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Objective Objective To investigate the changes in hippocampal astrocytes and neuronal primary cilia, and neuronal apoptosis in the offspring brain of advanced maternal age and the role of LKB1/AMPK pathway. Methods The 12-month-old SD female rats were mated with 3-month-old SD male rats to produce offspring as the advanced maternal age (AMA) group, and the 3-month-old SD female rats were mated with 3-month-old SD males to produce offspring as the appropriate age (Control, Ctl) group. The following studies were conducted on postnatal days 14, 28 and 60 (P14, P28 and P60) in the 2 groups (14 rats per group at each time point, half males and half females). HE staining and Nissl staining were used to observe the changes in the morphology and the number of hippocampal neurons and their internal Nissl bodies. Immunofluorescence assay was employed to detect the expression of hippocampal primary cilia marker, anti-ADP ribosylation factor-like protein-13B (ARL13B), and Western blotting was applied to measure the expression of hippocampal intraflagellar transport protein 88 (IFT88) to assess functional changes in primary ciliogenesis. TUNEL staining and Western blotting were performed to detect the expression levels of pro-apoptotic BAX, and anti-apoptotic protein, BCL-2 to observe the changes of apoptosis in the hippocampus. Western blotting was also used to detect the expression levels of liver kinase B1 (LKB1), adenosine monophosphate-activated protein kinase (AMPK), mammalian target of rapamycin (mTOR) and the levels of their corresponding phosphorylated proteins to assess LKB1/AMPK pathway changes. Results Compared with the Ctl group: HE staining and Nissl staining showed that the number of hippocampal neurons was significantly reduced in the AMA group at P14 (P < 0.05), and there were abnormal changes in hippocampal neuron morphology and Nissl body number and morphology in the AMA group at all time points; the incidence of ARL13B primary cilia was significantly decreased in the AMA group at both P14 (P < 0.05) and P28 (P < 0.001), and the length of ARL13B was obviously shortened in the AMA group at both P14 (P < 0.05) and P28 (P < 0.05); the hippocampal expression level of IFT88 was notably lower in the AMA group at the P14 (P < 0.01). TUNEL staining showed that the apoptotic rate of hippocampal neurons at P14 was remarkably higher in the AMA group (P < 0.05), while Western blotting indicated that the expression of BAX was significantly higher (P < 0.001) and that of BCL-2 was lower (P < 0.01). In the AMA group, the expression of p-LKB1 was significantly decreased at P14 (P < 0.05), that of p-AMPK was statistically elevated at P28 (P < 0.01) and P60 (P < 0.01), and that of p-mTOR was notably decreased at P60 (P < 0.05). Conclusion Neuronal damage, defective primary ciliogenesis and growth inhibition, and abnormal activation of apoptosis are present in the hippocampus of juvenile offspring brain of advanced maternal age. Meanwhile, the LKB1/AMPK pathway, which is regulated by primary cilia in hippocampal astrocytes and neurons of advanced maternal age offspring brain, is abnormally activated at all ages.

Investigation on the effects of Zr and quenching and tempering processes on the microstructure and properties of high-strength Ti-Mo microalloyed steel using SEM, TEM, mechanical property testing, and First-principles calculations. The results show that within the tempering temperature range of 550–650 °C, the microstructures of Ti-Mo microalloyed steel and Ti-Zr-Mo microalloyed steel consist of ultra-low carbon martensite and carbides. Specifically, the strength of Ti-Mo microalloyed steel initially increases and then decreases with the increase in tempering temperature, while the strength of Ti-Zr-Mo microalloyed steel increases with the increase in tempering temperature. During tempering, the addition of Zr element affects the diffusion of C element, delaying the martensitic tempering transformation process, and slowing down the nucleation, growth, and coarsening processes of alloy carbides. First-principles calculation results indicate that ZrC preferentially forms during tempering, resulting in a certain sequential gradient of precipitated microalloy carbides, thereby enhancing the tempering stability of microalloyed steel. Compared to Ti-Mo steel, Ti-Zr-Mo steel exhibits narrower lath martensite width and finer dispersed precipitation phases after tempering at 600 °C and 650 °C. [ABSTRACT FROM AUTHOR]

Aim: To identify the spectrum of autoimmune encephalitis antibody biomarkers (AE‐Abs) in children with suspected autoimmune encephalitis and explore the clinical features indicating AE‐Abs presence. Method: We included children with suspected autoimmune encephalitis who underwent AE‐Abs tests at the Children's Hospital of Chongqing Medical University between June 2020 and June 2022. Clinical features suggestive of AE‐Abs were analysed based on AE‐Abs test results. Results: A total of 392 children were tested for AE‐Abs with suspected autoimmune encephalitis. Of these, 49.5% were male, with a median age of 7 years 11 months (6 months–17 years 11 months); 93.6% (367/392) of all patients had both serum and cerebrospinal fluid (CSF) tests performed. The antibody‐positive rate in the cohort was 23.7% (93/392), the serum antibody‐positive rate was 21.9% (84/384), and the CSF antibody‐positive rate was 20.8% (78/375). Eleven different AE‐Abs were detected. Serum analysis revealed that N‐methyl‐D‐aspartate receptor immunoglobulin‐G (NMDAR‐IgG) (15.1%) was greater than myelin oligodendrocyte glycoprotein (MOG)‐IgG (14.6%) and glial fibrillary acidic protein (GFAP)‐IgG (3.3%). CSF analysis revealed that NMDAR‐IgG (16.3%) was greater than MOG‐IgG (13.8%) and GFAP‐IgG (3.3%). Compared with antibody‐negative patients, antibody‐positive patients were more often female (odds ratio [OR] 1.86, p = 0.03), with memory impairment (OR 2.91, p = 0.01) and sleep disorders (OR 2.08, p = 0.02). Interpretation: In children, the most frequent AE‐Abs detected were NMDAR‐IgG and MOG‐IgG. Female sex, memory impairment, and sleep disorders predict a higher likelihood of AE‐Abs. [ABSTRACT FROM AUTHOR]

Purpose: This study aimed to investigate whether minocycline could influence alterations of microglial subtypes, the morphology of dendrites and dendritic spines, the microstructures of synapses and synaptic proteins, or even cognition outcomes in immature male mice following status epilepticus (SE) induced by kainic acid. Methods: Golgi staining was performed to visualize the dendrites and dendritic spines of neurons of the hippocampus. The microstructures of synapses and synaptic proteins were observed using transmission electron microscopy and western blotting analysis, respectively. Microglial reactivation and their markers were evaluated using flow cytometry. The Morris water maze (MWM) test was used to analyze spatial learning and memory ability. Results: Significant partial spines increase (predominate in thin spines) was observed in the dendrites of neurons after acute SE and partial loss (mainly in thin spines) was presented by days 14 and 28 post‐SE. The postsynaptic ultrastructure was impaired on the 7th and 14th days after SE. The proportion of M1 microglia increased significantly only after acute SE Similarly, the proportion of M2 microglia increased in the acute stage with high expression levels of all surface markers. In contrast, a decrease in M2 microglia and their markers was noted by day 14 post‐SE. Minocycline could reverse the changes in dendrites and synaptic proteins caused by SE, and increase the levels of synaptic proteins. Meanwhile, minocycline could inhibit the reactivation of M1 microglia and the expression of their markers, except for promoting CD200R. In addition, treatment with minocycline could regulate the expression of M2 microglia and their surface markers, as well as ameliorating the impaired spatial learning and memory on the 28th day after SE. Conclusions: Dendritic spines and microglia are dynamically changed after SE. Minocycline could ameliorate the impaired cognition in the kainic acid‐induced mouse model by decreasing the damage to dendrites and altering microglial reactivation. [ABSTRACT FROM AUTHOR]

Interspecific variations in phenotypic plasticity of trees that are affected by climate change may alter the ecosystem function of forests. Seedlings of four common tree species (Castanopsis fissa , Michelia macclurei , Dalbergia odorifera and Ormosia pinnata) in subtropical plantations of southern China were grown in the field under rainout shelters and subjected to changing precipitation (48 L of water every 4 days in the dry season, 83 L of water every 1 day in the wet season; 4 g m−2 year−1 of nitrogen (N)), low N deposition (48 L of water every 2 days in the dry season, 71 L of water every 1 day in the wet season; 8 g m−2 year−1 N), high N deposition (48 L of water every 2 days in the dry season, 71 L of water every 1 day in the wet season; 10 g m−2 year−1 N) and their interactive effects. We found that the changes in seasonal precipitation reduced the light-saturated photosynthetic rate (A sat) for C. fissa due to declining area-based foliar N concentrations (Na). However, we also found that the interactive effects of changing precipitation and N deposition enhanced A sat for C. fissa by increasing foliar Na concentrations, suggesting that N deposition could alleviate N limitations associated with changing precipitation. Altered precipitation and high N deposition reduced A sat for D. odorifera by decreasing the maximum electron transport rate for RuBP regeneration (J max) and maximum rate of carboxylation of Rubisco (V cmax). Ormosia pinnata under high N deposition exhibited increasing A sat due to higher stomatal conductance and V cmax. The growth of D. odorifera might be inhibited by changes in seasonal precipitation and N deposition, while O. pinnata may benefit from increasing N deposition in future climates. Our study provides an important insight into the selection of tree species with high capacity to tolerate changing precipitation and N deposition in subtropical plantations. [ABSTRACT FROM AUTHOR]

A series of novel [Ir(tpy)(btp)Cl]+ complexes (Ir1–Ir4) have been reported to show excellent performance as photosensitizers. The introduction of electron-withdrawing groups increases visible light absorption and the lifetime of triplet states. To improve the photophysical properties, we theoretically design Ir5–Ir9 with electron-withdrawing groups (Cl, F, COOH, CN and NO2). Surprisingly, our findings indicate that the photosensitizer performance does not strictly increase with the electron-withdrawing ability of the substituents. In this work, the geometric and electronic structures, transition features, and photophysical properties of Ir1–Ir9 are investigated. The natural transition orbital (NTO) analysis indicates that the T1 and T2 states play a role in the photochemical pathways. Ultraviolet-visible (UV-vis) absorption spectra and charge-transfer spectra (CTS) have been investigated to show that the introduction of electron-withdrawing groups not only improves the visible light absorbing ability, but also changes the nature of electron excitation, providing a future molecular design strategy for similar series of photosensitizers. The rates of (reverse) intersystem crossing and the Huang–Rhys factors are evaluated to interpret the experimental results within the framework of Marcus theory. For complexes Ir1–Ir7, the introduction of electron-withdrawing groups leads to a lower efficiency of reverse intersystem crossing and a strong non-radiative process T2 → T1, resulting in a long triplet lifetime and excellent performance as a photosensitizer. Furthermore, some newly designed complexes (Ir7–Ir9) show great potential as thermally activated delayed fluorescence emitters, contrary to our initial expectations. [ABSTRACT FROM AUTHOR]