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The flow structures and the acoustic feedback loops of underexpanded round jets are investigated by numerical simulations. The jets have a Mach number of 1 at the nozzle exit and a diameter-based Reynolds number of $2.5 \\times {10^3}$. Three nozzle pressure ratios (NPRs) of 2.2, 2.4 and 2.6 are considered. The wavelengths of the screech tones are in good agreement with the experimental measurements on high-Reynolds-number jets in the literature. The screech tones are respectively at the A1 and B modes for the jets at NPRs of 2.2 and 2.6. Two screech tones at the A2 and B modes are identified in the jet at the NPR of 2.4 and the wavelet analyses conducted on the pressure fluctuations confirm that these two modes are contemporaneous. The amplitude and phase fields of fluctuating pressure at the screech frequencies are presented in the nozzle exit plane and azimuthal planes. The effective source locations of the screech tones are determined based on the distributions of the phase. The number of periods contained in the screech feedback loop is equal to the number of cells in the standing wave between the nozzle exit and the effective source. The screech frequencies estimated by the classical feedback model agree well with the numerical results at different modes. A modified model, in which the classical feedback model and the upstream-propagating acoustic wave mode of the jet are combined, shows that the screech feedback loops at the A1 and A2 modes are associated with the same acoustic wave mode. The modified model fails to estimate the screech frequencies at the B mode. Different feedback mechanisms lead to the coexistence of the A2 and B modes. The coherent structures corresponding to different screech modes are extracted by dynamic mode decomposition.

Quercetin, a prevalent flavonol compound, has gained attention for its multifaceted mechanisms of action against various cancers, highlighting its potential as an adjunctive therapy in cancer treatments. This review aims to systematically evaluate the structural optimization, mechanisms of action, and clinical applications of quercetin and its nano-derivatives in cancer treatment. Employing a bibliometric analysis of 6231 articles from the Web of Science Core Collection, we observed a notable increase in annual publications, particularly from the USA and China, indicating a growing interest in quercetin's therapeutic potential. Our findings reveal that quercetin enhances the efficacy of conventional therapies by modulating critical signaling pathways, thereby increasing cancer cell sensitivity while simultaneously protecting normal tissues from therapy-induced damage. Structural modifications, including glycosylation, methylation, sulfation, and glucuronidation, alongside nanoparticle formulation, significantly improve the stability, solubility, and bioavailability of quercetin, enabling targeted drug delivery. Despite the promising preclinical outcomes, the clinical translation of quercetin remains nascent, necessitating further rigorous research to validate its safety and efficacy in human subjects. In conclusion, while quercetin exhibits substantial anticancer properties and therapeutic potential, future studies should focus on expanding sample sizes, elucidating metabolic pathways, and conducting comprehensive clinical trials to inform its application in oncology.

CTRP1 (C1q/TNF-α [tumour necrosis factor-α]-related protein 1), an adiponectin paralog, is associated with diabetes and adverse events in cardiovascular disease. However, its effect on cardiac function post myocardial infarction (MI) is unclear. Our study aimed to explore the role of CTRP1 in cardiac function post MI. CTRP1 global knockout mice were subjected to left anterior descending ligation to establish the MI model. C57BL6J mice were also administered recombinant CTRP1 protein (200 μg/kg) 7 days post MI. As a result, mice with CTRP1 deficiency exhibited an increased survival rate, a reduced infarct area, improved cardiac function and decreased inflammation and oxidative stress levels at 4 weeks post MI compared with those of mice receiving the CRTP1 injection, whose conditions deteriorated. However, cardiomyocytes with either CTRP1 silencing or CTRP1 treatment showed few differences in inflammation and oxidative stress levels compared with those of the control under hypoxic conditions. The activation of macrophages isolated from CTRP1-deficient mice was decreased in response to interferon-γ, while CTRP1 enhanced the activation of macrophages in response to interferon-γ. Macrophage scavengers and clodronate liposomes antagonized the effects of CTRP1 injection in mice. We also found that CTRP1 regulated macrophage activation via adiponectin receptor 1, which binds to TLR4 on the macrophage membrane. TLR4 knockout also antagonized the effects of the CTRP1 protein on mice with MI. Taken together, these data indicate that CTRP1 supresses cardiac function post MI via TLR4 on macrophages. Targeting CTRP1 may become a promising therapeutic approach to cardiac dysfunction post MI.

Ovarian cancer's poor progression is closely associated with overexpression of matrix metalloproteinase 9 (MMP-9), which belongs to the class of enzymes believed to be involved in the degradation of extracellular matrix. However, the mechanisms underlying regulation of MMP-9 are not completely understood. STAT (signal transducer and activator of transcription) family of transcription factors is well known to be engaged in diverse cellular functions. Activation of STAT3 has been observed in a number of cancers, promoting tumorigenesis and metastasis via transcriptional activation of its target genes. In this study, we tested our hypothesis that STAT3 regulates MMP-9 gene expression in epithelial ovarian cancer. Using epithelial ovarian cancer cell lines as in vitro model, we show an abundance of phosphorylated STAT3 at Tyr705 (p-STAT3) in SKOV3 cell line. We further show that MMP-9 gene promoter was significantly enriched by p-STAT3, and IL-6 treatment led to a significant increase of MMP-9 at mRNA and protein levels, in addition to an association of p-STAT3 with MMP-9 gene. By using luciferase reporter assay, we determined that the STAT3 DNA responsive element of MMP-9 was sufficient to regulate transcriptional activity of a heterologous promoter. These results suggest that the phosphorylation of STAT3 regulates MMP-9 production in ovarian cancer, which might be responsible for its invasiveness and metastasis.

Ovarian cancer (OC) is among the most common gynecologic malignancies with a poor prognosis and a high mortality rate. Most patients are diagnosed at an advanced stage (stage III or IV), with 5-year survival rates ranging from 25% to 47% worldwide. Surgical resection and first-line chemotherapy are the main treatment modalities for OC. However, patients usually relapse within a few years of initial treatment due to resistance to chemotherapy. Cell-based therapies, particularly adoptive T-cell therapy and chimeric antigen receptor T (CAR-T) cell therapy, represent an alternative immunotherapy approach with great potential for hematologic malignancies. However, the use of CAR-T-cell therapy for the treatment of OC is still associated with several difficulties. In this review, we comprehensively discuss recent innovations in CAR-T-cell engineering to improve clinical efficacy, as well as strategies to overcome the limitations of CAR-T-cell therapy in OC.

Pain is a major symptom in cancer patients, and cancer-induced bone pain (CIBP) is the most common type of moderate and severe cancer-related pain. The current available analgesic treatments for CIBP have adverse effects as well as limited therapeutic effects. Acupuncture is proved effective in pain management as a safe alternative therapy. We evaluated the analgesic effect of acupuncture in treatment of cancer pain and try to explore the underlying analgesic mechanisms. Nude mice were inoculated with cancer cells into the left distal femur to establish cancer pain model. Electroacupuncture (EA) treatment was applied for the xenograft animals. Pain behaviors of mice were evaluated, followed by the detections of neuropeptide-related and inflammation-related indicators in peripheral and central levels. EA treatment alleviated cancer-induced pain behaviors covering mechanical allodynia, thermal hyperalgesia and spontaneous pain, and also down-regulated immunofluorescence expressions of neuropeptide CGRP and p75 in the skin of affected plantar area in xenograft mice, and inhibited expressions of overexpressed neuropeptide-related and inflammation-related protein in the lumbar spinal cord of xenograft mice. Overall, our findings suggest that EA treatment ameliorated cancer-induced pain behaviors in the mouse xenograft model of cancer pain, possibly through inhibiting the expressions of neuropeptide-related and inflammation-related protein in central level following tumor cell xenografts.

Great interest has been shown in mesenchymal stem cell (MSC) therapy in a wide variety of clinical domains. However, the therapeutic efficiency depends on the proliferation and migration of MSCs. Chemokine receptors are involved in regulating the proliferation and migration to the specific organs of MSCs in different microenvironments. CXC receptor seven (CXCR7), a newly discovered Chemokine ligand 12 (CXCL12) receptor, has organ specificity for tumour migration. We hypothesized that CXCR7 expression affects proliferation and migration of MSCs. In present study, we constructed long-term and stable mMSCs lines overexpressing and suppressing CXCR7 modifications with lentiviral vectors. The transduction efficiencies, mRNA and protein expression of CXCR7 were significantly regulated. CXCR7 gene overexpression promoted mMSCs proliferation and migration, whereas suppressing CXCR7 had the opposite effect. Additional CXCL12 improved the vertical migration of mMSCs. The overexpression of CXCR7 increased the MSC-secreted CXCL12, VCAM-1, CD44 and MMP2 levels, which contributed to the improvement of mMSC proliferation and migration. Therefore, overexpressing CXCR7 improved the proliferation and migration of mMSCs, which may be attributable to the CXCL12 secreted by MSCs, leading to a positive feedback loop for CXCL12/CXCR7 axis. Our results may provide a potential method for improving the treatment effectiveness of mMSCs by overexpressing CXCR7.

Urban parks are key to urban ecosystems, where soil microbe-plant-soil interactions sustain ecosystem services. Using high-throughput sequencing and multivariate statistics, this study explored how plant species diversity affects soil microbial community structure, functional diversity, and environmental drivers. Results showed that fungal and bacterial OTUs differed across plant diversity gradients, with Ascomycota (fungi) and Actinobacteriota/Proteobacteria (bacteria) dominant. Soil organic carbon (SOC) was positively correlated with Verrucomicrobia, while Acidobacteriota increased with lower SOC. Fungi were more sensitive to pH than bacteria. Partial Least Squares Path Modeling (PLS-PM) indicated that plant diversity was significantly positively associated with fungal community structure and was indirectly associated with bacterial diversity via soil factors (e.g., SOC, pH), with fungal community variation more explained than bacterial. Higher plant diversity was associated with elevated SOC and a higher relative abundance of putative nutrient-cycling taxa (e.g., Rhizobium), suggesting a potential enhancement of soil nutrient cycling capacity. This study demonstrates that plant diversity shapes microbial communities directly and via soil properties, highlighting synergistic effects. We propose arbor-shrub-herb composite vegetation in urban forest management to optimize microbial habitats and ecological services.

This study explored the chemical and pharmacological mechanisms of Shao Yao Gan Cao decoction (SYGC) in the treatment of Sphincter of Oddi Dysfunction (SOD) through ultra-high-performance liquid chromatography coupled with Quadrupole Exactive-Orbitrap high-resolution mass spectrometry (UHPLC-Q Exactive-Orbitrap HR-MS), network pharmacology, transcriptomics, molecular docking and in vivo experiments. First, we identified that SYGC improves SOD in guinea pigs by increased c-kit expression and decreased inflammation infiltration and ring muscle disorders. Then, a total of 649 SOD differential genes were found through RNA sequencing and mainly enriched in complement and coagulation cascades, the B cell receptor signaling pathway and the NF-kappa B signaling pathway. By combining UHPLC-Q-Orbitrap-HRMS with a network pharmacology study, 111 chemicals and a total of 52 common targets were obtained from SYGC in the treatment of SOD, which is also involved in muscle contraction, the B cell receptor signaling pathway and the complement system. Next, 20 intersecting genes were obtained among the PPI network, MCODE and ClusterOne analysis. Then, the molecular docking results indicated that four active compounds (glycycoumarin, licoflavonol, echinatin and homobutein) and three targets (AURKB, KIF11 and PLG) exerted good binding interactions, which are also related to the B cell receptor signaling pathway and the complement system. Finally, animal experiments were conducted to confirm the SYGC therapy effects on SOD and verify the 22 hub genes using RT-qPCR. This study demonstrates that SYGC confers therapeutic effects against an experimental model of SOD via regulating immune response and inflammation, which provides a basis for future research and clinical applications.