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Media companies in various countries are transforming and upgrading to improve their competitiveness in the digital economy. However, existing research only focuses on the issue of how media companies transform while ignoring whether internal governance mechanisms such as compensation incentives can promote corporate value during the transformation process. According to the principal-agent theory, we examined the incentive effects of the executive compensation system in terms of monetary compensation, equity compensation, and perks in a sample of Chinese media companies in the process of transformation and upgrading. The results have revealed that monetary compensation does not have a significant incentive effect, and equity compensation and perks have an incentive effect when they are in the suitable range. Based on the results, we proposed policy recommendations from three aspects: monetary compensation, equity compensation, and perks. This study complements the research content on the executive compensation system in media enterprises’ transformation and upgrading. It can provide a reference for setting the administrative compensation system for media companies in China and other emerging economies.

The COVID-19 pandemic has made treating renal anemia in chronic kidney disease (CKD) patients undergoing peritoneal dialysis (PD) difficult. The current study aims to compare roxadustat with erythropoiesis-stimulating agents (ESAs) during the COVID-19 pandemic. We conducted a single-center, retrospective study during the COVID-19 outbreak in China, from December 7, 2022, to January 31, 2023. The study involved patients undergoing PD who were divided based on the medication used to treat renal anemia; the roxadustat group (n = 34) and the ESAs group (n = 120). We analyzed the effectiveness of treating anemia, cost, medication adherence, and clinical outcomes related to COVID-19. Patients were followed up for 9 months. The baseline of hemoglobin levels was (110.03 ± 1.71 g/L in the roxadustat and 110.1 ± 1.52 g/L in the ESAs groups, respectively), after 9 months of inspections, the levels of hemoglobin were (121.26 ± 2.03 g/L in the roxadustat and 118.49 ± 1.35 g/L in the ESAs groups, respectively). The roxadustat subgroup analysis indicated that total cholesterol and low-density lipoprotein levels in the roxadustat group decreased from baseline in subjects not receiving statins (3.39 ± 0.12 vs. 4.2 ± 0.21 mmol/L and 2.21 ± 0.23 vs. 3.65 ± 0.37 mmol/L, P < 0.05). The Morisky score of the roxadustat group was higher [7 (5, 8) vs. 6 (4, 8), P < 0.01]. The drug cost of the roxadustat group was higher, but another additional cost for correcting anemia was significantly reduced. The infection rate of COVID-19 and the mortality rate caused by COVID-19 were lower in roxadustat group. During the COVID-19 pandemic, both roxadustat and ESAs effectively improved renal anemia in PD patients, however, the roxadustat group experienced less additional costs for anemia correction and better medication compliance.

T cell stimulatory and inhibitory molecules are critical for the regulation of immune responses. In this study, we identify a novel T cell co‐inhibitory molecule TAPBPL, whose amino acid sequence shares homology with known B7 family members. TAPBPL protein is expressed on resting and activated T cells, B cells, monocytes, and dendritic cells (DCs), as well as on some tumor tissues. The putative TAPBPL receptor is expressed on activated CD4 and CD8 T cells. A soluble recombinant human TAPBPL‐IgG Fc (hTAPBPL‐Ig) fusion protein inhibits the proliferation, activation, and cytokine production of both mouse and human T cells in vitro . In vivo administration of hTAPBPL‐Ig protein attenuates experimental autoimmune encephalomyelitis (EAE) in mice. Furthermore, an anti‐TAPBPL monoclonal antibody neutralizes the inhibitory activity of hTAPBPL‐Ig on T cells, enhances antitumor immunity, and inhibits tumor growth in animal models. Our results suggest that therapeutic intervention of the TAPBPL inhibitory pathway may represent a new strategy to modulate T cell‐mediated immunity for the treatment of cancer, infections, autoimmune diseases, and transplant rejection. Synopsis T cells play a critical role in immune response. This study identifies a novel B7 family‐related T cell inhibitory molecule TAPBPL. Targeting the TAPBPL pathway may represent a new strategy to modulate T cell‐mediated immunity to treat autoimmune disease and cancer. TAPBPL shares sequence and structural similarities with existing B7 family members. TAPBPL protein is expressed on antigen‐presenting cells and cancer cells, whereas its receptor is expressed on activated CD4 and CD8 T cells. TAPBPL‐IgG Fc (TAPBPL‐Ig) fusion protein inhibits the proliferation, activation and cytokine production of T cells in vitro . Administration of TAPBPL‐Ig protein attenuates experimental autoimmune encephalomyelitis in mice. Anti‐TAPBPL antibody neutralizes the inhibitory activity of TAPBPL‐Ig on T cells, enhances antitumor immunity and inhibits tumor growth in vivo . Graphical Abstract T cells play a critical role in immune response. This study identifies a novel B7 family‐related T cell inhibitory molecule TAPBPL. Targeting the TAPBPL pathway may represent a new strategy to modulate T cell‐mediated immunity to treat autoimmune disease and cancer.

Background: Surface-enhanced Raman scattering (SERS) has become a useful spectroscopic tool for studying biomolecule structures. The main types of plasmonic substrates used in biological systems are Au nanoparticles (AuNPs), whose surface plasmon resonance depends on the nanoparticle size, morphology, particle interspace, and so on. Methods: In this study, AuNP colloids with different sizes were synthesized and used as the sensors to probe SERS signals of different biomarkers and biomolecules. Results: The results showed that an AuNP colloid of ~50 nm had excellent SERS effects in probing various molecules, and could be preserved for about 3 months with excellent repeatability and reproducibility (RSD <5%) in terms of the probed signal intensity (rhodamine 6G and crystal violet). Meanwhile, the fabricated AuNPs were applied to study the SERS signals and structural information of bovine serum albumin (BSA) in aqueous solution. It was found that SERS could rapidly provide the structural information and vibration characteristics of BSA. Conclusion: It was concluded that biocompatible AuNP colloid may be a promising biosensor in the rapid and label-free detection of biological systems.

Polystyrene nanoplastics are a novel class of pollutants. They are easily absorbed by living organisms, and their potential toxicity has raised concerns. However, the impact of polystyrene nanoplastics on auditory organs remains unknown. Here, our results showed that polystyrene nanoplastics entered the cochlea of mice, HEI-OC1 cells, and lateral line hair cells of zebrafish, causing cellular injury and increasing apoptosis. Additionally, we found that exposure to polystyrene nanoplastics resulted in a significant elevation in the auditory brainstem response thresholds, a loss of auditory sensory hair cells, stereocilia degeneration and a decrease in expression of Claudin-5 and Occludin proteins at the blood-lymphatic barrier in mice. We also observed a significant decrease in the acoustic alarm response of zebrafish after exposure to polystyrene nanoplastics. Mechanistic analysis revealed that polystyrene nanoplastics induced up-regulation of the Nrf2/HO-1 pathway, increased levels of malondialdehyde, and decreased superoxide dismutase and catalase levels in cochlea and HEI-OC1 cells. Furthermore, we observed that the expression of ferroptosis-related indicators GPX4 and SLC7A11 decreased as well as increased expression of ACLS4 in cochlea and HEI-OC1 cells. This study also revealed that polystyrene nanoplastics exposure led to increased expression of the inflammatory factors TNF-α, IL-1β and COX2 in cochlea and HEI-OC1 cells. Further research found that the cell apoptosis, ferroptosis and inflammatory reactions induced by polystyrene nanoplastics in HEI-OC1 cells was reversed through the pretreatment with N-acetylcysteine, a reactive oxygen species inhibitor. Overall, our study first discovered and systematically revealed the ototoxicity of polystyrene nanoplastics and its underlying mechanism.

The advent of nanomedicine is profoundly revolutionizing conventional paradigms in cancer therapeutics. Selected formulations encompassing lipid nanoparticles and polymeric nanoparticles have already attained regulatory approval for clinical treatment. Nonetheless, achieving precise spatiotemporal control of exogenous nanomedicine within intricate physiological environments remains a formidable challenge. Drawing inspiration from evolutionarily optimized natural biological architectures, the development of biomembrane‐derived nanostructures with unique biological activities provides a new impetus for designing personalized antitumor drugs. Biomembrane‐derived constituents, particularly cell membrane, extracellular vesicles, and other bioactive payloads, have inherited their precise targeting, specific tumor killing, and dynamic tumor immunosuppressive microenvironments remodeling properties in antitumor intervention. Here, the diverse biomembrane engineering strategies to equip the biomembrane with plentiful functionalities are highlighted. Moreover, the cutting‐edge innovations of mammalian cells/bacteria/plants‐derived biomembrane nanostructures and their applications for advancing cancer nanomedicine development are systematically reviewed. Finally, the current challenges and future opportunities are proposed to realize the whole potential of biomembrane nanomedicine toward clinical transformation. Naturally derived biomembrane nanostructures by mimicking evolutionarily optimized biological architectures could effectively suppress tumor growth and have emerged as a compelling strategy in translational biomedicine. This review provides a systematic overview of rational design and underlying antitumor therapeutic mechanisms of mammalian cells/bacteria/plants‐derived biomembrane nanostructures for advancing antitumor nanomedicine development.

The immense complexity and interconnectedness of inflammation and metabolism in the primary tumor ecosystem and pre-metastatic niches (PMN) present an enormous challenge for developing advanced nano-medicines for cancer immunotherapy. Herein, an intelligent tumor- and PMN-tropic bioactive “nano-med-fireman” (PsiL@M1M) was developed to not only arouse an appropriate photothermal immune cascade but also to “extinguish” the accompanying excessive inflammation. Ultimately, it aims to revitalize the immunosuppressive tumor microenvironment (TME) to spatiotemporally and effectively inhibit tumor metastasis and recurrence. PsiL@M1M was devised by incorporating the siRNA of lactate dehydrogenase A (siLDHA) on the functionalized photothermal mesoporous polydopamine (mPDA) and coupled with an M1-type macrophage membrane (M1M) to enable the capacity of inflammation targeting and modulation. PsiL@M1M actively accumulated and destroyed the primary tumor via photothermal therapy and subsequently mitigated the photothermal therapy-induced inflammatory cascade (e.g., epithelial mesenchymal transition) via cytokine neutralization, eliminating the supply of tumor-derived secretory factors as “nutrients” for PMN. Concurrently, siLDHA interfered with lactate (LA) production, inhibited inflammation-LA communication and relieved immune checkpoint, thus profoundly reversing the immunosuppressive microenvironment of both the primary tumor and PMN. Through cooperation, PsiL@M1M initiated normalized hypo-inflammatory photo-immunotherapy against both local tumor growth and spontaneous metastasis/recurrence. Our study provides a paradigm for a new generation of photothermal nano-medicines for the whole process of tumor treatment. Schematic representation of (A) the construction of “nano-med-fireman” (PsiL@M1M) and (B) the elicited spatiotemporal and hypo-inflammatory photo-immunotherapy against primary tumor and lung metastasis by inflammation neutralization and LA metabolic modulation. [Display omitted] •A biomimetic “nano-med-fireman” PsiL@M1M combining cytokine neutralization and lactate metabolic regulation was developed.•PsiL@M1M homes to tumor and neutralizes PTT-released inflammatory cytokines to alleviate treatment-induced inflammation.•PsiL@M1M blocks inflammation-lactate metabolic crosstalk for reprogramming the TME and reinvigorating cytotoxic T cells.•PsiL@M1M further regulates PMN to prevent tumor “seed” colonization and resist tumor metastasis/recurrence.

Xuebijing injection (XBJ) has been widely recognized in the treatment of sepsis, however, inadequate information regarding XBJ's optimal dosage and frequency suffice. We aimed to assess the effectiveness of various doses and administration frequencies in patients with sepsis using a network meta-analysis (NMA) to offer therapeutic prescription guidance. We examined eight databases for 1,765 randomized controlled trials published before July 2024, organized the literature using NoteExpress software and extracted data using Microsoft Excel software. The literature's quality was assessed using the risk of bias evaluation approach endorsed by the Cochrane Collaboration. The analysis was conducted by NMA inside a frequency-based framework. Forty-three qualifying studies were included in the analysis, including 5,818 participants. Regarding the enhancement of 28-day mortality, 50 Milliliter (ml)-tie in die (tid) exhibited optimal efficacy, 100 ml-tid demonstrated superior efficacy in ameliorating APACHE II scores, 50 ml-bis in die (bid) proved more effective in enhancing the activated partial thromboplastin time (APTT), while 100 ml-quaque die (qd) significantly improved C-reactive protein (CRP) levels. Additional findings are displayed in net league tables, forest plots, and funnel plot. A daily dose of 100 ml of XBJ was associated with improvement in APTT and CRP levels in patients with sepsis, a daily dose of 150 ml may decrease 28-day mortality; while XBJ with a single-day dose of 300 ml is more effective at improving the APACHE II score, higher dosages correlated with improved prognosis in these patients compared to other doses.

The main purpose of this paper is to estimate the thickness of boundary layer for nonlinear evolution equations with damping and diffusion as the diffusion parameter β goes to zero. We prove that the thickness of layer is of the order O ( β γ ) with 0 < γ < 1 , thus improving the corresponding result in (Ruan and Zhu in Discrete Contin. Dyn. Syst. 32(1) 331-352, 2012 ) where 0 < γ < 1 / 2 is obtained.

The severity of ischemic stroke symptoms varies among patients and is a critical determinant of patient outcome. To date, the association between the number of stenotic intracranial arteries and stroke severity remains unclear. We aimed to investigate the association between the number of stenotic major intracranial arteries (NSMIA) and ischemic stroke severity, as well as the degree of stenosis and common stroke risk factors. We performed a retrospective analysis of patients with digital subtraction angiography (DSA)-confirmed ischemic stroke. Clinical stroke severity was measured using the National Institutes of Health Stroke Scale (NIHSS). The number of stenotic vessels was counted from the internal carotid arteries and vertebral arteries, bilaterally. Eighty three patients were recruited from a single center and included in the study. NSMIA was significantly correlated with stroke severity (Pearson Correlation Coefficient = 0.485, P < 0.001), but not with the degree of stenosis (Pearson Correlation Coefficient = 0.01, P = 0.90). Multivariate regression analysis revealed that NSMIA was significantly associated with the NIHSS score after adjusting for stroke risk factors. The adjusted odds ratio (per lateral) was 2.092 (95% CI, 0.865 to 3.308, P = 0.001). The degree of stenosis was also significantly associated with the NIHSS score after adjusting for common risk factors. The odds ratio (per 10%) was 0.712 (95% CI, 0.202 to 1.223, P = 0.007). The number of stenotic intracranial major arteries is associated with the severity of ischemic stroke independent of the degree of stenosis and other stroke risk factors. To the best of our knowledge, this has not been previosuly studied in great detail using DSA. Our data highlight the importance of examining all major arteries in stroke patients.