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Due to the lack of real-time planning for fire escape routes in large buildings, the current route planning methods fail to adequately consider factors related to the fire situation. This study introduces a real-time fire monitoring and dynamic path planning system based on an improved ant colony algorithm, comprising a hierarchical arrangement of upper and lower computing units. The lower unit employs an array of sensors to collect environmental data in real time, which is subsequently transmitted to an upper-level computer equipped with LabVIEW. Following a comprehensive data analysis, pertinent visualizations are presented. Capitalizing on the acquired fire situational awareness, a propagation model for fire spreading is developed. An enhanced ant colony algorithm is then deployed to calculate and plan escape routes by introducing a fire spread model to enhance the accuracy of escape route planning and incorporating the A* algorithm to improve the convergence speed of the ant colony algorithm. In response to potential anomalies in sensor data under elevated temperature conditions, a correction model for data integrity is proposed. The real-time depiction of escape routes is facilitated through the integration of LabVIEW2018 and MATLAB2023a, ensuring the dependability and safety of the path planning process. Empirical results demonstrate the system's capability to perform real-time fire surveillance coupled with efficient escape route planning. When benchmarked against the traditional ant colony algorithm, the refined version exhibits expedited convergence, augmented real-time performance, and effectuates an average reduction of 17.1% in the length of the escape trajectory. Such advancements contribute significantly to enhancing evacuation efficiency and minimizing potential casualties. [ABSTRACT FROM AUTHOR]

Objectives: Glioblastoma (GBM) is the most aggressive of intracranial gliomas. Despite the maximal treatment intervention, the median survival rate is still about 14–16 months. Nuclear receptor‐binding protein 1 (NRBP1) has a potential growth‐promoting role on biology function of cells. In this study, we investigated whether NRBP1 promotes GBM malignant phenotypes and the potential mechanisms. Methods: The correlation between NRBP1 and glioma grade, prognosis in TCGA/CGGA databases and our clinical data were analyzed. Next, we conducted knockout and overexpression of NRBP1 on GBM cells to verify that NRBP1 promoted cell proliferation, invasion, and migration in vitro and in vivo. Finally, we detected the impact of NRBP1 on PI3K/Akt signaling pathway and EMT. Results: There was a correlation between elevated NRBP1 expression and advanced stage glioma, as well as decreased overall and disease‐free survival. The suppression of proliferation, invasion, and migration of tumor cells was observed upon NRBP1 knockout, and in vitro studies also demonstrated the induction of apoptotic cell death. Whereas, its overexpression is associated with high multiplication rate, migration, invasion, and apoptotic escape. GO enrichment and KEGG analysis revealed that NRBP1 regulated differentially expressed gene clusters are involved in PI3K/Akt signaling pathway, as well as EMT mediated by this pathway. Moreover, the effects of NRBP1 knockdown and overexpression on GBM were mitigated by MK‐2206 and SC79, both of which respectively function as an inhibitor and an activator of the PI3K/Akt signaling pathway. Similarly, the suppression of NRBP1 led to a decrease in tumor growth, whereas its overexpression promoted tumor growth in a mouse model. Conclusions: This study shows that NRBP1 promotes malignant phenotypes in GBM by activating PI3K/Akt pathway. Hence, it can function as both a predictive indicator and a new target for therapies in GBM treatment. [ABSTRACT FROM AUTHOR]

PD-1 signaling on T cells is the major pathway that limits T cell immunity, but the efficacy of anti-PD-1 therapy has been limited to a small proportion of patients with advanced cancers. We fortuitously observed that anti-PD-1 therapy depends on IL-2 signaling, which raises the possibility that a lack of IL-2 limits anti-PD-1-induced effector T cell expansion. To selectively deliver IL-2 to [PD-1.sup.+] [CD8.sup.+] tumor-infiltrating lymphocytes (TILs), we engineered a low-affinity IL-2 paired with anti-PD-1 (PD-1-laIL-2), which reduced affinity to peripheral Treg cells but enhanced avidity to [PD-1.sup.+] [CD8.sup.+] TILs. PD-1-laIL-2 exerted better tumor control and lower toxicity than single or mixed treatments. Mechanistically, PD-1-laIL-2 could effectively expand dysfunctional and tumor-specific [CD8.sup.+] T cells. Furthermore, we discovered that presumably dysfunctional [PD-1.sup.+] [TIM3.sup.+] TILs are the dominant tumor-specific T cells responding to PD-1-laIL-2. Collectively, these results highlight that PD-1-laIL-2 can target and reactivate tumor-specific TILs for tumor regression as a unique strategy with stronger efficacy and lower toxicity., Introduction Increased levels of tumor-infiltrating lymphocytes (TILs) are associated with improved survival in patients with cancer (1-3). Anti-PD-1/PD-L1-based cancer immunotherapies have revolutionized the treatment of cancers (4-8), and TIL abundance [...]

A population of partially exhausted CXCR5.sup.+ CD8.sup.+ T cells, induced by chronic virus infection and residing in B-cell follicles, is shown to control viral replication. During chronic viral infection, virus-specific CD8.sup.+ T cells become exhausted, exhibit poor effector function and lose memory potential.sup.1,2,3,4. However, exhausted CD8.sup.+ T cells can still contain viral replication in chronic infections.sup.5,6,7,8,9, although the mechanism of this containment is largely unknown. Here we show that a subset of exhausted CD8.sup.+ T cells expressing the chemokine receptor CXCR5 has a critical role in the control of viral replication in mice that were chronically infected with lymphocytic choriomeningitis virus (LCMV). These CXCR5.sup.+ CD8.sup.+ T cells were able to migrate into B-cell follicles, expressed lower levels of inhibitory receptors and exhibited more potent cytotoxicity than the CXCR5.sup.- subset. Furthermore, we identified the Id2-E2A signalling axis as an important regulator of the generation of this subset. In patients with HIV, we also identified a virus-specific CXCR5.sup.+ CD8.sup.+ T-cell subset, and its number was inversely correlated with viral load. The CXCR5.sup.+ subset showed greater therapeutic potential than the CXCR5.sup.- subset when adoptively transferred to chronically infected mice, and exhibited synergistic reduction of viral load when combined with anti-PD-L1 treatment. This study defines a unique subset of exhausted CD8.sup.+ T cells that has a pivotal role in the control of viral replication during chronic viral infection., Author(s): Ran He [sup.1] [sup.9] , Shiyue Hou [sup.2] , Cheng Liu [sup.1] [sup.9] , Anli Zhang [sup.3] , Qiang Bai [sup.1] [sup.9] , Miao Han [sup.4] , Yu Yang [...]

Author(s): Ran He; Shiyue Hou; Cheng Liu; Anli Zhang; Qiang Bai; Miao Han; Yu Yang; Gang Wei; Ting Shen; Xinxin Yang; Lifan Xu; Xiangyu Chen; Yaxing Hao; Pengcheng Wang; Chuhong [...]

Anovel reassortant avian influenza A(H7N9) virus has emerged in eastern China and caused fatal infections in humans (1-3). The real-time reverse-transcription PCR (RT-PCR) is used as a diagnostic method for [...]

Targeting Treg cells: Depletion of regulatory T (Treg) cells is an attractive strategy to promote antitumor immunity. One strategy that could deplete Treg cells is blockade of the "do not eat me" signal, CD47, which prevents Treg cells from being targets of phagocytosis. However, CD47 is broadly expressed, making Treg cell–specific targeting difficult. To selectively deplete Treg cells, Zhang et al. designed a heterodimer that combines an anti–cytotoxic T lymphocyte antigen 4 (CTLA-4) antibody, which targets intratumoral Treg cells, and the CD47 ligand, signal regulatory protein α (SIRPα). Treatment with this heterodimer increased phagocytosis of Treg cells, leading to their depletion, and promoted antitumor immunity in mouse models. Thus, dual targeting of CD47 and CTLA-4 selectively depletes Treg cells and can promote immune responses against solid tumors. Blockade of CD47, the "do not eat me" signal, has limited effects in solid tumors despite its potent antitumor effects in hematopoietic malignancies. Taking advantage of the high expression of cytotoxic T lymphocyte–associated protein 4 (CTLA-4) on Treg cells and abundant Fc receptor–expressing active phagocytes inside the tumor microenvironment (TME), we designed and tested a heterodimer combining an anti–CTLA-4 antibody, which targets Treg cells, with the CD47 ligand, signal regulatory protein α (SIRPα), to selectively block CD47 on intratumoral Treg cells. We hypothesized that heterodimer treatment would increase antibody-dependent cellular phagocytosis of the targeted Treg cells. We found that anti–CTLA-4×SIRPα preferentially depleted ICOShigh immunosuppressive Treg cells in the TME and enhanced immunity against solid tumors, including MC38 and CT26 murine colon cancers. Mechanistically, we found that CD47 expression on Treg cells limited anti–CTLA-4–mediated depletion and Fc on the heterodimer-enhanced depletion. Furthermore, anti-human CTLA-4×SIRPα depleted tumor Treg cells and exhibits less toxicity than anti-human CTLA-4 in a humanized mouse model. Collectively, these results demonstrate that simultaneously modulating both "eat me" and do not eat me signals induces Treg cell depletion inside the TME and may be an effective strategy for treating solid tumors. [ABSTRACT FROM AUTHOR]