There have been several cases of large-scale wind generators (WGs) tripping off caused by untimely fault removing in recent years. Currently, the discoordination between the box-type transformer fuse protection (BTFP) and two-section collecting line current protection (CLCP) brings a security risk to wind farm. In order to ensure the selectivity, the first section (Sec-I) CLCP should be set a enough interval that is longer than the fuse melting time, and another interval is set for the Sec-II CLCP, which weakens the speed of the CLCP. When a fault occurs on the collecting line, there is no doubt that WGs cannot work too long in abnormal operation, which may cause WGs to be placed off the grid. For a power system with high penetration of wind power, large-scale WGs tripping off will cause a great power shortage, and affect the stability of the power system. The selectivity and sensitivity of the CLCP is analyzed in detail to make the CLCP speed better. Considering the fault ride-through ability of WGs, the fault clear time is an important factor to lead to large-scale WGs tripping off. Two main works are done in this paper. The first is to accelerate the speed of the Sec-I CLCP though reducing the protection zone. Another one is introduce the risk assessment module into the CLCP, which not only improve the speed of the CLCP but also ensure the safety of the wind farm during faults. According to the deference in trip-off causes of WGs, the matching functions are created to assess the trip-off risk of WGs on the spot. In the case of fault, the trip-off risk indicators of WGs are timely updated to data sharing center and open to the CLCPs. The set of risk indicators is divided into several subsets according to the risk range. The dynamic changes of the subsets during fault help to improved CLCP scheme. This scheme can accelerate protection speed based on the increasing risk of large-scale WGs tripping off in wind farms. Compared with traditional CLCP, this approach can make the CLCP combines selectivity and speed better based on the analysis of the ride- through ability of WGs.

Vaccines trigger a complicated immunological response that includes B and T cells, with B cells producing antibodies. SARS-CoV-2 immunity weakens over time after vaccination. Discovering key changes in antigen-reactive antibodies over time after vaccination could help improve vaccine efficiency. In this study, we collected data on blood antibody levels in a cohort of healthcare workers vaccinated for COVID-19 and obtained 73 antigens in samples from four groups according to the duration after vaccination, including 104 unvaccinated healthcare workers, 534 healthcare workers within 60 days after vaccination, 594 healthcare workers between 60 and 180 days after vaccination, and 141 healthcare workers over 180 days after vaccination. An efficient machine learning based framework containing four feature selection methods (least absolute shrinkage and selection operator, light gradient boosting machine, Monte Carlo feature selection, and maximum relevance minimum redundancy) and four classification algorithms (decision tree, k-nearest neighbor, random forest, and support vector machine) was designed to screen out essential antigens. Several efficient classifiers with weighted F1 value around 0.75 were constructed. This study revealed that S1+S2, S1.mFcTag, S1.HisTag, S1, S2, Spike.RBD.His.Bac, Spike.RBD.rFc, and S1.RBD.mFc were most highly ranked among all features, where S1 and S2 are the subunits of Spike, and the suffixes represent the tagging information of different recombinant proteins. Meanwhile, the classification rules were extracted from the optimal decision tree to explain quantitatively the roles of antigens in the classification. This study identified antibodies associated with decreased clinical immunity based on populations with different time spans after vaccination. These antibodies have important implications for maintaining long-term immunity to SARS-CoV-2.

Meiosis is a specialized cell division that produces haploid gametes from diploid germ cells, and the phosphorylation activity of cyclin-CDK complexes and Polo-like kinase is required for synaptonemal complex (SC) disassembly and metaphase I exit. Here, we identified a novel protein MSCDK (meiotic substrate of cyclin dependent kinase) that functions as a substrate of CDK1 in initiating SC disassembly and metaphase I transition during meiosis prophase I in mice. Deletion of MSCDK caused germ cell death and infertility in males but not females. Mechanistically, we show that MSCDK is sparsely localized as discrete foci along synaptic homologous chromosomes from the early zygotene to the early diplotene, and we confirm that MSCDK can be phosphorylated by CDK1 and dephosphorylated by the cell cycle exit regulator phosphatase PP1α. We also provide evidence that MSCDK is essential for SC disassembly based on its dephosphorylation-related function, which apparently promotes HSPA2 nuclear recruitment.

The development of a method to produce coumarins unsubstituted on the pyranic nucleus catalyzed from Wells–Dawson heteropolyacid (H₆P₂W₁₈O₆₂), phenol derivatives and ethyl 3,3-diethoxypropionate using Pechmann condensation under solvent-free conditions is described. This catalytic method was also applied successfully to synthesize various substituted coumarins, including the corresponding phenols and ethyl 3,3-diethoxypropionate. This work provides a novel, cheaper and safer way to syhthesize coumarins unsubstituted on the pyranic nucleus.

African swine fever virus (ASFV), a highly contagious pathogen characterized by a complex structure and a variety of immunosuppression proteins, causes hemorrhagic, acute, and aggressive infectious disease that severely injure the pork product and industry. However, there is no effective vaccine or treatment. The main reasons are not only the complex mechanisms that lead to immunosuppression, but also the unknown functions of various proteins. This review summarizes the interaction between ASFV and host immune system, along with the involvement of virulence related genes and proteins, as well as the corresponding molecular mechanism of immunosuppression of ASFV, encompassing pathways such as cGAS-STING, NF-κB, JAK/STAT, apoptosis, and other modulation. The aim is to summarize the dynamic process during the ASFV infection and entry into host cell, provide a rational insight into development of vaccine and a better clear knowledge of how ASFV impacts host.