Skin-Interfaced Wearable Sweat Sensors for Precision Medicine.

Wearable sensors hold great potential in empowering personalized health monitoring, predictive analytics, and timely intervention toward personalized healthcare. Advances in flexible electronics, materials science, and electrochemistry have spurred the development of wearable sweat sensors that enable the continuous and noninvasive screening of analytes indicative of health status. Existing major challenges in wearable sensors include: improving the sweat extraction and sweat sensing capabilities, improving the form factor of the wearable device for minimal discomfort and reliable measurements when worn, and understanding the clinical value of sweat analytes toward biomarker discovery. This review provides a comprehensive review of wearable sweat sensors and outlines state-of-the-art technologies and research that strive to bridge these gaps. The physiology of sweat, materials, biosensing mechanisms and advances, and approaches for sweat induction and sampling are introduced. Additionally, design considerations for the system-level development of wearable sweat sensing devices, spanning from strategies for prolonged sweat extraction to efficient powering of wearables, are discussed. Furthermore, the applications, data analytics, commercialization efforts, challenges, and prospects of wearable sweat sensors for precision medicine are discussed.

Staphylococcus aureus lysate induces an IgE response via memory B cells in nasal polyps.

BACKGROUND: Locally increased IgE levels plays a pathologic role in chronic rhinosinusitis with nasal polyps (CRSwNP). OBJECTIVE: This study aimed to investigate whether Staphylococcus aureus could induce aberrant IgE synthesis in CRSwNP and the potential mechanisms involved. METHODS: Total IgE, IL-4, IL-5, and IL-13 concentrations in the supernatants of the cultures stimulated with S aureus lysate were assessed by ELISA. S aureus-induced cellular responses were investigated by single-cell RNA sequencing. Flow cytometry and quantitative reverse transcription PCR were used to analyze B-cell subsets and stimulated cell ε-germline transcript expression, respectively. IgE-positive B-cell and germinal center localization were assessed by immunohistochemistry and immunofluorescence. RESULTS: S aureus lysate induced IgE production in the supernatants of nasal polyp (NP) tissues but not in those of healthy nasal mucosa. Moreover, IgE levels increased from days 2 to 4 after stimulation, paralleling the enhanced ε-germline transcript, IL-5, and IL-13 expression. Single-cell RNA sequencing revealed that there were increased IL-5 and IL-13 in group 2 innate lymphoid cells and identified a clonal overlap between unstimulated memory B cells and S aureus-stimulated plasma cells. The enriched IgE within NPs was mainly produced by IgE-negative memory B cells. Cellular evidence indicated that the IgE memory response to S aureus might also exist in the peripheral blood of CRSwNP patients. The S aureus-induced IgE memory response was associated with elevated IgE levels in NPs, asthma, and postoperative CRSwNP recurrence. CONCLUSIONS: S aureus induced an IgE response via IgE-negative memory B cells in CRSwNP patients, possibly contributing to CRSwNP development.

Mechanistic insights into enhancement or inhibition of phase separation by different polyubiquitin chains.

Ubiquitin-binding shuttle UBQLN2 mediates crosstalk between proteasomal degradation and autophagy, likely via interactions with K48- and K63-linked polyubiquitin chains, respectively. UBQLN2 comprises self-associating regions that drive its homotypic liquid-liquid phase separation (LLPS). Specific interactions between one of these regions and ubiquitin inhibit UBQLN2 LLPS. Here, we show that, unlike ubiquitin, the effects of multivalent polyubiquitin chains on UBQLN2 LLPS are highly dependent on chain types. Specifically, K11-Ub4 and K48-Ub4 chains generally inhibit UBQLN2 LLPS, whereas K63-Ub4, M1-Ub4 chains, and a designed tetrameric ubiquitin construct significantly enhance LLPS. We demonstrate that these opposing effects stem from differences in chain conformations but not in affinities between chains and UBQLN2. Chains with extended conformations and increased accessibility to the ubiquitin-binding surface promote UBQLN2 LLPS by enabling a switch between homotypic to partially heterotypic LLPS that is driven by both UBQLN2 self-interactions and interactions between multiple UBQLN2 units with each polyubiquitin chain. Our study provides mechanistic insights into how the structural and conformational properties of polyubiquitin chains contribute to heterotypic LLPS with ubiquitin-binding shuttles and adaptors.

Airways epithelial exposure to Streptococcus pneumoniae in the presence of the alarmin IL-33 induces a novel subset of pro-inflammatory ILC2s promoting a mixed inflammatory response.

BACKGROUND: We have previously shown that asthma-like airways inflammation may be induced by topical exposure to respiratory tract pathogens such as S. pneumoniae (SP) in concert with epithelial alarmins such as IL-33. Details of the pathogenesis of this murine surrogate remain however unexplored. METHODS: Airways inflammation was induced by repeated, intranasal exposure of Il-4-/-, Rag1-/- and Rag2-/-Il2rg-/- mice (in which B lymphocyte IgE switching, adaptive and innate immunity are respectively ablated) as well as wild type mice to inactivated SP, IL-33 or both. Airways pathological changes were analysed, and the subsets and functions of locally accumulated ILC2s investigated by single cell RNA sequencing and flow cytometry. RESULTS: In the presence of IL-33, repeated exposure of the airways to inactivated SP caused marked eosinophil- and neutrophil-rich inflammation and local accumulation of ILC2s, which was retained in the Il-4-/- and Rag1-/- deficient mice but abolished in the Rag2-/-Il2rg-/- mice, an effect partly reversed by adoptive transfer of ILC2s. Single cell sequencing analysis of ILC2s recruited following SP and IL-33 exposure revealed a Klrg1+Ly6a+subset, expressing particularly elevated quantities of the pro-inflammatory cytokine IL-6, type 2 cytokines (IL-5 and IL-13) and MHC class II molecules, promoting type 2 inflammation as well as involved in neutrophil-mediated inflammatory responses. CONCLUSION: Local accumulation of KLRG1+Ly6a+ ILC2s in the lung tissue is a critical aspect of the pathogenesis of airways eosinophilic and neutrophil-rich inflammation induced by repeated exposure to SP in the presence of the epithelial alarmin IL-33.

Bacterial antigens and asthma: a comparative study of common respiratory pathogenic bacteria.

Objective: In a previous study we have shown that, in the presence of interleukin (IL)-33, repeated, per-nasal challenge of murine airways with Streptococcus pneumoniae (S. pneumoniae) organisms induces human asthma-like airways inflammation. It is not clear, however, whether this effect is unique or manifest in response to other common respiratory pathogens.Methods: To explore this, airways of BALB/c mice were repeatedly challenged per-nasally with formaldehyde-inactivated bacterial bodies in the presence or absence of murine recombinant IL-33. Serum concentrations of S.pneumoniae, Moraxella catarrhalis (M.catarrhalis) and Haemophilus influenzae (H.influenzae) lysates-specific IgE were measured in patients with asthma and control subjects.Results: We showed that in the presence of IL-33, repeated, per-nasal airways exposure to the bodies of these bacteria induced airways hyperresponsiveness (AHR) in the experimental mice. This was accompanied by cellular infiltration into bronchoalveolar lavage fluid (BALF), eosinophilic infiltration and mucous hypertrophy of the lung tissue, with elevated local expression of some type 2 cytokines and elevated, specific IgG and IgE in the serum. The precise characteristics of the inflammation evoked by exposure to each bacterial species were distinguishable.Conclusions: These results suggest that in the certain circumstances, inhaled or commensal bacterial body antigens of both Gram-positive (S. pneumoniae) and Gram-negative (M. catarrhalis and H. influenzae) respiratory tract bacteria may initiate type 2 inflammation typical of asthma in the airways. In addition, we demonstrated that human asthmatic patients manifest elevated serum concentrations of M.catarrhalis- and H.influenzae-specific IgE.

Meta-analysis of the impact of laser interstitial hyperthermia on wound healing complications in brain tumors.

High-grade gliomas (HGGs) may be amenable to the neurosurgical technique known as laser interstitial thermal therapy (LITT), which delivers thermal energy to interstitial brain injuries and wounds with pinpoint accuracy. The purpose of this extensive meta-analysis was to evaluate the effects of LITT on wound complications among patients who have brain tumours. Diverse conclusions emerge from a systematic review of pertinent studies, necessitating a comprehensive examination. The meta-analysis, performed utilizing the meta library provided by the R package meta, reveals an initial significant overall effect (RR: -2.1262, 95% CI [-2.7466, -1.5059], p < 0.0001) accompanied by considerable heterogeneity among studies (I2 = 61.13%). Following analyses that specifically examined the incidence of wounds, a complex correlation was found (RR: 0.0471, 95% CI [0.0264, 0.0842], p < 0.0001), indicating that LITT has a discernible but insignificant effect on the occurrence of wounds. Although the meta-analysis emphasizes a notable decrease in wound complications subsequent to LITT treatment, additional research is warranted due to constraints in standardized reporting, data accessibility, and small sample sizes. The results of this study underscore the need for exhaustive protocols to analyse wound complications in patients with brain tumours undergoing LITT.

Exogenous c-di-GMP inhibited the biofilm formation of Vibrio splendidus.

Vibrio splendidus, a gram-negative bacterium that is ubiquitously present in marine environments, has been increasingly deemed an important opportunistic pathogen of marine animals. In this study, the biofilm formation of V. splendidus was quantitatively determined and morphologically characterized. Three stages of biofilm formation, including adhesion, aggregation and maturation were observed in the biofilm formed by V. splendidus. The inhibitory effect of exogenous bis (3',5')-cyclic dimeric guanosine monophosphate (c-di-GMP) on the biofilm formation from the scratch and preformed established biofilms of V. splendidus was determined. When 200 µmol/L c-di-GMP was added, the quantity of biofilm decreased by 88.1% or 66.7% under the two conditions. To explore the preliminary mechanism of exogenous c-di-GMP on the biofilm formed by V. splendidus, proteomic analysis was performed. GO enrichment analysis showed that exogenous c-di-GMP upregulated biological processes, including the tricarboxylic acid cycle, oxidation‒reduction reactions and organonitrogen compound catabolism and significantly downregulated tRNA threonylcarbamoyladenosine modification, protein dephosphorylation, and lactate transmembrane transporter activity. Sequence-specific DNA binding activity was the most markedly downregulated molecular function. KEGG analysis showed that the valine, leucine and isoleucine degradation pathway was the most enriched pathway, followed by nitrogen metabolism, among the 20 upregulated pathways. Among the downregulated pathways, a nonribosomal peptide structure pathway and the streptomycine, polyketide sugar unit, acarbose and validamycin biosynthesis pathways were significantly enriched. Our present study provides basic data for the biofilm formation of V. splendidus and the preliminary inhibitory mechanism of exogenous c-di-GMP on the biofilm formation of V. splendidus.

Synergistic toxicity of some food additives used in non-alcoholic beverages on renal tubular epithelial cells.

Evidences supported many food additives (FAs) possess toxicity to human health due to chronic excessive exposure. Global hygienic standards strictly limit the dosage of each FA and mixture of the same functional FAs. However, the synergetic effects caused by the combination of FAs with different functions require careful evaluation. In the present study, the content of each FA in beverages was determined by HPLC-UV-Vis detection. The cytotoxic effects of selected typical FAs alone or their combination were evaluated in human renal tubular epithelial cells. Mathematical Modeling and bioinformatics methods were employed to evaluate the toxicity of FAs and to predict the key target proteins of FAs on renal tubular cell toxicity, which were verified by western blot. The results indicated above 5 FAs were used in each surveyed beverage. The content of each FA and the respective ratios of the same functional FAs in each beverage did not exceed the maximum permitted level. But it was intensively shown that the significant synergistic cytotoxicity for the combination of FAs with lower concentration. The intercellular signaling transduction pathways including JNK/STAT, PI3P/AKT, and MAPK pathways, which could also be activated by PDGF signaling, were predicted to be involved in Fas-induced cytotoxicity. The increased expression of p-STAT3, p-JNK and p-AKT was associated with renal tubular injury. The current study implied the synergistic cytotoxic effect caused by multiple FAs at no toxic dosages via activated cellular transduction pathways regulating cell survival and apoptosis function, which warning of the synergistic toxic effects of different types of FAs.

Cloning and functional analysis of a pacifastin-like protein from the sea cucumber, Apostichopus japonicus.

Pacifastin family proteins play a crucial role in regulating innate immune responses such as phagocytosis in invertebrates. However, the function of the Ajpacifastin-like counterpart in the sea cucumber Apostichopus japonicus remains elusive. In this study, the pacifastin gene of A. japonicus was cloned, characterized and named Ajpacifastin-like. The open reading frame of Ajpacifastin-like is 1497 bp in length and encodes a polypeptide containing 498 amino acid residues. Structural analysis revealed that the protein encoded by Ajpacifastin-like contains two pacifastin light chain domains (amino acids 287-322 and amino acids 376-407). Real-time reverse transcriptase PCR showed that Ajpacifastin-like mRNA is ubiquitously expressed in all tissues examined, with the highest expression in muscle. Ajpacifastin-like mRNA expression was significantly upregulated to 3.27-fold after challenge with Vibrio splendidus for 24 h. To explore the function of the Ajpacifastin-like protein in the immune response of A. japonicus, dsRNA interference with Ajpacifastin-like expression and with the expression of its postulated target gene was performed. Flow cytometry analysis showed that the rate of phagocytosis by coelomocytes increased to 1.21-fold in individuals treated with specific Ajpacifastin-like siRNA. However, rate of phagocytosis by coelomocytes decreased to 86% in individuals treated with Ajphenoloxidase siRNA. These results show that the Ajpacifastin-like gene is ubiquitously expressed in almost all tissues and that Ajpacifastin-like protein acts as an immunomodulatory factor via phenoloxidase to mediate phagocytosis by coelomocytes in pathogen-challenged A. japonicus.

The absence of IL-9 reduces allergic airway inflammation by reducing ILC2, Th2 and mast cells in murine model of asthma.

Allergic asthma is an allergic inflammatory disease of the airways, in which numerous cell types and cytokines have been shown to contribute to pathogenesis of the disease. Although increased expression of IL-9 has been shown to influence the activity of structural as well as eosinophils and mast cells in asthma, the influence of IL-9 on function of ILC2 and Th2 cells remains unclear. This study therefore aimed to elucidate the role of IL-9 on ILC2 and Th2 cells using a murine model of asthma. A murine model of asthma was established using wild type (WT) and IL-9-deficient (Il9-/-) transgenic mice sensitized to house dust mite (HDM). Bronchoalveolar lavage fluid (BALF) and lung tissues were collected, and analysed for inflammatory cells (eosinophils, mast cells, Th2 cells and ILC2 cells), histopathological changes, and several cytokines. HDM challenge significantly increased accumulation of ILC2 cells, Th2 cells and mast cells, as well as goblet cell hyperplasia, and the expression of cytokines IL-4, IL-5 and IL-13, but not IFN-γ, in WT mice compared to saline-challenged control group. In contrast, all pathological changes, including infiltration of ILC2 cells, Th2 cells and mast cells, were significantly attenuated in HDM-challenged Il9-/- mice. Furthermore, the number of Ki67+ILC2 cells, Ki67+Th2 cells and Ki67+mast cells were significantly reduced in the absence of IL-9 signalling. These data suggest that IL-9 promotes the proliferation and type 2 cytokine production of type 2 cells in the murine models of asthma, and therefore might be a potential therapeutic target for asthma treatment.

Nursing Care of 26 Infants Born to Mothers With COVID-19.

BACKGROUND: Novel coronavirus disease (COVID-19) has spread throughout the world; yet, there are few reports of neonatal cases. Thus, information about related clinical care experience is scarce. CLINICAL FINDINGS: This case report includes 26 infants admitted to the neonatal intensive care unit (NICU) of Tongji Hospital in Wuhan City who were born to mothers with suspected/confirmed COVID-19. The nursing and medical staff implemented care of these infants in strict accordance with infection control measures. INTERVENTION: Emergency measures for the prevention and control of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection in the NICU were developed, and neonatal isolation, observation, and treatment were performed. OUTCOMES: Vital signs of the 26 infants remained stable during isolation and treatment, and no complications occurred. During the study period, neither the infants nor the nursing and medical staff were infected with SARS-CoV-2. PRACTICE RECOMMENDATIONS: Based on our strict practices, infants born to mothers with suspected/confirmed COVID-19 should receive care in a single-patient room to support infection control and provide enhanced observation. During initial contact and nursing care, increased attention should be given to the protection of infants born to mothers with suspected/confirmed COVID-19.

Perceived discrimination, ethnic identity, and ethnic-racial socialization in Chinese immigrant families before and after the COVID-19 outbreak: An exploratory natural experiment.

Emerging research from the United States indicates that people with an East Asian background experience COVID-19-related racial discrimination. There is some (although not consistent) evidence that these discrimination experiences can in turn have psychological and behavioral consequences, such as strengthening one's ethnic identity and influencing parents' ethnic-racial socialization practices. The current study presents a unique natural experiment examining self-reported perceived discrimination experiences, ethnic identity, and ethnic-racial socialization among 80 Chinese immigrant mothers in the Netherlands before and after the COVID-19 outbreak (39 mothers recruited before the start of the COVID-19 pandemic and 41 during). The main findings from our exploratory analyses indicated an impact of the pandemic with higher (subtle) discrimination and stronger ethnic identity among Chinese immigrant mothers living in the Netherlands, highlighting how personal experiences related to intergroup processes have changed as a result of the COVID-19 crisis in the European context.

Combined homologous recombination repair deficiency and immune activation analysis for predicting intensified responses of anthracycline, cyclophosphamide and taxane chemotherapy in triple-negative breast cancer.

BACKGROUND: Triple-negative breast cancer (TNBC) is a clinically aggressive disease with abundant variants that cause homologous recombination repair deficiency (HRD). Whether TNBC patients with HRD are sensitive to anthracycline, cyclophosphamide and taxane (ACT), and whether the combination of HRD and tumour immunity can improve the recognition of ACT responders are still unknown. METHODS: Data from 83 TNBC patients in The Cancer Genome Atlas (TCGA) was used as a discovery cohort to analyse the association between HRD and ACT chemotherapy benefits. The combined effects of HRD and immune activation on ACT chemotherapy were explored at both the genome and the transcriptome levels. Independent cohorts from the Molecular Taxonomy of Breast Cancer International Consortium (METABRIC) and Gene Expression Omnibus (GEO) were adopted to validate our findings. RESULTS: HRD was associated with a longer ACT chemotherapy failure-free interval (FFI) with a hazard ratio of 0.16 (P = 0.004) and improved patient prognosis (P = 0.0063). By analysing both HRD status and ACT response, we identified patients with a distinct TNBC subtype (ACT-S&HR-P) that showed higher tumour lymphocyte infiltration, IFN-γ activity and NK cell levels. Patients with ACT-S&HR-P had significantly elevated immune inhibitor levels and presented immune activation associated with the increased activities of both innate immune cells and adaptive immune cells, which suggested treatment with immune checkpoint blockade as an option for this subtype. Our analysis revealed that the combination of HRD and immune activation enhanced the efficiency of identifying responders to ACT chemotherapy (AUC = 0.91, P = 1.06e-04) and synergistically contributed to the clinical benefits of TNBC patients. A transcriptional HRD signature of ACT response-related prognostic factors was identified and independently validated to be significantly associated with improved survival in the GEO cohort (P = 0.0038) and the METABRIC dataset (P < 0.0001). CONCLUSIONS: These findings highlight that HR deficiency prolongs FFI and predicts intensified responses in TNBC patients by combining HRD and immune activation, which provides a molecular basis for identifying ACT responders.

Repeated exposure to inactivated Streptococcus pneumoniae induces asthma-like pathological changes in mice in the presence of IL-33.

While environmental aeroallergens and epithelial alarmins such as IL-33 are firmly implicated in asthma, the possible role of Streptococcus pneumoniae (S. pneumoniae) antigens is less clear. To explore this, wild-type BALB/c mice were repeatedly challenged per-nasally with IL-33 and inactivated S. pneumoniae, either agent alone or diluent control. Some animals were rested then later re-challenged with inactivated S. pneumoniae alone. Serum concentrations of S. pneumoniae lysates-specific IgE were measured in patients with asthma and control subjects. Interestingly, in the presence of IL-33, repeated exposure to inactivated S. pneumoniae induced asthma-like pathological changes accompanied by a systemic adaptive immune response. Subsequent re-exposure of the sensitized animals to inactivated S. pneumoniae alone was able to induce such changes. The concentration of S. pneumoniae lysates-specific IgE was significantly elevated in the asthma patients. These data suggest that antigens derived from infectious microorganisms may participate in generating the mucosal inflammation which characterizes asthma.

Structure, dynamics and functions of UBQLNs: at the crossroads of protein quality control machinery.

Cells rely on protein homeostasis to maintain proper biological functions. Dysregulation of protein homeostasis contributes to the pathogenesis of many neurodegenerative diseases and cancers. Ubiquilins (UBQLNs) are versatile proteins that engage with many components of protein quality control (PQC) machinery in cells. Disease-linked mutations of UBQLNs are most commonly associated with amyotrophic lateral sclerosis (ALS), frontotemporal dementia (FTD), and other neurodegenerative disorders. UBQLNs play well-established roles in PQC processes, including facilitating degradation of substrates through the ubiquitin-proteasome system (UPS), autophagy, and endoplasmic-reticulum-associated protein degradation (ERAD) pathways. In addition, UBQLNs engage with chaperones to sequester, degrade, or assist repair of misfolded client proteins. Furthermore, UBQLNs regulate DNA damage repair mechanisms, interact with RNA-binding proteins (RBPs), and engage with cytoskeletal elements to regulate cell differentiation and development. Important to the myriad functions of UBQLNs are its multidomain architecture and ability to self-associate. UBQLNs are linked to numerous types of cellular puncta, including stress-induced biomolecular condensates, autophagosomes, aggresomes, and aggregates. In this review, we focus on deciphering how UBQLNs function on a molecular level. We examine the properties of oligomerization-driven interactions among the structured and intrinsically disordered segments of UBQLNs. These interactions, together with the knowledge from studies of disease-linked mutations, provide significant insights to UBQLN structure, dynamics and function.

Clonal tumor mutations in homologous recombination genes predict favorable clinical outcome in ovarian cancer treated with platinum-based chemotherapy.

OBJECTIVE: Platinum-based chemotherapy remains the first-line treatment for ovarian carcinoma by inducing DNA damage. The therapeutic impact of clonal and subclonal somatic mutations in DNA damage repair (DDR) pathways remains unexplored. METHODS: We performed an integrated analysis to infer the clonality of somatic deleterious mutations in 385 ovarian carcinomas treated with platinum-based chemotherapy. The Kaplan-Meier method was performed for visualization and the differences between survival curves were calculated by log-rank test. Proportional hazards models were used to estimate relative hazards for platinum-free interval (PFI), progression-free survival (PFS) and overall survival (OS). RESULTS: We found that somatic deleterious mutations in DDR pathways exhibited widespread clonal heterogeneity, and that patients with DDR clonal mutations exhibited a "hypermutator phenotype". Clonal somatic mutations in homologous recombination repair (HRR) pathway were significantly associated with better OS (HR = 0.19 (95% CI, 0.06-0.59), P = 0.0044) and PFS (HR = 0.20 (95% CI, 0.08-0.49), P = 0.0005) than HRR wild-type, while HRR subclonal mutations were not associated with prognosis. Moreover, HRR clonal mutations were associated with significantly higher chemotherapy sensitive rate (P = 0.0027) and longer PFI (HR = 0.20 (95% CI, 0.08-0.49), P = 0.0005) than HRR wild-type, while HRR subclonal mutations were not. We validated our findings using an independent cohort of 93 ovarian cancer patients that received platinum-based chemotherapy. CONCLUSIONS: HRR clonal mutations, but not subclonal mutations, were associated with improved survival, chemotherapy response, and genome instability compared with HRR wild-type.

Wearable and flexible electronics for continuous molecular monitoring.

Wearable biosensors have received tremendous attention over the past decade owing to their great potential in predictive analytics and treatment toward personalized medicine. Flexible electronics could serve as an ideal platform for personalized wearable devices because of their unique properties such as light weight, low cost, high flexibility and great conformability. Unlike most reported flexible sensors that mainly track physical activities and vital signs, the new generation of wearable and flexible chemical sensors enables real-time, continuous and fast detection of accessible biomarkers from the human body, and allows for the collection of large-scale information about the individual's dynamic health status at the molecular level. In this article, we review and highlight recent advances in wearable and flexible sensors toward continuous and non-invasive molecular analysis in sweat, tears, saliva, interstitial fluid, blood, wound exudate as well as exhaled breath. The flexible platforms, sensing mechanisms, and device and system configurations employed for continuous monitoring are summarized. We also discuss the key challenges and opportunities of the wearable and flexible chemical sensors that lie ahead.

O/W Pickering emulsions stabilized by Flammulina velutipes polysaccharide nanoparticles as a fat substitute: the effects of phase separation on emulsified sausage's techno-functional and sensory quality.

BACKGROUND: The application of Pickering emulsion stabilized by food-derived particles is of great interest in the food field, including meat processing. However, the creaming phenomenon is a thorny problem and may impact the resulting product quality. Here, we used polysaccharide nanoparticles from Flammulina velutipes (FVPN) as a stabilizer to prepare a oil/water Pickering emulsion and partly replace the original fat of common emulsified sausage, focusing on exploring the influence of phase separation on the sausage's techno-functional and sensory quality, with the aim of developing a new alternative fat substitute. RESULTS: Reformulated sausages showed increases in moisture (53.24-64.85%) and protein content (11.97-12.76%), but were reduced in fat content (27.28-18.76%). The increased FPOE (FVPN-palm oil emulsion; substitution rate 5-37%) amount in sausages resulted in significantly reduced (P < 0.05) cooking loss (18.87-8.63%). Meanwhile, emulsion improved the springiness and cohesiveness of sausage and significantly reduced (P < 0.05) hardness and chewiness when the replacement amount was less than 20%. Experimental sausages attained a more compact pore structure without harming sensory characteristics. Compared with creaming emulsion, pristine emulsion resulted in a sausage with higher moisture content, lower cooking loss, better elasticity and denser structure. CONCLUSION: The characteristics of sausages could be influenced by emulsion stability. Emulsion, especially with no creaming, can be effectively used as fat substitute at a level of 20% or less without adversely affecting the sensory characteristics of emulsified sausages. The incorporation of FPOE provides the potential for developing a new alternative approach for animal fat improvement in meat products. © 2019 Society of Chemical Industry.

Photocatalytic Micro/Nanomotors: From Construction to Applications.

Synthetic micro/nanomotors (MNMs) are a particular class of micrometer or nanometer scale devices with controllable motion behavior in solutions by transferring various energies (chemical, optical, acoustic, magnetic, electric, etc.) into mechanical energy. These tiny devices can be functionalized either chemically or physically to accomplish complex tasks in a microcosm. Up to now, MNMs have exhibited great potential in various fields, ranging from environmental remediation, nanofabrication, to biomedical applications. Recently, light-driven MNMs as classic artificial MNMs have attracted much attention. Under wireless remote control, they can perform reversible and repeatable motion behavior with immediate photoresponse. Photocatalytic micro/nanomotors (PMNMs) based on photocatalysts, one of the most important light-driven MNMs, can utilize energy from both the external light source and surrounding chemicals to achieve efficient propulsion. Unlike other kinds of MNMs, the PMNMs have a unique characteristic: photocatalytic property. On one hand, since photocatalysts can convert both optical and chemical energy inputs into mechanical propulsion of PMNMs via photocatalytic reactions, the propulsion generated can be modulated in many ways, such as through chemical concentration or light intensity. In addition, these PMNMs can be operated at low levels of optical and chemical energy input which is highly desired for more practical scenarios. Furthermore, PMNMs can be operated with custom features, including go/stop motion control through regulating an on/off switch, speed modulation through varying light intensities, direction control through adjusting light source position, and so forth. On the other hand, as superoxide radicals can be generated by photocatalytic reactions of activated photocatalysts, the PMNMs show great potential in environment remediation, especially in organic pollutant degradation. In order to construct more practical PMNMs for future applications and further extend their application fields, the ideal PMNMs should be operated in a fully environmentally friendly system with strong propulsion. In the past decade, great progress in the construction, motion regulation, and application of PMNMs has been achieved, but there are still some challenges to realize the perfect system. In this Account, we will summarize our recent efforts and those of other groups in the development toward attractive PMNM systems. First, we will illustrate basic principles about the photocatalytic reactions of photocatalysts and demonstrate how the photocatalytic reactions affect the propulsion of PMNMs. Then, we will illustrate the construction strategies for highly efficient and biocompatible PMNMs from two key aspects: (1) Improvement of energy conversion efficiency to achieve strong propulsion of PMNMs. (2) Expansion of the usable wavelengths of light to operate PMNMs in environment-friendly conditions. Next, potential applications of PMNMs have been described. In particular, environment remediation has taken major attention for the applications of PMNMs due to their photocatalytic properties. Finally, in order to promote the development of PMNMs which can be operated in fully green environments for more practical applications, an outlook of key challenges and opportunities in construction of ideal PMNMs is presented.