Explore the vast range of titles available.

In this work, we establish the existence conditions and a universal upper bound on the radius of stable photon spheres (SPS) outside the event horizons of static, spherically symmetric, asymptotically flat black holes surrounded by matter fields. We prove that stable photon spheres exist if the external matter satisfies specific conditions. Furthermore, under the additional assumption of a monotonically decreasing mass-radius ratio m ( r ) / r 3 outside the horizon, we derive a strict upper bound on the radius r sps of any stable photon sphere: r sps < 6 M , where M is the asymptotic mass of the black hole. This bound is independent of specific black hole solutions and broadly applies to hairy black holes and other configurations with external matter fields meeting the stated energy conditions. Our results resolve fundamental questions regarding the existence and spatial constraints on stable photon orbits, with implications for gravitational lensing, accretion disk dynamics (e.g., the Aschenbach effect), and black hole shadow observations.

The spin-curvature coupling in the Mathisson–Papapetrou–Dixon (MPD) formalism induces non-geodesic motion, shifting the orbital parameters of spinning test particles in black hole spacetimes. We investigate whether these quantitative shifts alter the qualitative, global structure of the orbit manifold. Using a topological approach, we study timelike circular orbits (TCOs) for spinning particles in static, spherically symmetric spacetimes. By constructing an auxiliary vector field, we compute the topological winding number W in horizon-bounded regions of asymptotically flat, anti-de Sitter (AdS), and de Sitter (dS) backgrounds. We find that W is robust against both the magnitude and direction of the particle’s spin: between two horizons, W = - 1 , guaranteeing at least one unstable TCO; outside the outermost horizon in asymptotically flat and AdS spacetimes, W = 0 , enforcing that TCOs must appear in stable–unstable pairs or be absent. This spin independence reveals that the fundamental orbital structure is a property of spacetime geometry itself, not of the particle’s spin. We validate this with quantitative examples in Schwarzschild, Schwarzschild–AdS, and Schwarzschild–dS spacetimes, showing explicit spin-induced TCO shifts while confirming the invariant topology. This result provides a topological foundation for interpreting gravitational waveforms from extreme mass-ratio inspirals involving spinning secondaries.

With the acceleration of urbanization, opportunities for direct contact with nature have diminished, making mediated nature exposure a sustainable approach to promoting public health. Existing studies predominantly present natural stimuli from a first-person horizontal perspective, leaving it unclear whether different viewing perspectives lead to divergent restorative outcomes. To examine how environment type and perspective jointly influence cognitive and emotional restoration, this study employed a 2 (environmental type: forest vs. city) × 2 (perspective: first-person perspective (1PP) vs. third-person perspective (3PP)) × 2 (time: pre-test vs. post-test) mixed experimental design grounded in Attention Restoration Theory (ART). Results showed that viewing forest videos, compared to city videos, significantly improved directed attention and emotional state. More importantly, a functional decoupling of perspectives was observed: the first-person perspective primarily facilitated the restoration of directed attention, while the third-person perspective was more effective in alleviating negative mood. These findings provide empirical evidence for the design of sustainable interventions, guiding both the development of tailored digital nature solutions and the planning of green infrastructure that integrates multiple perspectives. Thereby, nature exposure can be transformed into an equitable public health resource, contributing to the development of resilient, sustainable cities.

The intracellular pathogen Legionella pneumophila delivers more than 330 effectors into host cells by its Dot/Icm secretion system. Those effectors direct the biogenesis of the Legionella -containing vacuole (LCV) that permits its intracellular survival and replication. It has long been documented that the LCV is associated with mitochondria and a number of Dot/Icm effectors have been shown to target to this organelle. Yet, the biochemical function and host cell target of most of these effectors remain unknown. Here, we found that the Dot/Icm substrate Ceg3 (Lpg0080) is a mono-ADP-ribosyltransferase that localizes to the mitochondria in host cells where it attacks ADP/ATP translocases by ADP-ribosylation, and blunts their ADP/ATP exchange activity. The modification occurs on the second arginine residue in the -RRRMMM- element, which is conserved among all known ADP/ATP carriers from different organisms. Our results reveal modulation of host energy metabolism as a virulence mechanism for L. pneumophila .

Legionella pneumophila strains harboring wild-type rpsL such as Lp02 rpsL WT cannot replicate in mouse bone marrow-derived macrophages (BMDMs) due to induction of extensive lysosome damage and apoptosis. The bacterial factor directly responsible for inducing such cell death and the host factor involved in initiating the signaling cascade that leads to lysosome damage remain unknown. Similarly, host factors that may alleviate cell death induced by these bacterial strains have not yet been investigated. Using a genome-wide CRISPR/Cas9 screening, we identified Hmg20a and Nol9 as host factors important for restricting strain Lp02 rpsL WT in BMDMs. Depletion of Hmg20a protects macrophages from infection-induced lysosomal damage and apoptosis, allowing productive bacterial replication. The restriction imposed by Hmg20a was mediated by repressing the expression of several endo-lysosomal proteins, including the small GTPase Rab7. We found that SUMOylated Rab7 is recruited to the bacterial phagosome via SulF, a Dot/Icm effector that harbors a SUMO-interacting motif (SIM). Moreover, overexpression of Rab7 rescues intracellular growth of strain Lp02 rpsL WT in BMDMs. Our results establish that L . pneumophila exploits the lysosomal network for the biogenesis of its phagosome in BMDMs.

Lethal encephalitis caused by rabies virus (RABV) in mammals is known to be associated with the production of several pro-inflammatory cytokines, but the mechanism of such induction remains unclear. In this study, we establish that the laboratory strain CVS-11 infects astrocytes which are the most abundant glial cell population and the dominant source of inflammatory factors in the central nervous system (CNS). A screen identifies the E3 ubiquitin ligase FBXL18 as a critical factor responsible for RABV-induced inflammation. Mechanistically, infection by RABV upregulates FBXL18, which induces K11-type ubiquitination of BST2 on Lys 109 and Lys 110 , two residues that are also ubiquitinated for degradation via K33-type ubiquitination by a yet unknown E3 ligase. FBXL18-mediated ubiquitination stabilizes BST2, leading to hyperphosphorylation of IκBα and excessive NF-κB activation. Knockdown of FBXL18 effectively inhibits IL-6 production and RABV replication in astrocytes and neurons, thereby mitigating the virulence of RABV in mice. Our findings suggest that targeting FBXL18 is a potentially effective strategy for rabies treatment. RABV upregulates FBXL18, which stabilizes BST2 via K11-linked ubiquitination at Lys109/110, thereby activating NF-κB. FBXL18 knockdown effectively suppresses inflammation and virulence, highlighting its potential as a therapeutic target for rabies.

The bacterial effector MavC modulates the host immune response by blocking Ube2N activity employing an E1-independent ubiquitin ligation, catalyzing formation of a γ-glutamyl-ε-Lys (Gln40 Ub -Lys92 Ube2N ) isopeptide crosslink using a transglutaminase mechanism. Here we provide biochemical evidence in support of MavC targeting the activated, thioester-linked Ube2N~ubiquitin conjugate, catalyzing an intramolecular transglutamination reaction, covalently crosslinking the Ube2N and Ub subunits effectively inactivating the E2~Ub conjugate. Ubiquitin exhibits weak binding to MavC alone, but shows an increase in affinity when tethered to Ube2N in a disulfide-linked substrate that mimics the charged E2~Ub conjugate. Crystal structures of MavC in complex with the substrate mimic and crosslinked product provide insights into the reaction mechanism and underlying protein dynamics that favor transamidation over deamidation, while revealing a crucial role for the structurally unique insertion domain in substrate recognition. This work provides a structural basis of ubiquitination by transglutamination and identifies this enzyme’s true physiological substrate. The Legionella pneumophila effector MavC inhibits the human ubiquitin-conjugating enzyme Ube2N. Here, the authors combine NMR, X-ray crystallography and biochemical assays and show that MavC catalyses the intramolecular transglutaminase reaction between the Ube2N and Ub subunits of the Ube2N∼Ub conjugate and present the substrate- and product-bound MavC crystal structures.

Angiogenesis is a pivotal mechanism driving tumor proliferation, and the epigenetic regulation of angiogenesis represents a cutting-edge area of current research in multiple myeloma (MM). High-throughput sequencing was carried out to detect the cargos of exosomes from clinical serum and U266 cells, then GSE108824 database was analyzed for the finding of differentially expressed genes (DEGs). The intersect set was made based on the three gene sets. The clinical features of Metastasis-Associated Lung Adenocarcinoma Transcript 1 (MALAT1)were verified through GEO and clinicopathological data analyses. Cell viability, tube formation assay, level of MALAT1 and VEGFA were used to evaluate the effect of U266 exosome pretreated with or without paeoniflorin (PF) on angiogenesis in HUVEC cells. Subcutaneous tumor-bearing mice were established by injection of U266 cells and exosomes derived from U266 cells which pretreated with or without PF. Tumor size, HE staining, analysis of MALAT1 and VEGFA levels, as well as IHC staining for VEGFA, CD31, and Ki67 were performed to evaluate the in vivo effects of PF. The interactions between MALAT1, VEGFA, and microRNAs were demonstrated by TargetScan, MiRanda databases and Luciferase reporter assay. Furthermore, network pharmacology and RROMO, Genecards, AnimalTFDB, JASPAR databases were combinedto predict transcription factors (TF) associated with MALAT1 and analyze the binding sites between PF and these transcription factors. The validation of PF effect on TF was conducted by WB and PCR. Clinical studies indicated a notable positive correlation between MALAT1 level and VEGFA, CD31 expression, moreover, the high MALAT1 level is closely related to poor prognosis of MM. We demonstrated that MALAT1 was the highest expression linear RNA in U266 exosomes and could be transported to HUVEC cells through exosomes, promoting HUVEC cells differentiation and angiogenesis by stimulating VEGFA expression. The tube formation could be blocked if we knockdown the MALAT1 in U266 exosome. It was also proved that this pathological process can be blocked by PF in vitro and in vivo experiments. The ceRNA mechanism in MALAT1/miR-17/VEGFA was predicted and then confirmed by luciferase reporter assay. 2548 PF target genes were retrieved from databases, and the intersections with MALAT1-related differentially expressed proteins, mRNA and TF gene were identified Venn diagaram. MEF2A binding sites were predicted JASPAR, finally molecular docking showed strong affinity between PF and MEF2A (-16.5 kcal/mol).Then the effect of PF on MEF2A/MALAT1 was confirmed by WB or PCR test. To summarize, our study revealed that myeloma cells can increase angiogenesis by releasing exosome to influence the endothelial cells. The MALAT1 from myeloma cells is the crucial factor in this pathological process. PF can obstruct this process by intervening in the MEF2A/MALAT1 in myeloma cells.

Given the rapid development of social media, effective extraction and analysis of the contents of social media for health care have attracted widespread attention from health care providers. As far as we know, most of the reviews focus on the application of social media, and there is a lack of reviews that integrate the methods for analyzing social media information for health care. This scoping review aims to answer the following 4 questions: (1) What types of research have been used to investigate social media for health care, (2) what methods have been used to analyze the existing health information on social media, (3) what indicators should be applied to collect and evaluate the characteristics of methods for analyzing the contents of social media for health care, and (4) what are the current problems and development directions of methods used to analyze the contents of social media for health care? A scoping review following Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines was conducted. We searched PubMed, the Web of Science, EMBASE, the Cumulative Index to Nursing and Allied Health Literature, and the Cochrane Library for the period from 2010 to May 2023 for primary studies focusing on social media and health care. Two independent reviewers screened eligible studies against inclusion criteria. A narrative synthesis of the included studies was conducted. Of 16,161 identified citations, 134 (0.8%) studies were included in this review. These included 67 (50.0%) qualitative designs, 43 (32.1%) quantitative designs, and 24 (17.9%) mixed methods designs. The applied research methods were classified based on the following aspects: (1) manual analysis methods (content analysis methodology, grounded theory, ethnography, classification analysis, thematic analysis, and scoring tables) and computer-aided analysis methods (latent Dirichlet allocation, support vector machine, probabilistic clustering, image analysis, topic modeling, sentiment analysis, and other natural language processing technologies), (2) categories of research contents, and (3) health care areas (health practice, health services, and health education). Based on an extensive literature review, we investigated the methods for analyzing the contents of social media for health care to determine the main applications, differences, trends, and existing problems. We also discussed the implications for the future. Traditional content analysis is still the mainstream method for analyzing social media content, and future research may be combined with big data research. With the progress of computers, mobile phones, smartwatches, and other smart devices, social media information sources will become more diversified. Future research can combine new sources, such as pictures, videos, and physiological signals, with online social networking to adapt to the development trend of the internet. More medical information talents need to be trained in the future to better solve the problem of network information analysis. Overall, this scoping review can be useful for a large audience that includes researchers entering the field.