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Abstract Background Nanosecond pulsed electric fields (nsPEF)‐based electroporation is a new therapy modality potentially synergized with radiation therapy to improve treatment outcomes. To verify its treatment accuracy intraoperatively, electroacoustic tomography (EAT) has been developed to monitor in‐vivo electric energy deposition by detecting ultrasound signals generated by nsPEFs in real‐time. However, utility of EAT is limited by image distortions due to the limited‐angle view of ultrasound transducers. Methods This study proposed a supervised learning‐based workflow to address the ill‐conditioning in EAT reconstruction. Electroacoustic signals were detected by a linear array and initially reconstructed into EAT images, which were then fed into a deep learning model for distortion correction. In this study, 56 distinct electroacoustic data sets from nsPEFs of different intensities and geometries were collected experimentally, avoiding simulation‐to‐real‐world variations. Forty‐six data were used for model training and 10 for testing. The model was trained using supervised learning, enabled by a custom rotating platform to acquire paired full‐view and single‐view signals for the same electric field. Results The proposed method considerably improved the image quality of linear array‐based EAT, generating pressure maps with accurate and clear structures. Quantitatively, the enhanced single‐view images achieved a low‐intensity error (RMSE: 0.018), high signal‐to‐noise ratio (PSNR: 35.15), and high structural similarity (SSIM: 0.942) compared to the reference full‐view images. Conclusions This study represented a pioneering stride in achieving high‐quality EAT using a single linear array in an experimental environment, which improves EAT's utility in real‐time monitoring for nsPEF‐based electroporation therapy.

Abstract Background Hepatocellular carcinoma (HCC) is a common gastrointestinal malignancy with a high incidence and poor prognosis. The subunits of the integrator complex (INTS1-14) play a crucial role in regulating genes dependent on RNA Polymerase II, which may be associated with cancer. However, the role of INTSs in HCC remains unclear. This study aims to comprehensively analyze the clinical value and potential role of INTS family genes in HCC through systematic bioinformatics analysis. Methods We employed various public databases, including UALCAN, HPA, Kaplan–Meier Plotter, GEPIA2, TNMplot, STRING, TIMER, and TISIDB, to investigate the expression levels, clinicopathological correlations, diagnostic and prognostic value, genetic alterations, co-expression network, molecular targets, and immune infiltration of INTSs in HCC. Additionally, Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were utilized to investigate the biological functions of genes associated with INTSs. Furthermore, Western blot, real-time fluorescence quantitative reverse transcription polymerase chain reaction (RT-qPCR), and immunohistochemistry techniques were employed to assess the expression of relevant proteins and genes. The proliferation of HCC cells was evaluated using the CCK8 assay. Results We found that in HCC, there was a significant upregulation of INTSs at the transcriptional level, particularly INTS1, INTS4, INTS7, and INTS8. Additionally, the protein levels of INTS1 and INTS8 were notably elevated. The overexpression of these INTSs was strongly correlated with tumor stages in HCC patients. INTS1, INTS4, INTS7, and INTS8 exhibited significant diagnostic and prognostic value in HCC. Moreover, their expression was associated with immune infiltrations and activated status, including B cells, CD8 + T cells, CD4 + T cells, NK cells, macrophages, and dendritic cells. Functional predictions indicated that INTS1, INTS4, INTS7, and INTS8 were involved in various cancer-related signaling pathways, such as TRAIL, IFN-gamma, mTOR, CDC42, Apoptosis, and the p53 pathway. Furthermore, we observed a significant upregulation of INTS1, INTS4, INTS7, and INTS8 expression in HCC cell lines compared to normal liver cell lines. The level of INTS1 protein was higher in cancerous tissues compared to adjacent non-cancerous tissues (n = 16), and the suppression of INTS1 resulted in a significant decrease in the proliferation of Huh7 cells. Conclusion These findings indicate the potential of INTS family genes as diagnostic biomarkers and therapeutic targets in HCC. Further research is needed to understand the underlying mechanisms and explore clinical applications.

Post-stroke depression (POSD) is a common difficulty and most predominant emotional syndrome after stroke often consequences in poor outcomes. In the present investigation, we have designed and studied the neurologically active celastrol/minocycline encapsulated with macrophages-derived exosomes functionalized PLGA nanoformulations (CMC-EXPL) to achieve enhanced anti-inflammatory behaviour and anti-depressant like activity in a Rat model of POSD. The animal model of POSD was established through stimulating process with chronic unpredictable mild stress (CUM) stimulations after procedure of middle cerebral artery occlusion (MCAO). Neuronal functions and Anti-inflammation behaviours were observed by histopathological (H&E) examination and Elisa analyses, respectively. The anti-depressive activity of the nanoformulations treated Rat models were evaluated by open-field and sucrose preference test methods. Microglial polarization was evaluated via flow-cytometry and qRT-PCR observations. The observed results exhibited that prepared nanoformulations reduced the POSD-stimulated depressive-like activities in rat models as well alleviated the neuronal damages and inflammatory responses in the cerebral hippocampus. Importantly, prepared CMC-EXPL nanoformulation effectively prevented the M1 pro-inflammatory polarization and indorsed M2 anti-inflammatory polarization, which indicates iNOS and CD86 levels significantly decreased and upsurged Arg-1 and CD206 levels. CMC-EXPL nanoformulation suggestively augmented anti-depressive activities and functional capability and also alleviated brain inflammation in POSD rats, demonstrating its therapeutic potential for POSD therapy.

By engaging in redox processes, ferroptosis plays a crucial role in sepsis-induced acute lung injury (ALI). Although iron stimulates calcium signaling through the stimulation of redox-sensitive calcium pathways, the function of calcium signals in the physiological process of ferroptosis in septic ALI remains unidentified. Iron homeostasis disequilibrium in ferroptosis is frequently accompanied by aberrant calcium signaling. Intracellular calcium overflow can be a symptom of dysregulation of the cellular redox state, which is characterized by iron overload during the early phase of ferroptosis. This can lead to disruptions in calcium homeostasis and calcium signaling. The mechanisms controlling iron homeostasis and ferroptosis are reviewed here, along with their significance in sepsis-induced acute lung injury, and the potential role of calcium signaling in these processes is clarified. We propose that the development of septic acute lung injury is a combined process involving the bidirectional interaction between iron homeostasis and calcium signaling. Our goal is to raise awareness about the pathophysiology of sepsis-induced acute lung injury and investigate the relationship between these mechanisms and ferroptosis. We also aimed to develop calcium-antagonistic therapies that target ferroptosis in septic ALI and improve the quality of survival for patients suffering from acute lung injury.

Abstract In this work, we studied four types of cosmological models with different mechanisms driving the accelerated expansion of the universe, include Braneworld models, Chaplygin Gas models, Emergent Dark Energy models, and cosmological torsion models. Considering that the dynamics of these models at low redshifts are very similar and difficult to distinguish, we used the latest and largest UV and X-ray measurements of quasars (QSOs) observations covering the range of redshift $$0.009

Highlights Janus quasi-solid electrolyte membranes with asymmetric porous structure were constructed, showing a high σLi+ of 1.5 × 10-4 S cm-1 and a high t + of 0.71. The solvation structures and ion transport dynamics in nanopores have been deciphered, manifesting a concentrated electrolyte-like structure and regulated transport behaviors. Quasi-solid NCM 622||Li cells have been demonstrated to stably cycle for 200 cycles at 1 C, and pouch cell has shown high tolerance for abuse.

Over the past decade, advancements in high-throughput sequencing technologies have led to a qualitative leap in our understanding of the role of the microbiota in human diseases, particularly in oncology. Despite the low biomass of the intratumoral microbiota, it remains a crucial component of the tumor immune microenvironment, displaying significant heterogeneity across different tumor tissues and individual patients. Although immunotherapy has emerged a major strategy for treating tumors, patient responses to these treatments vary widely. Increasing evidence suggests that interactions between the intratumoral microbiota and the immune system can modulate host tumor immune responses, thereby influencing the effectiveness of immunotherapy. Therefore, it is critical to gain a deep understanding of how the intratumoral microbiota shapes and regulates the tumor immune microenvironment. Here, we summarize the latest advancements on the role of the intratumoral microbiota in cancer immunity, exploring the potential mechanisms through which immune functions are influenced by intratumoral microbiota within and outside the gut barrier. We also discuss the impact of the intratumoral microbiota on the response to cancer immunotherapy and its clinical applications, highlighting future research directions and challenges in this field. We anticipate that the valuable insights into the interactions between cancer immunity and the intratumoral microbiota provided in this review will foster the development of microbiota-based tumor therapies.

Abstract Ulcerative colitis (UC) is a complicated and recurrent intestinal disease. Currently available drugs for UC treatment are scarce, therefore, novel therapeutic drugs for the UC are urgently to be developed. Gingerenone A (GA) is a phenolic compound known for its anti‐inflammatory effect, but its effect on UC remains unknown. Here, it is shown that GA protects mice against UC, which is closely associated with inhibiting intestinal mucosal inflammation and enhancing intestinal barrier integrity in vivo and in vitro. Of note, RNA sequencing analysis demonstrates an evident correlation with IL‐17 signaling pathway after GA treatment, and this effect is further corroborated by Western blot. Mechanistically, GA directly interacts with IL‐17RA protein through pull‐down, surface plasmon resonance analysis and molecular dynamics simulation. Importantly, lentivirus‐mediated IL‐17RA/Act1 knock‐down or GA co‐treatment with brodalumab/ixekizumab significantly impairs the protective effects of GA against DSS‐induced inflammation and barrier dysfunction, suggesting a critical role of IL‐17RA signaling for GA‐mediated protection against UC. Overall, these results indicate that GA is an effective agent against UC mainly through the direct binding of IL‐17RA to inhibit inflammatory signaling activation.

Establishing ecological management zones based on the supply-demand relationship of ecosystem services (ESs) is essential for fostering sustainable development within social-ecological systems and improving human well-being. In this study, the spatial pattern between supply and demand in five ESs (grain production (GP), carbon sequestration (CS), soil conservation (SC), water conservation (WC), and habitat quality (HQ)) is analyzed using the ESs supply-demand ratio (ESDR) method, the spatial autocorrelation method, and the coupled coordination degree model. Zoning is performed according to the differences in their spatial combinations, and differential zoning management policies are proposed. The following results were obtained: (1) In terms of the ESDR, except for a slight increase in GP surplus from 2010 to 2020, there is a decline in the surplus of the other four ESs. (2) CS, WC, and HQ are dominated by cluster types LH and HL. GP and SC are dominated by cluster types HH and LL. The average value of the coupling coordination degree (CCD) of comprehensive ESs supply and demand show five types: moderate disharmony, slight disharmony, near disharmony, basic coordination, and slight coordination. (3) Based on the multiple spatial heterogeneity of ESs supply and demand, differentiated ecological management strategies are proposed at the grid scale. Overall, this study discover the spatial pattern of mismatch between the supply and demand of ecosystem services (ESs) in mountainous urban areas. This contribution enhances the discourse surrounding sustainable development theory and advances research on the coupling of social-ecological systems. Furthermore, it offers valuable insights for the formulation of sustainable ecological management policies tailored to mountainous urban settings.

Fusobacterium vincentii brain abscesses are relatively rare. Here, we report our treatment of an anaerobic brain abscess caused by a mixed infection of Parvimonas micra, Streptococcus constellatus, Fusobacterium vincentii, and Bacteroides heparinolyticus diagnosed by metagenomic next-generation sequencing (mNGS). This is the first reported case of Fusobacterium vincentii in a brain abscess. This case highlights the possibility that oral anaerobic microbes can cause a brain abscess and demonstrates that mNGS has the potential to be deployed to provide rapid infection diagnosis and rationalize antimicrobial therapy for brain abscesses.

In this letter, we propose a novel cosmological model-independent method to determine cosmic curvature, combining the recent measurements of transverse and line-of-sight directions in the baryon acoustic oscillations (BAO) with cosmic chronometers (CC) datasets. Considering that the CC dataset is discrete and includes only 32 H(z) measurements, we apply Gaussian process (GP) regression to fit the CC dataset and reconstruct them. Our methodology, which does not need the calibration or selection of any cosmological model, provide multiple measurements of spatial curvature (ΩK) at different redshifts (depending on the redshift coverage of BAO dataset). For combination of all BAO data, we find that the constraint result on cosmic curvature is ΩK=−0.096−0.195+0.190 with 1σ observational uncertainty. Although the measured ΩK is in good agreement with zero cosmic curvature within 1σ confidence level, our result revels the fact of a closed universe. More importantly, our results show that the obtained ΩK measurements are almost unaffected by different priors of the Hubble constant. This could help solve the issue of the Hubble tension that may be caused by inconsistencies in the spatial curvature between the early and late universes.

Battery recycling is viewed in China as an important means of achieving primary sustainability goals and greater economic and environmental development. With the notice of high battery recycling intentions through relevant investigations, this study examine the influencing factors of these recycling behaviors of e-bikes citizens by incorporating the place identity and environmental concern into the Extended Normative Activation Model (NAM), which fill the research gap on how place identity and environmental concern affect the batteries recycling behavior. This study proposes that the consequence awareness, personal norms, and attitudes have mediating effect on place identity to the recycling behavior, and the environmental concern has moderating effect on consequence awareness, personal norms, and attitudes to the recycling behavior, respectively. Based on 1068 valid surveys, hypotheses were examined using partial least square structural equation modeling (PLS-SEM). The results show that personal norms and awareness of consequences positively impact e-bike users' intentions to recycle waste batteries, and environmental concerns have no moderating effect on attitude, recycling intention, personal norms, and recycling intention. Theoretical and practical implications are discussed at last.

Infrared small target detection (IRSTD) aims to segment small targets from infrared clutter background. Existing methods mainly focus on discriminative approaches, i.e., a pixel-level front-background binary segmentation. Since infrared small targets are small and low signal-to-clutter ratio, empirical risk has few disturbances when a certain false alarm and missed detection exist, which seriously affect the further improvement of such methods. Motivated by the dense prediction generative methods, in this article, we compensate pixel-level discriminant with mask posterior distribution modeling. Specifically, we propose a diffusion model framework for IRSTD. This generative framework maximizes the posterior distribution of the small target mask to surmount the performance bottleneck associated with minimizing discriminative empirical risk. This transition from the discriminative paradigm to generative one enables us to bypass the target-level insensitivity. Furthermore, we design a low-frequency isolation in wavelet domain to suppress the interference of intrinsic infrared noise on the diffusion noise estimation. The low-frequency component of the infrared image in the wavelet domain is processed by a neural network, and the high-frequency component is utilized to restore the targets information, to estimate the residuals of the enhanced features. Experiments show that the proposed method achieves competitive performance gains over state-of-the-art methods on NUAA-SIRST, NUDT-SIRST, and IRSTD-1 k datasets.

ABSTRACTMosquitoes carry a large number of known and unknown viruses, some of which could cause serious diseases in humans or animals. Metagenomic sequencing for mosquito viromes is crucial for understanding the evolutionary history of viruses and preventing emerging mosquito-borne diseases. We collected 1,598 mosquitoes belonging to four species from five counties in Shandong Province, China in 2021. They were grouped by species and sampling locations and subjected to metagenomic next-generation sequencing for the analysis of the viromes. A total of 233,317,352 sequencing reads were classified into 30 viral families and an unclassified group. Comparative analysis showed that mosquitoes in Shandong Province generally possessed host-specific virome. We detected mosquito-borne viruses including Japanese encephalitis virus, Getah virus, and Kadipiro virus in Culex tritaeniorhynchus and Anopheles sinensis samples. Phylogenetic analysis showed that these pathogenic viruses may have existed in mosquitoes in Shandong Province for a long time. Meanwhile, we identified 22 novel viruses belonging to seven families and the genus Negevirus. Our study comprehensively described the viromes of several common mosquito species in Shandong Province, China, and demonstrated the major role of host species in shaping mosquito viromes. Furthermore, the metagenomic data provided valuable epidemiological information on multiple mosquito-borne viruses, highlighting the potential risk of infection transmission.IMPORTANCEMosquitoes are known as the source of various pathogens for humans and animals. Culex tritaeniorhynchus, Armigeres subalbatus, and Anopheles sinensis have been found to transmit the Getah virus, which has recently caused increasing infections in China. Cx. tritaeniorhynchus and Culex pipiens are the main vectors of Japanese encephalitis virus and have caused epidemics of Japanese encephalitis in China in past decades. These mosquitoes are widely present in Shandong Province, China, leading to a great threat to public health and the breeding industry. This study provided a comprehensive insight into the viromes of several common mosquito species in Shandong Province, China. The metagenomic sequencing data revealed the risks of multiple pathogenic mosquito-borne viruses, including Japanese encephalitis virus, Getah virus, and Kadipiro virus, which are of great importance for preventing emerging viral epidemics.

Background: Epstein-Barr virus (EBV) is widely infected in humans and causes various diseases. Among them, microRNAs of EBV play a key role in the progression of EBV-associated febrile diseases. There're few specific indicators for rapid differential diagnosis of various febrile diseases associated with EBV, and the lack of more reliable screening methods with high diagnostic utility has led to spaces for improvement in the accurate diagnosis and efficient treatment of relevant patients, making EBV infection a complicated clinical problem. With recent advances in plasma microRNA testing, the apparent presence of EBV microRNAs in plasma can help screen for EBV infection. The gene networks targeted by these microRNAs can also indicate potential biomarkers of EBV-associated febrile diseases. This study aimed to identify some novel miRNAs as potential biomarkers for early diagnosis of respectively EBV-associated febrile diseases. Materials and methods: A total of 110 participants were recruited for this task. First, we performed high-throughput sequencing and preliminary PCR validation of differentially expressed miRNAs in 15 participants with EBV-associated fever (divided into 5 groups, common EBV carriers, infectious mononucleosis (IM) and chronic active EBV infection (CAEBV), EBV-associated Hemophagocytic Lymphohistiocytosis (EBV-HLH), and 3 healthy individuals). After a comprehensive analysis, 10 miRNAs with abnormal expression were screened, and then qRT-PCR was performed in the rest of 95 participants to detect the validation of miRNAs expression in plasma samples. Thereafter, we further investigated their potential for clinical application in EBV-related febrile diseases by using a combination of Gene Ontology analysis, Kyoto Encyclopedia of Genes and Genomes pathway analysis, and Protein-protein interaction network analysis. Results: Through identification and detailed analysis of the obtained data, we found significant differences in the expression of Hsa-miR-320d, EBV-miR-BART22, and EBV-miR-BART2-3p in blood samples from patients with different EBV-related febrile diseases. We found that the expression levels of Hsa-miR-320d, EBV-miR-BART22, and EBV-miR-BART2-3p in plasma are indicative of determining different disease types of EBV-related febrile diseases, while EBV-miR-BART22 and EBV-miR-BART2-3p may be potential therapeutic targets. Conclusion: The expression levels of Hsa-miR-320d, EBV-miR-BART22, and EBV-miR-BART2-3p suggest that they may be used as transcriptional features for early differential diagnosis of EBV-related febrile diseases, and EBV-miR-BART22 and EBV-miR-BART2-3p may be potential therapeutic targets.

Background. Atherosclerosis is an inflammatory cardiovascular disease. However, whether the association of immune cells in plaques promotes the progression of this disease has not yet been completely elucidated. Materials and Methods. Thus, this study aimed to investigate the relationship between C1q+ macrophages and CD8T cells through scRNA-seq data reanalysis, quantitative real-time PCR, and flow cytometry. Chromatin immunoprecipitation-quantitative polymerase chain reaction, western blot, and antibody-blocking experiments were performed to investigate the role of macrophage–CD8T interaction in atherosclerosis. An atherosclerotic mouse model was developed to confirm our findings. Results. Mechanistically, Spi1 expression induced by granulocyte–macrophage colony-stimulating factor promoted C1q expression in the macrophages. Moreover, C1q+ macrophages suppressed CD8T cell apoptosis by upregulating Slc7a7 expression to enhance the L-arginine uptake of CD8T cells. CD8T-derived interferon-γ promoted macrophage activation to induce atherosclerosis. Blockade of the C1q–C1qbp axis attenuated atherosclerosis. Conclusion. In conclusion, macrophages interacting with CD8T promote atherosclerosis development via the C1q–C1qbp axis.

We previously demonstrated that glycyrrhizin (GL) suppressed inflammation and carcinogenesis in an azoxymethane (AOM)/dextran sodium sulfate (DSS)-induced murine model of colorectal cancer (CC). In this study, we found an accumulation of regulatory T cells (Tregs) in the spleen and suppression by GL in model mice. ICR mice were divided into four groups: Control, GL, CC, and GL-treated CC (CC+GL), and were sacrificed 20 weeks after AOM/DSS treatment. We measured spleen weight, areas of white and red pulp, and CD8+ T cells (cytotoxic T lymphocytes, CTL), and CD11c-positive cells (dendritic cells) in splenic tissues and forkhead box protein 3 (FoxP3)-positive cells (Tregs) in colorectal and splenic tissues. In all cases, the CC group showed a significant increase compared with those in Control group, and GL administration significantly attenuated this increase. These results indicate that Tregs accumulated in the spleen may participate in inflammation-related carcinogenesis by suppressing CTL. We also suggest that GL which binds to high-mobility group box 1 (HMGB1), suppresses carcinogenesis with decreasing Tregs in the spleen. Furthermore, there was an expression of FoxP3 in cancer cells, indicating that it may be involved in the malignant transformation of cancer cells.

Primary ciliary dyskinesia (PCD) is a hereditary disease caused by genes related to motile cilia. We report two male pediatric cases of PCD caused by hemizygous pathogenic variants in the OFD1 centriole and centriolar satellite protein (OFD1) gene. The variants were NM_003611.3: c.[2789_2793delTAAAA] (p.[Ile930LysfsTer8]) in Case 1 and c.[2632_2635delGAAG] (p.[Glu878LysfsTer9]) in Case 2. Both cases had characteristic recurrent respiratory infections. Neither case had symptoms of oral-facial-digital syndrome type I. We identified a variant (c.2632_2635delGAAG) that has not been previously reported in any case of OFD1-PCD.

Climate change exerts significant impacts on regional agricultural production. This study assesses the implications of climate change on winter wheat yields in the Huang-Huai-Hai Plain (3H Plain), utilizing bias-corrected climate projections from the Coupled Model Intercomparison Project Phase 6 (CMIP6) for mid-21st century (2041–2060) and late 21st century (2081–2100) periods under two shared socioeconomic pathways (SSP2–4.5 and SSP5–8.5). These projections were incorporated into the decision support system for agrotechnology transfer (DSSAT) CERES-Wheat model to forecast potential alterations in winter wheat production. Initial findings reveal that uncorrected CMIP6 projections underestimated temperature and precipitation while overestimating solar radiation across the southern 3H Plain. Following bias correction through the equidistant cumulative distribution function (EDCDF) method, the regional average biases for temperature, precipitation, and solar radiation were reduced by 18.3%, 5.6%, and 30.7%, respectively. Under the SSP2–4.5 and SSP5–8.5 scenarios, mid-21st century simulations predicted a 13% increase in winter wheat yields. Late 21st century projections indicated yield increases of 11.3% and 3.6% under SSP2-4.5 and SSP5-8.5 scenarios, respectively, with a notable 8.4% decrease in yields south of 36° N under the SSP5-8.5 scenario. The analysis of climate change factors and winter wheat yields in the 3H Plain under both scenarios identified precipitation as the key contributing factor to yield increases in the northern 3H Plain, while temperature limitations were the primary constraint on yields in the southern region. Consequently, adaptive strategies are essential to mitigate climate change impacts, with a particular focus on addressing the challenges posed by elevated temperature in the southern 3H Plain.

Volatile organic compounds (VOCs) are important precursors of ozone (O3) generation. Understanding the characteristics, and emission sources of VOCs, and the relationship between VOCs and O3 during O3 pollution are of great significance for O3 pollution control. This study investigated the characteristics, sources, and effects of VOCs on O3 formation in Zhengzhou, Henan Province from 1st to 30th June 2023, and provided recommendations for O3 emission reduction strategies. Two O3 pollution events occurred during the observation period. During the observation period, the concentration of Total VOCs (TVOCs) varied from 9.9 to 60.3 ppbv, with an average of 22.8 ± 8.3 ppbv. The average concentration of TVOCs in the two pollution events were higher than that on the clean days. Six major VOCs sources were identified by using the Positive Matrix Factorization model. Vehicular exhaust (28%), solvent usage (27%), and industrial production (22%) were the main sources. An observation-based mode was applied to explore the O3-precursors relationship and observation-oriented O3 control strategies. The results of relative incremental reactivity (RIR) and empirical kinetics modeling approach showed that the O3 formation in Zhengzhou in June was in anthropogenic VOCs (AVOCs)-limited regimes. VOCs with the largest RIR values, while NOx had a negative RIR value. It was worth noting that the sensitivity of O3 generation to biogenic VOCs (BVOCs) was greater than that of AVOCs. From the perspective of the reduction effect, the reduction ratios of AVOCs/NOx should be no less than 3:1, which was conducive to the reduction of O3 formation. [ABSTRACT FROM AUTHOR]

This study proposes a novel method to prevent fatigue cracks at the root of fillet welds in steel bridge supports by inserting epoxy resin as an adhesive material. A total of 36 specimens, categorized into welded‐only and bonding‐assisted types, were subjected to a series of four‐point bending fatigue tests to simulate cyclic tensile stress conditions. Additionally, finite element analysis was employed to investigate the impact of epoxy insertion on stress distribution near the weld root. The results demonstrated that bonding‐assisted specimens exhibited significantly improved fatigue life compared to welded‐only specimens, with a notable reduction in tensile stress at the weld root. Furthermore, a displacement‐based method was employed to evaluate weld root fatigue performance, yielding consistent results. These findings highlight the potential of integrating adhesive bonding in fillet welds to improve the durability and service life of steel bridge structures by effectively mitigating fatigue‐related issues. [ABSTRACT FROM AUTHOR]

TRIM32 is often aberrantly expressed in many types of cancers. Kaposi’s sarcoma-associated herpesvirus (KSHV) is linked with several human malignancies, including Kaposi’s sarcoma and primary effusion lymphomas (PELs). Increasing evidence has demonstrated the crucial role of KSHV lytic replication in viral tumorigenesis. However, the role of TRIM32 in herpesvirus lytic replication remains unclear. Here, we reveal that the expression of TRIM32 is upregulated by KSHV in latency, and reactivation of KSHV lytic replication leads to the inhibition of TRIM32 in PEL cells. Strikingly, RTA, the master regulator of lytic replication, interacts with TRIM32 and dramatically promotes TRIM32 for degradation via the proteasome systems. Inhibition of TRIM32 induces cell apoptosis and in turn inhibits the proliferation and colony formation of KSHV-infected PEL cells and facilitates the reactivation of KSHV lytic replication and virion production. Thus, our data imply that the degradation of TRIM32 is vital for the lytic activation of KSHV and is a potential therapeutic target for KSHV-associated cancers. IMPORTANCE TRIM32 is associated with many cancers and viral infections; however, the role of TRIM32 in viral oncogenesis remains largely unknown. In this study, we found that the expression of TRIM32 is elevated by Kaposi’s sarcoma-associated herpesvirus (KSHV) in latency, and RTA (the master regulator of lytic replication) induces TRIM32 for proteasome degradation upon viral lytic reactivation. This finding provides a potential therapeutic target for KSHV-associated cancers. [ABSTRACT FROM AUTHOR]