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Facing the challenges of in-situ utilization of lunar regolith resources, applying an external electric field to manipulate lunar particles has become a promising method for space particle control, which mainly depends on the particle charging properties in the applied electric field. Using the surficial lunar regolith samples brought back from the Moon by the Chang’e-5 mission (CE5 LS), this work successively studied their charging properties, particle dynamics, and their collision damages to aerospace materials under the action of an external electric field in high-vacuum conditions. The results indicated that the charging process and electrostatic projection of lunar regolith particles under high-vacuum conditions were different from those under atmosphere conditions. The particle diameter range of CE5 LS used in the experiment is 27.7–139.0 μm. For electric field strength of 3–12 kV·cm−1, the charge obtained by CE5 LS is 4.8 × 10−15–4.7 × 10−13 C and the charge-to-mass ratio is 1.2 × 10−5–6.8 × 10−4 C·kg−1. The CE5 LS is easier to be negatively charged in an external electric field. Furthermore, significant damages were observed on the target impact surfaces, indicating severe influences of lunar regolith particles on aerospace materials. Our work contributes to a more comprehensive understanding of physical mechanisms controlling the lunar regolith shielding and utilization, and will inspire broad efforts to develop the lunar in-situ engineering solutions.

Summary: Hydroxycarboxylic acid receptor 3 (HCAR3), a class A G-protein-coupled receptor, is an important cellular energy metabolism sensor with a key role in the regulation of lipolysis in humans. HCAR3 is deeply involved in many physiological processes and serves as a valuable target for the treatment of metabolic diseases, tumors, and immune diseases. Here, we report four cryoelectron microscopy (cryo-EM) structures of human HCAR3-Gi1 complexes with or without agonists: the endogenous ligand 3-hydroxyoctanoic acid, the drug niacin, the highly subtype-specific agonist compound 5c (4-(n-propyl)amino-3-nitrobenzoic acid), and the apo form. Together with mutagenesis and functional analyses, we revealed the recognition mechanisms of HCAR3 for different agonists. In addition, the key residues that determine the ligand selectivity between HCAR2 and HCAR3 were also illuminated. Overall, these findings provide a structural basis for the ligand recognition, activation, and selectivity and G-protein coupling mechanisms of HCAR3, which contribute to the design of HCAR3-targeting drugs with high efficacy and selectivity.

The cost of building a lunar outpost can be greatly reduced by adopting melting of lunar regolith using concentrated solar energy beam based on in-situ additive manufacturing, there are still considerable obstacles to boosting the compactness and mechanical strength of the fabricated samples. The exploration of optimizing process parameters to address the above challenges are severely limited by solar time and space on Earth. Herein, a system for millimeter-scale energy beam melting of the lunar regolith simulant was set up to investigate the effects of process parameters, including laser power, scanning speed, hatching space (track overlapping ratio), and powder layer thickness (layer overlapping ratio) on the processes of single-track, multi-track, and multi-layer forming. The best range of single-track forming quality is the regular type with linear energy density of 27.5–100 J/mm. The surface is smooth and devoid of apparent fissures when the track overlapping rate is between 20% and 45% during the multi-track scanning procedure. For multi-layer sample forming, Samples with high density and few defects appear in the range of 45%–73% layer overlapping rate. The process parameters window for sample forming is determined by the combination of linear energy density, track overlapping rate, and layer overlapping rate. The relative density of single-track, multi-track, and multi-layer increases sequentially under the action of remelting, reaching 62.9%, 70%, and 86%, respectively. The average compressive strength of the test specimen is 5.6 MPa satisfies the specifications for the load-bearing structures on the moon. These results would provide essential data for the development of in-situ additive manufacturing.

Here, using cryo-electron microscopy and solution NMR, the authors reveal the structural and dynamic mechanisms underlying the signaling versatility of a muscarinic receptor regulated by orthosteric and allosteric ligands.

Melatonin receptors (MT1 and MT2) are the targets for melatonin, the major neurohormone involved in circadian rhythm and sleep regulation. Here the authors describe the structures of 2-iodomelatonin and ramelteon bound MT1–Gi and MT2-Gi, revealing that MT1 and MT2 possess distinctive features within the ligand-binding pocket.

Abstract Evidence has demonstrated that microRNA-342-5p (miR-342-5p) is implicated in atherosclerosis (AS), but little is known regarding its intrinsic regulatory mechanisms. Here, we aimed to explore the effect of miR-342-5p targeting Wnt3a on formation of vulnerable plaques and angiogenesis of AS. ApoE−/− mice were fed with high-fat feed for 16 w to replicate the AS vulnerable plaque model. miR-342-5p and Wnt3a expression in aortic tissues of AS were detected. The target relationship between miR-342-5p and Wnt3a was verified. Moreover, ApoE−/− mice were injected with miR-342-5p antagomir and overexpression-Wnt3a vector to test their functions in serum lipid levels, inflammatory and oxidative stress-related cytokines, aortic plaque stability and angiogenesis in plaque of AS mice. miR-342-5p expression was enhanced and Wnt3a expression was degraded in aortic tissues of AS mice and miR-342-5p directly targeted Wnt3a. Up-regulating Wnt3a or down-regulating miR-342-5p reduced blood lipid content, inflammatory and oxidative stress levels, the vulnerability of aortic tissue plaque and inhibited angiogenesis in aortic plaque of AS mice. Functional studies show that depleting miR-342-5p can stabilize aortic tissue plaque and reduce angiogenesis in plaque in AS mice via restoring Wnt3a.