Potassium-ion batteries (PIBs) are emerging as promising next-generation electrochemical storage systems for their abundant and low-cost potassium resource. The key point of applying PIBs is to exploit stable K-host materials to accommodate the large-sized potassium ion. In this work, a yolk−shell structured MoS 2 @hollow porous carbon-sphere composite (MoS 2 @HPCS) assembled by engineering HPCSconfined MoS 2 with expanded (002) planes is proposed for boosting potassium-ion storage. When used as a PIB anode, the as-synthesized MoS 2 @HPCS composite shows superior potassium storage performance. It delivers a reversible capacity of 254.9 mAh g −1 at 0.5 A g −1 after 100 discharge/charge cycles and maintains 126.2 mAh g −1 at 1 A g −1 over 500 cycles. The superior potassium-ion storage performance is ascribed to the elaborate yolk−shell nanoarchitecture and the expanded interlayer of the MoS 2 nanosheet, which could shorten the transport distance, enhance the electronic conductivity, relieve the volume variation, prevent the self-aggregation of MoS 2 , facilitate the electrolyte penetration, and boost the intercalation/deintercalation of K + . Moreover, the potential application of the MoS 2 @HPCS composite is also evaluated by assembled K-ion full cells with a perylenetetracarboxylic dianhydride cathode. Accordingly, the as-developed synthetic strategy can be extended to manufacture other host materials for PIBs and beyond.

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The balance between bone formation and bone resorption is closely related to bone homeostasis. Osteoclasts, originating from the monocyte/macrophage lineage, are the only cell type possessing bone resorption ability. Osteoclast overactivity is thought to be the major reason underlying osteoclast‐related osteolytic problems, such as Paget's disease, aseptic loosening of prostheses and inflammatory osteolysis; therefore, disruption of osteoclastogenesis is considered a crucial treatment option for these issues. WKYMVm, a synthetic peptide, which is a potent FPR2 agonist, exerts an immunoregulatory effect. This peptide inhibits the production of inflammatory cytokines, such as (IL)‐1β and TNF‐α, thus regulating inflammation. However, there are only few reports on the role of WKYMVm and FPR2 in osteoclast cytology. In the current study, we found that WKYMVm negatively regulates RANKL‐ and lipopolysaccharide (LPS)‐induced osteoclast differentiation and maturation in vitro and alleviates LPS‐induced osteolysis in animal models. WKYMVm down‐regulated the expression of osteoclast marker genes and resorption activity. Furthermore, WKYMVm inhibited osteoclastogenesis directly through reducing the phosphorylation of STAT3 and NF‐kB and indirectly through the CD9/gp130/STAT3 pathway. In conclusion, our findings demonstrated the potential medicinal value of WKYMVm for the treatment of inflammatory osteolysis.

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