The effect of different types of virtual influencers on consumers’ emotional attachment

A virtual influencer (VI) is a computer-generated, imagery-based digital character. It has become one of the hottest marketing trends, motivating researchers to investigate how consumers perceive VIs. However, consumers’ emotional attachment and benefit seeking behaviour to different types of VIs has remained under-investigated. Therefore, considering the level of perceived humanness and appearance realism, this research examines how consumers’ emotional attachment and benefit seeking differs across the three types of VI (i.e., mimic-human VI, animated-human VI, and non-human VI). We further propose that VIs may influence consumer emotional attachment and different benefit seeking behaviour through social presence because, specifically, when a VI shows a higher level of social presence, a higher level of emotional attachment and stronger benefit seeking behaviour will result. The experimental studies lend support to our theorization. This research provides insights into the different types of VIs in marketing literature and extends the context of social presence theory

Levo-Tetrahydropalmatine Attenuates Cocaine Self-Administration under a Progressive-Ratio Schedule and Cocaine Discrimination in Rats

Levo-tetrahydropalmatine (l-THP) is an alkaloid found in many traditional Chinese herbal preparations and has a unique pharmacological profile that includes dopamine receptor antagonism. Previously we demonstrated that l-THP attenuates fixed-ratio (FR) cocaine self-administration (SA) and cocaine-induced reinstatement in rats at doses that do not alter food-reinforced responding. This study examined the effects of l-THP on cocaine and food SA under progressive-ratio (PR) schedules of reinforcement and the discriminative stimulus effects of cocaine. In adult male Sprague–Dawley rats self-administering cocaine (0.5 or 1.0 mg/kg/inf), l-THP significantly reduced breaking points at the 1.875, 3.75 and 7.5 mg/kg doses. l-THP also reduced the breaking point and response rate for PR SA of sucrose-sweetened food pellets, although the decrease was significant only at the 7.5 mg/kg l-THP dose. In rats trained to discriminate cocaine (10 mg/kg, ip) from saline, l-THP (1.875, 3.75 and 7.5 mg/kg) produced a rightward shift in the dose–response curve for cocaine generalization. During generalization testing, l-THP reduced response rate, but only at the 7.5 mg/kg dose. l-THP also prevented substitution of the dopamine D2/D3 receptor agonist, (±) 7-OH-DPAT, for cocaine suggesting a potential role for antagonism of D2 and/or D3 receptors in the effects of l-THP. These data further demonstrate that l-THP attenuates the reinforcing and subjective effects of cocaine at doses that do not produce marked motor effects and provide additional evidence that l-THP may have utility for the management of cocaine addiction

Astrocyte-derived thrombospondins mediate the development of hippocampal presynaptic plasticity in vitro

Astrocytes contribute to many neuronal functions, including synaptogenesis, but their role in the development of synaptic plasticity remains unclear. Presynaptic muting of hippocampal glutamatergic terminals defends against excitotoxicity. Here we studied the role of astrocytes in the development of presynaptic muting at glutamatergic synapses in rat hippocampal neurons. We found that astrocytes were critical for the development of depolarization-dependent and G(i/o)-dependent presynaptic muting. The ability of cAMP analogues to modulate presynaptic function was also impaired by astrocyte deficiency. Although astrocyte deprivation resulted in postsynaptic glutamate receptor deficits, this effect appeared independent of astrocytes’ role in presynaptic muting. Muting was restored with chronic, but not acute, treatment with astrocyte-conditioned medium, indicating that a soluble factor is permissive for muting. Astrocyte-derived thrombospondins (TSPs) are likely responsible because TSP1 mimicked the effect of conditioned medium, and gabapentin, a high-affinity antagonist of TSP binding to the α2δ-1 calcium channel subunit, mimicked astrocyte deprivation. We found evidence that protein kinase A activity is abnormal in astrocyte-deprived neurons but restored by TSP1, so protein kinase A dysfunction may provide a mechanism by which muting is disrupted during astrocyte deficiency. In summary our results suggest an important role for astrocyte-derived TSPs, acting through α2δ-1, in maturation of a potentially important form of presynaptic plasticity

The era of multigene panels comes? The clinical utility of Oncotype DX and MammaPrint

The AJCC Cancer Staging Manual, eighth edition published in late 2016, will become the new global guideline for cancer diagnosis and treatment from January 1, 2018. The new edition for the tumor staging system has numerous updates, including building up the prognostic stage group of tumors for the first time and adding a large number of non-anatomical factors into the prognostic evaluation. Oncotype DX and MammaPrint are two of the genomic predictors that will be part of routine clinical practice in the future. Numerous studies have proved the clinical utility of multigene panels in predicting clinical outcome and treatment response. Here we present our review of the studies on these multigene panels and their application to breast cancer

Twist1 Controls Lung Vascular Permeability and Endotoxin-Induced Pulmonary Edema by Altering Tie2 Expression

Tight regulation of vascular permeability is necessary for normal development and deregulated vascular barrier function contributes to the pathogenesis of various diseases, including acute respiratory distress syndrome, cancer and inflammation. The angiopoietin (Ang)-Tie2 pathway is known to control vascular permeability. However, the mechanism by which the expression of Tie2 is regulated to control vascular permeability has not been fully elucidated. Here we show that transcription factor Twist1 modulates pulmonary vascular leakage by altering the expression of Tie2 in a context-dependent way. Twist1 knockdown in cultured human lung microvascular endothelial cells decreases Tie2 expression and phosphorylation and increases RhoA activity, which disrupts cell-cell junctional integrity and increases vascular permeability in vitro. In physiological conditions, where Ang1 is dominant, pulmonary vascular permeability is elevated in the Tie2-specific Twist1 knockout mice. However, depletion of Twist1 and resultant suppression of Tie2 expression prevent increase in vascular permeability in an endotoxin-induced lung injury model, where the balance of Angs shifts toward Ang2. These results suggest that Twist1-Tie2-Angs signaling is important for controlling vascular permeability and modulation of this mechanism may lead to the development of new therapeutic approaches for pulmonary edema and other diseases caused by abnormal vascular permeability

The role of JAM-B in cancer and cancer metastasis (Review)

The junctional adhesion molecule B (JAM-B) is a multifunctional transmembrane protein, which belongs to the immunoglobulin superfamily (IgSF). JAM-B is localized to cell-cell contacts and enriched at cell junctions in epithelial and endothelial cells, as well as on the surface of erythrocytes, leukocytes, and platelets. Recent research in this field has shown that JAM-B plays an important role in numerous cellular processes, such as tight junction assembly, spermatogenesis, regulation of paracellular permeability, leukocytic transmigration, angiogenesis, tumor metastasis and cell proliferation. This study provides a new research direction for the diagnosis and treatment of relevant diseases. In this review, we briefly focus on what is currently known about the structure, function, and mechanism of JAM-B, with particular emphasis on cancer

The effect of virtual mindfulness-based interventions on sleep quality: A systematic review of randomized controlled trials

PURPOSE OF REVIEW: We summarized peer-reviewed literature investigating the effect of virtual mindfulness-based interventions (MBIs) on sleep quality. We aimed to examine the following three questions: (1) do virtual MBIs improve sleep quality when compared with control groups; (2) does the effect persist long-term; and (3) is the virtual delivery method equally feasible compared to the in-person delivery method? RECENT FINDINGS: Findings suggest that virtual MBIs are equivalent to evidence-based treatments, and to a limited extent, more effective than non-specific active controls at reducing some aspects of sleep disturbance. Overall, virtual MBIs are more effective at improving sleep quality than usual care controls and waitlist controls. Studies provide preliminary evidence that virtual MBIs have a long-term effect on sleep quality. Moreover, while virtual MBI attrition rates are comparable to in-person MBI attrition rates, intervention adherence may be compromised in the virtual delivery method. This review highlights virtual MBIs as a potentially effective alternative to managing sleep disturbance during pandemic-related quarantine and stay-at-home periods. This is especially relevant due to barriers of accessing in-person interventions during the pandemic. Future studies are needed to explore factors that influence adherence and access to virtual MBIs, with a particular focus on diverse populations

LRP5 Regulates Development of Lung Microvessels and Alveoli through the Angiopoietin-Tie2 Pathway

Angiogenesis is crucial for lung development. Although there has been considerable exploration, the mechanism by which lung vascular and alveolar formation is controlled is still not completely understood. Here we show that low-density lipoprotein receptor-related protein 5 (LRP5), a component of the Wnt ligand-receptor complex, regulates angiogenesis and alveolar formation in the lung by modulating expression of the angiopoietin (Ang) receptor, Tie2, in vascular endothelial cells (ECs). Vascular development in whole mouse lungs and in cultured ECs is controlled by LRP5 signaling, which is, in turn, governed by a balance between the activities of the antagonistic Tie2 ligands, Ang1 and Ang2. Under physiological conditions when Ang1 is dominant, LRP5 knockdown decreases Tie2 expression and thereby, inhibits vascular and alveolar development in the lung. Conversely, when Ang2 dominates under hyperoxia treatment in neonatal mice, high LRP5 and Tie2 expression suppress angiogenesis and lung development. These findings suggest that the LRP5-Tie2-Ang signaling axis plays a central role in control of both angiogenesis and alveolarization during postnatal lung development, and that deregulation of this signaling mechanism might lead to developmental abnormalities of the lung, such as are observed in bronchopulmonary dysplasia (BPD)

Epithelial protein lost in neoplasm-α (EPLIN-α) is a potential prognostic marker for the progression of epithelial ovarian cancer

Epithelial protein lost in neoplasm-α (EPLIN-α) is a cytoskeletal protein whose expression is often lost or is aberrant in cancerous cells and tissues and whose loss is believed to be involved in aggressive phenotypes. This study examined this molecule in human epithelial ovarian tissues and investigated the cellular impact of EPLIN-α on ovarian cancer cells (EOC), SKOV3 and COV504. The expression of EPLIN-α in human ovarian tissues and EOC was assessed at both the mRNA and protein levels using reverse transcription-PCR (RT-PCR) and immunohistochemistry, respectively. In vitro assays for cellular matrix adhesion and migration (confirmed by an electrical cell substrate impedance sensing (ECIS) based method), invasion and cell growth were employed in order to assess the biological influence of EPLIN-α expression on EOC cells. Immunohistochemical analysis of ovarian cancer samples demonstrated that only a small number expressed EPLIN-α protein. Downregulation of EPLIN-α protein in EOC cell lines increased the growth, invasion, adhesion and migration in vitro. This EPLIN-α downregulation may have a prognostic value. From these data, we conclude that downregulation of EPLIN-α may be associated with poorer patient prognosis, and that this molecule appears to play a tumour suppressor role by inhibition of EOC growth and migration

Effect of junctional adhesion molecule-2 expression on cell growth, invasion and migration in human colorectal cancer

The junctional adhesion molecule (JAMs) family belongs to the immunoglobulin subfamily involved in the formation of tight junctions (TJ) in both endothelial and epithelial cells. Aberrant expression of JAM-2 is associated with cancer progression but little work has been carried out in discovering how this affects changes in cell behaviour. The present study aimed to examine the expression of JAM-2 in human colon cancer specimens and cell lines and its role in the development of colon cancer. JAM-2 expression in human colon cancer specimens (normal, n=75; cancer, n=94) and cell lines was analysed using quantitative real-time PCR and conventional RT-PCR. Colon cancer cells were stably transfected with a mammalian expression vector to overexpress JAM-2-Flag. The effect on growth, adhesion and migration following overexpression of JAM-2 was then investigated using in vitro models. TJ function was assessed using a trans-epithelial resistance assay (TER, with an EVOM voltammeter). JAM-2 was lowly expressed in colon cancer cells such as RKO, HT115. JAM-2 overexpression in RKO cells (RKO-JAM-2) and HT115 cells (HT115-JAM-2) showed retarded adhesion (P<0.05). An in vivo tumour model showed that RKO-JAM-2 had significantly reduced growth (P<0.05), invasion (P<0.05) and migration (P<0.05) as well as in HT115-JAM-2, except on proliferation and migration. Expression of JAM-2 resulted in a significant increase in TER and decrease in permeability of polarized monolayers (P<0.05). Further analysis of JAM-2 transcript levels against clinical aspects demonstrated that the decreasing JAM-2 expression correlated to disease progression, metastasis and poor survival. Taken together, JAM-2 may function as a putative tumour suppressor in the progression and metastasis of colorectal cance