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Regulatory T (Treg) cells are crucial for peripheral immune tolerance and prevention of autoimmunity and tissue damage. Treg cells are inherently defined by the expression of the transcription factor Foxp3, which enforces lineage development and immune suppressive function of these cells. Under various conditions as observed in autoimmunity, cancer and non-lymphoid tissues, a proportion of Treg cells respond to specific environmental signals and display altered stability, plasticity and tissue-specific heterogeneity, which further shape their context-dependent suppressive functions. Recent studies have revealed that metabolic programs play pivotal roles in controlling these processes in Treg cells, thereby considerably expanding our understanding of Treg cell biology. Here we summarize these recent advances that highlight how cell-extrinsic factors, such as nutrients, vitamins and metabolites, and cell-intrinsic metabolic programs, orchestrate Treg cell stability, plasticity, and tissue-specific heterogeneity. Understanding metabolic regulation of Treg cells should provide new insight into immune homeostasis and disease, with important therapeutic implications for autoimmunity, cancer, and other immune-mediated disorders.

Fused Deposition Modeling (FDM) can be used to manufacture any complex geometry and internal structures, and it has been widely applied in many industries, such as the biomedical, manufacturing, aerospace, automobile, industrial, and building industries. The purpose of this research is to characterize the polylactic acid (PLA) and polyethylene terephthalate glycol (PETG) materials of FDM under four loading conditions (tension, compression, bending, and thermal deformation), in order to obtain data regarding different printing temperatures and speeds. The results indicated that PLA and PETG materials exhibit an obvious tensile and compression asymmetry. It was observed that the mechanical properties (tension, compression, and bending) of PLA and PETG are increased at higher printing temperatures, and that the effect of speed on PLA and PETG shows different results. In addition, the mechanical properties of PLA are greater than those of PETG, but the thermal deformation is the opposite. The above results will be a great help for researchers who are working with polymers and FDM technology to achieve sustainability.

Background Dysfunctions of long non-coding RNA (lncRNAs) have been associated with the initiation and progression of hepatocellular carcinoma (HCC), but the clinicopathologic significance and potential role of lncRNA PTTG3P (pituitary tumor-transforming 3, pseudogene) in HCC remains largely unknown. Methods We compared the expression profiles of lncRNAs in 3 HCC tumor tissues and adjacent non-tumor tissues by microarrays. In situ hybridization (ISH) and quantitative real-time polymerase chain reaction (qRT-PCR) were applied to assess the level of PTTG3P and prognostic values of PTTG3P were assayed in two HCC cohorts ( n  = 46 and 90). Artificial modulation of PTTG3P (down- and over-expression) was performed to explore the role of PTTG3P in tumor growth and metastasis in vitro and in vivo. Involvement of PTTG1 (pituitary tumor-transforming 1), PI3K/AKT signaling and its downstream signals were validated by qRT-PCR and western blot. Results We found that PTTG3P was frequently up-regulated in HCC and its level was positively correlated to tumor size, TNM stage and poor survival of patients with HCC. Enforced expression of PTTG3P significantly promoted cell proliferation, migration, and invasion in vitro, as well as tumorigenesis and metastasis in vivo. Conversely, PTTG3P knockdown had opposite effects. Mechanistically, over-expression of PTTG3P up-regulated PTTG1, activated PI3K/AKT signaling and its downstream signals including cell cycle progression, cell apoptosis and epithelial-mesenchymal transition (EMT)-associated genes. Conclusions Our findings suggest that PTTG3P, a valuable marker of HCC prognosis, promotes tumor growth and metastasis via up-regulating PTTG1 and activating PI3K/AKT signaling in HCC and might represent a potential target for gene-based therapy.

Helium (He) bubbles are typical radiation defects in structural materials in nuclear reactors after high dose energetic particle irradiation. In the past decades, extensive studies have been conducted to explore the dynamic evolution of He bubbles under various conditions and to investigate He-induced hardening and embrittlement. In this review, we summarize the current understanding of the behavior of He bubbles in metals; overview the mechanisms of He bubble nucleation, growth, and coarsening; introduce the latest methods of He control by using interfaces in nanocrystalline metals and metallic multilayers; analyze the effects of He bubbles on strength and ductility of metals; and point out some remaining questions related to He bubbles that are crucial for design of advanced radiation-tolerant materials.

Vibronic coupling is a central issue in molecular spectroscopy. Here we investigate vibronic coupling within a single pentacene molecule in real space by imaging the spatial distribution of single-molecule electroluminescence via highly localized excitation of tunneling electrons in a controlled plasmonic junction. The observed two-spot orientation for certain vibronic-state imaging is found to be evidently different from the purely electronic 0–0 transition, rotated by 90°, which reflects the change in the transition dipole orientation from along the molecular short axis to the long axis. Such a change reveals the occurrence of strong vibronic coupling associated with a large Herzberg–Teller contribution, going beyond the conventional Franck–Condon picture. The emergence of large vibration-induced transition charges oscillating along the long axis is found to originate from the strong dynamic perturbation of the anti-symmetric vibration on those carbon atoms with large transition density populations during electronic transitions. Vibronic coupling is a key feature of molecular electronic transitions, but its visualization in real space is an experimental challenge. Here the authors, using scanning tunneling microscopy induced luminescence, resolve the effect of vibronic coupling with different modes on the electron distributions in real space in a single pentacene molecule.

Lysosome is a key subceilular organelle in the execution of the autophagic process and at present little is known whether lysosomal function is controlled in the process of autophagy. In this study, we first found that suppression of mammalian target of rapamycin （mTOR） activity by starvation or two mTOR catalytic inhibitors （PP242 and To- rinl）, but not by an allosteric inhibitor （rapamycin）, leads to activation of lysosomal function. Second, we provided evidence that activation of lysosomal function is associated with the suppression of mTOR complex 1 （mTORC1）, but not mTORC2, and the mTORC1 localization to lysosomes is not directly correlated to its regulatory role in lysosomal function. Third, we examined the involvement of transcription factor EB （TFEB） and demonstrated that TFEB acti- vation following mTORC1 suppression is necessary but not sufficient for lysosomal activation. Finally, Atg5 or Atg7 deletion or blockage of the autophagosome-lysosome fusion process effectively diminished lysosomal activation, sug- gesting that lysosomal activation occurring in the course of autophagy is dependent on autophagosome-lysosome fu- sion. Taken together, this study demonstrates that in the course of autophagy, lysosomal function is upregulated via a dual mechanism involving mTORC1 suppression and autophagosome-lysosome fusion.

Circular RNAs (circRNAs) is one type of important non-coding RNAs that participate in tumorigenesis and cancer progression. In our previous study, we performed a microarray analysis of circRNAs between the tumor tissues and the adjacent normal tissues of hepatocellular carcinoma (HCC) patients, and found that the circRNA hsa_circ_0007456 is significantly downregulated in the tumor tissues and correlated with the prognosis of HCC. We further investigated the relationship between the expression levels of hsa_circ_0007456 in HCC and the susceptibility of NK cells, and found that the expression levels of hsa_circ_0007456 in HCC cell lines significantly influenced their susceptibility to NK cells. Through a series of screening and validation, we found that hsa_circ_0007456 mainly functioned through sponging miR-6852-3p and regulating the expression of intercellular adhesion molecule-1 (ICAM-1) in HCC. The miR-6852-3p/ICAM-1 axis is essential for the NK cytotoxicity toward HCC mediated by hsa_circ_0007456. In conclusion, we identify here hsa_circ_0007456 as a promising biomarker of HCC, and highlight hsa_circ_0007456/miR-6852-3p/ICAM-1 axis as an important signaling pathway in the process of tumor immune evasion and the tumorigenesis of HCC.

Hawking radiation is one of the quantum features of a black hole that can be understood as a quantum tunneling across the event horizon of the black hole, but it is quite difficult to directly observe the Hawking radiation of an astrophysical black hole. Here, we report a fermionic lattice-model-type realization of an analogue black hole by using a chain of 10 superconducting transmon qubits with interactions mediated by 9 transmon-type tunable couplers. The quantum walks of quasi-particle in the curved spacetime reflect the gravitational effect near the black hole, resulting in the behaviour of stimulated Hawking radiation, which is verified by the state tomography measurement of all 7 qubits outside the horizon. In addition, the dynamics of entanglement in the curved spacetime is directly measured. Our results would stimulate more interests to explore the related features of black holes using the programmable superconducting processor with tunable couplers. Recently, the theory of Hawking radiation of a black hole has been tested in several analogue platforms. Shi et al. report a fermionic-lattice model realization of an analogue black hole using a chain of superconducting transmon qubits with tuneable couplers and show the stimulated Hawking radiation.