On par with lithium-ion
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ToF-SIMS sputter depth profiling of interphases and coatings on lithium metal surfaces
Lithium metal as a negative electrode material offers ten times the specific capacity of graphitic electrodes, but its rechargeable operation poses challenges like excessive and continuous interphase formation, high surface area lithium deposits and safety issues. Improving the lithium | electrolyte interface and interphase requires powerful surface analysis techniques, such as ToF-SIMS sputter depth profiling.This study investigates lithium metal sections with an SEI layer by ToF-SIMS using different sputter ions. An optimal sputter ion is chosen based on the measured ToF-SIMS sputter depth profiles and SEM analysis of the surface damage. Further, this method is adapted to lithium metal foil with an intermetallic coating. ToF-SIMS sputter depth profiles in both polarities provide comprehensive insights into the coating structure. Both investigations highlight the value of ToF-SIMS sputter depth profiling in lithium metal battery research and offer guidance for future studies.
STING directly interacts with PAR to promote apoptosis upon acute ionizing radiation-mediated DNA damage
Acute ionizing radiation (IR) causes severe DNA damage, leading to cell cycle arrest, cell death, and activation of the innate immune system. The role and signaling pathway of stimulator of interferon genes (STING) in IR-induced tissue damage and cell death are not well understood. This study revealed that STING is crucial for promoting apoptosis in response to DNA damage caused by acute IR both in vitro and in vivo. STING binds to poly (ADP‒ribose) (PAR) produced by activated poly (ADP‒ribose) polymerase-1 (PARP1) upon IR. Compared with that in WT cells, apoptosis was suppressed in Stinggt-/gt- cells. Excessive PAR production by PARP1 due to DNA damage enhances STING phosphorylation, and inhibiting PARP1 reduces cell apoptosis after IR. In vivo, IR-induced crypt cell death was significantly lower in Stinggt-/gt- mice or with low-dose PARP1 inhibitor, PJ34, resulting in substantial resistance to abdominal irradiation. STING deficiency or inhibition of PARP1 function can reduce the expression of the proapoptotic gene PUMA, decrease the localization of Bax on the mitochondrial membrane, and thus reduce cell apoptosis. Our findings highlight crucial roles for STING and PAR in the IR-mediated induction of apoptosis, which may have therapeutic implications for controlling radiation-induced apoptosis or acute radiation symptoms.
The evolution of lithium-ion battery recycling
Demand for lithium-ion batteries (LIBs) is increasing owing to the expanding use of electrical vehicles and stationary energy storage. Efficient and closed-loop battery recycling strategies are therefore needed, which will require recovering materials from spent LIBs and reintegrating them into new batteries. In this Review, we outline the current state of LIB recycling, evaluating industrial and developing technologies. Among industrial technologies, pyrometallurgy can be broadly applied to diverse electrode materials but requires operating temperatures of over 1,000 °C and therefore has high energy consumption. Hydrometallurgy can be performed at temperatures below 200 °C and has material recovery rates of up to 93% for lithium, nickel and cobalt, but it produces large amounts of wastewater. Developing technologies such as direct recycling and upcycling aim to increase the efficiency of LIB recycling and rely on improved pretreatment processes with automated disassembly and cleaner mechanical separation. Additionally, the range of materials recovered from spent LIBs is expanding from the cathode materials recycled with established methods to include anode materials, electrolytes, binders, separators and current collectors. Achieving an efficient recycling ecosystem will require collaboration between recyclers, battery manufacturers and electric vehicle manufacturers to aid the design and automation of battery disassembly lines.
Improving the fast-charging capability of NbWO-based Li-ion batteries
The discovery of Nb-W-O materials years ago marks the milestone of charging a lithium-ion battery in minutes. Nevertheless, for many applications, charging lithium-ion battery within one minute is urgently demanded, the bottleneck of which largely lies in the lack of fundamental understanding of Li+ storage mechanisms in these materials. Herein, by visualizing Li+ intercalated into representative Nb16W5O55, we find that the fast-charging nature of such material originates from an interesting rate-dependent lattice relaxation process associated with the Jahn-Teller effect. Furthermore, in situ electron microscopy further reveals a directional, [010]-preferred Li+ transport mechanism in Nb16W5O55 crystals being the “bottleneck” toward fast charging that deprives the entry of any desolvated Li+ through the prevailing non-(010) surfaces. Hence, we propose a machine learning-assisted interface engineering strategy to swiftly collect desolvated Li+ and relocate them to (010) surfaces for their fast intercalation. As a result, a capacity of ≈ 116 mAh g−1 (68.5% of the theoretical capacity) at 80 C (45 s) is achieved when coupled with a Li negative electrode.
RECQL4 requires PARP1 for recruitment to DNA damage, and PARG dePARylation facilitates its associated role in end joining
RecQ helicases, highly conserved proteins with pivotal roles in DNA replication, DNA repair and homologous recombination, are crucial for maintaining genomic integrity. Mutations in RECQL4 have been associated with various human diseases, including Rothmund–Thomson syndrome. RECQL4 is involved in regulating major DNA repair pathways, such as homologous recombination and nonhomologous end joining (NHEJ). RECQL4 has more prominent single-strand DNA annealing activity than helicase activity. Its ability to promote DNA damage repair and the precise role of its DNA annealing activity in DNA repair are unclear. Here we demonstrate that PARP1 interacts with RECQL4, increasing its single-stranded DNA strand annealing activity. PARP1 specifically promoted RECQL4 PARylation at both its N- and C-terminal regions, promoting RECQL4 recruitment to DNA double-strand breaks (DSBs). Inhibition or depletion of PARP1 significantly diminished RECQL4 recruitment and occupancy at specific DSB sites on chromosomes. After DNA damage, PARG dePARylated RECQL4 and stimulated its end-joining activity. RECQL4 actively displaced replication protein A from single-stranded DNA, promoting microhomology annealing in vitro. Furthermore, depletion of PARP1 or RECQL4 substantially impacted classical-NHEJ- and alternative-NHEJ-mediated DSB repair. Consequently, the combined activities of PARP1, PARG and RECQL4 modulate DNA repair.
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