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In this work, the spectra of the prospective exotic hidden-charm and hidden-bottom baryonium, viz. the baryon–antibaryon states, with J PC = 0 - - and 0 + - are investigated in the framework of QCD sum rules. The non-perturbative contributions up to dimension 12 are taken into account. Numerical results indicate that there might exist 3 possible 0 - - hidden-charm baryonium states with masses ( 5.22 ± 0.26 ) , ( 5.52 ± 0.25 ) , and ( 5.46 ± 0.24 ) GeV, and 5 possible 0 + - hidden-charm baryonium states with masses ( 4.76 ± 0.28 ) , ( 5.24 ± 0.28 ) , ( 5.16 ± 0.27 ) , ( 5.52 ± 0.27 ) , and ( 5.69 ± 0.27 ) GeV, respectively. The corresponding hidden-bottom partners are found lying in the range of 11.68 - 12.28 GeV and 11.38 - 12.33 GeV, respectively. The possible baryonium decay modes are analyzed, which are hopefully measurable in LHC experiments.

METTL3 has been shown to be involved in regulating a variety of biological processes. However, the relationship between METTL3 expression and glycolysis, cuproptosis‐related genes and the ceRNA network in oesophageal carcinoma (ESCA) remains unclear. ESCA expression profiles from databases were obtained, and target genes were identified using differential analysis and visualization. Immunohistochemistry (IHC) staining assessed METTL3 expression differences. Functional enrichment analysis using GO, KEGG and GSEA was conducted on the co‐expression profile of METTL3. Cell experiments were performed to assess the effect of METTL3 interference on tumour cells. Correlation and differential analyses were carried out to assess the relationship between METTL3 with glycolysis and cuproptosis. qRT‐PCR was used to validate the effects of METTL3 interference on glycolysis‐related genes. Online tools were utilized to screen and construct ceRNA networks based on the ceRNA theory. METTL3 expression was significantly higher in ESCA compared to the controls. The IHC results were consistent with the above results. Enrichment analysis revealed that METTL3 is involved in multiple pathways associated with tumour development. Significant correlations were observed between METTL3 and glycolysis‐related genes and cuproptosis‐related gene. Experiments confirmed that interfered with METTL3 significantly inhibited glucose uptake and lactate production in tumour cells, and affected the expression of glycolytic‐related genes. Finally, two potential ceRNA networks were successfully predicted and constructed. Our study establishes the association between METTL3 overexpression and ESCA progression. Additionally, we propose potential links between METTL3 and glycolysis, cuproptosis and ceRNA, presenting a novel targeted therapy strategy for ESCA.

It remains unclear whether the necessity of calcified mellitus induced by high inorganic phosphate (Pi) is required and the roles of autophagy plays in aldosterone (Aldo)‐enhanced vascular calcification (VC) and vascular smooth muscle cell (VSMC) osteogenic differentiation. In the present study, we found that Aldo enhanced VC both in vivo and in vitro only in the presence of high Pi, alongside with increased expression of VSMC osteogenic proteins (BMP2, Runx2 and OCN) and decreased expression of VSMC contractile proteins (α‐SMA, SM22α and smoothelin). However, these effects were blocked by mineralocorticoid receptor inhibitor, spironolactone. In addition, the stimulatory effects of Aldo on VSMC calcification were further accelerated by the autophagy inhibitor, 3‐MA, and were counteracted by the autophagy inducer, rapamycin. Moreover, inhibiting adenosine monophosphate‐activated protein kinase (AMPK) by Compound C attenuated Aldo/MR‐enhanced VC. These results suggested that Aldo facilitates high Pi‐induced VSMC osteogenic phenotypic switch and calcification through MR‐mediated signalling pathways that involve AMPK‐dependent autophagy, which provided new insights into Aldo excess‐associated VC in various settings.

In this paper, we investigate the spectra of the prospective hidden-bottom and -charm hexaquark states with quantum numbers J PC = 0 + + , 0 - + , 1 + + and 1 - - in the framework of QCD sum rules. By constructing appropriate interpreting currents, the QCD sum rules analyses are performed up to dimension 12 of the condensates. Results indicate that there exist two possible baryonium states in b -quark sector with masses 11.84 ± 0.22 GeV and 11.72 ± 0.26 GeV for 0 + + and 1 - - , respectively. The corresponding hidden-charm partners are found lying respectively at 5.19 ± 0.24 GeV and 4.78 ± 0.23 GeV. Note that these baryonium states are all above the dibaryon thresholds, which enables their dominant decay modes could be measured at BESIII, BELLEII, and LHCb detectors.

The Monte Carlo method is the most commonly used dose calculation method in the field of boron neutron capture therapy (BNCT). General-purpose Monte Carlo (MC) code (e.g., MCNP) has been used in most treatment planning systems (TPS) to calculate dose distribution, which takes overmuch time in radiotherapy planning. Based on this, we developed COMPASS (COMpact PArticle Simulation System), an MC engine specifically for BNCT dose calculation. Several optimization algorithms are used in COMPASS to make it faster than general-purpose MC code. The parallel computation of COMPASS is performed by the message passing interface (MPI) library and OpenMP commands, which allows the user to increase computational speed by increasing the computer configurations. The physical dose of each voxel is calculated for developing a treatment plan. Comparison results show that the computed dose distribution of COMPASS is in good agreement with MCNP, and the computational efficiency is better than MCNP. These results validate that COMPASS has better performance than MCNP in BNCT dose calculation.

Collectin-11 (CL-11), a recently described soluble C-type lectin, has been shown to stimulate cell proliferation in fibroblasts and melanoma cells. However, its broader influence on fibroblast functions and the specific receptors mediating CL-11's effects remain to be elucidated. The EDU proliferation assay and WB detection of PCNA protein levels were used to evaluate the fibroblast proliferative effect after CL-11 stimulated. The qRT-PCR and WB detection of fibronectin and collagen I were used to evaluate the ECM production. The qRT-PCR detection of Il-6, Il-11, Tnfa, Il1b, Cxcl1, Egf, Tgfb1, Pdgfb were used to evaluate the cytokine production. The WB detection of ERK, AKT, STAT3, mTOR, SMAD2 and ACTIN were used to evaluate the activation of signaling pathway. The WB detection of ERK, AKT, STAT3, mTOR, SMAD2 and ACTIN were used to evaluate the activation of signaling pathway. The immunofluorescence and molecular docking experiments were used to detect the binding of CL-11 to EGFR/TGFRII. In this study, we demonstrate that CL-11 not only promotes fibroblast proliferation but also modulates their activation status and extracellular matrix (ECM) synthesis. Specifically, treatment with recombinant CL-11 (rCL-11) significantly upregulated the production of ECM proteins (fibronectin, collagen I), growth factors (EGF, TGF-β1), and proinflammatory cytokines/chemokines (IL-6, TNF-α, IL-11, IL-1β, CXCL1) in renal fibroblasts. Additionally, rCL-11 activated multiple intracellular signaling pathways, including ERK, AKT/mTOR, STAT3, and SMAD2. Further, EGFR and TGF-βRII were found to be abundantly expressed in renal fibroblasts, and molecular docking analysis along with immunofluorescence/confocal microscopy confirmed CL-11's interaction with these receptors. Our findings provide strong evidence that CL-11 plays a critical role in renal fibroblast proliferation and activation via engagement with EGFR and TGF-βRII, shedding light on the mechanisms by which CL-11 stimulates cellular activation and proliferation.

Microecology is an emerging discipline in recent years. The female reproductive tract is an important microecological region, and its microecological environment can directly affect women’s cervical health. This meta-analysis aimed to analyze the effects of vaginal microecology on Human papillomavirus (HPV) infection and cervical intraepithelial neoplasia (CIN). PubMed and Web of Science were systematically searched for eligible publications from January 2000 to December 2017. Articles were selected on the basis of specific inclusion and exclusion criteria. The design and quality of all studies were evaluated using the Newcastle-Ottawa Scale (NOS). Odds ratios (ORs) with a 95% confidence interval (95% CI) were calculated. Thirteen eligible studies were selected to evaluate the association of vaginal microecology with HPV infection and CIN. The factors related to HPV infection were bacterial vaginosis (BV) (OR 2.57, 95% CI 1.78–3.71, P<0.05), Candida albicans (VVC) (OR 0.63, 95% CI 0.49–0.82, P  < 0.05), Chlamydia trachomatis (CT) (OR 3.16, 95% CI 2.55–3.90, P  < 0.05), and Ureaplasma urealyticum (UU) (OR 1.35, 95% CI 1.20–1.51, P  < 0.05). BV was also related to CIN (OR 1.56, 95% CI 1.21–2.00, P  < 0.05). This meta-analysis of available literature suggested an intimate association of vaginal microecology and HPV infection with CIN. BV, CT and UU were associated to increased HPV infection, VVC was associated to decreased HPV infection, Lactobacillus is not associated to increased HPV infection, BV was associated to increased CIN development risk. Further large-scale studies are needed to confirm our findings.

NeuMANTA is a new generation boron neutron capture therapy (BNCT)-specific treatment planning system developed by the Neuboron Medical Group and upgraded to an important feature, a Hounsfield unit (HU)-based material conversion algorithm. The range of HU values was refined to 96 specific groups and established corresponding to tissue information. The elemental compositions and mass densities have an important effect on the calculated dose distribution. The region of interest defined in the treatment plan can be converted into multiple material compositions based on HU values or assigned specified single material composition in NeuMANTA. Different material compositions may cause normal tissue maximum dose rates to differ by more than 10% in biologically equivalent doses and to differ by up to 6% in physically absorbed doses. Although the tumor has a lower proportion of BNCT background dose, the material composition difference may affect the minimum dose of biologically equivalent dose and physically absorbed dose by more than 3%. In addition, the difference in material composition could lead to a change in neutron moderation as well as scattering. Therefore, the material composition has a significant impact on the assessment of normal tissue side effects and tumor control probability. It is essential for accurate dose estimation in BNCT.

Most treatment planning systems of boron neutron capture therapy perform dose calculations based on the assumption of a homogeneous boron distribution in tumors, which leads to dose distortion due to the difference between the tumor-to-normal tissue ratio (TNR) range measured in positron emission tomography images (PET) and the target delineation in computed tomography images of the treatment plan. The heterogeneous boron distribution in the target of the treatment plan can be obtained by image fusion. This study provides a way to quantify a heterogeneous boron distribution based on PET images. Theoretically, the same mean TNR for dose calculation by homogeneous or heterogeneous boron distribution should get almost the same mean dose. However, slightly different mean doses are found due to the partial volume effect for a small target volume. The wider the boron distribution is, the higher the impact on the dose-volume histogram distribution is. Dose distribution with homogeneous boron distribution may be overestimated in low boron uptake regions by wrong boron concentration and neutron flux depression. To accurately give the tumor prescription dose and achieve better tumor control, for low dose regions of the tumor should be considered more boron neutron capture therapy treatments or combined with other treatment modalities. The heterogeneous boron distribution must be taken into consideration to have an accurate dose estimation. Therefore, the way how medical physicists and clinicians process the TNR in gross tumor volume should be refined, and the method demonstrated in the work provides a good reference.

Background: Fucoidan (FPS) has been widely used to treat renal fibrosis (RF) in patients with diabetic kidney disease (DKD); however, the precise therapeutic mechanisms remain unclear. Recently, research focusing on inflammation-derived podocyte pyroptosis in DKD has attracted increasing attention. This phenomenon is mediated by the activation of the nucleotide-binding oligomerization domain (Nod)-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, leading to RF during DKD progression. Therefore, we designed a series of experiments to investigate the ameliorative effects of FPS on RF in DKD and the mechanisms that are responsible for its effect on NLRP3 inflammasome-mediated podocyte pyroptosis in the diabetic kidney. Methods: The modified DKD rat models were subjected to uninephrectomy, intraperitoneal injection of streptozotocin, and a high-fat diet. Following induction of renal injury, the animals received either FPS, rapamycin (RAP), or a vehicle for 4 weeks. For in vitro research, we exposed murine podocytes to high glucose and MCC950, an NLRP3 inflammasome inhibitor, with or without FPS or RAP. Changes in the parameters related to RF and inflammatory podocyte injury were analyzed in vivo . Changes in podocyte pyroptosis, NLRP3 inflammasome activation, and activation of the adenosine monophosphate-activated protein kinase (AMPK)/mammalian target of rapamycin complex 1 (mTORC1)/NLRP3 signaling axis involved in these changes were analyzed in vivo and in vitro . Results: FPS and RAP ameliorated RF and inflammatory podocyte injury in the DKD model rats. Moreover, FPS and RAP attenuated podocyte pyroptosis, inhibited NLRP3 inflammasome activation, and regulated the AMPK/mTORC1/NLRP3 signaling axis in vivo and in vitro . Notably, our data showed that the regulative effects of FPS, both in vivo and in vitro , on the key signaling molecules, such as p-AMPK and p-raptor, in the AMPK/mTORC1/NLRP3 signaling axis were superior to those of RAP, but similar to those of metformin, an AMPK agonist, in vitro . Conclusion: We confirmed that FPS, similar to RAP, can alleviate RF in DKD by inhibiting NLRP3 inflammasome-mediated podocyte pyroptosis via regulation of the AMPK/mTORC1/NLRP3 signaling axis in the diabetic kidney. Our findings provide an in-depth understanding of the pathogenesis of RF, which will aid in identifying precise targets that can be used for DKD treatment.