As hot topics in the chemical conversion of CO2, the photo‐/electrocatalytic reduction of CO2 and use of CO2 as a supporter for energy storage have shown great potential for the utilization of CO2. However, many obstacles still exist on the road to realizing highly efficient chemical CO2 conversion, such as inefficient uptake/activation of CO2 and mass transport in catalysts. Covalent organic frameworks (COFs), as a kind of porous material, have been widely explored as catalysts for the chemical conversion of CO2 owing to their unique features. In particular, COF‐based functional materials containing diverse active sites (such as single metal sites, metal nanoparticles, and metal oxides) offer great potential for realizing CO2 conversion and energy storage. This Minireview discusses recent breakthroughs in the basic knowledge, mechanisms, and pathways of chemical CO2 conversion strategies that use COF‐based functional catalysts. In addition, the challenges and prospects of COF‐based functional catalysts for the efficient utilization of CO2 are also introduced.

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The objective of this study was to develop a novel scaffold imitating the ingredients and their ratios of natural dermal matrix and to evaluate its biological activity. We applied different ratios and different synthetic methods to fabricate nine kinds of cross-linked (CL) collagen/chondroitin sulfate/hyaluronic acid (Co/CS/HA) scaffolds for dermal tissue engineering. On the basis of comparison among the morphology, mechanical properties, and biodegradation rates of scaffolds, we selected the novel scaffold that was fabricated under unique procedures. In the procedures, Co, CS, and HA were firstly synthesized together in the ratio of 9:1:1 to form a membrane that was then CL with 5 mM of 1-ethyl-3-3-dimethylaminopropylcarbodiimide hydrochloride (EDC) (Co-CS-HA/CL 9:1:1). From the results of comparison, we also found that the ratio of 9:1:1 was better than other ratios. So the scaffold of Co-CS-HA/CL 9:1:1 was used as experimental group with the scaffolds of Co-HA/CS CL 9:1:1 and Co-CS/HA CL 9:1:1 as control groups to evaluate their characteristics in vitro. A control group of an open wound without scaffold was supplemented to evaluate their effects on promoting wound healing in vivo. Morphological observation showed that the novel Co-CS-HA/CL 9:1:1 scaffold had uniform and widely interconnected pores with mean diameters of 109 +/- 11 microm and adequate porosity of about 94%. Mechanical property and biodegradation assessment indicated that it had more degradation-resistant and higher elastic modulus than other scaffolds. Metabolic activity assay showed that it could more strongly promote cellular attachment and proliferation. When scaffolds were seeded with allogenic skin fibroblasts and implanted on the dorsum of Sprague-Dawley rats for 6 weeks, the novel Co-CS-HA/CL 9:1:1 skin equivalent could more successfully repair full thickness skin defects in Sprague-Dawley rats. The histology was more approximate to normal skin than those of the controls within 6 weeks. These results demonstrated that the novel CoCS-HA/CL 9:1:1 tri-copolymer has the potential to be used as a scaffold for dermal tissue engineering.

Cancer cell–intrinsic programmed cell death protein-1 (PD-1) has emerged as a tumor regulator in an immunity-independent manner, but its precise role in modulating tumor behaviors is complex, and how PD-1 is regulated in cancer cells is largely unknown. Here, we identified PD-1 as a direct target of tumor suppressor p53. Notably, p53 acetylation at K120/164 played a critical role in p53-mediated PD-1 transcription. Acetylated p53 preferentially recruited acetyltransferase cofactors onto PD-1 promoter, selectively facilitating PD-1 transcription by enhancing local chromatin acetylation. Reexpression of PD-1 in cancer cells inhibited tumor growth, whereas depletion of cancer cell–intrinsic PD-1 compromised p53-dependent tumor suppression. Moreover, histone deacetylase inhibitor (HDACi) activated PD-1 in an acetylated p53–dependent manner, supporting a synergistic effect by HDACi and p53 on tumor suppression via stimulating cancer cell–intrinsic PD-1. Our study reveals a mechanism for activating cancer cell–intrinsic PD-1 and indicates that p53-mediated PD-1 activation is critically involved in tumor suppression in an immunity-independent manner.

Canavan disease (CD) is a leukodystrophy caused by aspartoacylase (ASPA) gene mutation with no cure so far. In this study, a functional ASPA was introduced into patient iPSC‐derived neural progenitor cells (iNPCs) and the engineered ASPA iNPCs could rescue major pathological features of CD in a disease mouse model. These patient iPSC‐derived cellular products are promising cell therapies for CD patients. [Image designed and prepared by Olivia Sun]

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Eight new sesquiterpenoids (1-8), two new diterpenoids (9 and 10), and 17 known sesqui- and diterpenoids (11-27) were isolated from the radix of Curcuma aromatica. Among these compounds, 1 is an unprecedented guaiane with unique cyclopropane and furan functionalities, and 9 is the first atisane diterpenoid isolated from a Curcuma species. Their 2D and 3D structures were established using HRESIMS and spectroscopic methods, including ECD and IECD data. The antioxidant activities of compounds 1-27 were evaluated based on their ability to protect PC12 cells against HO-induced damage, with 1, 2, 5-8, 11, 12, 14, 16, 18, and 19 exhibiting notable antioxidant effects on oxidative injury induced by HO.