Neurodegenerative diseases (NDs) are characterized by degenerative nerve damage, and available therapeutic drugs cannot prevent or slow down their progression. The pathogenesis of NDs is related to the brain-gut axis, but the regulatory mechanisms are not yet fully understood. The vagus nerve, the main neural pathway of the brain-gut axis, plays a crucial role in the occurrence and development of NDs. This study summarizes the molecular mechanisms by which the vagus nerve regulates intestinal immunity and neuroinflammatory homeostasis of NDs to improve movement disorders and mental disorders. Intestinal immune dysregulation promotes the transfer of metabolites through the vagus nerve to the brain, leading to a general imbalance between the central immune response and the peripheral immune response and enhancing the level of systemic inflammatory stress. Intestinal immune responses and metabolic imbalances cause brain immune imbalances mediated by the vagus nerve and brain-gut communication. Targeted strategies of vagus nerve and brain-gut communication, including intelligent engineered strains systems, genetic-engineering strain modification, artificial intelligence dynamic monitoring, vagus nerve stimulation, polysaccharides, and natural small molecules, can help improve the symptoms of NDs. This study emphasizes that vagus nerve and brain-gut communication can serve as novel targets for NDs.

In this paper, we study minimal power transmission for uplink systems of LTE with constraints on mean queuing delay. Power consumption is important concern for multimedia services of mobile station of LTE. The power minimizing scheduler adapts power and rate of transmission based on the queue and channel state. Our extensive simulations show that small increases in average delay can lead to substantial savings in transmission power, thereby providing another avenue for mobile devices to save on battery power. We propose a low-complexity scheduler that has near-optimal performance.

Background: Parkinson’s disease (PD) is a neurodegenerative disease whose cause and molecular mechanism remain unclear. Dingzhen pill (DZP), a water extract from crude herbs, is thought to possibly play a neuroprotective role in PD. However, the underlying pharmacological mechanisms of the DZP and its impact on the potential pathways against PD have not been elucidated. Aim: The aim of this study was to explore the effect and molecular mechanism of DZP treatment on PD by quantitative proteomic and metabolomic analysis. Methods: The effect of DZP on the behavior of movement disorders in a mouse model of MPTP-induced was first evaluated. Secondary metabolomics for TCM resolved the components of DZP and its metabolites distributed in the serum of PD mice. Proteomics was used to resolve the effects of DZP on proteins in brain tissue in mice with PD. Network pharmacology and molecular docking analysis were used to screen and validate the binding relationships of components and targets. Immunofluorescence and western blot analysis verified the pathway affected by DZP. Results: Our study showed that DZP improved the movement disorder of PD mice and promoted the recovery of dopaminergic neurons in substantia nigra. Secondary metabolomics showed that 460 kinds of secondary metabolites existed in serum of PD mice after DZP treatment. Proteomics analysis showed that DZP affected the expression of 9393 proteins, 87 of which were up-regulated and 120 down-regulated. Through target prediction and molecular docking, a total of 8 compounds were found to interact with 8 pathological PD targets, playing a significant role in neuronal protection. In addition, DZP inhibits neuronal ferroptosis and neuroinflammation by inhibiting the cGAS-STING pathway. Conclusion: This study is helpful to understand the molecular mechanism of the multi-component, multi-target neuroprotective effect of DZ, and may contribute to the development of DZP as a new therapeutic strategy for clinical application in PD.

In this paper, we focus on the Markov model of IEEE 802.11 distributed coordination function with power saving mode. The throughput evaluation is based on the model, with the comparison with the simulation result for validation. Furthermore, we notice that after each beacon transmission, there're more stations in contention than usual. Excessive contention results in high collision probability and low throughput. To solve this problem, we propose a downlink access scheme which can be used in both the basic access scheme and the access scheme with RTS/CTS. This novel scheme enables AP to constrain the number of stations in contention to be an optimal value. Simulation results prove the performance improvement declared. The proposed scheme can be extended for multi-rate or multi-service WLANs.

Adverse childhood experiences (ACEs) are a high risk factor for depression and anxiety in adulthood and are associated with the alterations in the hypothalamic‒pituitary‒adrenal (HPA) axis and monoamine neurotransmitters. This study aimed to elucidate the behavioral, neuroendocrine, and neural circuit mechanisms underlying the impact of ACEs effect on adult second-hit stress. We employed a "two-hit" mouse model that combines maternal separation (MS) with restraint stress (RS). To investigate the potential pathological effects of ACEs on depressive- and anxiety-like behaviors in second-hit model mice. The mice were assessed through the behaviors test of sucrose preference test (SPT), tail suspension test (TST), open field test (OFT) and elevated zero maze (EZM). We analyzed the neural circuits in mice by immunohistochemical (IHC) technique, and detected the neuroendocrine changes of the HPA axis and monoamine neurotransmitters by ELISA, flow cytometry (FCM), and high performance liquid chromatography-electrochemical detection (HPLC-ECD). Mice in the RS and MS + RS groups exhibited depressive- and anxiety-like behaviors in the SPT, TST, OFT and EZM. Serum levels of GR, CORT, ACTH and CRH levels were decreased in the RS and MS + RS groups. Limbic‑system‑related neural circuits were activated in short- and long-term stress, with the expression of c-Fos decreasing and that of FosB increasing. Moreover, the concentrations of 5‑HT, dopamine (DA), norepinephrine (NE), and epinephrine (E) were lowered in the prefrontal cortex, amygdala, hippocampus, and hypothalamus. Maternal separation exerts a time-dependent dual effect on adult mice's response to restraint stress: initially enhancing resilience, but later increasing susceptibility to depressive- and anxiety-like behaviors. These effects are likely mediated by neuroendocrine regulation of neural circuits involving HPA axis hormones and monoamine neurotransmitters. This study provides a novel two-hit mouse model for exploring how ACEs shape adult respond to stress.

Maternal separation (MS) is an early life stress model that is often studied to determine how early life stress affects brain development and psychopathological adaptation. As society has developed, public health problems have become increasingly prominent, and this research area has attracted significant attention. However, to date, there has been no systematic bibliometric study on MS. The aim of this study was to analyze the trends and frontiers in MS using bibliometrics and provide a scientific reference to researchers in the field. Utilizing VOSviewer, CiteSpace, and Microsoft Excel, examined data obtained from the WoSCC, which encompasses the years 2002–2021. In this bibliometric study, we analyzed 6209 articles related to MS authored by 24,174 researchers across 121 countries and regions and published in 2219 journals. The United States had the most publications (2,232, 35.95%) and both the United States and the United Kingdom had the highest h-index. Institutions in the United States and France had the most published articles and citations. Keyword clustering analysis revealed associations between MS and adverse early life experiences, the hypothalamic–pituitary–adrenal (HPA) axis, stress, gene expression, and depression. This bibliometric analysis highlights the current research focus on the long-term effects of MS on emotional cognition, the HPA axis, epigenetic changes, and their links to gut microbiome imbalances. Future research may expand on these findings to investigate the underlying mechanisms and broader health and societal implications of MS. These results provide a comprehensive overview of the current research landscape in MS and offer valuable insights for researchers to guide future investigations in this field.