The structure characterization of two new polysaccharides from Agrocybe aegerita (AA-P) and Hygrophorus olivaceoalbus (HO-P) by HPGPC, GC-MS, NMR and FT-IR indicated that AA-P was composed of Galactose, Glucose and Arabinose, in the ratio of 3:2:1. Its skeleton structure was consisted of (1→4)-Arap, (1→4,6)-Glup and (1→6)-Galp with one branched chain. The HO-P was consisted of mannose, galactose and glucose in a ratio of 1:1:2. Its skeleton structure was consisted of (1→6)-Galactose residues, (→1)-glucose residues, (1→4)-glucose residues and (1→4,6)-D-mannose residues. There were two branched chains connected to the main chain. AA-P and HO-P had the best stimulation effect on B cells and RAW264.7 cells, respectively, and could both mainly by impacting and reducing G0/G1 phase which lead to a significant proliferation of B cells, T cells and RAW264.7 cells. In addition, AA-P and HO-P could significantly promote the secretion of TNF-α from T cells, the secretion of IgA, IgD, IgE, IgG and IgM from B cells, and the secretion of TNF-α from RAW264.7 cells, but neither of them could impact the secretion of IL-1β from RAW264.7 cells.

Background: Infertility can affect a couple's mental health, marital and social relationships. The study aimed to investigate the prevalence of depression among infertile couples and the relationships with other factors. Methods: This study employed a cross-sectional survey. Validated tools were used to assess anxiety and depression, marital satisfaction, personality traits and sufficiency economy. The Actor-Partner Interdependence Model (APIM) was used for dyadic analysis. Results: The prevalence of depression in infertile couples was 6.7%. Aggression, extraversion, and neuroticism were significantly correlated with depression, whereas the expectation of having children, marital satisfaction, and sufficiency economy were negatively correlated with depression. The APIM model suggested that neuroticism and marital satisfaction were significant predictors of depression. Partner effect between the expectation of having children and depression was observed (p = .039). Conclusions: Like other populations, depression in infertile couples seems to be associated with aggression, extraversion, and neuroticism. However, there are specific variables related to infertility that impact the depression levels of these couples. For instance, the expectation of having children can affect the partners of infertile couples, while the role of sufficiency economy is a new factor that has been examined for depression in this sample and requires further exploration.

Cerebral ischemia, which is a leading cause of disability and mortality worldwide, sets off a chain of molecular and cellular pathologies that are associated with some central nervous system (CNS) disorders, mainly including ischemic stroke, Alzheimer's disease (AD), Parkinson's disease (PD), epilepsy and other CNS diseases. In recent times, despite significant advancements in the treatment of the pathological processes underlying various neurological illnesses, effective therapeutic approaches specifically targeted at minimizing the damage of such diseases remain absent. Remarkably, ischemia causes severe damage to cells in Ischemia-associated CNS Diseases. Cerebral ischemia initiates oxygen and glucose deprivation, which subsequently promotes mitochondrial dysfunction, including MPTP opening, mitophagy dysfunction, and excessive mitochondrial fission, triggering various forms of cell death, such as autophagy, apoptosis, as well as ferroptosis. Ferroptosis, a novel type of regulated cell death (RCD), is characterized by iron-dependent accumulation of lethal reactive oxygen species and lipid peroxidation. Mitochondrial dysfunction and ferroptosis both play critical roles in the pathogenic progression of Ischemia-associated CNS Diseases. In recent years, growing evidence has indicated that mitochondrial dysfunction interplays with ferroptosis to aggravate cerebral ischemia injury. However, the potential connections between mitochondrial dysfunction and ferroptosis in Cerebral Ischemia have not yet been clarified. Thus, we analyze the underlying mechanism between mitochondrial dysfunction and ferroptosis in Ischemia-associated CNS Diseases. We also discovered that GSH depletion and GPX4 inactivation cause lipoxygenase activation and calcium influx following cerebral ischemia injury, resulting in MPTP opening and mitochondrial dysfunction. Additionally, dysfunction in mitochondrial electron transport and an imbalanced fusion-to-fission ratio can lead to the accumulation of reactive oxygen species and iron overload, which further contribute to the occurrence of ferroptosis. This creates a vicious cycle that continuously worsens cerebral ischemia injury. In this study, our focus is on exploring the interplay between mitochondrial dysfunction and ferroptosis, which may offer new insights into potential therapeutic approaches for the treatment of Ischemia-associated CNS Diseases.