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1,612 result(s) for "Wang, Yu-Han"
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Oxygen Defect Engineering Promotes Synergy Between Adsorbate Evolution and Single Lattice Oxygen Mechanisms of OER in Transition Metal‐Based (oxy)Hydroxide
The oxygen evolution reaction (OER) activity of transition metal (TM)‐based (oxy)hydroxide is dominated by the number and nature of surface active sites, which are generally considered to be TM atoms occupying less than half of surface sites, with most being inactive oxygen atoms. Herein, based on an in situ competing growth strategy of bimetallic ions and OH − ions, a facile one‐step method is proposed to modulate oxygen defects in NiFe‐layered double hydroxide (NiFe‐LDH)/FeOOH heterostructure, which may trigger the single lattice oxygen mechanism (sLOM). Interestingly, by only varying the addition of H 2 O 2 , one can simultaneously regulate the concentration of oxygen defects, the valence of metal sites, and the ratio of components. The proper oxygen defects promote synergy between the adsorbate evolution mechanism (AEM, metal redox chemistry) and sLOM (oxygen redox chemistry) of OER in NiFe‐based (oxy)hydroxide, practically maximizing the use of surface TM and oxygen atoms as active sites. Consequently, the optimal NiFe‐LDH/FeOOH heterostructure outperforms the reported non‐noble OER catalysts in electrocatalytic activity, with an overpotential of 177 mV to deliver a current density of 20 mA cm −2 and high stability. The novel strategy exemplifies a facile and versatile approach to designing highly active TM‐LDH‐based OER electrocatalysts for energy and environmental applications.
Galectin-9 interacts with PD-1 and TIM-3 to regulate T cell death and is a target for cancer immunotherapy
The two T cell inhibitory receptors PD-1 and TIM-3 are co-expressed during exhausted T cell differentiation, and recent evidence suggests that their crosstalk regulates T cell exhaustion and immunotherapy efficacy; however, the molecular mechanism is unclear. Here we show that PD-1 contributes to the persistence of PD-1 + TIM-3 + T cells by binding to the TIM-3 ligand galectin-9 (Gal-9) and attenuates Gal-9/TIM-3-induced cell death. Anti-Gal-9 therapy selectively expands intratumoral TIM-3 + cytotoxic CD8 T cells and immunosuppressive regulatory T cells (T reg cells). The combination of anti-Gal-9 and an agonistic antibody to the co-stimulatory receptor GITR (glucocorticoid-induced tumor necrosis factor receptor-related protein) that depletes T reg cells induces synergistic antitumor activity. Gal-9 expression and secretion are promoted by interferon β and γ, and high Gal-9 expression correlates with poor prognosis in multiple human cancers. Our work uncovers a function for PD-1 in exhausted T cell survival and suggests Gal-9 as a promising target for immunotherapy. Galectin-9 regulates several cellular processes including TIM-3-mediated T cell death. Here the authors show that co-expressed PD-1 protects TIM-3 + T cells from galectin-9-induced cell death and that anti-galectin-9 in combination with GITR agonism promotes an anti-tumor immune response.
Consumer attitudes and purchase intentions towards internet celebrity self-brands: an integrated view of congruence, brand authenticity and internet celebrity involvement
Purpose Internet celebrities have become key resources for consumers making purchase decisions. An increasing number of internet celebrities have begun to exert their influence by creating self-branded products. This study aims to examine the antecedents of consumer attitudes and purchase intentions towards internet celebrity self-brands by integrating cognitive consistency theory, cue utilisation theory and the literature on brand authenticity and celebrity involvement. Design/methodology/approach Two sub-samples of different social media brand communities were collected via online surveys of consumers with experience purchasing targeted internet celebrity self-brands. Partial least squares structural equation modelling (PLS-SEM) was used to analyse the data. Findings The results of the two sub-samples provide convergent evidence that brand–consumer congruence, brand authenticity and internet celebrity involvement have positive correlations with consumer attitudes towards internet celebrity self-brands, which then positively correlate with purchase intentions in both psychological (Sub-sample 1) and social (Sub-sample 2) brand communities. Originality/value To the best of the authors’ knowledge, this research is the first to develop a comprehensive model of consumers’ attitudes towards internet celebrity self-brands, which predict purchase intentions. The model is empirically tested in different social media brand communities, and the convergent results show the power of the proposed model. Internet celebrity involvement is proposed as a key driver of brand attitudes, which has received little attention. We conceptualise internet celebrity involvement and develop a scale to measure it. Based on the findings, we propose strategies to improve the marketing effectiveness of internet celebrity self-brands.
Adipocyte-derived kynurenine promotes obesity and insulin resistance by activating the AhR/STAT3/IL-6 signaling
Aberrant amino acid metabolism is a common event in obesity. Particularly, subjects with obesity are characterized by the excessive plasma kynurenine (Kyn). However, the primary source of Kyn and its impact on metabolic syndrome are yet to be fully addressed. Herein, we show that the overexpressed indoleamine 2,3-dioxygenase 1 (IDO1) in adipocytes predominantly contributes to the excessive Kyn, indicating a central role of adipocytes in Kyn metabolism. Depletion of Ido1 in adipocytes abrogates Kyn accumulation, protecting mice against obesity. Mechanistically, Kyn impairs lipid homeostasis in adipocytes via activating the aryl hydrocarbon receptor (AhR)/Signal transducer and activator of transcription 3 /interleukin-6 signaling. Genetic ablation of AhR in adipocytes abolishes the effect of Kyn. Moreover, supplementation of vitamin B6 ameliorated Kyn accumulation, protecting mice from obesity. Collectively, our data support that adipocytes are the primary source of increased circulating Kyn, while elimination of accumulated Kyn could be a viable strategy against obesity. Kynurenine, a tryptophan metabolite, is increased in the circulating plasma of obese individuals, but the source has been unclear. Here, the authors show in mice that mature adipocytes produce kynurenine, with vitamin B6 administration preventing accumulation and protecting against high-fat diet.
Implications of Angiogenesis Involvement in Arthritis
Angiogenesis, the growth of new blood vessels, is essential in the pathogenesis of joint inflammatory disorders such as rheumatoid arthritis (RA) and osteoarthritis (OA), facilitating the invasion of inflammatory cells and increase in local pain receptors that contribute to structural damage and pain. The angiogenic process is perpetuated by various mediators such as growth factors, primarily vascular endothelial growth factor (VEGF) and hypoxia-inducible factors (HIFs), as well as proinflammatory cytokines, various chemokines, matrix components, cell adhesion molecules, proteases, and others. Despite the development of potent, well-tolerated nonbiologic (conventional) and biologic disease-modifying agents that have greatly improved outcomes for patients with RA, many remain resistant to these therapies, are only partial responders, or cannot tolerate biologics. The only approved therapies for OA include symptom-modifying agents, such as analgesics, non-steroidal anti-inflammatory drugs (NSAIDs), steroids, and hyaluronic acid. None of the available treatments slow the disease progression, restore the original structure or enable a return to function of the damaged joint. Moreover, a number of safety concerns surround current therapies for RA and OA. New treatments are needed that not only target inflamed joints and control articular inflammation in RA and OA, but also selectively inhibit synovial angiogenesis, while preventing healthy tissue damage. This narrative review of the literature in PubMed focuses on the evidence illustrating the therapeutic benefits of modulating angiogenic activity in experimental RA and OA. This evidence points to new treatment targets in these diseases.
Understanding Senior Adults’ Needs, Preferences, and Experiences of Commercial Exergames for Health: Usability Study
Many senior adults are at risk of mental and physical disorders due to a lack of sufficient exercise. Therefore, adherent exercise should be urgently promoted to improve senior adults' muscle strength, preventing falls and conditions caused by physical and cognitive decline. However, off-the-shelf exercise games, so-called exergames, are mainly targeted at the younger generation or children, while senior adults are neglected, when this age group strongly needs exercise. Exergames could serve as a health intervention for promoting exercise. This study aimed to investigate senior adults' experience, perceptions, and acceptance of game technology to promote exercise in order to suggest game design guidelines. In this usability study, participants engaged in playing Nintendo Switch and Xbox Kinect games, after which semistructured interviews were conducted. Before the gameplay, the participants provided their background information, exercise habits, and use of technology products. Next, all participants completed a workshop including 3 activities (brief instructions on how to play the games: 20 minutes; playing the selected exergames: 80 minutes; semistructured interviews: 20 minutes) for 2 hours a day for 3 days each. The participants played the latest Nintendo Switch games (eg, Just Dance, Boxing, Ring Fit Adventure) and Xbox Kinect games (eg, Kinect Adventures!, Mini Games). Just Dance, Zumba, and Boxing were played in activity 1; Ring Fit Adventure and Mini Games in activity 2; and Kinect Adventures! in activity 3. Reflexive thematic analysis was applied to identify the relative themes generated from the interviews. In total, 22 participants (mean age 70.4, SD 6.1 years) were enrolled in the workshop in May 2021. The results of the generated themes included incomprehension of game instructions, psychological perception of game technology, and game art preferences. The subthemes generated from game art preferences included favorite game genres, characters, and scenes. There is a significant need for customized game tutorials considering senior adults' cognitive and physical aging. Furthermore, the adventure game genre is preferable to other games. Humanlike game characters are preferable, especially those with a fit and healthy body shape. Nature scenes are more enjoyable than indoor stages or rooms. Furthermore, the game intensity design and playing time should be carefully planned to meet the World Health Organization's criteria for physical activity in older adults. Intelligent recommendation systems might be helpful to support older adults with various health conditions. The guidelines suggested in this study might be beneficial for game design, exercise training, and game technology adoption of exergames for older adults to improve health.
Stout camphor tree genome fills gaps in understanding of flowering plant genome evolution
We present reference-quality genome assembly and annotation for the stout camphor tree ( Cinnamomum kanehirae (Laurales, Lauraceae)), the first sequenced member of the Magnoliidae comprising four orders (Laurales, Magnoliales, Canellales and Piperales) and over 9,000 species. Phylogenomic analysis of 13 representative seed plant genomes indicates that magnoliid and eudicot lineages share more recent common ancestry than monocots. Two whole-genome duplication events were inferred within the magnoliid lineage: one before divergence of Laurales and Magnoliales and the other within the Lauraceae. Small-scale segmental duplications and tandem duplications also contributed to innovation in the evolutionary history of Cinnamomum . For example, expansion of the terpenoid synthase gene subfamilies within the Laurales spawned the diversity of Cinnamomum monoterpenes and sesquiterpenes. A high-quality reference genome of the stout camphor tree reveals its genome evolution and supports that magnoliid and eudicot lineages share more common ancestry relative to monocots.
Effective six-band model and unconventional spin-singlet pairing in Kagome superconductor CsV3Sb5
Recently synthesized Kagome compounds AV3Sb5 attract great attention due to the unusual coexistence of the topology, charge density wave, and superconductivity. In this work, based on the band structures for CsV3Sb5 in the pristine phase, we construct an effective six-band model for the low-energy processes; utilizing the random phase approximation on the effective six-band model, we show that the E1u (p wave) pairing dominates in the region of 0
A 4‐month‐old female infant with complete colonic duplication presenting with stool leaking out of the vestibule
Complete colonic duplication (Figure 1E) and double appendixes (Figure 1F) were discovered through the laparoscopy. [...]instead of excision of the duplicated colon, the patient was treated with anastomosis of the duplicated colon to the native colon (Figure 1E), alongside ligation of the fistula and resection of the duplicated appendix. Colonic and rectal duplications are rare congenital malformations, accounting for less than 20% of all enteric duplications. 1 Hindgut duplications, which include colonic and rectal duplications, can be categorized into three classes: small intra-mesenteric duplications, presacral midline masses, and side-by-side tubular duplications. CONFLICT OF INTEREST STATEMENT The authors declare no conflict of interest.
Repression of JAK2-STAT1 and PD-L1 by CEP-33779 ameliorates the LPS-induced decline in phagocytic activity of alveolar macrophages and mitigates lung injury in mice
BackgroundThe role of the JAK2-STAT1/PD-L1 pathway in the phagocytic activity of alveolar macrophages (AMs) during LPS-induced acute lung injury in mice remains poorly understood. This study aims to explore whether the JAK2-STAT1/PD-L1 pathway is upregulated on AMs in LPS-induced mice acute lung injury and to further explore the impact of the JAK2-specific inhibitor CEP-33779 on the LPS-induced impairment of AMs phagocytic activity and lung injury.MethodsALI was induced in mice via intratracheal administration of LPS, followed by intragastric administration of JAK2 inhibitor CEP-33779 suspension. Immunohistochemistry was conducted to assess PD-L1 expression in lung tissue, as well as p-JAK2, p-STAT1, and PD-L1 expression on AMs in bronchoalveolar lavage fluid (BALF) using immunofluorescence. Levels of TNF-α and IL-6, as well as protein concentration in BALF, were measured using enzyme-linked immunosorbent assay and Bicinchoninic acid assays, respectively. Hematoxylin-eosin staining and lung injury score were employed to evaluate pathological changes in mouse lungs. Total cell count in BALF was determined using a cell counter. Furthermore, western blot and immunofluorescence was conducted to assess the effect of JAK2 and STAT1 inhibitor on JAK2-STAT1 pathway activation and PD-L1 expression, while confocal microscopy with latex beads rabbit IgG FITC complex was used to observe MH-S cells phagocytic ability.ResultsThe study revealed that LPS stimulation triggered the activation of the JAK2-STAT1 pathway and an upregulation of PD-L1 on AMs in both LPS-induced acute lung injury mice and MH-S cell lines. Moreover, treatment with the JAK2 and STAT1 inhibitor effectively reduced the activation of JAK2-STAT1 signaling, downregulated PD-L1 expression on AMs in BALF from LPS-induced ALI mice and LPS-stimulated MH-S cells, and significantly improved the LPS-induced reduction in phagocytic activity in MH-S cells. Most notably, CEP-33779 treatment significantly mitigated the pulmonary inflammatory response and lung injury in mice with LPS-induced ALI.ConclusionsCollectively, these findings imply that the JAK2-STAT1 pathway plays a role in the upregulation of PD-L1, which in turn is associated with the diminished phagocytic activity in LPS-induced AMs as well as lung injury. Furthermore, our study highlights that CEP-33779 treatment can effectively improve the reduced phagocytic activity of AMs and relieve lung injury induced by LPS through suppression of the JAK2-STAT1/PD-L1 pathway.