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Psoriasis is a common chronic skin disease characterized by epidermal hyperplasia and inflammation. However, the pathogenesis of psoriasis is multifactorial and is not fully understood. MicroRNAs (miRNAs) represent a promising class of small, noncoding RNA molecules that have a large impact on cellular functions by regulating gene expression. Here we reported that microRNA‐187 (miR‐187), which is one of the most dynamic microRNAs identified in the deep screening miRNAs profile, is downregulated in inflammatory cytokines‐stimulated keratinocytes and psoriatic skins. By luciferase activity assay and gain‐of‐function studies, we showed that miR‐187 inhibits keratinocytes hyperproliferation by targeting CD276. Moreover, overexpression of miR‐187 decreases acanthosis and reduces the disease severity in psoriasis mouse models. Taken together, the results of our study implies miR‐187 as a critical factor in psoriasis pathogenesis, which could be a potent target for psoriasis treatment. MicroRNA‐187, which is declined in the inflammatory cytokines‐stimulated keratinocytes and psoriatic skins, can contribute to keratinocytes hyperproliferation by promoting CD276‐STAT3 signaling. [ABSTRACT FROM AUTHOR]

In this work, we study the trans influence of boryl ligands and other commonly used non-boryl ligands in order to search for a more active catalyst than the ruthenium dihydride complex Ru(PNP)(CO)H2 for the hydrogenation of CO2. The theoretical calculation results show that only the B ligands exhibit a stronger trans influence than the hydride ligand and are along increasing order of trans influence as follows: –H < –BBr2 < –BCl2 ≈ –B(OCH)2 < –Bcat < –B(OCH2)2 ≈ –B(OH)2 < –Bpin < –B(NHCH2)2 < –B(OCH3)2 < –B(CH3)2 < –BH2. The computed activation free energy for the direct hydride addition to CO2 and the NBO analysis of the property of the Ru–H bond indicate that the activity of the hydride can be enhanced by the strong trans influence of the B ligands through the change in the Ru–H bond property. The function of the strong trans influence of B ligands is to decrease the d orbital component of Ru in the Ru–H bond. The design of a more active catalyst than the Ru(PNP)(CO)H2 complex is possible. [ABSTRACT FROM AUTHOR]

Advances in transcriptome sequencing have revealed that the genome fraction largely encodes for thousands of non‐coding RNAs. Long non‐coding RNAs (lncRNAs), which are a class of non–protein‐coding RNAs longer than approximately 200 nucleotides in length, are emerging as key epigenetic regulators of gene expression recently. Intensive studies have characterized their crucial roles in cutaneous biology and diseases. In this review, we address the promotive or suppressive effects of lncRNAs on cutaneous physiological processes. Then, we focus on the pathogenic role of dysfunctional lncRNAs in a variety of proliferative skin diseases. These evidences suggest that lncRNAs have indispensable roles in the processes of skin biology. Additionally, lncRNAs might be promising biomarkers and therapeutic targets for cutaneous disorders. [ABSTRACT FROM AUTHOR]

Summary of main observation and conclusion: A dual‐templating method was used to synthesize a series of hierarchical carbon supports containing different proportions of spherical macropores (ca. 200 nm in diameter) and mesoporous channels (ca. 4 nm in diameter). These and some other conventional carbon materials were subsequently impregnated with Ni and tested for the conversion of glycerol. The hierarchical catalysts exhibited a significantly higher conversion (96%) and selectivity (77%) to 1,2‐propanediol, and the specificity selectivity coefficient (6.1) towards 1,2‐propanediol against lactic acid was three times higher than that observed over a conventional Ni/Cmicro catalyst (2.1). The enhanced performance of these materials, compared with the Ni nanoparticles supported on conventional carbon supports, was attributed to their high surface areas (> 1110 m2∙g−1) and large pore volumes (ca. 0.4 cm3∙g−1) permitting greater accessibility of substrate and/or intermediates to Ni active sites. Given that the concentration of accessible Ni sites in these materials is higher, a competitive benzilic‐acid‐rearrangement reaction to produce lactic acid was suppressed, leading to an enhanced hydrogenation selectivity to 1,2‐propanediol. This study evidences the potential benefits, which can be established from utilizing hierarchical support materials in the valorization of biomass. [ABSTRACT FROM AUTHOR]

Herein we report an efficient and recyclable catalytic system for tandem CO 2 capture and N-formylation to value-added chemicals. CO 2 is apt to be captured by morpholine solution, while a highly efficient heterogeneous catalyst, isolated iridium atoms supported over nanadiamond/graphene, is discovered to be highly reactive for the formylation of morpholine, leading to the formation of N-formylmorpholine with excellent productivity (with a turnover number of 5 120 000 in a single batch reaction) and selectivity (>99 %). In addition, the CO 2 captured by morpholine under atmospheric conditions can be converted to N-formylmorpholine with decent conversion (51 %), which realizes the integration of CO 2 capture and conversion to value-added chemicals., (© 2022 Wiley-VCH GmbH.)

N 6 -methyladenosine (m 6 A) modification, the addition of a methylation decoration at the position of N6 of adenosine, is one of the most prevalent modifications among the over 100 known chemical modifications of RNA. Numerous studies have recently characterized that RNA m 6 A modification functions as a critical post-transcriptional regulator of gene expression through modulating various aspects of RNA metabolism. In this review, we will illustrate the current perspectives on the biological process of m 6 A methylation. Then we will further summarize the vital modulatory effects of m 6 A modification on immunity, viral infection, and autoinflammatory disorders. Recent studies suggest that m 6 A decoration plays an important role in immunity, viral infection, and autoimmune diseases, thereby providing promising biomarkers and therapeutic targets for viral infection and autoimmune disorders., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2021 Tang, Wei, Li, Chen, Dai, Lu and Zheng.)

Overstimulation of NMDA-type glutamate receptors is believed to be responsible for neuronal death of the CNS in various disorders, including cerebral and spinal cord ischemia. However, the intrinsic and physiological mechanisms of modulation of these receptors are essentially unknown. Here we report that cholestane-3β,5α,6β-triol (triol), a major metabolite of cholesterol, is an endogenous neuroprotectant and protects against neuronal injury both in vitro and in vivo via negative modulation of NMDA receptors. Treatment of cultured neurons with triol protects against glutamate-induced neurotoxicity, and administration of triol significantly decreases neuronal injury after spinal cord ischemia in rabbits and transient focal cerebral ischemia in rats. An inducible elevation of triol is associated with ischemic preconditioning and subsequent neuroprotection in the spinal cord of rabbits. This neuroprotection is effectively abolished by preadministration of a specific inhibitor of triol synthesis. Physiological concentrations of triol attenuate [Ca(2+)]i induced by glutamate and decrease inward NMDA-mediated currents in cultured cortical neurons and HEK-293 cells transiently transfected with NR1/NR2B NMDA receptors. Saturable binding of [(3)H]triol to cerebellar granule neurons and displacement of [(3)H]MK-801 binding to NMDA receptors by triol suggest that direct blockade of NMDA receptors may underlie the neuroprotective properties. Our findings suggest that the naturally occurring oxysterol, the major cholesterol metabolite triol, functions as an endogenous neuroprotectant in vivo, which may provide novel insights into understanding and developing potential therapeutics for disorders in the CNS., (Copyright © 2014 the authors 0270-6474/14/3411426-13$15.00/0.)