The Role of Social Media Influencers in China Beauty Industry: Consumers’ Perspective

This study aims to explore the role of social media influencers in China beauty industry from the perspective of consumers. Existing literature on the topic mainly focus on the role of social media influencers in promoting products or building consumers customer relationships and brand awareness. The primary platforms being studied by scholars are also some social media platforms in the Western. Therefore, this study emphasizes on the beauty industry in the context of the Chinese market, including probing the social media platforms Chinese consumers use, consumers’ psychological mechanism in using beauty products, and the role social media influencers play in consumers selecting and purchasing beauty products. The study utilises in-depth interview technique of qualitative research method to seek consumers’ perceptions about the aspects mentioned above. The findings give clear answers about the social media platforms that Chinese consumers use. It also reveals that consumers are relying on using beauty products to construct self-identification and enhance self-esteem. As indicated from the data, consumers are more goal-driven and utility-driven while following social media influencers. They perceive the type of content shared by influencers, the personality and appearance of influencers as crucial factors that influence their attention to different social media influencers. Although consumers admit the importance of social media influencers for them to gain beauty products information, to learn makeup skills and attain entertainment, consumers’ trust to influencers is declining. On the one hand, experienced users are becoming more rational and rely less on social media influencers while consuming beauty products. Therefore, they tend to search for the information while they need rather than regularly follow the updates of influencers. On the other hand, there are too many commercials in influencers’ content, and some of the influencers are perceived unprofessional while sharing products or teaching skills, which also lowered the credibility of social media influencers. The findings also reflect a trend that consumers may incline more to word-of-mouth communication and professional help from specialized medical institutions

Japanese Encephalitis Virus wild strain infection suppresses dendritic cells maturation and function, and causes the expansion of regulatory T cells

<p>Abstract</p> <p>Background</p> <p>Japanese encephalitis (JE) caused by Japanese encephalitis virus (JEV) accounts for acute illness and death. However, few studies have been conducted to unveil the potential pathogenesis mechanism of JEV. Dendritic cells (DCs) are the most prominent antigen-presenting cells (APCs) which induce dual humoral and cellular responses. Thus, the investigation of the interaction between JEV and DCs may be helpful for resolving the mechanism of viral escape from immune surveillance and JE pathogenesis.</p> <p>Results</p> <p>We examined the alterations of phenotype and function of DCs including bone marrow-derived DCs (bmDCs) <it>in vitro </it>and spleen-derived DCs (spDCs) <it>in vivo </it>due to JEV P3 wild strain infection. Our results showed that JEV P3 infected DCs <it>in vitro </it>and <it>in vivo</it>. The viral infection inhibited the expression of cell maturation surface markers (CD40, CD80 and CD83) and MHCⅠ, and impaired the ability of P3-infected DCs for activating allogeneic naïve T cells. In addition, P3 infection suppressed the expression of interferon (IFN)-α and tumor necrosis factor (TNF)-α but enhanced the production of chemokine (C-C motif) ligand 2 (CCL2) and interleukin (IL)-10 of DCs. The infected DCs expanded the population of CD4+ Foxp3+ regulatory T cell (Treg).</p> <p>Conclusion</p> <p>JEV P3 infection of DCs impaired cell maturation and T cell activation, modulated cytokine productions and expanded regulatory T cells, suggesting a possible mechanism of JE development.</p

The relationship between self-efficacy and aggressive behavior in boxers: the mediating role of self-control

P. 1-9El comportamiento agresivo ha sido uno de los temas centrales de la psicología deportiva, mientras que el comportamiento agresivo de los boxeadores ha recibido una atención limitada. Aunque algunas publicaciones informaron que la autoeficacia se relaciona con el comportamiento agresivo, el mecanismo por el cual la autoeficacia afecta el comportamiento agresivo no está claro. El presente estudio investigó la relación entre la autoeficacia y el comportamiento agresivo, así como el efecto del autocontrol como factor mediador. Este estudio utiliza la Escala de autoeficacia para atletas, el Cuestionario de autocontrol para atletas y el Cuestionario de agresión de Buss-Perry. Esta relación se explora a través de medidas auto-informadas de N = 414 boxeadores profesionales chinos, n = 243 eran hombres y n = 171 mujeres, la edad promedio fue M = 17.72 años (SD = 3.147), los participantes, el número promedio de los años de ejercicio fueron M = 3.89 años (SD = 2.734); Los resultados mostraron que los boxeadores masculinos reportaron mayor agresividad que las boxeadoras; se encontró que la autoeficacia y el autocontrol mejoraron a medida que aumentaba la edad de los participantes; A mayor nivel de competencia, mayores niveles de autoeficacia y autocontrol; La autoeficacia se relacionó negativamente con el comportamiento agresivo y se correlacionó positivamente con el autocontrol. El autocontrol también se correlacionó negativamente con el comportamiento agresivo entre los boxeadores. El autocontrol tuvo un efecto de mediación total en la relación entre la autoeficacia y el comportamiento agresivoS

Time series study on the effect of low air pollution level NO2 On the death of residents from cardiovascular and cerebrovascular diseases

Objective: To explore the impact of low-level atmospheric nitrogen dioxide (NO2) on the death risk of cardiovascular and cerebrovascular diseases in Enshi City, so as to provide scientific basis for locating sensitive populations and formulating population health policiesmethods the monitoring of air pollutants, meteorological factors and death data of residents from cardiovascular and cerebrovascular diseases in Enshi City from 2015 to 2018 were collected. The generalized additive model based on Poisson distribution was used to analyze the impact of low air pollution level NO2 on the death risk of cardiovascular and cerebrovascular diseases in Enshi City, and subgroup analysis was carried out on age, gender and seasonresults the average concentrations of major gaseous pollutants in Enshi from 2015 to 2018 were NO2 (21.40 μg/m3), sulfur dioxide (so, 9.68 μg/m3). Carbon oxide (CO, 0.88 mg/m3) and ozone (O, 61.21 μg/m3). The results of single pollutant model analysis show that every increase of NO2 concentration in the total population μg/m, the risk of death from cardiovascular and cerebrovascular diseases on the same day (lag0) will increase by 0.33% (-0.06%~0.72%) (P&gt;0.05); In the female population, every 1% increase in NO2 concentration μg/m, the death risk of cardiovascular and cerebrovascular diseases with cumulative lag of 1 day (lag01) will increase by 0.92% (0.26%~1.56%) (P &lt; 0.05); In the cold season, every increase of NO2 concentration μg/m, the death risk of cardiovascular and cerebrovascular diseases in the whole population on the same day (lag0) will increase by 0.62% (0.12%~1.12%) (P &lt; 0.05). The results of the two pollutant model show that after controlling other gaseous pollutants (SO2, Co or O3), the impact of NO2 on the death risk of cardiovascular and cerebrovascular diseases in women and the whole population in cold season still exists. Conclusion: Low pollution level of NO2 in Enshi City will increase the death risk of cardiovascular and cerebrovascular diseases among women and the whole population in cold season. Attention should be paid to the health protection of special populations in low pollution areas and in special seasons

MRI-based radiomics features uncover the micro-change of dorsal root ganglia lesion for patients with post-herpetic neuralgia

ObjectiveTo create and authenticate MRI-based radiomic signatures to identify dorsal root ganglia (DRG) lesions in post-herpetic neuralgia (PHN) patients generalizable and interpretable.MethodThis prospective diagnostic study was conducted between January 2021 and February 2022. Lesioned DRG in patients with PHN and normal DRG in age-, sex-, height-, and weight-matched healthy controls were selected for assessment and divided into two groups (8:2) randomly: training and testing sets. The least absolute shrinkage and selection operator algorithm was employed to generate feature signatures and construct a model, followed by the assessment of model efficacy using the area under the curve (AUC) of the receiver operating characteristic (ROC), as well as sensitivity and specificity metrics.ResultsThe present investigation involved 30 patients diagnosed with postherpetic neuralgia (PHN), consisting of 18 males and 12 females (mean age 60.70 ± 10.18 years), as well as 30 healthy controls, comprising 18 males and 12 females (mean age 58.13 ± 10.54 years). A total of 98 DRG were randomly divided into two groups (8:2), namely a training set (n = 78) and a testing set (n = 20). Five radiomic features were chosen to construct the models. In the training dataset, the area under the curve (AUC) was 0.847, while the sensitivity and specificity were 71.79 and 97.44%, respectively. In the test dataset, the AUC was 0.87, and the sensitivity and specificity were 80.00 and 100.00%, respectively.ConclusionAn MRI-based radiomic signatures model has the capacity to uncover the micro-change of damaged DRG in individuals afflicted with postherpetic neuralgia

Resveratrol Enhances Autophagic Flux and Promotes Ox-LDL Degradation in HUVECs via Upregulation of SIRT1

Oxidized low-density lipoprotein- (Ox-LDL-) induced autophagy dysfunction in human vascular endothelial cells contributes to the development of atherosclerosis (AS). Resveratrol (RSV) protects against Ox-LDL-induced endothelium injury. The objective of this study was to determine the mechanisms underlying Ox-LDL-induced autophagy dysfunction and RSV-mediated protection in human umbilical vein endothelial cells (HUVECs). The results showed that Ox-LDL suppressed the expression of sirtuin 1 (SIRT1) and increased LC3-II and sequestosome 1 (p62) protein levels without altering p62 mRNA levels in HUVECs. Pretreatment with bafilomycin A1 (BafA1) to inhibit lysosomal degradation abrogated the Ox-LDL-induced increase in LC3-II protein level. Ox-LDL increased colocalization of GFP and RFP puncta in mRFP-GFP-tandem fluorescent LC3- (tf-LC3-) transfected cells. Moreover, Ox-LDL decreased the expression of mature cathepsin D and attenuated cathepsin D activity. Pretreatment with RSV increased the expression of SIRT1 and LC3-II and increased p62 protein degradation. RSV induced RFP-LC3 aggregation more than GFP-LC3 aggregation. RSV restored lysosomal function and promoted Ox-LDL degradation in HUVECs. All the protective effects of RSV were blocked after SIRT1 was knocked down. These findings demonstrated that RSV upregulated the expression of SIRT1, restored lysosomal function, enhanced Ox-LDL-induced impaired autophagic flux, and promoted Ox-LDL degradation through the autophagy-lysosome degradation pathway in HUVECs

Evidence for an oncogenic role of HOXC6 in human non-small cell lung cancer

Background Identification of specific biomarkers is important for the diagnosis and treatment of non-small cell lung cancer (NSCLC). HOXC6 is a homeodomain-containing transcription factor that is highly expressed in several human cancers; however, its role in NSCLC remains unknown. Methods The expression and protein levels of HOXC6 were assessed in NSCLC tissue samples by Quantitative real-time PCR (qRT-PCR) and immunohistochemistry, respectively. HOXC6 was transfected into the NSCLC cell lines A549 and PC9, and used to investigate its effect on proliferation, migration, and invasion using CFSE, wound healing, and Matrigel invasion assays. Next-generation sequencing was also used to identify downstream targets of HOXC6 and to gain insights into the molecular mechanisms underlying its biological function. Results HOXC6 expression was significantly increased in 66.6% (20/30) of NSCLC tumor samples in comparison to normal controls. HOXC6 promoted proliferation, migration, and invasion of NSCLC cells in vitro. RNA-seq analysis demonstrated the upregulation of 310 and 112 genes in A549-HOXC6 and PC9-HOXC6 cells, respectively, and the downregulation of 665 and 385 genes in A549-HOXC6 and PC9-HOXC6 cells, respectively. HOXC6 was also found to regulate the expression of genes such as CEACAM6, SPARC, WNT6, CST1, MMP2, and KRT13, which have documented pro-tumorigenic functions. Discussion HOXC6 is highly expressed in NSCLC, and it may enhance lung cancer progression by regulating the expression of pro-tumorigenic genes involved in proliferation, migration, and invasion. Our study highlighted the oncogenic potential of HOXC6, and suggests that it may be a novel biomarker for the diagnosis and treatment of NSCLC