Objective: Stress is a known trigger for seizures in patients with epilepsy (PWE). However, the association between stress and seizures has not been thoroughly investigated. In December 2019, an outbreak of coronavirus disease (COVID-19) occurred in Wuhan, Hubei province, China, causing tremendous collateral stress. This study was designed to evaluate the influence of the COVID-19 outbreak on seizures in PWE in the most severely affected area, Wuhan, and its surrounding cities. Methods: In this single-center, cross-sectional study, PWE were surveyed via online questionnaires between February 23 and March 5, 2020. Collected data included demographic information, epilepsy-related characteristics (seizure type, frequency, antiepileptic drugs [AEDs], and medication management), direct and perceived threat of COVID-19, and changes in seizures during the outbreak. Psychological comorbidities were evaluated by the Patient Health Questionnaire-9, Generalized Anxiety Disorder-7 items, and Insomnia Severity Index (ISI). Multivariate logistic regression was used to identify precipitants for seizure exacerbation. Results: We received 362 completed questionnaires after excluding 12 duplicates (response rate = 63.51%). A total of 31 (8.56%) patients had increased seizures during the outbreak. Exposure history to COVID-19 (P = .001), uncontrolled seizure after AED therapy (P = .020), seizure frequency of two or more times per month before the outbreak (P = .005), change of AED regimen during the outbreak (AED reduction, withdrawal, replacement, skipping altogether; P = .002), and worry about the adverse effect of the outbreak on overall seizure-related issues (severity = moderate to critical; P = .038) were risk factors for increased seizures. Significance: A minority of PWE experienced seizure exacerbation during the outbreak of COVID-19. Stress, uncontrolled seizures, and inappropriate change in AED regimen were associated with increased seizures. Based on these findings, stress might be an independent precipitant for triggering seizures in some PWE.

Despite increasing recognition of the importance of GM-CSF in autoimmune disease, it remains unclear how GM-CSF is regulated at sites of tissue inflammation. Using GM-CSF fate reporter mice, we show that synovial NK cells produce GM-CSF in autoantibody-mediated inflammatory arthritis. Synovial NK cells promote a neutrophilic inflammatory cell infiltrate, and persistent arthritis, via GM-CSF production, as deletion of NK cells, or specific ablation of GM-CSF production in NK cells, abrogated disease. Synovial NK cell production of GM-CSF is IL-18–dependent. Furthermore, we show that cytokine-inducible SH2-containing protein (CIS) is crucial in limiting GM-CSF signaling not only during inflammatory arthritis but also in experimental allergic encephalomyelitis (EAE), a murine model of multiple sclerosis. Thus, a cellular cascade of synovial macrophages, NK cells, and neutrophils mediates persistent joint inflammation via production of IL-18 and GM-CSF. Endogenous CIS provides a key brake on signaling through the GM-CSF receptor. These findings shed new light on GM-CSF biology in sterile tissue inflammation and identify several potential therapeutic targets.

Natural killer (NK) cells are a specialised population of innate lymphoid cells (ILCs) that help control local immune responses. Through natural cytotoxicity, production of cytokines and chemokines, and migratory capacity, NK cells play a vital immunoregulatory role in the initiation and chronicity of inflammatory and autoimmune responses. Our understanding of their functional differences and contributions in disease settings is evolving owing to new genetic and functional murine proof‐of‐concept studies. Here, we summarise current understanding of NK cells in several classic autoimmune disorders, particularly in rheumatoid arthritis (RA), multiple sclerosis (MS), systemic lupus erythematosus (SLE) and type 1 diabetes mellitus (T1DM), but also less understood diseases such as idiopathic inflammatory myopathies (IIMs). A better understanding of how NK cells contribute to these autoimmune disorders may pave the way for NK cell‐targeted therapeutics.

Tens of miRNAs were previously established as being arsenic (As) stress responsive in rice. However, their functional role in As tolerance remains unclear. This study demonstrates that transgenic plants overexpressing miR528 (Ubi::MIR528) were more sensitive to arsenite [As(III)] compared with wild-type (WT) rice. Under normal and stress conditions, miR528-5p and -3p were highly up-regulated in both the roots and leaves of transgenic plants, which exhibited a negative correlation with the expression of seven target genes. Compared with WT plants, Ubi::MIR528 plants showed excessive oxidative stress generation and remarkable amino acid content changes in the roots and leaves upon As(III) exposure. Notably, the expression profiles of diverse functional genes were clearly different between WT and transgenic plants. Thus, the observed As(III) sensitivity of Ubi::MIR528 plants was likely due to the strong alteration of antioxidant enzyme activity and amino acid profiles and the impairment of the As(III) uptake, translocation, and tolerance systems of rice.

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Boron neutron capture therapy (BNCT) was first proposed as early as 1936, and research on BNCT has progressed relatively slowly but steadily. BNCT is a potentially useful tool for cancer treatment that selectively damages cancer cells while sparing normal tissue. BNCT is based on the nuclear reaction that occurs when 10B capture low-energy thermal neutrons to yield high-linear energy transfer (LET) α particles and recoiling 7Li nuclei. A large number of 10B atoms have to be localized within the tumor cells for BNCT to be effective, and an adequate number of thermal neutrons need to be absorbed by the 10B atoms to generate lethal 10B (n, α)7Li reactions. Effective boron neutron capture therapy cannot be achieved without appropriate boron carriers. Improvement in boron delivery and the development of the best dosing paradigms for both boronophenylalanine (BPA) and sodium borocaptate (BSH) are of major importance, yet these still have not been optimized. Here, we present a review of this treatment modality from the perspectives of radiation oncology, biology, and physics. This manuscript provides a brief introduction of the mechanism of cancer-cell-selective killing by BNCT, radiobiological factors, and progress in the development of boron carriers and neutron sources as well as the results of clinical study.