While controlling the chirality and modulating the helicity is a challenging task, it attracts great research interest for gaining a better understanding of the origin of chirality in nature. Herein, structurally similar azobenzene (Azo) vinyl monomers were designed in which the alkyl chains comprised the chiral stereocenter with different achiral tail lengths. Combining the synchronous polymerization, supramolecular stacking and self-assembly, the multiple chiroptical inversion of the Azo-polymer supramolecular assemblies can be modulated by the tail length and DP of Azo blocks during in situ polymerization. The DP-, UV light-, temperature-, aging timedependent chiroptical properties and liquid-crystalline (LC) characterization indicated that the amorphous-to-LC phase transition and biphasic LC interconversion allow the transcription of intra-chain p-p stacking, inter-chain H-and Jaggregation, thereby controlling the dynamic multiple reversal of supramolecular chirality.

Several drugs are effective in attenuating intestinal ischemia-reperfusion injury (IRI); however little is known about the effect of montelukast. Fifty rats were randomly assigned to 3 groups: model group (operation with clamping), sham group (operation without clamping), and study group (operation with clamping and 0.2, 2 and 20 mg/kg montelukast pretreatment). Intestinal ischemia-reperfusion was performed by occlusion (clamping) of the arteria mesenterica anterior for 45 min, followed by 24 h reperfusion. Intestinal IRI in the model group led to severe damage of the intestinal mucosa, liver and kidney. The Chiu scores of the intestines from the study group (2 and 20 mg/kg) were lower than that of the model group. Intestinal IRI induced a marked increase in CysLTR1, Caspase-8 and -9 expression in intestine, liver and kidney, which were markedly reduced by preconditioning with 2 mg/kg montelukast. Preconditioning with 2 g/kg montelukast significantly attenuated hepatic tissue injury and kidney damage, and decreased plasma interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) levels in plasma after intestinal IRI. In conclusion, preconditioning with montelukast could attenuate intestinal IRI and the subsequent systemic inflammatory response in rats.

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Magnetic anisotropy is a fundamental key parameter of magnetic materials that determines their applications. For ferromagnetic materials, the magnetic anisotropy can be easily detected by using conventional magnetic characterization techniques. However, due to the magnetic compensated structure in antiferromagnetic materials, synchrotron measurements, such as X-ray magnetic linear dichroism, are often needed to probe their magnetic properties. In this work, we observed an imprinted fourfold magnetic anisotropy in the amorphous ferromagnetic layer of FeRh/CoFeB heterostructures. The MOKE and ferromagnetic resonance measurements show that the easy magnetization axes of the CoFeB layer are along the FeRh〈110〉 and FeRh〈100〉 directions for the epitaxially grown FeRh layer in the antiferromagnetic and ferromagnetic states, respectively. The combined Monte Carlo simulation and first-principles calculation indicate that the fourfold magnetic anisotropy of the amorphous CoFeB layer is imprinted due to the interfacial exchange coupling between the CoFeB and FeRh moments from the magnetocrystalline anisotropy of the epitaxial FeRh layer. This observation of imprinting the magnetocrystalline anisotropy of antiferromagnetic materials on easily detected ferromagnetic materials may be applied to probe the magnetic structures of antiferromagnetic materials without using synchrotron methods.