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Acoustic imaging method is a critical task in various applications since it can locate the sound sources. However, the resolution of the method becomes low at low frequencies. This paper proposes a novel method to realize high-resolution acoustic imaging based on block sparsity constraint. By dividing the focusing area into blocks, the block sparse property of sound sources can be utilized to improve the resolution of the result. In this study, a block orthogonal matching pursuit method is introduced to deal with source localization problem with block sparsity constraint. To evaluate the performance of the proposed method, it is tested through numerical simulations and an experiment. The results of simulations prove that the proposed acoustic imaging method based on block sparsity constraint can localize sound sources accurately and performs better than that based on sparsity constraint. The results of the experiment further validate these findings. [ABSTRACT FROM AUTHOR]

Sound source localization is a critical task in various applications. However, it becomes challenging when the sound sources are not directly visible to the sensors due to obstacles or other environmental factors. This paper proposes a novel approach for locating sound sources in non-line-of-sight environments by combining the equivalent source method (ESM) with the time reversal method (TRM). The ESM is used to compute the frequency responses between the focusing points and the measurement points numerically. These frequency responses are then substituted to the TRM to localize the sound sources. To evaluate the performance of the proposed method, it is tested through numerical simulations and an experiment. The results prove that the ESM can compute the frequency responses accurately, and the combination of TRM and ESM effectively localizes sound sources in non-line-of-sight environments. [ABSTRACT FROM AUTHOR]

Introduction: Diabetes has been recognized as an independent risk factor for periodontitis. Increasing evidences indicate that hyperglycemia aggravates inflammatory response of human periodontal ligament cells (hPDLCs). Carbon monoxide-releasing molecule-3 (CORM-3) is a water-soluble compound that can release carbon monoxide (CO) in a controllable manner. CORM-3 has been shown the anti-inflammatory effect in different cell lineages. Methods: We stimulated periodontal ligament cells with LPS and high glucose. The expression of inflammatory cytokine was detected by ELISA. RT-qPCR, Western blot and immunofluorescence were used to detect the expression of TLR2, TLR4, RAGE and the activation of NF-κB pathway. We performed silencing and overexpression treatment of RAGE targeting the role of RAGE. We performed the immunostaining of paraffin sections of the periodontitis model in diabetes rats. Results: The results showed that CORM-3 significantly inhibited the expression of inflammatory cytokine in hPDLCs stimulated with LPS and high glucose. CORM-3 also inhibited LPS and high glucose-induced expression of RAGE/NF-κB pathway and TLR2/TLR4/NF-κB pathway. Silence of RAGE resulted in significantly decreased expression of proteins above. Overexpression of RAGE significantly enhanced the expression of these factors. CORM-3 abrogated the effect of RAGE partially. In animal model, CORM-3 suppressed the inflammatory response of periodontal tissues in experimental periodontitis of diabetic rats. Discussion: Our research proved CORM-3 reduced the inflammatory response via RAGE/NF-κB pathway and TLR2/TLR4/NF-κB pathway in the process of high glucose exacerbated periodontitis. These findings demonstrated the role of RAGE in the process of high glucose exacerbated periodontitis and suggested that CORM3 be a potential therapeutic strategy for the treatment of diabetes patients with periodontitis. [ABSTRACT FROM AUTHOR]

Background: Our study investigated the role of experimental periodontitis on tumor growth, local and systemic immunosuppressive status, and programmed death receptor 1 (PD-1) / programmed death ligand 1 (PD-L1) expression in oral squamous cell carcinoma (OSCC) and prostate cancer., Methods: Mouse oral or prostate cancer xenograft models were divided into control, periodontitis and periodontitis + anti-PD-1 groups. Tumor volume and weight were recorded and the levels of relevant immune-suppressive cells and T cells were detected by flow cytometry or immunofluorescence. THP-1 cells were stimulated using conditioned media of LPS-stimulated Cal-27 cells and PD-L1 expression was measured by quantitative real-time PCR, western blotting and immunofluorescence. Tumor specimens from OSCC patients with or without periodontitis were also collected for immunofluorescence., Results: Periodontitis significantly promoted tumor volume and weight. Compared to the control, the proportions of tumor-associated macrophages (TAMs), regulatory T cells (Tregs), PD-L1 + TAMs and PD-1 + CD8 + T cells increased, while CD8 + T cells decreased in the periodontitis group. Immunofluorescence demonstrated that there was an increase in PD-L1 + TAMs and PD-1 + CD8 + T cells, but a decrease in IFN-γ + CD8 + T cells in both xenografts and clinical OSCC samples with periodontitis. In vitro, LPS-stimulated Cal-27 cells had a stronger potential to induce PD-L1 expression in macrophages compared with unstimulated Cal-27 cells. And the promoting effect of periodontitis on tumor growth and immune evasion was significantly attenuated after anti-PD-1 therapy., Conclusion: Periodontitis may facilitate tumor growth and immune escape evidenced by the increased immune-suppressive cells and the decreased functional T cells, via enhancing PD-1/PD-L1 expression in the tumor microenvironment., Competing Interests: Declarations Conflict of interest The authors declare that they have no conflict of interest. Ethics approval All animal research was performed in accordance with the Basel Declaration and approved by the ethics committee of Stomatological Hospital of Shandong University (No. 20220907). The use of human samples for this study was performed in accordance with the Declaration of Helsinki and approved by the ethics committee of scientific research of Shandong University Qilu Hospital (No. KYLL-2017–256)., (© 2024. The Author(s).)