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In this paper, we try to design the joint waveform and passive beamforming within the context of dual-function radar–communication (DFRC) systems. Focusing on the intricate trade-off between stringent radar beampattern constraints and their desired performance, we introduce a novel manifold idea based on the alternating direction method of multipliers (ADMM) framework. Specifically, our proposed method, named DFRC-MA, could address the challenge of constant modulus waveform design in a multiple-input–multiple-output (MIMO) DFRC system. Firstly, our methodology begins by formulating the reference waveform to achieve an optimal radar beamforming pattern. Subsequently, we define the DFRC optimization problem to mitigate the multi-user interference (MUI) under the constant modulus constraint. Through a series of simulations, we evaluate the efficacy of DFRC-MA, where the integrated waveform designed by DFRC-MA exhibits superior performance over some prevalent ones. [ABSTRACT FROM AUTHOR]

With the continuous increase in the scale of distribution network construction and operation, a large number of electricity load control problems have emerged, especially the weakening of sample time series characteristics in electricity load data analysis, resulting in incomplete acquisition of local load characteristics, making it impossible for the distribution network electricity load prediction system to maintain the balance of energy in the power grid. In the past, the impact of "source-load" uncertainty was also rarely considered in the distribution network electricity load processing and distribution, which can easily lead to low probability of electricity load classification recognition, significant errors in electricity load prediction, and long-term problems such as high generation costs and insufficient distribution balance. In response to the above situation, the uncertainty of "source" and "load" was conducted research through probability distribution functions. A multi-objective function composed of two probability distribution functions was set as the constraint conditions for the coordinated output balance. The improved cluster eddy current search algorithm was used to solve the problem, and a coordinated control scheme for electricity load was obtained. The test results show that at 17: 00, the power of photovoltaic device 1 is 1 050 kW, at 11: 00, the power of photovoltaic device 2 is 980 kW, based on the source-load uncertainty root-mean-square error of less than 0.7%. The cost of the scheme based on "source-load" uncertainty is 453 200 yuan, and the balance degree is 0.94. The collaborative control method based on "source-load" uncertainty has a higher balance than the collaborative control method without "source-load" uncertainty, and the collaborative control technology is more reasonable. [ABSTRACT FROM AUTHOR]

Aims: Colony stimulating factor 1 receptor (CSF1R)‐related leukoencephalopathy is a rapidly progressing neurodegenerative disease caused by CSF1R gene mutations. This study aimed to identify and investigate the effect of a novel intronic mutation (c.1754‐3C>G) of CSF1R on splicing. Methods: A novel intronic mutation was identified using whole‐exome sequencing. To investigate the impact of this mutation, we employed various bioinformatics tools to analyze the transcription of the CSF1R gene and the three‐dimensional structure of its encoded protein. Furthermore, reverse transcription polymerase chain reaction (RT‐PCR) was performed to validate the findings. Results: A novel mutation (c.1754‐3C>G) in CSF1R was identified, which results in exon 13 skipping due to the disruption of the 3′ splice site consensus sequence NYAG/G. This exon skipping event was further validated in the peripheral blood of the mutation carrier through RT‐PCR and Sanger sequencing. Protein structure prediction indicated a disruption in the tyrosine kinase domain, with the truncated protein showing significant structural alterations. Conclusions: Our findings underscore the importance of intronic mis‐splicing mutations in the diagnosis and management of CSF1R‐related leukoencephalopathy. [ABSTRACT FROM AUTHOR]

Background: To date, most existing models for predicting neuromyelitis optica spectrum disorder (NMOSD) are based primarily on clinical characteristics. Blood‐based NMOSD severity and prognostic predictive immune‐ and inflammation‐related biomarkers are needed. We aimed to investigate the associations between plasma inflammatory biomarkers and relapse and attack severity in NMOSD. Methods: This two‐step, single‐center prospective cohort study included discovery and validation cohorts. We quantified 92 plasma inflammatory proteins by using Olink's proximity extension assay and identified differentially expressed proteins in the relapse group (relapse within 1 year of follow‐up) and severe attack group. To define a new molecular prognostic model, we calculated the risk score of each patient based on the key protein signatures and validated the results in the validation cohort. Results: The relapse prediction model, including FGF‐23, DNER, GDNF, and SLAMF1, predicted the 1‐year relapse risk. The severe attack prediction model, including PD‐L1 and MCP‐2, predicted the severe clinical attack risk. Both the relapse and severe attack prediction models demonstrated good discriminative ability and high accuracy in the validation cohort. Conclusions: Our discovered biomarker signature and prediction models may complement current clinical risk stratification approaches. These inflammatory biomarkers could contribute to the discovery of therapeutic interventions and prevent NMOSD progression. [ABSTRACT FROM AUTHOR]

Maternal histone methyltransferase is critical for epigenetic regulation and development of mammalian embryos by regulating histone and DNA modifications. Here, we reported a novel mechanism by revealing the critical effects of maternal Ezh1/2 deletion on mitochondria in MII oocytes and early embryos in mice. We found that Ezh1/2 knockout in mouse MII oocytes impaired the structure of mitochondria and decreased its number, but membrane potential and respiratory function of mitochondrion were increased. The similar effects of Ezh1/2 deletion have been observed in 2‐cell and morula embryos, indicating that the effects of maternal Ezh1/2 deficiency on mitochondrion extend to early embryos. However, the loss of maternal Ezh1/2 resulted in a severe defect of morula: the number, membrane potential, respiratory function, and ATP production of mitochondrion dropped significantly. Content of reactive oxygen species was raised in both MII oocytes and early embryos, suggesting maternal Ezh1/2 knockout induced oxidative stress. In addition, maternal Ezh1/2 ablation interfered the autophagy in morula and blastocyst embryos. Finally, maternal Ezh1/2 deletion led to cell apoptosis in blastocyst embryos in mice. By analyzing the gene expression profile, we revealed that maternal Ezh1/2 knockout affected the expression of mitochondrial related genes in MII oocytes and early embryos. The chromatin immunoprecipitation‐polymerase chain reaction assay demonstrated that Ezh1/2 directly regulated the expression of genes Fxyd6, Adpgk, Aurkb, Zfp521, Ehd3, Sgms2, Pygl, Slc1a1, and Chst12 by H3K27me3 modification. In conclusion, our study revealed the critical effect of maternal Ezh1/2 on the structure and function of mitochondria in oocytes and early embryos, and suggested a novel mechanism underlying maternal epigenetic regulation on early embryonic development through the modulation of mitochondrial status. [ABSTRACT FROM AUTHOR]