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Macrophages are crucial members of the innate immune response and important regulators. The differentiation and activation of macrophages require the timely regulation of gene expression, which depends on the interaction of a variety of factors, including transcription factors and epigenetic modifications. Epigenetic changes also give macrophages the ability to switch rapidly between cellular programs, indicating the ability of epigenetic mechanisms to affect phenotype plasticity. In this review, we focus on key epigenetic events associated with macrophage fate, highlighting events related to the maintenance of tissue homeostasis, responses to different stimuli and the formation of innate immune memory. Further understanding of the epigenetic regulation of macrophages will be helpful for maintaining tissue integrity, preventing chronic inflammatory diseases and developing therapies to enhance host defense.

For robot swarm applications, accurate positioning is one of the most important requirements for avoiding collisions and keeping formations and cooperation between individuals. However, in some worst cases, the GNSS (Global Navigation Satellite System) signals are weak due to the crowd being in a swarm or blocked by a forest, mountains, and high buildings in the environment. Thus, relative localization is an indispensable way to provide position information for the swarm. In this paper, we review the status and development of relative localization. It is first assessed that relative localization to obtain spatio-temporal relationships between individuals is necessary to achieve the stable operation of the group. After analyzing typical relative localization systems and algorithms from the perspective of functionality and practicality, this paper concludes that the UWB-based (ultra wideband) system is suitable for the relative localization of robots in large-scale applications. Finally, after analyzing the current challenges in the field of fully distributed localization for robotic swarms, a complete mechanism encompassing the relative localization process and the relationship between local and global localization that can be a possible direction for future research is proposed.

Suc transporters (SUTs) play a key role in the allocation and partitioning of photosynthetically fixed carbon in plants. While a function could be assigned to many members of the SUT family, almost no information is available on their regulation. Here, the transcriptional regulation of SUTs in response to various environmental stimuli in the leaves of five dicots (Arabidopsis [Arabidopsis thaliana], soybean [Glycine max], potato [Solanum tuberosum], tomato [Solanum lycopersicum], and poplar [Populus spp.]) and four monocots (maize [Zea mays], rice [Oryza sativa], wheat [Triticum aestivum], and barley [Hordeum vulgare]) was investigated. Extensive data on expression of SUTs in relation to changes of environmental conditions were obtained through a global analysis of 168 transcriptomics data sets. Results were validated by quantitative PCR measurements and extended by the measurement of photosynthesis rate and phloem sugar content to draw insight on the correlation of SUT expression and sugar export from leaves. For the apoplasmic phloem loaders, a clear difference in transcriptional regulation in response to different environmental stimuli was observed. The consistent patterns of SUT expression under abiotic stress indicates which types of SUTs are involved in the regulation of leaf sugar status and in stress signaling. Furthermore, it is shown that down-regulation of phloem loading is likely to be caused by transcriptional regulation of SUTs, while up-regulation depends on post-transcriptional regulation. In poplar, expression of PtaSUT4 was found to consistently respond to environmental stimuli, suggesting a significant role in the regulation of sugar export from leaves in this passive symplasmic phloem loader.

Kaposiform hemangioendothelioma (KHE) is a rare vascular neoplasm with high morbidity and mortality. The initiating mechanism during the pathogenesis of KHE has yet to be discovered. The main pathological features of KHE are abnormal angiogenesis and lymphangiogenesis. KHEs are clinically heterogeneous and may develop into a life-threatening thrombocytopenia and consumptive coagulopathy, known as the Kasabach-Merritt phenomenon (KMP). The heterogeneity and the highly frequent occurrence of disease-related comorbidities make the management of KHE challenging. Currently, there are no medications approved by the FDA for the treatment of KHE. Multiple treatment regimens have been used with varying success, and new clinical trials are in progress. In severe patients, multiple agents with variable adjuvant therapies are given in sequence or in combination. Recent studies have demonstrated a satisfactory efficacy of sirolimus, an inhibitor of mammalian target of rapamycin, in the treatment of KHE. Novel targeted treatments based on a better understanding of the pathogenesis of KHE are needed to maximize patient outcomes and quality of life. This review summarizes the epidemiology, etiology, pathophysiology, clinical features, diagnosis and treatments of KHE. Recent new concepts and future perspectives for KHE will also be discussed.

Inflammation has accompanied human beings since the emergence of wounds and infections. In the past decades, numerous efforts have been undertaken to explore the potential role of inflammation in cancer, from tumor development, invasion, and metastasis to the resistance of tumors to treatment. Inflammation-targeted agents not only demonstrate the potential to suppress cancer development, but also to improve the efficacy of other therapeutic modalities. In this review, we describe the highly dynamic and complex inflammatory tumor microenvironment, with discussion on key inflammation mediators in cancer including inflammatory cells, inflammatory cytokines, and their downstream intracellular pathways. In addition, we especially address the role of inflammation in cancer development and highlight the action mechanisms of inflammation-targeted therapies in antitumor response. Finally, we summarize the results from both preclinical and clinical studies up to date to illustrate the translation potential of inflammation-targeted therapies.

Spatial transcriptomics technologies are used to profile transcriptomes while preserving spatial information, which enables high-resolution characterization of transcriptional patterns and reconstruction of tissue architecture. Due to the existence of low-resolution spots in recent spatial transcriptomics technologies, uncovering cellular heterogeneity is crucial for disentangling the spatial patterns of cell types, and many related methods have been proposed. Here, we benchmark 18 existing methods resolving a cellular deconvolution task with 50 real-world and simulated datasets by evaluating the accuracy, robustness, and usability of the methods. We compare these methods comprehensively using different metrics, resolutions, spatial transcriptomics technologies, spot numbers, and gene numbers. In terms of performance, CARD, Cell2location, and Tangram are the best methods for conducting the cellular deconvolution task. To refine our comparative results, we provide decision-tree-style guidelines and recommendations for method selection and their additional features, which will help users easily choose the best method for fulfilling their concerns. This study comprehensively benchmarks 18 state-of-the-art methods for cellular deconvolution of spatial transcriptomics and provide decision-tree-style guidelines and recommendations for method selection.

Background Drug-resistance and severe side effects of chemotherapeutic agents result in unsatisfied survival of patients with lung cancer. CXCLs/CXCR2 axis plays an important role in progression of cancer including lung cancer. However, the specific anti-cancer mechanism of targeting CXCR2 remains unclear. Methods Immunohistochemical analysis of CXCR2 was performed on the microarray of tumor tissues of clinical lung adenocarcinoma and lung squamous cell carcinoma patients. CCK8 test, TUNEL immunofluorescence staining, PI-Annexin V staining, β-galactosidase staining, and Western blot were used to verify the role of CXCR2 in vitro. Animal models of tail vein and subcutaneous injection were applied to investigate the therapeutic role of targeting CXCR2. Flow cytometry, qRT-PCR, enzyme-linked immunosorbent assay (ELISA), and immunohistochemistry analysis were performed for further mechanistic investigation. Results The expression of CXCR2 was elevated in both human lung cancer stroma and tumor cells, which was associated with patients’ prognosis. Inhibition of CXCR2 promoted apoptosis, senescence, epithelial-to-mesenchymal transition (EMT), and anti-proliferation of lung cancer cells. In vivo study showed that tumor-associated neutrophils (TANs) were significantly infiltrate into tumor tissues of mouse model, with up-regulated CXCLs/CXCR2 signaling and suppressive molecules, including Arg-1 and TGF-β. SB225002, a selective inhibitor of CXCR2 showed promising therapeutic effect, and significantly reduced infiltration of neutrophils and enhanced anti-tumor T cell activity via promoting CD8 + T cell activation. Meanwhile, blockade of CXCR2 could enhance therapeutic effect of cisplatin via regulation of neutrophils infiltration. Conclusions Our finds verify the therapeutic effects of targeting CXCR2 in lung cancer and uncover the potential mechanism for the increased sensitivity to chemotherapeutic agents by antagonists of CXCR2.

The electric automotive transition is crucial for achieving carbon neutrality, especially in emerging economies like China. However, the scarcity of critical materials in lithium-ion batteries (LIBs) challenges electric vehicle (EV) deployment targets. Our work delivers a comprehensive framework of EV battery recycling, considering resource compensation, environmental performance, geospatial optimization, and cost feasibility of closed-loop LIB recycling under China’s carbon neutrality. Our findings show that meeting EV deployment targets will widen the supply-demand gap, with cobalt and manganese demand exceeding 2022 production levels by 54-fold and 116-fold, respectively. Battery recycling is crucial for mitigating material scarcity, necessitating a minimum 84% collection rate to stabilize supply by 2060. Battery recycling remains economically viable in most scenarios, generating a net profit of US$58 billion in the optimal scenario. Here, our work underscores inherent trade-offs among integrated metrics, informing battery recycling strategies to strengthen supply chain resilience and advance automotive electrification under decarbonization goals. This study assesses the material, environmental, and economic performance of closed-loop lithium-ion battery (LIB) recycling amid China’s electric vehicle ambitions, indicating that a minimum 84% LIB collection rate is needed to stabilize material supply.

To summarize the existing evidence from double-blind randomized controlled trials (RCTs) and cohort studies regarding the effects of biologic agents for the treatment of large vessel vasculitis (LVV). A systematic review and meta-analysis was conducted using MEDLINE, Embase, Cochrane Central Registry of Controlled Trials, and ClinicalTrials.gov covering the period from database inception to May 3rd, 2023. Double-blind RCTs and cohort studies reporting biologic therapies' effects on LVV including giant cell arteritis (GCA) and Takayasu's arteritis (TAK) with outcomes of interest in English were included. The primary outcome of interest was relapse rates during glucocorticoid tapering. The Cochrane Risk of Bias tool 2.0 and the Risk of Bias In Non-randomized Studies of Interventions tool were used for the quality assessment. Random-effects models were used for meta-analysis. Of the 4599 references retrieved, 10 RCTs regarding GCA, 6 cohort studies, and 2 RCTs regarding TAK were included, comprising 997 participants in total. All the included RCTs were of low risk of bias, while the 6 cohort studies were of moderate to serious risk of bias. Meta-analysis suggested a significant superiority of biologic agents in prolonging relapse-free survival, increasing glucocorticoid taper rate, and decreasing cumulative glucocorticoids dose for both GCA and TAK. Additionally, GCA patients using biologic agents had significantly lower relapse rates and ESR levels with higher remission rates. Trends of favoring biologic agents in reducing relapse rate, ITAS-2010, ITAS-A, ESR, and CRP along with increased remission rate for TAK were also observed. Biologic agents significantly improved clinical outcomes in LVV by reducing relapse rates, enhancing remission, and enabling safer glucocorticoid tapering, offering an important therapeutic advantage for managing both GCA and TAK. Further well-designed studies and corresponding meta-analyses are needed to validate their long-term efficacy and safety.

Over the last decades, the growing understanding on DNA damage response (DDR) pathways has broadened the therapeutic landscape in oncology. It is becoming increasingly clear that the genomic instability of cells resulted from deficient DNA damage response contributes to the occurrence of cancer. One the other hand, these defects could also be exploited as a therapeutic opportunity, which is preferentially more deleterious in tumor cells than in normal cells. An expanding repertoire of DDR‐targeting agents has rapidly expanded to inhibitors of multiple members involved in DDR pathways, including PARP, ATM, ATR, CHK1, WEE1, and DNA‐PK. In this review, we sought to summarize the complex network of DNA repair machinery in cancer cells and discuss the underlying mechanism for the application of DDR inhibitors in cancer. With the past preclinical evidence and ongoing clinical trials, we also provide an overview of the history and current landscape of DDR inhibitors in cancer treatment, with special focus on the combination of DDR‐targeted therapies with other cancer treatment strategies. In this review, we sought to summarize the complex network of DNA repair machinery in cancer cells and discuss the underlying mechanism for the application of DDR inhibitors in cancer. With the past preclinical evidence and ongoing clinical trials, we also provide an overview of the history and current landscape of DDR inhibitors in cancer treatment, with especial focus on the combination of DDR‐targeted therapies with other cancer treatment strategies.