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Even though the presence and use of mobile augmented reality (MAR) technology has become increasingly popular in the field of marketing and advertising in recent years, it has largely been neglected in the study of consumer behavior research. This paper utilizes a single-group posttest-only quasi-experimental design to investigate how the feature of mobile augmented reality application influences consumers’ attitude and purchasing intention as explained by the dimensions of persuasion (i.e., consumers’ cognitive, affective, and conative dimensions). Structural Equation Modeling (SEM) with SPSS and AMOS is used to analyze the psychometric survey data collected from 179 participants. The results supported the prediction that MAR application’s real-time interactivity and entertainment increase cognition and affection, respectively; while irritation with MAR application decreases affection. The unsupported hypothesis, which predicted a positive relationship between informativeness and cognition, came as a surprise. The overall result of the study demonstrates the positive influence of MAR application in enhancing consumers’ purchasing intention. Finally, implications and future research directions are discussed.

Poly ADP-ribosylation (PARylation) is a post-translational modification process. Following the discovery of PARP-1, numerous studies have demonstrated the role of PARylation in the DNA damage and repair responses for cellular stress and DNA damage. Originally, studies on PARylation were confined to PARP-1 activation in the DNA repair pathway. However, the interplay between PARylation and DNA repair suggests that PARylation is important for the efficiency and accuracy of DNA repair. PARylation has contradicting roles; however, recent evidence implicates its importance in inflammation, metabolism, and cell death. These differences might be dependent on specific cellular conditions or experimental models used, and suggest that PARylation may play two opposing roles in cellular homeostasis. Understanding the role of PARylation in cellular function is not only important for identifying novel therapeutic approaches; it is also essential for gaining insight into the mechanisms of unexplored diseases. In this review, we discuss recent reports on the role of PARylation in mediating diverse cellular functions and homeostasis, such as DNA repair, inflammation, metabolism, and cell death.

Protease-activated receptor 1 (PAR1), a G protein-coupled receptor, plays a central role in coordinating multiple phases of cutaneous wound healing, including hemostasis, cell proliferation, migration, and extracellular matrix remodeling. Despite its therapeutic potential, PAR1-selective positive allosteric modulators (PAMs) remain limited. Here, we characterized the wound healing efficacy of gestodene, a third-generation progestin previously identified as a selective PAM of PAR1. Gestodene exhibited no intrinsic agonist activity but selectively potentiated PAR1-activating peptide (PAR1-AP)-induced calcium signaling without affecting PAR2 or PAR4 responses. Consistently, gestodene induced a concentration-dependent leftward shift in the PAR1-AP dose-response curve. Notably, gestodene enhanced PAR1-dependent cell proliferation, migration, and ERK1/2 activation, effects abolished by PAR1 knockout or pharmacological inhibition with vorapaxar in human keratinocytes (HaCaT) and dermal fibroblasts (HDF). Gestodene also potentiated the expression of wound healing-associated genes, including matrix metalloproteinases (MMP-1, -2, -3, -10), fibronectin, and type I collagen (COL1A1). In a murine wound model, topical administration of gestodene accelerated wound closure, achieving complete re-epithelialization by Day 8 and significantly enhancing collagen deposition, effects reversed by vorapaxar. Collectively, these findings demonstrate that gestodene accelerates cutaneous wound healing through PAR1-selective positive allosteric modulation and supports its potential as a drug repositioning candidate for wound repair.

The evolution of mobile communication technology has brought about significant changes in the way people communicate. However, the lack of nonverbal cues in computer-mediated communication can make the accurate interpretation of emotions difficult. This study proposes a novel approach for using emotions as active input in mobile systems. This approach combines psychological and neuroscientific principles to accurately and comprehensively assess an individual’s emotions for use as input in mobile systems. The proposed technique combines facial and heart rate information to recognize users’ five prime emotions, which can be implemented on mobile devices using a front camera and a heart rate sensor. A user evaluation was conducted to verify the efficacy and feasibility of the proposed technique, and the results showed that users could express emotions faster and more accurately, with average recognition accuracies of 90% and 82% for induced and intended emotional expression, respectively. The proposed technique has the potential to enhance the user experience and provide more personalized and dynamic interaction with mobile systems.

IntroductionCytokine Release Syndrome (CRS) is a life-threatening complication of T-cell-engaging immunotherapies, causing vascular leakage and multi-organ dysfunction. Standard Interleukin-6 (IL-6) blockade often fails in severe cases by leaving the upstream initiator, Tumor Necrosis Factor-α (TNF-α), unchecked. TNF-α drives early macrophage activation and endothelial injury, whereas IL-6 amplifies systemic inflammation. To decisively interrupt this inflammatory feedback loop, we developed IDC007, a novel bispecific antibody simultaneously neutralizing TNF-α and IL-6 receptor (IL-6R).MethodsWe evaluated the neutralizing effects of IDC007 in an in vitro CRS model utilizing OKT3/R848-stimulated human peripheral blood mononuclear cells and human umbilical vein endothelial cells. Furthermore, we utilized an OKT3-induced humanized CRS mouse model to assess in vivo target engagement and therapeutic efficacy.ResultsIn vitro, IDC007 effectively suppressed pro-inflammatory cytokine secretion (e.g., TNF-α, IFN-γ) and prevented endothelial barrier dysfunction. In vivo, IDC007 successfully engaged both targets. Administration mitigated physiological deterioration, including hypothermia and weight loss, leading to improved survival. Dual inhibition effectively prevented immune hyperactivation, evidenced by the significant attenuation of splenomegaly and lung-specific organ damage.DiscussionThese findings serve as a preclinical proof-of-concept demonstrating that dual targeting of TNF-α and IL-6R offers a potent mechanistic approach to attenuate severe CRS by preserving vascular endothelial integrity and overcoming the therapeutic limitations of conventional monotherapies.

Systemic lupus erythematosus (SLE) is a chronic autoimmune disease that affects multiple organs. Recent studies suggest relevance between cysteine protease cathepsin S (CTSS) expression and SLE. To investigate the mechanism of CTSS in SLE, CTSS-overexpressing transgenic (TG) mice were generated, and induced lupus-like symptoms. Eight months later, the TG mice spontaneously developed typical SLE symptoms regardless of the inducement. Furthermore, we observed increased toll-like receptor 7 (TLR7) expression with increased monocyte and neutrophil populations in the TG mice. In conclusion, overexpression of CTSS in mice influences TLR7 expression, autoantibodies and IFN-α, which leads to an autoimmune reaction and exacerbates lupus-like symptoms.

The inner ear is the hub where hair cells (HCs) transduce sound, gravity, and head acceleration stimuli to the brain. Hearing and balance rely on mechanosensation, the fastest sensory signals transmitted to the brain. The mechanoelectrical transducer (MET) channel is the entryway for the sound-balance-brain interface, but the channel-complex composition is not entirely known. Here, we report that the mouse utilizes Piezo1 (Pz1) and Piezo2 (Pz2) isoforms as MET-complex components. The Pz channels, expressed in HC stereocilia, and cell lines are co-localized and co-assembled with MET complex partners. Mice expressing non-functional Pz1 and Pz2 at the ROSA26 locus have impaired auditory and vestibular traits that can only be explained if the Pzs are integral to the MET complex. We suggest that Pz subunits constitute part of the MET complex and that interactions with other MET complex components yield functional MET units to generate HC MET currents. The identity of hair cells’ mechanoelectrical transduction (MET) channel-complex components is unknown. Here, the authors used multiple biochemical, genetic, and functional approaches to show that mouse hair cells utilize Piezo1 and Piezo2 isoforms as part of the MET-complex component.

The mitochondrial glutamine transporter SLC1A5ᵥar plays a central role in the metabolic reprogramming of cancer cells by facilitating glutamine import into mitochondria for energy production and redox homeostasis. Despite its critical function, the development of effective and selective inhibitors targeting SLC1A5ᵥar has remained a significant challenge. Here, we introduce iMQT₀20, a selective allosteric inhibitor identified through structure-based screening. iMQT₀20 disrupts the trimeric assembly of SLC1A5ᵥar, causing metabolic crisis in cancer cells and selectively suppressing their growth. Mechanistically, iMQT₀20 reduces glutamine anaplerosis and oxidative phosphorylation, resulting in a broad disruption of cancer metabolism. Additionally, iMQT₀20 treatment epigenetically upregulates PD-L1 expression, enhancing the efficacy of combination therapies with anti-PD-L1 immune checkpoint inhibitors. These findings highlight the therapeutic potential of targeting SLC1A5ᵥar as a critical metabolic vulnerability in cancer and demonstrate that targeting allosteric interprotomer interactions is a novel and promising therapeutic strategy for cancer treatment. Glutamine addiction is a hallmark of many cancers. iMQT₀20, a first-in-class allosteric inhibitor of the mitochondrial glutamine transporter SLC1A5ᵥar, disrupts glutamine-dependent mitochondrial metabolism, selectively killing cancer cells and enhancing immune checkpoint inhibitor efficacy.

Myelosuppression is a major adverse effect of chemotherapy. With the increasing number of cancer patients worldwide, there is a growing interest in therapeutic approaches that reduce the adverse effects of chemotherapy. Nakai (AGN) roots have been widely used in oriental medicine to treat blood-related diseases, including cancer. However, the effects of AGN on myelosuppression have not been studied. Here, we investigated the effects of AGN ethanol extract (AGNEX) on cyclophosphamide-induced myelosuppression. AGNEX treatment significantly decreased white blood cell levels while increasing red blood cell and platelet levels in the peripheral blood. It inhibited thymus and spleen atrophy. It also enhanced serum levels of interleukin (IL)-6 and tumor necrosis factor (TNF)-α. qRT-PCR results showed that AGNEX decreased the expression of IL-1b and stem cell factor (SCF) in the bone marrow (BM) while increasing the mRNA expression of IL-3 and IL-6 in the spleen. Although AGNEX did not significantly decrease apoptosis and cell cycle arrest in the BM and splenocytes, AGNEX plays a positive role in cyclophosphamide-induced myelosuppression. AGNEX administration increased BM cells in the femur while decreasing apoptotic BM cells. These findings suggest that AGNEX could be used to treat myelosuppression and as a combination therapy in cancer patients.

Lapachone is a natural naphthoquinone-derived compound found in . It is well-known for its analgesic, anti-inflammatory, anti-microbial, diuretic, and anti-cancerous effects. However, the wound-healing effects of this compound are not known yet. The aim of this study was to investigate the wound healing activity of naphthoquinones (α-lapachone and β-lapachone) from . Expression of Sirt3, migration-related proteins (Rac1, Cdc42, α-Pak) and angiogenesis-related protein of vascular endothelial growth factor (VEGF) was monitored using western blot analysis. Blood vessel formation and tissue development were monitored by angiogenesis assay and hematoxylin & eosin (H & E) staining, respectively on mouse skin tissue samples. Both α-lapachone and β-lapachone increased Sirt3 expression , but only β-lapachone increased Sirt3 expression Both the compounds accelerated wound healing in cultured skin cells as well as mouse skin; however, β-lapachone was more effective at lower concentrations. Both of the compounds increased the expression of migration-related proteins both and . Similarly, α-lapachone and β-lapachone increased VEGF expression, tissue development and blood vessel formation in mouse skin. These findings indicated that α-lapachone and β-lapachone are novel Sirt3 activators, and Sirt3 has a role in wound healing. Thus, Sirt3 and its regulators come out as a novel target and potential drug candidates, respectively in the important field of cutaneous wound healing.