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The remotely controlled shape memory behaviors of a two-dimensional (2D) sheet to controlled helix structure upon external stimuli is of great significance in the field of smart materials. Herein, we devise a strategy to fabricate a series of shape memory polycaprolactone/[W.sub.18][O.sub.49] nanowire film via highly efficient UV-triggered thiol-acrylate click chemistry. The resultant polymer composites exhibited desirable photothermal transfer efficiency and can enable rapid temperature increase over the melting temperature of polymeric matrix, thus remotely actuating shape transformation within 8 s. Owing to the well- defined architecture of the polymer network, the fabricated elastic composite film exhibited a high degree of crystallinity and showed excellent shape memory properties with [R.sub.f] of 93.12% and [R.sub.r] of 95.32%. Remarkably, under a 160 mW/[cm.sup.2] simulated sunlight illumination, the transformation of flat 2D film into 3D chiral actuators is driven by designing anisotropic bilayer thin sheet, and it yields right- and left-handed helix. This work will pave the way for designing biomimetic flexible actuators toward multifunctional shape-shifting devices. Highlights * Shape memory polycaprolactone/[W.sub.18][O.sub.49] nanowires composite film is fabricated via UV-triggered thiol-ene click chemistry. * Polymer composites exhibit light-activated shape memory behaviors. * The composite films show excellent shape fixity and shape recovery ratio based on the well-defined network. * The shape morphing behaviors of a flexible 2D bilayer strip into 3D chiral actuators are achieved. KEYWORDS flexible actuators, polycaprolactone, shape memory polymers, stimuli- responsive polymers, 1 | INTRODUCTION Stimuli-responsive morphing materials belong to one kind of molecules with 'intelligent' behavior, which can generate corresponding response signals upon the stimuli of heat, light, electric field, etc. [...]

Hazy conditions have a significant impact on the environment and societal development. Their occurrence and persistence depend largely on climatological conditions, including the important role of climate change. Based on monthly data from 15 Coupled Model Intercomparison Project Phase 6 (CMIP6) models under three Tier 1 scenarios (SSP1–2.6, SSP2–4.5, and SSP5–8.5), the meteorological potential for winter haze pollution over Beijing was assessed during periods of peak carbon emissions (PCP; 2021–2030) and carbon neutrality (approximate net‐zero emissions) (PCN; 2051–2060) in China. The results show that a possible high‐emission strategy during PCP may not obviously enhance winter hazy conditions over Beijing in the near future. Rather, the high‐emission scenario in this period may decrease the meteorological potential that is favourable for the enhanced Beijing haze pollution by inducing a Northeast Asia cyclonic anomaly, compared to situations under SSP2–4.5, with medium emissions. Further analyses indicated that, under the continued sustainable pathway (SSP1–2.6 in PCN plus SSP1–2.6 in PCP; the better pathway simulating the effects of approximate net‐zero emissions during PCN through model results), atmospheric conditions such as the East Asian winter monsoon as well as decadal oceanic forcings of the mega‐El Niño and the warm Atlantic Multidecadal Oscillation, which are conducive to more frequent Beijing haze, are significantly suppressed in the farther future PCN. Under such circumstances, in situ haze pollution is highly repressed, suggesting a critical and positive role for the low‐carbon policy advocated by China during PCN in suppressing longer‐term hazy conditions over Beijing. In contrast, Beijing haze pollution during PCN is frequent under the discontinued sustainable pathway (SSP2–4.5/SSP5–8.5 in PCN plus SSP1–2.6 in PCP). Our findings demonstrate the possible insignificant impact of the high‐emission strategy of China during the near‐future PCP on Beijing haze exacerbation, and an important role for carbon neutrality advocated by China to suppress the haze potential in the farther future PCN, highlighting the significance of future pathway selections. [ABSTRACT FROM AUTHOR]

BackgroundMethodsResultsConclusionGout is a chronic inflammatory diseases caused by monosodium urate crystal deposition. However, the role of interleukin (IL)-36 in gout has not dbeen elucidated.We enrolled 75 subjects, including 20 healthy controls (HC), 30 patients with acute gout attack and 25 patients in remission. Baseline data were obtained through clinical interrogation and laboratory data were obtained through tests of blood samples. Serum levels of IL-36α were detected using enzyme-linked immunosorbent assay. Spearman correlation analysis was used to investigate the correlation of IL-36α with other parameters. The diagnostic value of IL-36α was demonstrated using a receiver operating characteristic curve.The serum IL-36α level of gout patients in acute attack and remission stage was significantly higher than that of HC. Serum IL-36α was positively correlated with alanine transaminase (ALT) and aspartate transaminase (AST). Serum amyloid A (SAA) levels positively correlated with C-reactive protein levels and erythrocyte sedimentation rates. Glutamyl transpeptidase levels positively correlated with AST and ALT levels.In conclusion, serum IL-36α levels were elevated in patients with gout and correlated with the clinical markers of inflammation. Our findings suggest that IL-36α may be a novel inflammatory indicator for gout. [ABSTRACT FROM AUTHOR]

Diabetes mellitus is a metabolic disease caused by a combination of genetic and environmental factors. The importance of the inflammatory response occurring in the pancreas and adipose tissue in the occurrence and progression of diabetes has been gradually accepted. Excess blood glucose and free fatty acids produce large amounts of inflammatory cytokines and chemokines through oxidative stress and endoplasmic reticulum stress. There is sufficient evidence that proinflammatory mediators, such as interleukin (IL)-1β, IL-6, macrophage chemotactic protein-1, and tumor necrosis factor-α, are engaged in insulin resistance in peripheral adipose tissue and the apoptosis of pancreatic β-cells. IL-36, IL-37, and IL-38, as new members of the IL-1 family, play an indispensable role in the regulation of immune system homeostasis and are involved in the pathogenesis of inflammatory and autoimmune diseases. Recently, the abnormal expression of IL-36, IL-37, and IL-38 in diabetes has been reported. In this review, we discuss the emerging functions, potential mechanisms, and future research directions on the role of IL-36, IL-37, and IL-38 in diabetes mellitus and its complications., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)