A key factor for successful design of bioactive complex, organic-inorganic hybrid biomaterials is the facilitation and control of adhesion at interfaces, as many current synthetic biomaterials are inert, lacking interfacial bio activity. In this regard, the development of a simple, unified way to bio functionalize diverse organic and inorganic materials toward biomineralization remains a critical challenge. In this report, a universal biomimetic mineralization route that can be applied to virtually any type and morphology of scaffold materials is provided to induce nucleation and growth of hydroxyapatite (HAp) crystals based on phase-transited lysozyme (PTL) coating. Surface-anchored abundant functional groups in the PTL enrich the interface with strongly bonded calcium ions, facilitating the formation of HAp crystals in simulated body fluid with the morphology and alignment being similar to that observed in natural HAp in mineralized tissues. By the adhesion of amyloid contained in the PTL, such protein assembly could readily integrate HAp on ceramics, metals, semiconductors, and synthetic polymers irrespective of their size and morphology, with robust bonding stability and corresponding ultralow wear extent under normal bone pressure. This strategy successfully improves the in vivo osteoconductivity of Ti-based implant, underpinning the expectation for such biomaterial in future biointerface and tissue engineering.

In situ regeneration of the enamel‐like structure of hydroxyapatite (HAp) crystals under oral conditions is significant for dental caries treatment. However, it is still a challenge for dentists to duplicate the elegant and well‐aligned apatite structure bonding to the surface of demineralized enamel. A biocompatible amelogenin‐inspired matrix, a phase‐transited lysozyme (PTL) film mimicking an N‐terminal amelogenin with central domain (N‐Ame) combined with synthetic peptide (C‐AMG) based on the functional domains of C‐terminal telopeptide (C‐Ame) is shown here, which is formed by amyloid‐like lysozyme aggregation at the enamel interface through a rapid one‐step aqueous coating process. In the PTL/C‐AMG matrix, C‐AMG facilitated the oriented arrangement of amorphous calcium phosphate (ACP) nanoparticles and their transformation to ordered enamel‐like HAp crystals, while PTL served as a strong interfacial anchor to immobilize the C‐AMG peptide and PTL/C‐AMG matrix on versatile substrate surfaces. PTL/C‐AMG film‐coated enamel induced both of the in vivo and in vitro synthesis of HAp crystals, facilitated epitaxial growth of HAp crystals and recovered the highly oriented structure and mechanical properties to levels nearly identical to those of natural enamel. This work underlines the importance of amyloid‐like protein aggregates in the biomineralization of enamel, providing a promising strategy for treating dental caries.

The extraction of gold from ores and electronic waste is an important topic worldwide, as this precious metal has immense value in a variety of fields. However, serious environmental pollution and high energy consumption due to the use of toxic oxidation reagents and harsh reaction conditions is a well-known problem in the gold industry. Herein, we report a new chemical method based on the combined use of N-bromosuccinimide (NBS) and pyridine (Py), which has a greatly decreased environmental impact and reagent cost, as well as mild reaction requirements. This method can directly leach Au from gold ore and electronic waste to form Au in water. The process is achieved in a yield of approximately 90 % at room temperature and a nearly neutral pH. The minimum dose of NBS/Py is as low as 10 mm, which exhibits low toxicity towards mammalian cells and animals as well as aquatic creatures. The high leaching selectivity of Au over other metals during gold leaching is demonstrated, showing that this method has great potential for practical industrial application towards the sustainable refining of gold from ores and electronic waste.

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Arachidonic acid-derived epoxyeicosatrienoic acids (EETs) are important regulators of cardiac remodeling; manipulation of their levels is a potentially useful pharmacological strategy. EETs are hydrolyzed by soluble epoxide hydrolase (sEH) to form the corresponding diols, thus altering and reducing the activity of these oxylipins. To better understand the phenotypic impact of sEH disruption, we compared the effect of EPHX2 gene knockout (EPHX2 −/−) and sEH inhibition in mouse models. Measurement of plasma oxylipin profiles confirmed that the ratio of EETs/DHETs was increased in EPHX2 −/− and sEH-inhibited mice. However, plasma concentrations of 9, 11, 15, 19-HETE were elevated in EPHX2 −/− but not sEH-inhibited mice. Next, we investigated the role of this difference in cardiac dysfunction induced by Angiotensin II (AngII). Both EPHX2 gene deletion and inhibition protected against AngII-induced cardiac hypertrophy. Interestingly, cardiac dysfunction was attenuated by sEH inhibition rather than gene deletion. Histochemical staining revealed that compared with pharmacological inhibition, EPHX2 deletion aggravated AngII-induced myocardial fibrosis; the mRNA levels of fibrotic-related genes were increased. Furthermore, cardiac inflammatory response was greater in EPHX2 −/− than sEH-inhibited mice with AngII treatment, as evidenced by increased macrophage infiltration and expression of MCP-1 and IL-6. In vitro, AngII-upregulated MCP-1 and IL-6 expression was significantly attenuated by sEH inhibition but promoted by EPHX2 deletion in cardiofibroblasts. Thus, compared with pharmacological inhibition of sEH, EPHX2 deletion caused the shift in arachidonic acid metabolism, which may led to pathological cardiac remodeling, especially cardiac fibrosis.