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Indoor fires pose significant threats in terms of casualties and economic losses globally. Thus, it is vital to accurately detect indoor fires at an early stage. To improve the accuracy of indoor fire detection for the resource-constrained embedded platform, an indoor fire detection method based on multi-sensor fusion and a lightweight convolutional neural network (CNN) is proposed. Firstly, the Savitzky–Golay (SG) filter is used to clean the three types of heterogeneous sensor data, then the cleaned sensor data are transformed by means of the Gramian Angular Field (GAF) method into matrices, which are finally integrated into a three-dimensional matrix. This preprocessing stage will preserve temporal dependency and enlarge the characteristics of time-series data. Therefore, we could reduce the number of blocks, channels and layers in the network, leading to a lightweight CNN for indoor fire detection. Furthermore, we use the Fire Dynamic Simulator (FDS) to simulate data for the training stage, enhancing the robustness of the network. The fire detection performance of the proposed method is verified through an experiment. It was found that the proposed method achieved an impressive accuracy of 99.1%, while the number of CNN parameters and the amount of computation is still small, which is more suitable for the resource-constrained embedded platform of an indoor fire detection system.

Widespread measles cases following the COVID-19 pandemic have threatened human health and progress towards measles elimination. While we know that the pandemic has disrupted routine measles vaccination worldwide, most settings still lack quantification of post-pandemic population immunity gaps and the feasibility of closing these gaps through supplementary immunisation activities. Using serological data (15,405 antibody measurements from 3,674 individuals) in southern China between 2013-2024, we analyse pre- and post-pandemic susceptibility profile changes in the pediatric population, and explore underlying differences and mechanisms of measles-specific immunity. We show that childbearing-age women born at a time of low measles infection risk (born between 1990-2005) had 0.39 (95% CI 0.38-0.42) log mIU/ml lower mean log-concentration in 2021-2024 compared to those born during high-risk periods (born between 1984-1989). This in turn resulted in a 0.29 (95% CI 0.27-0.52) log mIU/ml lower mean log-concentration at birth and faster antibody waning in their infants. We also observe that 9.5-10.7% pediatric susceptibility was attributed to waning vaccine-induced immunity during 2013-2024. We project a 23.5–50.0% immunity increase (from 66.6% to 92.7%) in children under 15 years following non-selective supplementary immunisation activities, supporting the key role of supplementary immunisation activities in restoring robust population immunity. Measles vaccination was interrupted globally during the COVID-19 pandemic. Here, the authors use data on measles antibody levels from Hunan province, China, to quantify the immunity gap and model the potential impact of supplementary immunisation activities.

Group 3 innate lymphoid cells (ILC3s) are key players in intestinal homeostasis. ER stress is linked to inflammatory bowel disease (IBD). Here, we used cell culture, mouse models, and human specimens to determine whether ER stress in ILC3s affects IBD pathophysiology. We show that mouse intestinal ILC3s exhibited a 24-hour rhythmic expression pattern of the master ER stress response regulator inositol-requiring kinase 1α/X-box-binding protein 1 (IRE1α/XBP1). Proinflammatory cytokine IL-23 selectively stimulated IRE1α/XBP1 in mouse ILC3s through mitochondrial ROS (mtROS). IRE1α/XBP1 was activated in ILC3s from mice exposed to experimental colitis and in inflamed human IBD specimens. Mice with Ire1α deletion in ILC3s (Ire1αΔRorc) showed reduced expression of the ER stress response and cytokine genes including Il22 in ILC3s and were highly vulnerable to infections and colitis. Administration of IL-22 counteracted their colitis susceptibility. In human ILC3s, IRE1 inhibitors suppressed cytokine production, which was upregulated by an IRE1 activator. Moreover, the frequencies of intestinal XBP1s+ ILC3s in patients with Crohn's disease before administration of ustekinumab, an anti-IL-12/IL-23 antibody, positively correlated with the response to treatment. We demonstrate that a noncanonical mtROS-IRE1α/XBP1 pathway augmented cytokine production by ILC3s and identify XBP1s+ ILC3s as a potential biomarker for predicting the response to anti-IL-23 therapies in IBD.

The patient, a 43-year-old male, was admitted to the hospital with gradually aggravated exertional palpitations and chest tightness over a 2-day period. Upon hospital admission, a cardiac ultrasound revealed aortic valve redundancy, however multiple blood culture investigations came back negative. Blood mNGS was perfected, revealing Coxiella burnetii , and the diagnosis of Q fever (query fever) was established. The temperature and inflammatory indices of the patient were all normal with the treatment of vancomycin before cardiac surgery. But for the potential liver damage of and the Coxiella burnetii was still positive in the anti-phase II IgG titer, the doxycycline and hydroxychloroquine instead of vancomycin were applied for the patient. Despite receiving standardized anti-infective therapy of doxycycline combined with hydroxychloroquine, this patient had fever and increased leukocytes following surgery. After the addition of vancomycin as an anti-infective treatment, the temperature and leukocytes improved quickly. During the treatment of vancomycin, a discovery of liver injury may have resulted. These findings provide new therapy options for future professionals.

Introduction Myocardial hypoxia is an important factor causing myocardial infarction (MI). Interestingly, many unknown factors in the molecular mechanism of MI remain unclear. Our study explored the role of lncRNA growth arrest‐specific 5 (GAS5) in cell injury under hypoxia. Methods AS5 expression was assessed in MI and human cardiomyocytes under hypoxia through RT‐qPCR assay. Methyl thiazolyl tetrazolium assay, flow cytometry assay, and transwell assay was carried out for cell viability, cell apoptosis, cell migration, and invasion, respectively. The regulatory target of GAS5 was explored through a dual‐luciferase reporter assay. Results Our findings indicated that the upregulation of GAS5 was related to hypoxia. Downregulation of GAS5 expression could decrease hypoxia‐induced cell apoptosis and increase cell migration and invasion. Moreover, GAS 5 targeted miR‐21, which regulated the phosphatase and tension homology deleted on chromosome ten gene (PTEN) expression. Furthermore, the knockdown of miR‐21 eliminated the effect of GAS5 silencing on cell injury. Conclusion These results indicated that lncRNA GAS5 silencing decreased cardiomyocyte injury by hypoxia‐induced through regulating miR‐21/PTEN. Our results indicate that GAS5 can regulate the process of myocardial infarction (MI) by targeting the miR‐21/PTEN axis. Therefore, both GAS5 and miR‐21/PTEN may become key targets for the treatment of MI in the future.

Characterizing the long-term kinetics of maternally derived and vaccine-induced measles immunity is critical for informing measles immunization strategies moving forward. Based on two prospective cohorts of children in China, we estimate that maternally derived immunity against measles persists for 2.4 months. Following two-dose series of measles-containing vaccine (MCV) at 8 and 18 months of age, the immune protection against measles is not lifelong, and antibody concentrations are extrapolated to fall below the protective threshold of 200 mIU/ml at 14.3 years. A catch-up MCV dose in addition to the routine doses between 8 months and 5 years reduce the cumulative incidence of seroreversion by 79.3–88.7% by the age of 6 years. Our findings also support a good immune response after the first MCV vaccination at 8 months. These findings, coupled with the effectiveness of a catch-up dose in addition to the routine doses, could be instrumental to relevant stakeholders when planning routine immunization schedules and supplemental immunization activities. The timing of measles vaccination in infants affects the risk of infection in young children and the duration of protection provided. Here, the authors investigate optimal vaccination timing by characterising antibody kinetics following different vaccine schedules in two cohorts of children in southern China.

ObjectivesTo explore the temporal and causal relationships underlying brain structural changes in post-radiotherapy (RT) nasopharyngeal carcinoma (NPC) patients.MethodsA total of 38 post-radiotherapy NPC patients (33 males, 5 females; median age: 50.0 years, range: 27–63 years; median time post-RT: 17.2 months, range: 0.5–108 months) and 23 healthy controls (16 males, 7 females; median age: 37 years, range: 24–61 years) underwent T1-weighted magnetic resonance (MR) images, and their images were evaluated. The causal structural covariance network (CaSCN) analysis approach was applied to assess the causal relationships underlying radiation-induced brain structural alterations in these patients. Granger causality (GC) analysis was employed to morphometric data derived from T1-weighted MR images, which were ordered by the time elapsed post-RT.ResultsThe source-like directed associations were observed in the bilateral parahippocampal gyrus (PHG), the right gyrus rectus (REC.R), and the right caudate nucleus (CAU.R). The directed network analysis revealed that the parahippocampal gyrus (PHG), REC.R and CAU.R exhibited typical source-like characteristics, and their structural changes exerted a key regulatory effect on GM volume alterations across multiple brain regions. While the left precuneus (PCUN.L), left temporal pole: middle temporal gyrus (TPOmid.L) and the left inferior temporal gyrus (ITG.L) were typical sink-like brain region that mainly received regulatory effects from source-like brain regions, acting as major target regions of structural damage.ConclusionOver time, post-radiotherapy NPC patients exhibited progressive changes in GM volume, where the PHG.L, PHG.R, REC.R and CAU.R were core source-like brain regions. The PCUN.L, TPOmid.L, and ITG.L show distinct sink-like features, which mainly receive regulatory effects from source-like brain regions.

During January-February 2020, coronavirus disease (COVID-19) and tuberculosis were diagnosed for 3 patients in Wuhan, China. All 3 patients had COVID-19 pneumonia. One severely ill patient died after acute respiratory distress syndrome developed. Clinicians and public health officials should be aware of underlying chronic infections such as tuberculosis in COVID-19 patients.

Background The dysfunction of type I interferon (IFN) signaling is an important mechanism of immune escape and metastasis in tumors. Increased NOS1 expression has been detected in melanoma, which correlated with dysfunctional IFN signaling and poor response to immunotherapy, but the specific mechanism has not been determined. In this study, we investigated the regulation of NOS1 on the interferon response and clarified the relevant molecular mechanisms. Methods After stable transfection of A375 cells with NOS1 expression plasmids, the transcription and expression of IFNα-stimulated genes (ISGs) were assessed using pISRE luciferase reporter gene analysis, RT-PCR, and western blotting, respectively. The effect of NOS1 on lung metastasis was assessed in melanoma mouse models. A biotin-switch assay was performed to detect the S-nitrosylation of HDAC2 by NOS1. ChIP-qPCR was conducted to measure the binding of HDAC2, H4K16ac, H4K5ac, H3ac, and RNA polymerase II in the promoters of ISGs after IFNα stimulation. This effect was further evaluated by altering the expression level of HDAC2 or by transfecting the HDAC2-C262A/C274A site mutant plasmids into cells. The coimmunoprecipitation assay was performed to detect the interaction of HDAC2 with STAT1 and STAT2. Loss-of-function and gain-of-function approaches were used to examine the effect of HDAC2-C262A/C274A on lung metastasis. Tumor infiltrating lymphocytes were analyzed by flow cytometry. Results HDAC2 is recruited to the promoter of ISGs and deacetylates H4K16 for the optimal expression of ISGs in response to IFNα treatment. Overexpression of NOS1 in melanoma cells decreases IFNα-responsiveness and induces the S-nitrosylation of HDAC2-C262/C274. This modification decreases the binding of HDAC2 with STAT1, thereby reducing the recruitment of HDAC2 to the ISG promoter and the deacetylation of H4K16. Moreover, expression of a mutant form of HDAC2, which cannot be nitrosylated, reverses the inhibition of ISG expression by NOS1 in vitro and decreases NOS1-induced lung metastasis and inhibition of tumor infiltrating lymphocytes in a melanoma mouse model. Conclusions This study provides evidence that NOS1 induces dysfunctional IFN signaling to promote lung metastasis in melanoma, highlighting NOS1-induced S-nitrosylation of HDAC2 in the regulation of IFN signaling via histone modification.

Endogenous nitric oxide (NO) produced by nitric oxide synthases (NOSs) plays an important immunosuppressive role in the tumor microenvironment. In melanoma, NOS1 expression increases with tumor progression and correlates with tumor immune escape through the inhibition of type I interferon (IFN) signaling. However, the immune regulatory role and related mechanisms of NOS1, as well as its impacts on immune therapies such as immune checkpoint blockade (ICB) in melanoma, remain unclear. Here, we found that NOS1 expression induces IRF7 modification by S-nitrosylation at the C435 site in mice (C481 in humans), which functionally promoted tumor growth in mouse models. Mechanistically, IRF7-C435-SNO inhibited IFNβ transcription under PRR signal activation, leading to a disorder in the initiation of the type I interferon response in melanoma cells. In a melanoma mouse model, IRF7-C435-SNO decreased the infiltration and activation of CD8 + T cells in the tumor microenvironment by reducing antigen presentation processes in tumor cells and inhibiting the maturation of DC1. Clinically, high expression of NOS1 correlated with poor survival prognosis and resistance to ICB anti-tumor therapies in melanoma cases with less immune cell infiltration. Our study suggests that NOS1 expression in melanoma characterizes IFN-I signal disorders in response to innate immune stimulation through IRF7 s-nitrosylation. Targeting NOS1 signaling might be beneficial for overcoming immune therapeutically resistance, particularly in immune-cold melanoma phenotype.