Search

In this work, the perovskite fluorescent nanocrystals (CsPbBr 3) were successfully synthesized and wrapped with SiO 2 shell, utilized for the assembly of solid-state detection strip capable of conveniently and specifically detection of aflatoxin B 1 (AFB 1). The SiO 2 coating aimed to enhance the stability of CsPbBr 3 nanocrystals. The resulting CsPbBr 3 @SiO 2 material exhibited remarkable fluorescence properties, and further self-assembled onto solid-state plate, generating AFB 1 -specific quenched fluorescence at a specific wavelength of 515 nm. When combined with the capture of AFB 1 by magnetic nanoparticles conjugated with aptamers (MNPs-Apt), it was achieved the good separation and specific detection of AFB 1 toxin in food matrices. The constructed fluorescent solid-state detection strip based on CsPbBr 3 @SiO 2 exhibited good response to AFB 1 toxin within a linear range of 0.1–100 ng mL−1 and an impressive detection limit as low as 0.053 ng mL−1. This presents a new strategy for the rapid screening and convenient detection of highly toxic AFB 1. • Fluorescent CsPbBr 3 nanocrystals coated with SiO 2 to improve the stability. • Self-assembly CsPbBr 3 @SiO 2 -based fluorescent solid-state strip for detecting AFB 1. • Remarkable linear response and sensitivity to AFB 1 with portable solid-state strip. • Good recovery and precision for magnetic aptasensing detection of AFB 1 in foods. [ABSTRACT FROM AUTHOR]

Triple negative breast cancer (TNBC) is highly malignant and prone to recurrence and metastasis. Patients with TNBC usually have poor prognosis. Hence, it is urgent to develop new comprehensive treatments for TNBC. The combination of heat shock protein (HSP) inhibitor and the photothermal agent can reduce the temperature required to kill tumor cells, thus achieving mild-temperature photothermal therapy (PTT). Compared with traditional PTT, mild-temperature PTT not only decreases tumor thermoresistance introduced by the overexpression of HSP, but also reduces the damage to normal tissues. Meanwhile, Azo initiator 2,2-azobis[2-(2-imidazolin-2-yl) propane]-dihydroch-loride (AIPH) can be thermally decomposed to generate oxygen-independent free radicals. Herein, a new therapeutic multifunctional nanoplatform (M-17AAG-AIPH) by loading heat shock protein 90 (HSP90) inhibitor (17AAG) and AIPH incorporated into mesoporous polydopamine (MPDA) was successfully constructed for mild-temperature PTT combined with oxygen-independent cytotoxic free radicals against TNBC. Under 808 nm laser irradiation, the mild-temperature PTT arising from the combined effects of 17AAG and MPDA induced a rapid release and decomposition of AIPH, promoting the apoptosis of cancer cells in hypoxic microenvironments. Both in vitro and in vivo results showed that the designed nanoplatform can significantly inhibit tumor growth and provided an efficient new therapeutic strategy for TNBC. There is still an urgent need for new strategies for the treatment of triple negative breast cancer (TNBC). In this work, we successfully constructed a new therapeutic multifunctional nanoplatform (M-17AAG-AIPH) by co-carrying heat shock protein 90 (HSP90) inhibitor (17AAG) and AIPH on mesoporous polydopamine (MPDA). MPDA owned good biocompatibility and outstanding photothermal-conversion ability. The loading of 17AAG can reduce the heat resistance of tumor cells via specifically inhibiting the activity of HSP90, so as to achieve mild-temperature PTT. Meanwhile, 17AAG and MPDA mediated mild-temperature PTT promoted the decomposition of AIPH into oxygen-independent cytotoxic free radicals. Both in vitro and in vivo results showed that M-17AAG-AIPH can significantly inhibit tumor growth and provided an efficient new therapeutic strategy for TNBC. [Display omitted] [ABSTRACT FROM AUTHOR]

Intumescent fire-retardants (IFR) are widely applied in fire protection coatings of steel and wooden structures. The addition of inorganic fillers, such as layered ionic clays, can improve the fireproof performance of IFR coatings. However, a fundamental insight of how these filler materials synergistically interact with the IFR materials remains elusive. In this study, we address this fundamental knowledge gap by systematically investigating the synergy between the IFR fire protection coatings and the CaAlCO 3 -layer double hydroxide (LDH) or montmorillonite (MMT) fillers, which render substantially longer fire resistance (>20 min), reduced specific extinction area (by 54.7 and 44.1 m2 kg−2, respectively), and reduced heat release (by 0.9 and 0.7 MJ m−2, respectively). Combining experimental results and density functional theory calculations, we show for the first time that the superior fireproof performance of the MMT-IFR fire coating originates from the chemical modifications of the char layer by Si-doping. The chemical stabilisation of the silicon- and nitrogen-doped graphene (Si–N-G) structures improves the oxidation resistance of the char layer. Additionally, the formation of the Si–N-G structures with limited lattice deformation stabilised the porous morphology of the char layer, thereby promoting its heat-shielding performance. [Display omitted] [ABSTRACT FROM AUTHOR]

Photodynamic therapy (PDT) is an effective noninvasive therapeutic strategy that can convert oxygen to highly cytotoxic singlet oxygen (1O 2) through the co-localization of excitation light and photosensitizers. However, compromised by the hypoxic tumor microenvironment, the therapeutic efficacy of PDT is reduced seriously. Herein, to overcome tumor-associated hypoxia, and further achieve tumor-targeted synergistic chemotherapy/PDT/photothermal therapy (PTT), we have constructed a biodegradable oxygen-producing nanoplatform (named Ini@PM-HP), which was composed of the porous metal-organic framework (PCN-224(Mn)), the poly (ADP-ribose) polymerase (PARP) inhibitor (Iniparib), and the polydopamine-modified hyaluronic acid (HA-PDA). Since HA can specifically bind to the overexpressed HA receptors (cluster determinant 44, CD44) on tumor cell, Ini@PM-HP prefers to accumulate at the tumor site once injected intravenously. Then iniparib can be released in tumor environment (TME), thereby dysfunctioning DNA damage repair and promoting cell apoptosis. At the same time, the chelating of Mn and tetrakis(4-carboxyphenyl) porphyrin (Mn-TCPP) can generate O 2 in situ by reacting with endogenous H 2 O 2 , relieving the hypoxic TME and achieving enhanced PDT. Moreover, owing to the high photothermal conversion efficiency of PDA, PTT can be driven by the 808 nm laser irradiation. As systematically demonstrated in vitro and in vivo , this nanotherapeutic approach enables the combined therapy with great inhibition on tumor. Overall, the as-prepared nanoplatform provide a promising strategy to overcome tumor-associated hypoxia, and shows great potential for combination tumor therapy. A delicately designed biodegradable oxygen-producing nanoplatform Ini@PM-HP is constructed to achieve combination therapy of solid tumors. Taking advantage of the active-targeting, PTT, enhanced PDT and PARPi, this nanotherapeutic approach successfully enables the combined chemo/photothermal/photodynamic therapy with great inhibition of solid tumors. [Display omitted] [ABSTRACT FROM AUTHOR]

LPS-induced injury in lung epithelial cells is a crucial part of the process of acute lung injury (ALI). The aim of this study is to explore whether Xanthorrhizol, a medicine that has antioxidant and anti-inflammatory activity, could mitigate the injury of lung epithelial cells caused by LPS. Mouse lung epithelial cell line (MLE-12 cells) were treated with LPS in the absence and presence of Xanthorrhizol. As a results, we observed that LPS could induce MLE-12 cells death, mitochondrial dysfunction, oxidative stress and inflammation, and activate MAPK signaling pathways. However, Xanthorrhizol mitigated the injury in MEL-12 caused by LPS by promoting cell viability and MDA, GSH production as well as inhibiting LDH release, mitochondria damage, IL-1β, IL-6 and TNF-α production and the phosphorylation levels of ERK, P38 and JNK. Our results indicated that Xanthorrhizol could protect lung epithelial cells from LPS-induced injury, more likely by inhibiting the phosphorylation of MAPK pathway related proteins. • Xanthorrhizol mitigates LPS-induced death in lung epithelial cells. • Xanthorrhizol alleviates the damage of mitochondria in lung epithelial cells induced by LPS. • Xanthorrhizol diminish oxidative stress and inflammation in lung epithelial cell caused by LPS. • Xanthorrhizol inhibits MAPK pathway activation in LPS-induced lung epithelial cell. [ABSTRACT FROM AUTHOR]