How Online Extended Reality (XR) Promotes Consumer Offline Engagement

Using extended-reality (XR) simulation to replicate physical surroundings has become increasingly prevalent in engaging online consumers with offline businesses. However, the efficacy of this XR technology remains ambiguous. To justify the huge investments in XR-related technologies, we investigate the impacts of extended surroundings on consumers’ offline engagement with associated businesses. Specifically, we utilize a natural experimental design on a leading housing platform that applies XR simulation to present the surrounding environment of housing estates. By combining propensity score matching and difference-in-differences, our findings indicate that extended surroundings increase consumer offline engagement outcomes, particularly word-of-mouth volume, and valence. Furthermore, we examine the heterogeneous effects moderated by three business characteristics. To our knowledge, this is the first to examine the impacts of XR simulation of extended surroundings. Therefore, this research offers significant implications for the literature and practice related to XR and omnichannel marketing

Fixed Point Theory and Positive Solutions for a Ratio-Dependent Elliptic System

We consider a ratio-dependent predator-prey model under zero Dirichlet boundary condition. By using topological degree theory and fixed index theory, we study the necessary and sufficient conditions for the existence of positive solutions. Then we present the asymptotic behavior analysis of positive solutions, by bifurcation theory and energy estimates

Comparison of antidiabetic drugs added to sulfonylurea monotherapy in patients with type 2 diabetes mellitus: A network meta-analysis.

AIMS:This study aimed to investigate the efficacy and safety of dual therapy comprising sulfonylurea (SU) plus antidiabetic drugs for the treatment of type 2 diabetes mellitus (T2DM). METHODS:We searched the PubMed, Cochrane library, and Embase databases for randomized clinical trials (≥24 weeks) published up to December 28, 2017. Subsequently, we conducted pairwise and network meta-analyses to calculate the odds ratios (ORs) and mean differences (MDs) with 95% confidence intervals (CIs) of the outcomes. RESULTS:The final analyses included 24 trials with a total of 10,032 patients. Compared with placebo, all treatment regimens were associated with a significantly higher risk of hypoglycemia, except the combinations of SU plus sodium-glucose co-transporter-2 inhibitor (SGLT-2i) [OR, 1.35 (95% CI: 0.81 to 2.25)] or alpha-glucosidase inhibitor (AGI) [OR, 1.16 (95% CI: 0.55 to 2.44)]. Notably, the combination of SU plus glucagon-like peptide-1 receptor agonist (GLP-1RA) was associated with the most significant increase in the risk of hypoglycemia. Furthermore, all SU-based combination regimens reduced the glycated hemoglobin (HbA1c) and fasting plasma glucose levels (FPG). However, only combinations containing SGLT-2i [MD, -1.00 kg (95% CI: -1.73 to -0.27)] and GLP-1RA [MD, -0.56 kg (95% CI: -1.10 to -0.02)] led to weight loss. CONCLUSIONS:Our findings highlight the importance of considering the risk of hypoglycemia when selecting antidiabetic drugs to be administered concomitantly with SU. Although all classes of antidiabetic drugs improved glucose control when administered in combination with SU, SGLT-2i might be the best option with respect to factors such as hypoglycemia and body weight

Agonist-induced activation of human FFA1 receptor signals to extracellular signal-regulated kinase 1 and 2 through Gq- and Gi-coupled signaling cascades

Abstract Background FFA1 is abundantly expressed in the liver, skeletal muscle, monocytes and nervous system, but is particularly abundant in pancreatic β cells. It is widely believed that FFA1 exerts its regulatory roles in a variety of physiological and pathological functions. In response to oleic acid, FFA1 has been shown to induce the activation of extracellular signal-regulated kinase 1 and 2 (ERK1/2) through a mechanism involving EGFR transactivation in a breast cancer cell line. However, the underlying molecular mechanism for ERK1/2 activation mediated by n-6 free fatty acid (LA) in HEK293 cells remains to be further elucidated. Methods A FLAG-FFA1 vector was stably expressed in HEK293 cells. Western blot analysis was applied to investigate the change in LA-induced ERK1/2 phosphorylation change in response to kinase inhibitors. Arrestin-2/3-specific siRNA was used to analyze the effect of arrestin-2/3 knockdown on FFA1-mediated ERK1/2 activation. Results We proved that activation of ERK1/2 by LA was rapid, peaking at 5 min. Further experiments proved that FFA1 couples to a Gq protein and activates PI-PLC, which induces the IP3/Ca2+ and DAG/PKC signal pathways, both of which are involved in ERK1/2 activation. We also showed that there is no EGFR transactivation, arrestin-2/3 or Gβγ pathway participation in ERK1/2 phosphorylation. Treating cells with PTX abolished ERK1/2 activation at a late time point (≥20 min), indicating a critical role for Gi subunits in FFA1-mediated ERK1/2 activation. Conclusions Our study provides a detailed delineation of the LA-mediated activation of ERK1/2 in HEK293 cells that are stably transfected with human FFA1. We also present evidence of Gi/Gq-induced synergism in the regulation of ERK1/2 phosphorylation. These observations may provide new insights into the pharmacological effects of FFA1 and the physiological functions modulated by FFA1-mediated activation of ERK1/2

Additional file 1: Figure S1. of Agonist-induced activation of human FFA1 receptor signals to extracellular signal-regulated kinase 1 and 2 through Gq- and Gi-coupled signaling cascades

Forskolin did not mimic the effect of PTX. A. Serum-starved FFA1-HEK293 cells were pretreated with DMSO or Forskolin (10μM) for 1h, and the cells were then stimulated with 10μM LA for the indicated time. ERK1/2 phosphorylation was assessed by Western blot as described in the Experimental Procedures and corresponding immunoblots were quantified by Bio-Rad Quantity One Imaging system. B. FFA1-HEK293 and HEK293 cells were exposed to PTX(100ng/ml) for indicated time, and than cell viabilities were evaluated by CCK8 assay at OD450nm. Error bars represent the SEM for three replicates. The data shown are representative of at least three replicate independent experiments. Data were analyzed using Student’s t-test (* p<0.001). (DOC 2835 kb