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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]

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]

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]