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Depression is the most common complication of childhood epilepsy, leading to a poor prognosis for seizure control and poor quality of life. However, the molecular mechanisms underlying epileptic depression have not been completely elucidated. Increasing evidence suggests that oxidative stress and neuroinflammation are major contributors to depression. The positive effects of dietary supplementation with docosahexaenoic acid (DHA) and eicosapentaenoic acid (EPA) on depression have been previously reported. However, knowledge regarding the effects of EPA and DHA in managing depressive symptoms in pediatric patients with epilepsy is limited. Therefore, this study aims to investigate the effects of EPA and DHA on epileptic depression in a pentylenetetrazole (PTZ)-treated young mouse model. Three-week-old mice were fed a DHA- or EPA-enriched diet for 21 days and treated with PTZ (35 mg/kg, i.p.) every other day for a total of 10 times. EPA was more effective than DHA at alleviating PTZ-induced depressive symptoms. Pathological results revealed that DHA and EPA significantly improved neuronal degeneration in the hippocampus. Analysis of the mechanism revealed that DHA and EPA mitigated PTZ-induced myelin damage by increasing the protein levels of CNPase, Olig2, and MBP. Furthermore, both DHA and EPA reduced neuroinflammation by promoting microglial M2 polarization and suppressing the LCN2-NLRP3 inflammasome pathway. Notably, EPA polarized microglia towards the M2 phenotype. In addition, DHA and EPA decreased oxidative stress by inhibiting NOX2 and enhancing mitochondrial metabolism through the increased expression of mitochondrial respiratory chain complex I-V proteins. These findings suggest that DHA and EPA can be used as effective interventions to improve depression in children with epilepsy, with EPA being a particularly favorable option.

BackgroundInternet gaming disorder (IGD) has become a social problem in children. Evidence from previous studies has proven that anxiety is associated with IGD. However, IGD was always assessed as a whole based on total scores, and the fine-grained relationship between anxiety and IGD was hidden.ObjectiveThe present study aims to investigate the fine-grained relationship between anxiety and IGD in elementary school students during the COVID-19 lockdown, and to identify potential targets for psychological interventions.MethodsDuring the lockdown caused by the COVID-19 pandemic, 667 children from a primary school in China were investigated by the Spence Children’s Anxiety Scale-Short Version and Internet Gaming Disorder Scale. R4.1.1 software was used to construct a network model, assess bridge centrality, and test the robustness of the network and conduct a network.ResultsThere were 23 cross-community edges (weight ranged from −0.03 to 0.12), and each node of anxiety was connected to different nodes of IGD. The nodes with the top 80th percentile bridge expected influence were A2 “social phobia” (0.20), A3 “panic disorder” (0.21) and IGD5 “escape” (0.22). The robustness of the network was acceptable.ConclusionFrom the perspective of network analysis, the present study explored the correlation pathways between anxiety and IGD in children and identified social phobia and panic disorder as the best targets for intervention to reduce IGD.

ABSTRACT Enveloped virus entry requires fusion of the viral envelope with a host cell membrane. Herpes simplex virus 1 (HSV-1) entry is mediated by a set of glycoproteins that interact to trigger the viral fusion protein glycoprotein B (gB). In the current model, receptor-binding by gD signals a gH/gL heterodimer to trigger a refolding event in gB that fuses the membranes. To explore functional interactions between gB and gH/gL, we used a bacterial artificial chromosome (BAC) to generate two HSV-1 mutants that show a small plaque phenotype due to changes in gB. We passaged the viruses to select for restoration of plaque size and analyzed second-site mutations that arose in gH. HSV-1 gB was replaced either by gB from saimiriine herpesvirus 1 (SaHV-1) or by a mutant form of HSV-1 gB with three alanine substitutions in domain V (gB3A). To shift the selective pressure away from gB, the gB3A virus was passaged in cells expressing gB3A. Sequencing of passaged viruses identified two interesting mutations in gH, including gH-H789Y in domain IV and gH-S830N in the cytoplasmic tail (CT). Characterization of these gH mutations indicated they are responsible for the enhanced plaque size. Rather than being globally hyperfusogenic, both gH mutations partially rescued function of the specific gB version present during their selection. These sites may represent functional interaction sites on gH/gL for gB. gH-H789 may alter the positioning of a membrane-proximal flap in the gH ectodomain, whereas gH-S830 may contribute to an interaction between the gB and gH CTs. IMPORTANCE Enveloped viruses enter cells by fusing their envelope with the host cell membrane. Herpes simplex virus 1 (HSV-1) entry requires the coordinated interaction of several viral glycoproteins, including gH/gL and gB. gH/gL and gB are essential for virus replication and both proteins are targets of neutralizing antibodies. gB fuses the membranes after being activated by gH/gL, but the details of how gH/gL activates gB are not known. This study examined the gH/gL-gB interaction using HSV-1 mutants that displayed reduced virus entry due to changes in gB. The mutant viruses were grown over time to select for additional mutations that could partially restore entry. Two mutations in gH (H789Y and S830N) were identified. The positions of the mutations in gH/gL may represent sites that contribute to gB activation during virus entry.

Sleep deprivation (SD) is one of the main risk factors for Alzheimer’s disease (AD), but the underlying mechanism is still unclear. Ketogenic diet (KD) has been shown widely neuroprotective effects but less known about its effect on SD-induced AD. In the present study, a continuous 21 days SD mouse model with or without KD was established. The changes of cognitive function, pathological hallmarks of AD, ferroptosis, and intracellular signal pathways in mice were detected by Morris water maze, ThS staining, diaminobenzidine (DAB)-enhanced Perls’ stain, antioxidant assay, immuno-histochemistry, and western blot. The results showed that KD can prevent the cognitive deficiency, amyloid deposition and hyperphosphorylated tau induced by chronic SD. Analysis of ferroptosis revealed that KD can inhibit iron dyshomeostasis by down-regulating the expression of TfR1 and DMT1 and up-regulating the expression of FTH1, FPN1. Meanwhile, KD alleviated oxidative stress with elevated xCT/GPX4 axis, FSP1 and reduced MDA. In addition, KD could promote neuronal repair by enhancing BDNF and DCX. Further studies demonstrated that KD activated Sirt1/Nrf2 signaling pathway in the hippocampus in SD-exposed mice. Our finding firstly suggested that KD could prevent chronic SD-induced AD by inhibiting ferroptosis and improving the neuronal repair ability via Sirt1/Nrf2 signaling pathway.

Epilepsy is a chronic neurological disorder that is more prevalent in children, and recurrent unprovoked seizures can lead to cognitive impairment. Numerous studies have reported the benefits of docosahexaenoic acid (DHA) on neurodevelopment and cognitive ability, while comparatively less attention has been given to eicosapentaenoic acid (EPA). Additionally, little is known about the effects and mechanisms of DHA and EPA in relation to seizure-induced cognitive impairment in the young rodent model. Current research indicates that ferroptosis is involved in epilepsy and cognitive deficiency in children. Further investigation is warranted to determine whether EPA or DHA can mitigate seizure-induced cognitive deficits by inhibiting ferroptosis. Therefore, this study was conducted to compare the effects of DHA and EPA on seizure-induced cognitive deficiency and reveal the underlying mechanisms focused on ferroptosis in a pentylenetetrazol (PTZ)-kindling young mice model. Mice were fed a diet containing DHA-enriched ethyl esters or EPA-enriched ethyl esters for 21 days at the age of 3 weeks and treated with PTZ (35 mg/kg, i.p.) every other day 10 times. The findings indicated that both EPA and DHA exhibited ameliorative effects on seizure-induced cognitive impairment, with EPA demonstrating a superior efficacy. Further mechanism study revealed that supplementation of DHA and EPA significantly increased cerebral DHA and EPA levels, balanced neurotransmitters, and inhibited ferroptosis by modulating iron homeostasis and reducing lipid peroxide accumulation in the hippocampus through activating the Nrf2/Sirt3 signal pathway. Notably, EPA exhibited better an advantage in ameliorating iron dyshomeostasis compared to DHA, owing to its stronger upregulation of Sirt3. These results indicate that DHA and EPA can efficaciously alleviate seizure-induced cognitive deficiency by inhibiting ferroptosis in PTZ-kindled young mice.

To explore the change of brain connectivity in schizophrenics (SCZ), the resting-state EEG source functional connections of SCZ and healthy control (HC) were investigated in this paper. Different band single-layer networks, multilayer networks, and improved multilayer networks were constructed and their topological attributes were extracted. The topological attributes of SCZ and HC were automatically distinguished using ensemble learning methods called Ensemble Learning based on Trees and Soft voting method, and the effectiveness of different network construction methods was compared based on the classification accuracy. The results showed that the classification accuracy was 89.38% for α band network, 82.5% for multilayer network, and 86.88% for improved multilayer network. Comparing patients with SCZ to those with Alzheimer’s disease (AD), the classification accuracy of improved multilayer network was the highest, which was 88.12%. The power spectrum in the α band of SCZ was significantly lower than HC, whereas there was no significant difference between SCZ and AD. This indicated that the improved multilayer network can effectively distinguish SCZ and other groups not only when their power spectrum was significantly different. The results also suggested that the improved multilayer topological attributes were regarded as biological markers in the clinical diagnosis of patients with schizophrenia and even other mental disorders.

Fault tolerance is essential for the maneuverability of self-propelled biomimetic robotic fish in real-world aquatic applications. This paper explores the fault-tolerance control problem of a free-swimming robotic fish with multiple moving joints and a stuck tail joint. The created control system is composed of two main components: a feedback controller and a feedforward compensator. Specifically, the bio-inspired central pattern generator-based feedback controller is designed to make the robotic fish robust to external disturbances, while the feedforward compensator speeds up the convergence of the overall control system. Simulations are performed for control system analysis and performance validation of the faulty robotic fish. The experimental results demonstrate that the proposed fault-tolerant control method is able to effectively regulate the faulty robotic fish, allowing it to complete the desired motion in the presence of damage and thereby improving both the stability and the lifetime of the real robotic system. Keywords: Fault-tolerant control, Robotic fish, Motion control, Feedback controller, Feedforward compensator

The study investigated the semi-hibernation and critical temperature of grass carp based on gradient cooling, and explore the effects of temperature (12–24 ℃) on the survival of grass carp and the concentration of ammonia nitrogen in the water. The temperature was reduced from room temperature (23–25 ℃) to the semi-dormant temperature (16 ℃) at cooling rate of 1, 3, or 5 ℃/h. The control group was reared at room temperature, and sampling was conducted after 0, 12, 24, 36, and 48 h. Serum biochemical and antioxidant parameters were measured to obtain the maximum cooling rate for grass crap. The results showed that the semi-dormant temperature of grass carp was 16 ℃, the critical temperature was 6–8 ℃, and the optimal cooling rate was 3 ℃/h. At 16 ℃, grass carp exhibited delayed stress response and decreased metabolism, and lower concentrations of ammonia nitrogen in the water. Except for aspartate aminotransferase level, the maximum values of other serum biochemical indexes at the cooling rate of 3 ℃/h, were significantly lower than those at 1 and 5 ℃/h (P < 0.05). The activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) exhibited a trend of initially increasing and then decreasing with survival time, whereas the content of malondialdehyde (MDA) showed an opposite trend, reaching a minimum value of 5.27 mmol/mg after 36 h. Compared to the control group, the contents of all biochemical and antioxidant indexes in the three cooling groups showed significant changes with survival time. Therefore, cooling grass carp at a rate of 3 ℃/h could reduce the stress response and allowed it to enter a semi-hibernation state at a more suitable time. The results from this study provide key parameters for the temporary cultivation and transport of grass carp, as well as useful guidelines for reducing the transport mortality.