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We found that the Wigner-Yanase skew information, which has been recently proposed as a measure of coherence in Girolami (2014), can increase under a class of operations which may be interpreted as incoherent following the framework of Baumgratz et al., while being phase sensitive. [ABSTRACT FROM AUTHOR]

Abstract: Let , be von Neumann algebras with no central summands of type . For , define a new product of T and S. In this note, it is proved that a not necessarily linear bijective map satisfies for all if and only if Φ is the direct sum of a linear ⁎-isomorphism and a conjugate linear ⁎-isomorphism. [Copyright &y& Elsevier]

Abstract: Let , be factors. If is a multiplicative ∗-Lie isomorphism, then Φ is of the form , where σ is a linear ∗-isomorphism, or a conjugate linear ∗-isomorphism, or the negative of a linear ∗-anti-isomorphism, or the negative of a conjugate linear ∗-anti-isomorphism of onto and τ is a mapping of into which maps commutators into zero. [Copyright &y& Elsevier]

Let H, K be infinite-dimensional complex Hilbert spaces. And let p(t) be a complex polynomial with deg(p)⩾2. In this paper we give a sufficient and necessary condition for a surjective linear or additive map Φ :B(H)→B(K) to preserve operators annihilated by p in both directions and answer a question raised by Sˇemrl affirmatively. [Copyright &y& Elsevier]

• Cryptotanshinone (CTS) is a specific inhibitor for NLRP3 inflammasome. • CTS blocks Ca2+ signaling and the induction of mtROS, the important upstream signalings of NLRP3 inflammasome activation. • CTS exhibits protective effect in inflammasome-mediated diseases such as endotoxemia syndrome and MCD-diet-induced NASH. NLRP3 inflammasome activation is implicated in the pathogenesis of a wide range of inflammatory diseases, but medications targeting the NLRP3 inflammasome are not available for clinical use. Here, we demonstrate that cryptotanshinone (CTS), a major component derived from the traditional medicinal herb Salvia miltiorrhiza Bunge, is a specific inhibitor for the NLRP3 inflammasome. Cryptotanshinone inhibits NLRP3 inflammasome activation in macrophages, but has no effects on AIM2 or NLRC4 inflammasome activation. Mechanistically, cryptotanshinone blocks Ca2+ signaling and the induction of mitochondrial reactive oxygen species (mtROS), which are important upstream signals of NLRP3 inflammasome activation. In vivo , cryptotanshinone attenuates caspase-1 activation and IL-1β secretion in mouse models of NLRP3 inflammasome-mediated diseases such as endotoxemia syndrome and methionine- and choline-deficient-diet-induced nonalcoholic steatohepatitis (NASH). Our findings suggest that cryptotanshinone may be a promising therapeutic agent for the treatment of NLRP3 inflammasome-mediated diseases. [ABSTRACT FROM AUTHOR]

• DCL inhibits NLRP3 inflammasome activation in primary BMDMs and hPBMCs. • DCL reduces the NLRP3-dependent inflammation in LPS-induced sepsis model. • DCL is a novel and potent drug for treating NLRP3-associated diseases. Uncontrolled activation of NLRP3 inflammasome initiates a series of human inflammatory diseases. Targeting NLRP3 inflammasome has attracted considerable attention in developing potential therapeutic interventions. Here, we reported that dehydrocostus lactone (DCL), a main component of Saussurea lappa from the traditional Chinese medicine, inhibited NLRP3 inflammasome-mediated caspase-1 activation and subsequent interleukin (IL)-1β production in primary mouse macrophages and human peripheral blood mononuclear cells and exerted an inhibitory effect on NLRP3-driven inflammation. Mechanistically, DCL significantly blocked the ASC oligomerization, which is essential for the assembly of activated inflammasome. Importantly, in vivo experiments showed that DCL reduced IL-1β secretion and peritoneal neutrophils recruitment in LPS-mediated inflammation mouse model, which is demonstrated to be NLRP3 dependent. These results suggest that DCL is a potent pharmacological inhibitor of NLRP3 inflammasome and may be developed as a therapeutic drug for treating NLRP3-associated diseases. [ABSTRACT FROM AUTHOR]