The Investigation of Hedonic Consumption, Impulsive Consumption and Social Sharing in E-commerce Live-streaming Videos

The use of online live-streaming videos to promote brands and products in e-commerce is “exploding” in China. Whereas, little is known about the mechanism underlying viewers/ audience participating behavior in the rapidly growing online live-streaming videos for commerce phenomenon. Based on the stimulus–organism–response paradigm, this study endeavors to investigate the effects of content and social features (information quality, broadcaster attractiveness and para-social interaction) of on customers cognitive and emotional state (cognitive assimilation and emotional energy) and the subsequently their responses (hedonic consumption, impulsive consumption, and social sharing). 200 valid respondents were collected via cross-sectional online survey websites. The research results provide empirical evidences to support most of our hypotheses, indicating that hedonic consumption and social sharing behavior are determined by emotional energy and cognitive assimilation. These cognitive and emotional states, are influenced by information quality, broadcaster attractiveness, and para-social interaction. Impulsive consumption is only determined by emotional energy

GPER-induced signaling is essential for the survival of breast cancer stem cells.

G protein-coupled estrogen receptor-1 (GPER), a member of the G protein-coupled receptor (GPCR) superfamily, mediates estrogen-induced proliferation of normal and malignant breast epithelial cells. However, its role in breast cancer stem cells (BCSCs) remains unclear. Here we showed greater expression of GPER in BCSCs than non-BCSCs of three patient-derived xenografts of ER- /PR+ breast cancers. GPER silencing reduced stemness features of BCSCs as reflected by reduced mammosphere forming capacity in vitro, and tumor growth in vivo with decreased BCSC populations. Comparative phosphoproteomics revealed greater GPER-mediated PKA/BAD signaling in BCSCs. Activation of GPER by its ligands, including tamoxifen (TMX), induced phosphorylation of PKA and BAD-Ser118 to sustain BCSC characteristics. Transfection with a dominant-negative mutant BAD (Ser118Ala) led to reduced cell survival. Taken together, GPER and its downstream signaling play a key role in maintaining the stemness of BCSCs, suggesting that GPER is a potential therapeutic target for eradicating BCSCs

α-Lactosylceramide Protects Against iNKT-Mediated Murine Airway Hyperreactivity and Liver Injury Through Competitive Inhibition of Cd1d Binding.

Invariant natural killer T (iNKT) cells, which are activated by T cell receptor (TCR)-dependent recognition of lipid-based antigens presented by the CD1d molecule, have been shown to participate in the pathogenesis of many diseases, including asthma and liver injury. Previous studies have shown the inhibition of iNKT cell activation using lipid antagonists can attenuate iNKT cell-induced disease pathogenesis. Hence, the development of iNKT cell-targeted glycolipids can facilitate the discovery of new therapeutics. In this study, we synthesized and evaluated α-lactosylceramide (α-LacCer), an α-galactosylceramide (α-GalCer) analog with lactose substitution for the galactose head and a shortened acyl chain in the ceramide tail, toward iNKT cell activation. We demonstrated that α-LacCer was a weak inducer for both mouse and human iNKT cell activation and cytokine production, and the iNKT induction by α-LacCer was CD1d-dependent. However, when co-administered with α-GalCer, α-LacCer inhibited α-GalCer-induced IL-4 and IFN-γ production from iNKT cells. Consequently, α-LacCer also ameliorated both α-GalCer and GSL-1-induced airway hyperreactivity and α-GalCer-induced neutrophilia when co-administered in vivo. Furthermore, we were able to inhibit the increases of ConA-induced AST, ALT and IFN-γ serum levels through α-LacCer pre-treatment, suggesting α-LacCer could protect against ConA-induced liver injury. Mechanistically, we discerned that α-LacCer suppressed α-GalCer-stimulated cytokine production through competing for CD1d binding. Since iNKT cells play a critical role in the development of AHR and liver injury, the inhibition of iNKT cell activation by α-LacCer present a possible new approach in treating iNKT cell-mediated diseases

A Fungal Glycosphingolipid Directly Activates Natural Killer T Cells and Rapidly Induces Airways Disease

Aspergillus fumigatusis a saprophytic fungus that is ubiquitous in the environment and commonly associated with allergic sensitization and severe asthma in humans. Although A. fumigatus is recognized by multiple microbial pattern recognition receptors, we identified and synthesized an A. fumigatus glycosphingolipid, asperamide B, that directly activated invariant natural killer T (iNKT) cells in vitro in a CD1d-restricted, MyD88- and dectin-1-independent fashion. Moreover, asperamide B, when loaded into CD1d, directly stained, and was sufficient to activate, iNKT cells. In vivo, asperamide B rapidly induced airway hyperreactivity, a cardinal feature of asthma, by activating pulmonary iNKT cells in an IL-33-ST2-dependent fashion. Asperamide B is thus the first fungal glycolipid found to directly activate iNKT cells. These results extend the range of microorganisms that can be directly detected by iNKT cells to the Kingdom of Fungi, and may explain the effectiveness of A. fumigatus in causing severe chronic respiratory diseases in humans

Extract from Periostracum cicadae

Periostracum cicadae is widely used for the treatment of skin diseases such as eczema, pruritus, and itching. The current study sought to evaluate the effect of P. cicadae extract on ultraviolet B (UVB) irradiation and identify the mechanisms involved. Photodamage-protective activity of P. cicadae extracts against oxidative challenge was screened using HaCaT keratinocytes. P. cicadae extracts did not affect cell viability but decreased reactive oxygen species (ROS) production. The extract attenuates the expression of interleukin-6 (IL-6), matrix metalloproteinase-2 (MMP-2), and MMP-9 in UVB-treated HaCaT cells. Also, P. cicadae abrogated UVB-induced activation of NF-κB, p53, and activator protein-1 (AP-1). The downmodulation of IL-6 by P. cicadae was inhibited by the p38 inhibitor (SB203580) or JNK inhibitor (SP600125). Moreover, the extract attenuated the expression of NF-κB and induced thrombomodulin in keratinocytes and thereby effectively downregulated inflammatory responses in the skin. The nuclear accumulation and expression of NF-E2-related factor (Nrf2) were increased by P. cicadae treatment. Furthermore, treatment with P. cicadae remarkably ameliorated the skin’s structural damage induced by irradiation. This study demonstrates that P. cicadae may protect skin cells against oxidative insult by modulating ROS concentration, IL-6, MMPs generation, antioxidant enzymes activity, and cell signaling pathways

Low-cell-number, single-tube amplification (STA) of total RNA revealed transcriptome changes from pluripotency to endothelium

Table S1. Summary of the sequencing results. The alignments against the GRCh38 genome assembly (Aligned Reads) were counted for exon reads (exon) and transcript reads based on GENCODE v22. Intronic counts (intron) were defined by transcript counts minus exon ones. Nontranscript reads were used to obtain tRNA counts (tRNA) based on the tRNA database of GENCODE v22. Nontranscript and non-tRNA reads were used for counts on repetitive sequences (repeats) based on RepeatMasker. Those not belonging to any category were defined as unannotated reads (unannotated). The counting of exonic features was based on the “gene_type” attribute in GENCODE v22. The percentages of mature miRNA reads were defined by reads aligned exclusively to the mature “miRNA” feature divided by reads aligned to the “miRNA_primary_transcript” feature of miRBase v21. (DOCX 42 kb

Facile bioactive transformation of magnesium alloy surfaces for surgical implant applications

The market for orthopedic implant alloys has seen significant growth in recent years, and efforts to reduce the carbon footprint of medical treatment (i.e., green medicine) have prompted extensive research on biodegradable magnesium-based alloys. Magnesium alloys provide the mechanical strength and biocompatibility required of medical implants; however, they are highly prone to corrosion. In this study, Mg-9Li alloy was immersed in cell culture medium to simulate degradation in the human body, while monitoring the corresponding effects of the reaction products on cells. Variations in pH revealed the generation of hydroxyl groups, which led to cell death. At day-5 of the reaction, a coating of MgCO3 (H2O)3, HA, and α -TCP appeared on sample surfaces. The coating presented three-dimensional surface structures (at nanometer to submicron scales), anti-corrosion effects, and an altered surface micro-environment conducive to the adhesion of osteoblasts. This analysis based on bio-simulation immersion has important implications for the clinical use of Mg alloys to secure regenerated periodontal tissue