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A novel photothermal probe, o-phenylenediamine trimer (triOPD)-Ni2+ aggregates with a photothermal conversion efficiency of up to 74.4%, was prepared by CuNi–BTC catalytic oxidation and assembly of OPD. Based on the specific inhibition activity of thiophanate-methyl toward CuNi–BTC, a direct and background-free photothermal sensing platform was fabricated. [ABSTRACT FROM AUTHOR]

The domain of science and engineering relies heavily on an in-depth comprehension of fluid dynamics, given the prevalence of fluids such as water, air, and interstellar gas in the universe. Euler equations form the basis for the study of fluid motion. This paper is concerned with the Cauchy problem of isentropic compressible Euler equations away from the vacuum. We use the integration method with the general test function f = f (r) , proving that there exist the corresponding blowup results of C 1 irrotational solutions for Euler equations and Euler equations with time-dependent damping in R n ( n ≥ 2 ), provided the density-independent initial functional is sufficiently large. We also provide two simple and explicit test functions f (r) = r and f (r) = 1 + r , to demonstrate the blowup phenomenon in the one-dimensional case. In particular, our results are applicable to the non-radial system. [ABSTRACT FROM AUTHOR]

Type I interferons (IFN‐Is) are a class of proinflammatory cytokines produced in response to viruses and environmental stimulations, resulting in chronic inflammation and even carcinogenesis. However, the connection between IFN‐I and p53 mutation is poorly understood. Here, we investigated IFN‐I status in the context of mutant p53 (p53N236S, p53S). We observed significant cytosolic double‐stranded DNA (dsDNA) derived from nuclear heterochromatin in p53S cells, along with an increased expression of IFN‐stimulated genes. Further study revealed that p53S promoted cyclic GMP‐AMP synthase (cGAS) and IFN‐regulatory factor 9 (IRF9) expression, thus activating the IFN‐I pathway. However, p53S/S mice were more susceptible to herpes simplex virus 1 infection, and the cGAS–stimulator of IFN genes (STING) pathway showed a decline trend in p53S cells in response to poly(dA:dT) accompanied with decreased IFN‐β and IFN‐stimulated genes, whereas the IRF9 increased in response to IFN‐β stimulation. Our results illustrated the p53S mutation leads to low‐grade IFN‐I‐induced inflammation via consistent low activation of the cGAS–STING‐IFN‐I axis, and STAT1‐IRF9 pathway, therefore, impairs the protective cGAS–STING signalling and IFN‐I response encountered with exogenous DNA attack. These results suggested the dual molecular mechanisms of p53S mutation in inflammation regulation. Our results could be helping in further understanding of mutant p53 function in chronic inflammation and provide information for developing new therapeutic strategies for chronic inflammatory diseases or cancer. [ABSTRACT FROM AUTHOR]