Intermediate-statistics quantum bracket, coherent state, oscillator, and representation of angular momentum (su(2)) algebra

In this paper, we first discuss the general properties of an intermediate-statistics quantum bracket, $[ u,v]_{n}=uv-e^{i2\pi /(n+1)}vu$, which corresponds to intermediate statistics in which the maximum occupation number of one quantum state is an arbitrary integer, $n$. A further study of the operator realization of intermediate statistics is given. We construct the intermediate-statistics coherent state. An intermediate-statistics oscillator is constructed, which returns to bosonic and fermionic oscillators respectively when $n\to \infty$ and $n=1$. The energy spectrum of such an intermediate-statistics oscillator is calculated. Finally, we discuss the intermediate-statistics representation of angular momentum ($su(2)$) algebra. Moreover, a further study of the operator realization of intermediate statistics is given in the Appendix.Comment: 12 pages, no figures. Revte

Valosin-containing protein regulates the proteasome-mediated degradation of DNA-PKcs in glioma cells.

DNA-dependent protein kinase (DNA-PK) has an important role in the repair of DNA damage and regulates the radiation sensitivity of glioblastoma cells. The VCP (valosine-containing protein), a chaperone protein that regulates ubiquitin-dependent protein degradation, is phosphorylated by DNA-PK and recruited to DNA double-strand break sites to regulate DNA damage repair. However, it is not clear whether VCP is involved in DNA-PKcs (DNA-PK catalytic subunit) degradation or whether it regulates the radiosensitivity of glioblastoma. Our data demonstrated that DNA-PKcs was ubiquitinated and bound to VCP. VCP knockdown resulted in the accumulation of the DNA-PKcs protein in glioblastoma cells, and the proteasome inhibitor MG132 synergised this increase. As expected, this increase promoted the efficiency of DNA repair in several glioblastoma cell lines; in turn, this enhanced activity decreased the radiation sensitivity and prolonged the survival fraction of glioblastoma cells in vitro. Moreover, the VCP knockdown in glioblastoma cells reduced the survival time of the xenografted mice with radiation treatment relative to the control xenografted glioblastoma mice. In addition, the VCP protein was also downregulated in ~25% of GBM tissues from patients (WHO, grade IV astrocytoma), and the VCP protein level was correlated with patient survival (R(2)=0.5222, P<0.05). These findings demonstrated that VCP regulates DNA-PKcs degradation and increases the sensitivity of GBM cells to radiation

Frontiers of Energy Storage Technologies

Energy storage technologies (ESTs) play a crucial role in ensuring energy security and addressing the challenges posed by climate change. They enable us to overcome the mismatch between energy supply and demand caused by the intermittent and unpredictable nature of renewable energy sources. The identification of research frontiers in ESTs has primarily relied on expert experience and has been limited to specific areas of study. However, there is a relative lack of data-driven approaches to identify these frontiers. In this study, we employed an integrated technique combining bibliographic coupling and sliding window analysis to identify the research frontiers in ESTs and understand their evolution over time. Our study reveals 19 research frontiers in ESTs distributed across four knowledge domains: electrochemical energy storage, electrical energy storage, chemical energy storage, and energy storage systems. Among these frontiers, two noteworthy areas are aqueous zinc batteries (AZBs) and two-dimensional transition metal carbon-nitride composites (MXenes). By identifying these research frontiers, our study provides insights into the potential future directions for research and development (R&D) deployment in energy storage technologies

Imidazole-thiazolidinone inhibits oesophageal cancer cell proliferation via induction of apoptosis and cell cycle arrest at S phase

Purpose: To investigate the effect of imidazole-thiazolidinone on oesophageal cancer (OC) cell proliferation, and the mechanism of action involved.Methods: Human OC cells (HCE-6 and KYSE-1170) were cultured in Dulbecco's modified Eagle's medium (DMEM) supplemented with 10 % fetal bovine serum (FBS) and 1 % penicillin/streptomycin solution at 37 ˚C for 24 h in a humidified atmosphere of 5 % CO2 and 95 % air. After attaining 60 -  70 % confluency, the cells were treated with serum-free medium and graded concentrations of imidazolethiazolidinone (up to 160 μM) for 24 h. Normal cell culture without imidazole-thiazolidinone served as control. Cells in logarithmic growth phase were selected and used in this study. Cell proliferation and apoptosis were assessed using 3 (4,5 dimethyl thiazol 2 yl) 2,5 diphenyl 2H tetrazolium bromide (MTT), and flow cytometric assays, respectively. The levels of expression of apoptosis-related proteins were determined using Western blotting.Results: Treatment of HCE-6 and KYSE-1170 cells with imidazole-thiazolidinone for 48 h led to significant and dose-dependent reduction in their  proliferation, as well as significant and dosedependent increase in the number of apoptotic cells (p < 0.05). Light microscopy revealed significantreduction in HCE-6 cell count, detached cells, reduced cell size and irregular cytoplasmic vacuoles. Imidazole-thiazolidinone treatment significantly and dose-dependently decreased HCE-6 and KYSE-1170 cell migration, and arrested HCE-6 cell cycle at S phase (p < 0.05). In HCE-6 cells, imidazolethiazolidinone treatment significantly and dose-dependently upregulated the expressions of cleaved caspase-3/8/9 and bax, but down-regulated bcl-2 expression significantly and dose-dependently (p < 0.05). However, metalloproteinases 2 and 9 (MMP-2 and MMP-9) expressions in HCE-6 and KYSE-1170 cells were significantly and dose-dependently down-regulated by imidazole-thiazolidinone treatment (p < 0.05).Conclusion: The results obtained in this study suggest that imidazole-thiazolidinone suppresses OC cell proliferation via induction of apoptosis and arrest of cell cycle at S phase. Keywords: Imidazole-thiazolidinone, Oesophageal cancer, Metastasis, Cell cycle arrest, Apoptosi