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This study presents a stable oxygen isotope (δ18O) record in daily precipitation from two sites located to the northeast of the Tibetan Plateau (TP): Yushu on the eastern TP and Xi'an on the eastern Chinese Loess Plateau. It attempts to reveal the unique features associated with variations in atmospheric circulation patterns over inland China. For δ18O in daily precipitation at both stations, temperature effect is significant (p < 0.01) only during non-monsoon, while amount effect is significant only during monsoon. This suggests the coexistence of local recycling with large-scale atmospheric circulation on regional precipitation, which is further verified by the significant correlation of relative humidity with δ18O at both stations during monsoon season. The similarity of δ18O in regions under the supposedly same atmospheric circulation streams is tested for Yushu with that at Lhasa, Lulang and Delingha, demonstrating the lag days of δ18O depletion at Yushu with that at Lulang as varying from 15 to 25 d. This confirms the Bay of Bengal monsoon dominance over Yushu. Daily δ18O at Xi'an is compared with contemporary data at Changsha and Guangzhou, featuring a close correlation with the East Asian summer monsoon evolution processes over eastern China, and reflecting the Meiyu-Baiu front influence during July. Back-trajectory analysis in October–November at Xi'an identified the combined effect of cooling of the atmospheric column by the colder air from the west and the lifting of the warmer air from the east, which coexists with local water vapour source. Interactions of the three result in condensation at lower temperatures that is coupled with the long-distance transport of 2/3 of the available water vapour, thus leading to extremely low δ18O values in the post-monsoon precipitation.

Increasing penetration of electric vehicles (EVs) gives rise to the challenges in the secure operation of power systems. The EV charging loads should be distributed among charging stations in a fair and incentive-compatible manner while ensuring that power transmission and transformation facilities are not overloaded. This paper first proposes a charging right (or charging power ration) trading mechanism and model based on blockchain. Considering all kinds of random factors of charging station loads, we use Monte Carlo modeling to determine the charging demand of charging stations in the future. Based on the charging demand of charging stations, a charging station needs to submit the charging demand for a future period. The blockchain first distributes initial charging right in a just manner and ensures the security of facilities. Given that the charging urgency and elasticity differences vary by charging stations, all charging stations then proceed with double auction and peer-to-peer (P2P) transaction of charging right. Bids and offers are cleared via double auctions if bids are higher than offers. The remaining bids and offers are cleared via the P2P market. Then, this paper designs the charging right allocation and trading platform and smart contract based on the Ethernet blockchain to ensure the safety of the distribution network (DN) and the transparency and efficiency of charging right trading. Simulation results based on the Ethereum private blockchain show the fairness and efficiency of the proposed mechanism and the effectiveness of the method and the mechanism.

Parkinson's disease (PD) is characterized by age-dependent neurodegeneration and the accumulation of toxic phosphorylated α-synuclein (pS129-α-syn). The mechanisms underlying these crucial pathological changes remain unclear. Mutations in parkin RBR E3 ubiquitin protein ligase (PARK2), the gene encoding parkin that is phosphorylated by PTEN-induced putative kinase 1 (PINK1) to participate in mitophagy, cause early onset PD. However, current parkin-KO mouse and pig models do not exhibit neurodegeneration. In the current study, we utilized CRISPR/Cas9 technology to establish parkin-deficient monkey models at different ages. We found that parkin deficiency leads to substantia nigra neurodegeneration in adult monkey brains and that parkin phosphorylation decreases with aging, primarily due to increased insolubility of parkin. Phosphorylated parkin is important for neuroprotection and the reduction of pS129-α-syn. Consistently, overexpression of WT parkin, but not a mutant form that cannot be phosphorylated by PINK1, reduced the accumulation of pS129-α-syn. These findings identify parkin phosphorylation as a key factor in PD pathogenesis and suggest it as a promising target for therapeutic interventions. [ABSTRACT FROM AUTHOR]

Neuronal death plays a crucial role in early brain injury after subarachnoid hemorrhage (SAH). PANoptosis is a programmed form of cell death regulated by the PANoptosome, which possesses key characteristics of pyroptosis, apoptosis and necroptosis. Phosphoglycerate mutase family member 5 (PGAM5) has specific phosphatase activity that phosphorylates or dephosphorylates serine and threonine residues on bound proteins such as receptor-interacting protein kinase 1 (RIPK1), which are involved in programmed cell death. This study aimed to explore whether PANoptosis occurs after subarachnoid hemorrhage and to investigate the role of PGAM5 in early brain injury after SAH. A monofilament perforation SAH model in Sprague–Dawley rats was established, and PGAM5 siRNA (siPGAM5) was administered via intracerebroventricular injection 48 h before SAH modeling. The efficacy of siPGAM5 treatment was assessed via neurological scoring, and the impact of siPGAM5 on PANoptosis was evaluated via Western blotting, TUNEL staining and ELISA. To investigate its potential mechanism, the RIPK1 activator birinapant was administered intraperitoneally 0.5 h after SAH. The role of RIPK in PGAM5-mediated PANoptosis was evaluated by Western blotting and coimmunoprecipitation. Our findings indicate that PANoptosis occurs in neurons after SAH and that reducing PGAM5 in the cytosol after SAH can reduce PANoptosis and enhance the short-term and long-term neurological functions of SAH rats. Mechanistically, we discovered that PGAM5 can directly bind to and phosphorylate and activate RIPK1 (ser 166), triggering the assembly of the RIPK1-PANoptosome complex. In conclusion, our study revealed that the increased PGAM5 in the mitochondria-free cytosol after SAH can bind to and activate RIPK1 (ser 166), driving the assembly of the RIPK1-PANoptosome and mediating PANoptosis after SAH. PGAM5 and PANoptosis might be novel therapeutic targets for SAH. [Display omitted] • PGAM5 is increased in the cytosol after SAH. • PANoptosis occurs in brain tissue neurons after SAH. • PGAM5 can directly phosphorylate and activate RIPK1 (ser 166). • PGAM5 and RIPK1 mediate the occurrence of PANoptosis after SAH. [ABSTRACT FROM AUTHOR]