Search

Abstract In this article, we study in detail the double-J/ψ yield through Z decay at the next-to-leading-order (NLO) QCD accuracy within the nonrelativistic QCD factorization. At the tree level, the pure QCD diagrams predict a branching ratio of B Z → J / ψ + J / ψ $$ {\mathcal{B}}_{Z\to J/\psi +J/\psi } $$ ~ 10 −12; however, the inclusion of the QED diagrams would augment this prediction by approximately 2–3 orders of magnitude. After incorporating the QCD corrections, the QCD results exhibit a considerable increase, whereas the QED results undergo a substantial reduction. Combining the QCD and QED contributions at NLO in α s , it is observed that the prediction of B Z → J / ψ + J / ψ $$ {\mathcal{B}}_{Z\to J/\psi +J/\psi } $$ = ( 1.110 − 0.241 − 0.001 + 0.334 + 0.054 $$ {1.110}_{-0.241-0.001}^{+0.334+0.054} $$ ) × 10 −10, which displays a fairly steady dependence on the renormalization scale, is significantly lower than the upper limits released by CMS.

Abstract In this paper, we study the X(3860) production associated with $$J/\psi $$ J / ψ via $$e^{+}e^{-}$$ e + e - annihilation at the next-to-leading-order (NLO) accuracy in $$\alpha _s$$ α s , within the nonrelativistic QCD (NRQCD) framework. With the hypothesis of $$J^{PC}_{X(3860)}=0^{++}$$ J X ( 3860 ) PC = 0 + + , the predictions of $$\sigma _{e^{+}e^{-} \rightarrow J/\psi +X(3860)}$$ σ e + e - → J / ψ + X ( 3860 ) agree well with the Belle measurements, whereas the results following the $$2^{++}$$ 2 + + assignment significantly undershoot the data. This is consistent with the Belle’s conclusion that the $$0^{++}$$ 0 + + hypothesis is favored over the $$2^{++}$$ 2 + + hypothesis for X(3860). Despite fitting the data of the total cross section, the NRQCD predictions seem to be incompatible with the measured $$J/\psi $$ J / ψ angular distributions. We simultaneously calculate the cross section of $$e^{+}e^{-} \rightarrow J/\psi +X(3940)$$ e + e - → J / ψ + X ( 3940 ) under the assumption of $$J^{PC}_{X(3940)}=0^{-+}$$ J X ( 3940 ) PC = 0 - + , discovering the consistency of the NRQCD predictions with the light-cone results as well as the experiment.

Proteomic profiling of extracellular vesicles (EVs) represents a promising approach for early detection and therapeutic monitoring of diseases such as cancer. The focus of this study was to apply robust EV isolation and subsequent data-independent acquisition mass spectrometry (DIA-MS) for urinary EV proteomics of prostate cancer and prostate inflammation patients. Urinary EVs were isolated by functionalized magnetic beads through chemical affinity on an automatic station, and EV proteins were analyzed by integrating three library-base analyses (Direct-DIA, GPF-DIA, and Fractionated DDA-base DIA) to improve the coverage and quantitation. We assessed the levels of urinary EV-associated proteins based on 40 samples consisting of 20 cases and 20 controls, where 18 EV proteins were identified to be differentiated in prostate cancer outcome, of which three (i.e., SERPINA3, LRG1, and SCGB3A1) were shown to be consistently upregulated. We also observed 6 out of the 18 (33%) EV proteins that had been developed as drug targets, while some of them showed protein-protein interactions. Moreover, the potential mechanistic pathways of 18 significantly different EV proteins were enriched in metabolic, immune, and inflammatory activities. These results showed consistency in an independent cohort with 20 participants. Using a random forest algorithm for classification assessment, including the identified EV proteins, we found that SERPINA3, LRG1, or SCGB3A1 add predictable value in addition to age, prostate size, body mass index (BMI), and prostate-specific antigen (PSA). In summary, the current study demonstrates a translational workflow to identify EV proteins as molecular markers to improve the clinical diagnosis of prostate cancer.

Hepatocellular carcinoma (HCC) is a major cause of cancer-related deaths worldwide. Emerging evidence has revealed the vital functions of microRNAs (miRNAs) in cancer malignant progressions. miR-375 has been verified to serve as an antioncogene in tumorigenesis and a potential therapeutic target in various types of cancer. In this study, we aimed to determine the role of miR-375 in the regulation of chemoresistance and metastasis of HCC. Differentially expressed miR-375 and NCAPG2 were externally validated using expression data from The Cancer Genome Atlas (TCGA) database. Quantitative real-time polymerase chain reaction (qRT-PCR) was performed to detect the expression levels of miR-375 in HCC tissues and cell lines. miR-375 mimics and NCAPG2-overexpression were transfected into HepG2 and Huh7 cells to establish miR-375 overexpression models. Cell Counting Kit-8, Transwell, and flow cytometry experiments were conducted to monitor cell proliferation, migration, and apoptosis. The targeting relationship between miR-375 and non-SMC condensin II complex subunit G 2 (NCAPG2) was determined by qRT-PCR, western blot, and luciferase reporter gene assay. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analyses were conducted using Gene Set Enrichment Analysis (GSEA). The pathway enrichment analysis was used to predict the potential pathways for further study. miR-375 was significantly downregulated in HCC tissues and cells compared to adjacent tissue and normal hepatocyte cell line respectively while NCAPG2 was upregulated. The targeting relationship was verified by luciferase reporting assay, and miR-375 could target the 3'UTR of NCAPG2 mRNA and effectively suppress NCAPG2 protein expression. Replenishing of miR-375 significantly repressed HCC cell proliferation and migration, and induced cell apoptosis. Overexpression of NCAPG2 recovered those biological abilities in miR-375 overexpressed cells. Collective data suggested that miR-375 served as a tumor suppressor via regulating NCAPG2. Replenishing of miR-375 or knockout of NCAPG2 could be therapeutically exploited for HCC. [ABSTRACT FROM AUTHOR]