16 research outputs found

    Integrative analysis of disulfidptosis and immune microenvironment in hepatocellular carcinoma: a putative model and immunotherapeutic strategies

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    BackgroundHepatocellular carcinoma (HCC) is a malignant tumor with a high rate of recurrence and m metastasis that does not respond well to current therapies and has a very poor prognosis. Disulfidptosis is a novel mode of cell death that has been analyzed as a novel therapeutic target for HCC cells.MethodsThis study integrated bulk ribonucleic acid (RNA) sequencing datasets, spatial transcriptomics (ST), and single-cell RNA sequencing to explore the landscape of disulfidptosis and the immune microenvironment of HCC cells.ResultsWe developed a novel model to predict the prognosis of patients with HCC based on disulfidptosis. The model has good stability, applicability, and prognostic and immune response prediction abilities. N-myc downregulated gene1 (NDRG1) may contribute to poor prognosis by affecting macrophage differentiation, thus allowing HCC cells to evade the immune system.ConclusionOur study explores the disulfidptosis of HCC cells through multi-omics and establishes a new putative model that explores possible targets for HCC treatment

    Growth of Pentacene-Doped p-Terphenyl Crystals Using SSVBT and Doping Effects in p-Terphenyl Molecular Crystals

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    High-quality pentacene-doped p-terphenyl bulk crystals were grown by the selective self-seeding vertical Bridgman technique (SSVBT). The lattice structure and crystal properties of the samples of different doping concentrations and their relations with p-terphenyl single crystals were tested and analyzed. The doping effects of pentacene doping at different concentrations in p-terphenyl molecular crystals are discussed. The powder X-ray diffraction, FTIR, and 1H NMR studies show that no additional peaks (except for p-terphenyl) are observed in the spectra of two doped crystals. The results indicate that guest molecules appear as defects in the form of irregularly oriented molecules which do not significantly change the crystal structures. As the doping concentration increases, the average crystallite size decreases, and the crystallinity declines. The ultraviolet–visible absorption and fluorescence spectra show that with added pentacene molecules, the characteristic peak intensities decrease in the spectra owing to the p-terphenyl molecular transition. Meanwhile, characteristic peaks appear due to the pentacene molecular transition. Moreover, with the increase of doping concentration, the intensities of characteristic peaks of host molecules decrease continuously, and those of guest molecules increase accordingly

    Expression and prognostic analyses of early growth response proteins (EGRs) in human breast carcinoma based on database analysis

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    Background Early growth response proteins (EGRs), as a transcriptional regulatory family, are involved in the process of cell growth, differentiation, apoptosis, and even carcinogenesis. However, the role of EGRs in tumors, their expression levels, and their prognostic value remain unclear. Methods Using the Oncomine database, Kaplan–Meier Plotter, bcGenExMiner v4.2, cBioPortal, and other tools, the association between the survival data of breast carcinoma (BC) patients and transcriptional levels of four EGRs was investigated. Results According to the Oncomine database, in comparison to normal tissues, the expression level of EGR2/3 mRNA in BC tissues was decreased, but there was no difference in the expression level of EGR4 mRNA. On the basis of the Scarff-Bloom-Richardson (SBR) grading system, the downregulated expression level of EGR1/2/3 and upregulated expression level of EGR4 were correlated with an increased histological differentiation level, with significant differences (p < 0.05). Kaplan–Meier curves suggest that a reduction in EGR2/3 mRNA expression is related to recurrence-free survival (RFS) in BC patients. In addition, the mRNA expression level of EGR1/2/3 was related to metastatic relapse-free survival (MRFS) in BC patients with metastatic recurrence (p < 0.05). Conclusion EGR1/2/3 can be utilized as an important factor for evaluating prognosis and may be relevant to diagnosis. EGR4 may play a role in the occurrence and development of BC. The specific function and mechanism of EGRs in BC deserve further study

    Taurochenodeoxycholic Acid Inhibited AP-1 Activation via Stimulating Glucocorticoid Receptor

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    Taurochenodeoxycholic acid (TCDCA) as a primary bioactive substance of animal bile has been shown to exert good anti-inflammatory and immunomodulatory functions in adjuvant arthritis in rats. The anti-inflammatory and immunomodulatory properties of TCDCA have exhibited interesting similarities with the effects of glucocorticoids (GCs). To investigate the potential mechanisms of TCDCA in anti-inflammation and immunomodulation, we used a luciferase reporter assay to evaluate the activation of the glucocorticoid receptor (GR) stimulated by TCDCA. Our results showed that GR was activated by TCDCA in a concentration-dependent manner. Moreover, the elevated expressions of c-Fos and phosphorylated c-Jun induced by interleukin-1&beta; (IL-1&beta;) were reversed by TCDCA. The inhibition of TCDCA on the transactivation of activator protein-1 (AP-1) was observed as well. However, the suppression of TCDCA on the phosphorylation of c-Jun was blocked incompletely by GR inhibitor RU486. These results have indicated that the anti-inflammatory and immunomodulatory functions of TCDCA involve multiple pathways, with contributions from GR and its related AP-1 signaling pathway

    A High-Performance InGaAs Vertical Electron–Hole Bilayer Tunnel Field Effect Transistor with P<sup>+</sup>-Pocket and InAlAs-Block

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    To give consideration to both chip density and device performance, an In0.53Ga0.47As vertical electron–hole bilayer tunnel field effect transistor (EHBTFET) with a P+-pocket and an In0.52Al0.48As-block (VPB-EHBTFET) is introduced and systematically studied by TCAD simulation. The introduction of the P+-pocket can reduce the line tunneling distance, thereby enhancing the on-state current. This can also effectively address the challenge of forming a hole inversion layer in an undoped InGaAs channel during device fabrication. Moreover, the point tunneling can be significantly suppressed by the In0.52Al0.48As-block, resulting in a substantial decrease in the off-state current. By optimizing the width and doping concentration of the P+-pocket as well as the length and width of the In0.52Al0.48As-block, VPB-EHBTFET can obtain an off-state current of 1.83 × 10−19 A/μm, on-state current of 1.04 × 10−4 A/μm, and an average subthreshold swing of 5.5 mV/dec. Compared with traditional InGaAs vertical EHBTFET, the proposed VPB-EHBTFET has a three orders of magnitude decrease in the off-state current, about six times increase in the on-state current, 81.8% reduction in the average subthreshold swing, and stronger inhibitory ability on the drain-induced barrier-lowering effect (7.5 mV/V); these benefits enhance the practical application of EHBTFETs

    Interplay between Gut Microbiota and NLRP3 Inflammasome in Intracerebral Hemorrhage

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    The pathophysiological process of intracerebral hemorrhage (ICH) is very complex, involving various mechanisms such as apoptosis, oxidative stress and inflammation. As one of the key factors, the inflammatory response is responsible for the pathological process of acute brain injury and is associated with the prognosis of patients. Abnormal or dysregulated inflammatory responses after ICH can aggravate cell damage in the injured brain tissue. The NOD-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome is a multiprotein complex distributed in the cytosol, which can be triggered by multiple signals. The NLRP3 inflammasome is activated after ICH, thus promoting neuroinflammation and aggravating brain edema. In addition, there is evidence that the gut microbiota is crucial in the activation of the NLRP3 inflammasome. The gut microbiota plays a key role in a variety of CNS disorders. Changes in the diversity and species of the gut microbiota affect neuroinflammation through the activation of the NLRP3 inflammasome and the release of inflammatory cytokines. In turn, the gut microbiota composition can be influenced by the activation of the NLRP3 inflammasome. Thereby, the regulation of the microbe&ndash;gut&ndash;brain axis via the NLRP3 inflammasome may serve as a novel idea for protecting against secondary brain injury (SBI) in ICH patients. Here, we review the recent evidence on the functions of the NLRP3 inflammasome and the gut microbiota in ICH, as well as their interactions, during the pathological process of ICH

    sj-docx-1-tej-10.1177_20417314221125310 – Supplemental material for Expanding tubular microvessels on stiff substrates with endothelial cells and pericytes from the same adult tissue

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    Supplemental material, sj-docx-1-tej-10.1177_20417314221125310 for Expanding tubular microvessels on stiff substrates with endothelial cells and pericytes from the same adult tissue by Xiuyue Song, Yali Yu, Yu Leng, Lei Ma, Jie Mu, Zihan Wang, Yalan Xu, Hai Zhu, Xuefeng Qiu, Peifeng Li, Jing Li and Dong Wang in Journal of Tissue Engineering</p
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