbles can generate on-demand 3-D propulsion through microstreaming when they are selectively excited at their individual resonance frequencies that depend on the bubble sizes. In order to equip the drone with highly stable maneuverability, a non-uniform mass distribution of the drone body is carefully designed to spontaneously restore the drone to the upright position from disturbances. A mathematical model of the restoration mechanism is developed to predict the restoration behavior showing a good agreement with the experimental data. The present swimming microdrone potentially lends itself to a robust 3-D maneuverable microscale mobile cargo navigating in vitro and in vivo for biomedical applications.

Arsenic represses airway epithelial mucin expression by affecting retinoic acid signaling pathway.

Arsenic is a ubiquitous environmental toxicant, found in high concentrations worldwide. Although abundant research has dealt with arsenic-induced cancers, studies on mechanisms of non-malignant lung diseases have not been complete. In addition, decades of research have mostly concentrated on high-dose arsenic exposure, which has very limited use in modeling the biological effects of today's low-dose exposures. Indeed, accumulated evidence has shown that low-dose arsenic exposure (i.e. ≤100 ppb) may also alter lung homeostasis by causing host susceptibility to viral infection. However, the underlying mechanism of this alteration is unknown. In this study, we found that low-dose sodium arsenite (As (III)) repressed major airway mucins-MUC5AC and MUC5B at both mRNA and protein levels. We further demonstrated that this repression was not caused by cellular toxicity or mediated by the reduction of a common mucin-inducing pathway-EGFR. Other established mucin activators- dsRNA, IL1ß or IL17 were not able to override As (III)-induced mucin repression. Interestingly, the suppressing effect of As (III) appeared to be partially reversible, and supplementation of all trans retinoic acid (t-RA) doses dependently restored mucin gene expression. Further analyses indicated that As (III) treatment significantly reduced the protein level of retinoic acid receptors (RARα, γ and RXRα) as well as RARE promoter reporter activity. Therefore, our study fills in an important knowledge gap in the field of low-dose arsenic exposure. The interference of RA signaling, and mucin gene expression may be important pathogenic factors in low-dose arsenic induced lung toxicity.

Trehalose Alleviates Crystalline Silica-Induced Pulmonary Fibrosis via Activation of the TFEB-Mediated Autophagy-Lysosomal System in Alveolar Macrophages.

Silicosis is an occupational lung disease characterized by persistent inflammation and irreversible fibrosis. Crystalline silica (CS) particles are mainly phagocytized by alveolar macrophages (AMs), which trigger apoptosis, inflammation, and pulmonary fibrosis. Previously, we found that autophagy-lysosomal system dysfunction in AMs was involved in CS-induced inflammation and fibrosis. Induction of autophagy and lysosomal biogenesis by transcription factor EB (TFEB) nuclear translocation can rescue fibrotic diseases. However, the role of TFEB in silicosis is unknown. In this study, we found that CS induced TFEB nuclear localization and increased TFEB expression in macrophages both in vivo and in vitro. However, TFEB overexpression or treatment with the TFEB activator trehalose (Tre) alleviated lysosomal dysfunction and enhanced autophagic flux. It also reduced apoptosis, inflammatory cytokine levels, and fibrosis. Both pharmacologically inhibition of autophagy and TFEB knockdown in macrophages significantly abolished the antiapoptotic and anti-inflammatory effects elicited by either TFEB overexpression or Tre treatment. In conclusion, these results uncover a protective role of TFEB-mediated autophagy in silicosis. Our study suggests that restoration of autophagy-lysosomal function by Tre-induced TFEB activation may be a novel strategy for the treatment of silicosis.