Advances in Research on Water-in-Water Emulsions Based on the Stabilization Mechanism of Pickering Emulsions

Water-in-water emulsions, which have a very low interfacial tension and a thick interfacial layer, are formed by two thermodynamically incompatible hydrophilic macromolecules in a certain proportion. It has been reported that the system cannot be stabilized by surfactants, but can avoid macroscopic phase separation by gelation of one or two phases. Recently, it has been found that the stability of water-in-water emulsions can be improved by the irreversible adsorption of solid particles at the interface based on the stabilization mechanism of oil-in-water Pickering emulsions. In this review, we summarize recent advances in research on the stabilization of water-in-water emulsions, and focus on the stability of Pickering emulsions stabilized by solid particles and its influential factors, as well as its applications in the food field. It is expected that this review will provide new ideas for food structure design based on the stabilization of water-in-water emulsions

Simultaneous suppression of PKM2 and PHGDH elicits synergistic anti-cancer effect in NSCLC

Metabolic reprogramming is a hallmark of human cancer. Cancer cells exhibit enhanced glycolysis, which allows glycolytic intermediates to be diverted into several other biosynthetic pathways, such as serine synthesis. Here, we explored the anti-cancer effects of the pyruvate kinase (PK) M2 inhibitor PKM2-IN-1 alone or in combination with the phosphoglycerate dehydrogenase (PHGDH) inhibitor NCT-503 in human NSCLC A549 cells in vitro and in vivo. PKM2-IN-1 inhibited proliferation and induced cell cycle arrest and apoptosis, with increased glycolytic intermediate 3-phosphoglycerate (3-PG) level and PHGDH expression. The combination of PKM2-IN-1 and NCT-503 further suppressed cancer cell proliferation and induced G2/M phase arrest, accompanied by the reduction of ATP, activation of AMPK and inhibition of its downstream mTOR and p70S6K, upregulation of p53 and p21, as well as downregulation of cyclin B1 and cdc2. In addition, combined treatment triggered ROS-dependent apoptosis by affecting the intrinsic Bcl-2/caspase-3/PARP pathway. Moreover, the combination suppressed glucose transporter type 1 (GLUT1) expression. In vivo, co-administration of PKM2-IN-1 and NCT-503 significantly inhibited A549 tumor growth. Taken together, PKM2-IN-1 in combination with NCT-503 exhibited remarkable anti-cancer effects through induction of G2/M cell cycle arrest and apoptosis, in which the metabolic stress induced ATP reduction and ROS augmented DNA damage might be involved. These results suggest that the combination of PKM2-IN-1 and NCT-503 might be a potential strategy for the therapy of lung cancer

Advances in Gel Stability Improvement of Yoghurt

Yoghurt has high nutritional value and health-promoting functions; however, its quality defects such as whey syneresis and poor coagulation affect the sensory experience of consumers. Researchers commonly use food macromolecules to improve the gel stability and sensory properties of yoghurt by modifying the formation of gel networks or inducing the gelation of milk protein. In this review, we summarize the texture defects of yogurt, the factors influencing them, and the strategies to improve the gel stability of yogurt as well as the underlying mechanism. Also, we discuss future trends. This review will provide important guidance for improving the quality and stability of yoghurt products

FoxG1 Directly Represses Dentate Granule Cell Fate During Forebrain Development

The cortex consists of 100s of neuronal subtypes that are organized into distinct functional regions; however, the mechanisms underlying cell fate determination remain unclear. Foxg1 is involved in several developmental processes, including telencephalic patterning, cell proliferation and cell fate determination. Constitutive disruption of Foxg1 leads to the transformation of cortical neurons into Cajal-Retzius (CR) cells, accompanied by a substantial expansion of the cortical hem through the consumption of the cortex. However, rather than the induction of a cell fate switch, another group has reported a large lateral to medial repatterning of the developing telencephalon as the explanation for this change in cell type output. Here, we conditionally disrupted Foxg1 in telencephalic progenitor cells by crossing Foxg1fl/fl mice with Nestin-CreERTM mice combined with tamoxifen (TM) induction at distinct developmental stages beginning at E10.5 to further elucidate the role of FoxG1 in cell fate determination after telencephalon pattern formation. The number of dentate gyrus (DG) granule-like cells was significantly increased in the cortex. The increase was even detected after deletion at E14.5. In vivo mosaic deletion and in vitro cell culture further revealed a cell-autonomous role for FoxG1 in repressing granule cell fate. However, the cortical hem, which is required for the patterning and the development of the hippocampus, was only slightly enlarged and thus may not contribute to the cell fate switch. Lef1 expression was significantly upregulated in the lateral, cortical VZ and FoxG1 may function upstream of Wnt signaling. Our results provide new insights into the functions of FoxG1 and the mechanisms of cell fate determination during telencephalic development

Neural oscillations during acupuncture imagery partially parallel that of real needling

IntroductionTasks involving mental practice, relying on the cognitive rehearsal of physical motors or other activities, have been reported to have similar patterns of brain activity to overt execution. In this study, we introduced a novel imagination task called, acupuncture imagery and aimed to investigate the neural oscillations during acupuncture imagery.MethodsHealthy volunteers were guided to watch a video of real needling in the left and right KI3 (Taixi point). The subjects were then asked to perform tasks to keep their thoughts in three 1-min states alternately: resting state, needling imagery left KI3, and needling imagery right KI3. Another group experienced real needling in the right KI3. A 31-channel-electroencephalography was synchronously recorded for each subject. Microstate analyses were performed to depict the brain dynamics during these tasks.ResultsCompared to the resting state, both acupuncture needling imagination and real needling in KI3 could introduce significant changes in neural dynamic oscillations. Moreover, the parameters involving microstate A of needling imagery in the right KI3 showed similar changes as real needling in the right KI3.DiscussionThese results confirm that needling imagination and real needling have similar brain activation patterns. Needling imagery may change brain network activity and play a role in neural regulation. Further studies are needed to explore the effects of acupuncture imagery and the potential application of acupuncture imagery in disease recovery

Loss of Smad7 Promotes Inflammation in Rheumatoid Arthritis

Objective: Smad7 is an inhibitory Smad and plays a protective role in many inflammatory diseases. However, the roles of Smad7 in rheumatoid arthritis (RA) remain unexplored, which were investigated in this study.Methods: The activation of TGF-β/Smad signaling was examined in synovial tissues of patients with RA. The functional roles and mechanisms of Smad7 in RA were determined in a mouse model of collagen-induced arthritis (CIA) in Smad7 wild-type (WT) and knockout (KO) CD-1 mice, a strain resistant to autoimmune arthritis induction.Results: TGF-β/Smad3 signaling was markedly activated in synovial tissues of patients with RA, which was associated with the loss of Smad7, and enhanced Th17 and Th1 immune response. The potential roles of Smad7 in RA were further investigated in a mouse model of CIA in Smad7 WT/KO CD-1 mice. As expected, Smad7-WT CD-1 mice did not develop CIA. Surprisingly, CD-1 mice with Smad7 deficiency developed severe arthritis including severe joint swelling, synovial hyperplasia, cartilage damage, massive infiltration of CD3+ T cells and F4/80+ macrophages, and upregulation of proinflammatory cytokines IL-1β, TNFα, and MCP-1. Further studies revealed that enhanced arthritis in Smad7 KO CD-1 mice was associated with increased Th1, Th2 and, importantly, Th17 over the Treg immune response with overactive TGF-β/Smad3 and proinflammatory IL-6 signaling in the joint tissues.Conclusions: Smad7 deficiency increases the susceptibility to autoimmune arthritis in CD-1 mice. Enhanced TGF-β/Smad3-IL-6 signaling and Th17 immune response may be a mechanism through which disrupted Smad7 causes autoimmune arthritis in CD-1 mice

Causal analysis of coach and bus accidents in China based on road alignments

Given the complexity and the difficulty of controlling contributors effectively, road passenger transport often results in serious injuries and fatalities. The purpose of this study is to identify the main contributors to coach and bus accidents and to provide policy recommendations for making improvements in accident prevention. The Driving Reliability and Error Analysis Method 3.0 (DREAM 3.0) was modified and used to analyze the contributing factors (i.e. phenotypes and genotypes in DREAM) and their casual mechanisms. By having statistical analysis and social network analysis (SNA) adopted, the main genotypes and phenotypes of the DREAM charts were identified. The results of the study showed that A2.1 (too high speed) was the key phenotype and the main genotypic process chain leading to the phenotype was “inadequate safety management → inadequate training → inadequate skills/knowledge → misjudgment of the situation → too high speed” on all types of road. For A2.1 (too high speed), C2 (misjudgment of the situation) was the dominant genotype, while N5 (inadequate safety management) was the root cause of most genotypes. This suggests that road passenger transport companies, as the responsible parties, often fail to implement or violate safety prevention and control systems. Government regulators should promote the policy system and incentivize them to fulfil their safety management responsibilities. The government should also educate the public and improve the road environment to reduce passenger-related risks and the impact of environmental factors on drivers

Recent Progress in Research on [2.2]Paracyclophane-Based Dyes

In recent years, the [2.2]paracyclophane (PCP) ring has attracted extensive attention due to its features of providing not only chirality and electron-donating ability but also steric hindrance, which reduces intermolecular π–π stacking interactions and thereby improves the fluorescence properties of dyes. To date, some circularly polarized luminescence (CPL)-active small organic molecules based on the PCP skeleton have been reviewed; however, the application of the PCP ring in improving the photophysical properties of fluorescent dyes is still limited, and new molecular design strategies are still required. This review summarizes and promotes the application of PCP in fluorescent dye design, fluorescence detection, and CPL modulation. We expect that this review will provide readers with a comprehensive understanding of the PCP skeleton and lead to further improvement in fluorescent dye design

The Pekin duck programmed death ligand-2: cDNA cloning, genomic structure, molecular characterization and expression analysis

Programmed death-1 (PD-1), upon engagement by its ligands, programmed death ligand-1 (PD-L1) and programmed death ligand-2 (PD-L2), provides signals that attenuate adaptive immune responses. Here we describe the identification of the Pekin duck PD-L2 (duPD-L2) and its gene structure. The duPD-L2 cDNA encodes a 321 amino acid protein that has an amino acid identity of 76% and 35% with chicken and human PD-L2, respectively. Mapping of the duPD-L2 cDNA with duck genomic sequences revealed an exonic structure similar to that of the human Pdcd1lg2 gene. Homology modelling of the duPD-L2 protein was compatible with the murine PD-L2 ectodomain structure. Residues known to be important for PD-1 receptor binding of murine PD-L2 were mostly conserved in duPD-L2 within sheets A and G and partially conserved within sheets C and F. DuPD-L2 mRNA was constitutively expressed in all tissues examined with highest expression levels in lung, spleen, cloaca, bursa, cecal tonsil, duodenum and very low levels of expression in muscle, kidney and brain. Lipopolysaccharide treatment of adherent duck PBMC upregulated duPD-L2 mRNA expression. Our work shows evolutionary conservation of the PD-L2 ectodomain structure and residues important for PD-1 binding in vertebrates including fish. The information provided will be useful for further investigation of the role of duPD-L2 in the regulation of duck adaptive immunity and exploration of PD-1-targeted immunotherapies in the duck hepatitis B infection model. Keywords: Programmed death ligand-2, Gene cloning, Genomic organization, Homology modelling, Expression analysis, Pekin duc