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The study of high-order harmonic generation (HHG) in confined quantum systems is essential for developing a comprehensive physical description of harmonic generation from atoms to bulk solids. Using the time-dependent density-functional theory, we demonstrate how the symmetry of the system modulates the generation of high-order harmonic in fullerene C60 molecules along different orthogonal directions, as well as the effects of amplitude and photon energy of a linearly polarized laser on high-order harmonics generation. We found that the generation of high-order harmonics perpendicular to the laser polarization direction (LPD) is related to the symmetry of molecules along the LPD and the symmetry of molecules perpendicular to the LPD. Within a certain parameter range, the cut-off energy is linearly proportional to the laser amplitude and the laser photon energy. [ABSTRACT FROM AUTHOR]

Recently, zero-dimensional (0D) lead-free Cs3Cu2I5 materials have become one of the most attractive research hotspots in the optoelectronic field owing to their simple preparation method and long-term air stability. However, the photoluminescence quantum yield (PLQY) of the blue luminescence of Cs3Cu2I5 still lags behind those of the green and red luminescence of lead halide perovskites. Herein, 0D lead-free Cs3Cu2I5 films modulated by hydroiodic acid (HI) with a high PLQY of blue luminescence are addressed. The results show that the particle size of the Cs3Cu2I5 films decreases as the added amount of HI increases, from 223.3 (without HI) to 200.7 nm (with 0.076 mmol HI). The Cs3Cu2I5 films with 0.038 mmol HI display the lowest root-mean-square roughness of 14.7 nm. Moreover, the as-prepared films all exhibit blue luminescence at 445 nm, and the PLQY of Cs3Cu2I5 films reaches 85.3% when 0.038 mmol HI is added. Most importantly, the obtained films demonstrate long-term air stability under an ambient atmosphere, and the crystal structure and PLQY of Cs3Cu2I5 films have no obvious variation after 150 days. This air-stable lead-free blue luminescence with high PLQY provides a new strategy to promote the blue luminescence optical property of halide perovskite materials. [ABSTRACT FROM AUTHOR]

As a primary active ingredient of safflor yellow, hydroxysafflor yellow A (HSYA) exhibits notable antioxidative and neuroprotective effects. The aim of the present study was to investigate the protective effects of HSYA in mesenchymal stem cells (MSCs) exposed to hypoxia (5% O2) and serum deprivation (H/SD), and to explore the mechanisms underlying HSYA-mediated protection. Under H/SD conditions, HSYA was applied to protect MSCs against injury. Cell viability, proliferation, apoptosis and reactive oxygen species (ROS) levels were determined using an 5-ethynyl-2'-deoxyuridine assay, MTT assay, Hoechst 33342/propidium iodide and 2',7'-dichlorodihydrofluorescein diacetate staining, respectively. The results revealed that 160 mg/l HSYA significantly reduced apoptosis and ROS levels compared with the H/SD group; however, HSYA demonstrated minimal effects on cell proliferation. A western blot assay demonstrated that HSYA reduced cleaved caspase-3 expression and cytC release from the mitochondria to the cytoplasm when compared with the H/SD group. In addition, western blotting and RT-qPCR analyses revealed that HSYA treatment significantly increased the expression of hypoxia inducible factor-1α (HIF-1α) and vascular endothelial growth factor (VEGF). In conclusion, the results of the current study demonstrated that HSYA exerts protective effects against H/SD-induced apoptosis in MSCs potentially via activation of the HIF-1α/VEGF signaling pathway and stabilization of the mitochondrial membrane. [ABSTRACT FROM AUTHOR]

Mutations in TGF-β-activated kinase 1 binding protein 2 (TAB2) have been implicated in the pathogenesis of dilated cardiomyopathy and/or congenital heart disease in humans, but the underlying mechanisms are currently unknown. Here, we identified an indispensable role for TAB2 in regulating myocardial homeostasis and remodeling by suppressing receptor-interacting protein kinase 1 (RIPK1) activation and RIPK1-dependent apoptosis and necroptosis. Cardiomyocyte-specific deletion of Tab2 in mice triggered dilated cardiomyopathy with massive apoptotic and necroptotic cell death. Moreover, Tab2-deficient mice were also predisposed to myocardial injury and adverse remodeling after pathological stress. In cardiomyocytes, deletion of TAB2 but not its close homolog TAB3 promoted TNF-α-induced apoptosis and necroptosis, which was rescued by forced activation of TAK1 or inhibition of RIPK1 kinase activity. Mechanistically, TAB2 critically mediates RIPK1 phosphorylation at Ser321 via a TAK1-dependent mechanism, which prevents RIPK1 kinase activation and the formation of RIPK1-FADD-caspase-8 apoptotic complex or RIPK1-RIPK3 necroptotic complex. Strikingly, genetic inactivation of RIPK1 with Ripk1-K45A knockin effectively rescued cardiac remodeling and dysfunction in Tab2-deficient mice. Together, these data demonstrated that TAB2 is a key regulator of myocardial homeostasis and remodeling by suppressing RIPK1-dependent apoptosis and necroptosis. Our results also suggest that targeting RIPK1-mediated cell death signaling may represent a promising therapeutic strategy for TAB2 deficiency-induced dilated cardiomyopathy. [ABSTRACT FROM AUTHOR]

Background: Programmed cell death, including apoptosis, mitochondria-mediated necrosis, and necroptosis, is critically involved in ischemic cardiac injury, pathological cardiac remodeling, and heart failure progression. Whereas apoptosis and mitochondria-mediated necrosis signaling is well established, the regulatory mechanisms of necroptosis and its significance in the pathogenesis of heart failure remain elusive.Methods: We examined the role of tumor necrosis factor receptor-associated factor 2 (Traf2) in regulating myocardial necroptosis and remodeling using genetic mouse models. We also performed molecular and cellular biology studies to elucidate the mechanisms by which Traf2 regulates necroptosis signaling.Results: We identified a critical role for Traf2 in myocardial survival and homeostasis by suppressing necroptosis. Cardiac-specific deletion of Traf2 in mice triggered necroptotic cardiac cell death, pathological remodeling, and heart failure. Plasma tumor necrosis factor α level was significantly elevated in Traf2-deficient mice, and genetic ablation of TNFR1 largely abrogated pathological cardiac remodeling and dysfunction associated with Traf2 deletion. Mechanistically, Traf2 critically regulates receptor-interacting proteins 1 and 3 and mixed lineage kinase domain-like protein necroptotic signaling with the adaptor protein tumor necrosis factor receptor-associated protein with death domain as an upstream regulator and transforming growth factor β-activated kinase 1 as a downstream effector. It is important to note that genetic deletion of RIP3 largely rescued the cardiac phenotype triggered by Traf2 deletion, validating a critical role of necroptosis in regulating pathological remodeling and heart failure propensity.Conclusions: These results identify an important Traf2-mediated, NFκB-independent, prosurvival pathway in the heart by suppressing necroptotic signaling, which may serve as a new therapeutic target for pathological remodeling and heart failure. [ABSTRACT FROM AUTHOR]

Corrosion fatigue (CF) tests of 316LN weld metal were investigated in high-temperature water at different strain rates (0.0004–0.4%/s) under strain amplitude of 0.6%. Relationship between CF life and strain rate was proposed and environmental fatigue correction factor F en was also calculated. It was found that the γ/δ phase boundary was more susceptible to cracking at low strain rates and δ-ferrite worked as a barrier to retard the crack growth at high strain rates. Mechanisms of CF damage involving the effects of strain rate, hydrogen, δ-ferrite and residual strain on crack growth are also discussed. • Quantitative relation between fatigue life of 316LN weld metal and strain rate is purposed. • Effect of δ-ferrite changed with strain rate due to the interaction between localized deformation and environmental damage. • Mechanisms of CF damage involving the effects of hydrogen and residual strain on crack growth are proposed. [ABSTRACT FROM AUTHOR]

TAK1 (TGFβ-activated kinase-1) signaling is essential in regulating a number of important biological functions, including innate immunity, inflammatory response, cell growth and differentiation, and myocardial homeostasis. The precise role of TAK1 in the adult heart under pathological conditions remains largely unknown. Importantly, we observed that TAK1 is upregulated during compensatory hypertrophy but downregulated in end-stage heart failure. Here we generated transgenic mice with inducible expression of an active TAK1 mutant (TAK1ΔN) in the adult heart. TAK1ΔN transgenic mice developed greater cardiac hypertrophy compared with control mice after transverse aortic constriction (TAC), which was largely blocked by ablation of calcineurin Aβ. Expression of TAK1ΔN also promoted NFAT (nuclear factor of activated T-cells) transcriptional activity in luciferase reporter mice at baseline, which was further enhanced after TAC. Our results revealed that activation of TAK1 promoted adaptive cardiac hypertrophy through a cross-talk between calcineurin-NFAT and IKK-NFκB pathways. More significantly, adult-onset inducible expression of TAK1ΔN protected the myocardium from adverse remodeling and heart failure after myocardial infarction or long-term pressure overload, by preventing cardiac cell death and fibrosis. Mechanistically, TAK1 exerts its cardioprotective effect through activation of NFAT/NFκB, downregulation of Bnip3, and inhibition of cardiac cell death. [ABSTRACT FROM AUTHOR]