Objective To investigate the effects and underlying molecular mechanisms of typhaneoside (TYP) on lung adenocarcinoma based on network pharmacology and in vitro experiments. Methods TYP-lung adenocarcinoma-related genes were obtained from the prediction target website SwissTargetPrediction, The Cancer Genome Atlas (TCGA) database, GeneCards database, and Gene Expression Omnibus (GEO) database. Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed on the obtained TYP-lung adenocarcinoma-related genes. Protein-protein network interactions analysis was carried out using the String database, and molecular docking was conducted with the Vina software. These network pharmacological analysis methods were employed to explore the theoretical action pathways of TYP on lung adenocarcinoma. PC9 cells were divided into control group (normal culture), low-TYP group (treated with 50 μmol/L TYP for 48 h), high-TYP group (treated with 100 μmol/L TYP for 48 h), and ferrostatin-1 (Fer-1)+TYP group (treated with 1 μmol/L Fer-1+100 μmol/L TYP for 48 h). The cell viability was detected by the CCK-8 assay, the cell proliferation ability was detected by the EdU assay, and the cell migration and invasion ability was detected by scratch assay, Transwell migration assay and Transwell invasion assay. The occurrence of ferroptosis was detected by reduced glutathione (GSH) assay kit, reactive oxygen species (ROS) assay kit, mitochondrial membrane potential assay kit, ferrous ion fluorescent probe, and transmission electron microscopy. Protein and mRNA expression levels of ferroptosis-related key molecules, solute carrier family 7 member 11 (SLC7A11) and glutathione peroxidase 4 (GPX4), were measured by Western blotting and reverse transcription-quantitative PCR (RT-qPCR). PC9 cells were transfected with SLC7A11 overexpression plasmid and divided into vector group (transfected with empty plasmid), vector+TYP group (transfected with empty plasmid and treated with 100 μmol/L TYP for 48 h), OE-SLC7A11 group (transfected with SLC7A11 overexpression plasmid) and OE-SLC7A11+TYP group (transfected with SLC7A11 overexpression plasmid and treated with 100 μmol/L TYP for 48 h). The molecular mechanism of SLC7A11 in the effect of TYP on PC9 was verified by CCK-8 assay, ferrous ion fluorescence probe, and protein expression levels of SLC7A11 and GPX4. Results A total of 73 TYP-lung adenocarcinoma-related target genes were predicted. GO analysis showed that the target genes were mainly involved in biological processes such as positive regulation of kinase activity, and were enriched in cellular components like transferase complex (transferring phosphorus-containing groups), revealing molecular functions such as transmembrane receptor protein tyrosine kinase activity. KEGG analysis identified 124 related pathways, mainly including epidermal growth factor receptor (EGFR) tyrosine kinase inhibitor resistance pathway. Protein-protein interaction network analysis obtained 7 core targets such as serine/threonine kinase 1 (Akt1). Molecular docking results showed that the binding energies of TYP with core target genes and the ferroptosis-related proteins (SLC7A11 and GPX4) were all ≤-5.0 kcal/mol, indicating significant binding activity. CCK-8 assay showed that TYP significantly inhibited PC9 cell viability (P<0.05). EdU assay demonstrated that the proportion of proliferating cells in TYP group was significantly lower than that in control group (P<0.05). Scratch assay, Transwell migration assay, and invasion assay revealed that, compared with control group, the migration and invasion abilities of PC9 cells in TYP group significantly decreased (P<0.05), and GSH content and mitochondrial membrane potential in TYP group also significantly decreased (P<0.05), while ROS and Fe²⁺ contents increased significantly (P<0.01), and protein and mRNA expression levels of SLC7A11 and GPX4 decreased significantly (P<0.05). Transmission electron microscopy results showed that cells in TYP group exhibited specific ferroptosis-related changes such as reduced mitochondrial cristae and increased membrane density, compared with control group. Compared with vector+TYP group, OE-SLC7A11+TYP group had higher cell viability (P<0.05), lower Fe²⁺ content (P<0.05), and higher protein expression levels of SLC7A11 and GPX4 (P<0.05). Conclusion TYP may induce ferroptosis in lung adenocarcinoma cells and inhibit their malignant behaviors such as proliferation, migration and invasion by regulating the SLC7A11-GPX4 axis.

Objective To investigate the effects of a 100 mT static magnetic field (SMF) on emotional behavior and brain damage-related molecules in mice. Methods Fifty-eight C57BL/6N mice were randomly divided into control group (n=25) and observation group (n=33). Mice in observation group were exposed to a 100 mT SMF for 0.5 h/d over 14 consecutive days, while mice in control group underwent pseudo-exposure. On the 7 and 14 days of exposure, anxiety-like behavior was assessed using open field and elevated plus maze tests. Cerebral blood flow was monitored using laser speckle imaging, and the levels of tumor necrosis factor-α(TNF-α), interleukin (IL)-1β, IL-4, central nervous system specific protein β (S100β), neuron-specific enolase (NSE), and brain-derived neurotrophic factor (BDNF) were measured by radioimmunoassay. BDNF expression in the brain was detected by immunofluorescence. Results On the 7 and 14 days of SMF exposure, the open field and elevated plus maze tests showed no statistically significant differences between observation and control groups in the frequencies, durations, and distance entering the central area of the open field and the open arm of the elevated plus maze (P>0.05). Laser speckle imaging revealed no significant difference in cerebral cortical perfusion compared with pre-exposure period (P>0.05). The results of radioimmunoassay showed that compared with control group, on the 7 d of SMF exposure, the serum IL-1β, NSE and S100β levels were significantly increased (P<0.05), the serum BDNF level was significantly decreased (P<0.05), and the IL-1β and TNF-α contents in brain tissues were significantly increased in observation group (P<0.01). On the 14 d of SMF exposure, serum IL-1β, TNF‑α, NSE, and S100β levels were significantly increased (P<0.05, P<0.0001), and the brain IL-1β and TNF‑α levels were significantly increased (P<0.01) in observation group. No statistically significant differences were found in anti-inflammatory cytokine IL-4 level of serum and brain tissue or BDNF content of brain tissue between the two groups (P>0.05). Conclusion Continuous exposure to a 100 mT SMF for 14 d at 0.5 h/d induces neuroinflammation and brain damage in mice, without inducing anxiety-like behavior.

Objective To compare the effects of different exercise acclimatization (EA) durations on liver injury and inflammatory response in mice with exertional heatstroke (EHS). Methods A total of 168 male C57BL/6 mice were randomly assigned to four groups using a random number table: no exercise acclimation group (EA0W, n=54), 1-week exercise acclimation group (EA1W, n=54), 2-week exercise acclimation group (EA2W, n=54), and blank control group (n=6). The blank control group did not undergo acclimatization training or EHS modeling. The EA1W and EA2W groups underwent daily 2-hour exercise training at a speed of 10 m/min in an environment maintained at (26.0±0.5) ℃ for 1 and 2 weeks, respectively, followed by a 2-day rest after training completion. EHS modeling was performed in mice of EA0W, EA1W, and EA2W groups through running at 10 m/min under controlled environmental conditions (39.5 ℃ ambient temperature, 65% relative humidity). The modeling endpoint was defined as loss of consciousness accompanied by a core body temperature ≥42.7 ℃. All modeling procedures were systematically documented. Following modeling, 18 mice from EA0W, EA1W, and EA2W groups underwent 24-hour survival analysis. Blood samples from the abdominal aorta and liver tissues were collected at 6, 12 and 24 hours post-modeling (6 mice per time point for each group). Plasma levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), and creatine kinase (CK) were quantified. Interleukin (IL)-1β and IL-6 concentrations were determined using enzyme-linked immunosorbent assay (ELISA). Liver tissue specimens underwent hematoxylin-eosin (HE) staining and pathological scoring. Results The EHS model was successfully established in all EA groups. When all mice in EA0W group developed EHS (65 min after the modeling initiation), the incidence rates in EA1W and EA2W groups were 50.0% and 22.2%, respectively, with a statistically significant difference between EA0W group and the latter two groups (P<0.05). When all mice in the three groups developed EHS, the time to EHS onset was significantly longer in both EA1W and EA2W groups compared to EA0W group, with EA2W group showing a longer onset time than EA1W group (P<0.05). Survival analysis revealed a significantly higher 24-hour survival rate in EA2W group (61.1%) compared to EA0W group (33.3%) (P<0.05), while no significant difference was observed between EA1W group and the other two groups (P>0.05). The levels of IL-1β, IL-6, and CK were highest at 6 h post-modeling in all EA groups (P<0.05), and liver injury was most severe at 12 h post-modeling (P<0.05). Compared to EA0W group, the levels of ALT, AST, and IL-1β, as well as liver pathology scores, were significantly lower at 12 h post-modeling in both EA1W and EA2W groups (P<0.05), with EA2W group showing significantly lower ALT and AST levels, as well as liver pathology scores than EA1W group (P<0.05). At 6 h post-modeling, CK levels were significantly higher in EA1W and EA2W groups compared to EA0W group (P<0.05), with EA2W group exhibiting higher CK levels than in EA1W group (P<0.05). Conclusions Exercise acclimation helps reduce the incidence of EHS. Following EHS onset, the survival rate of exercise-acclimated mice is higher than that non-acclimated mice, with a significantly higher survival rate in mice acclimated for 2 weeks compared to non-acclimated mice. However, no significant difference in survival rate is observed between mice acclimated for 1 week and non-acclimated mice. Additionally, exercise acclimation for 2 weeks is more effective in reducing liver injury and inflammatory responses compared to 1-week acclimation.

Good endometrial receptivity is an essential factor for embryo implantation, and gene expression in endometrial tissue during the window of implantation (WOI) is closely related to receptivity. Transcriptome sequencing technology enables the identification of gene expression profiles of endometrium during different menstrual phases, as well as microRNAs and long-chain non-coding RNA sequences involved in regulating gene expression. Combining this technology with bioinformatics analysis provides a better understanding of specific gene expression during the receptive period and offers technical support for studying its regulatory mechanism. Moreover, gene expression profiles of the endometrium during different menstrual phases hold significant clinical application value for accurately assessing endometrium receptivity in infertility patients and those with repeated implantation failure, thereby guiding individualized embryo transfer strategies. This review summarizes the progress of transcriptome sequencing in evaluating human endometrial receptivity and discusses future research directions. This review aims to understand the complex molecular mechanisms of endometrial receptivity formation and regulation from the transcriptional level, in order to improve the implantation rate of embryos in assisted reproductive technology and reduce the abortion rate.

Heat stroke is a heat-related illness caused by an imbalance between the body's heat production and heat dissipation, which could lead to multiple organ dysfunction syndrome with a high mortality rate. Rapid and effective reduction of core body temperature is key to successful treatment. This article reviews recent progress in the treatment of heat stroke, including new understandings of organ injury mechanisms, the timing, velocity and goals of cooling treatment, evaluation and selection of traditional cooling techniques (such as cold water immersion), and scientific evaluation of new cooling technologies (such as blood purification technology and intravascular heat exchange cooling technology), aiming to promote understanding and treatment of heat stroke.

The inflammatory status in patients with chronic kidney disease (CKD) is closely associated with cardiovascular events, infections, and other complications, and is a powerful indicator for prognosis assessment. The core view of the "gut-kidney axis" theory reveals the relationship among inflammatory state, microbiota dysbiosis, and deterioration of renal function. The microbiota alters the microenvironment through structural changes and metabolites with different properties, subsequently leading to microbiota translocation, inducing inflammatory lesions, and damaging the kidneys. Recent studies have proposed that targeted microbiota intervention strategies such as probiotics, prebiotics, and synbiotics can modulate the microbiota structure, regulate the microenvironment, relieve renal inflammation, and affect the progression of renal disease, representing a potentially promising research direction in the future. This review discusses the characteristics of how intestinal microbiota influence the inflammatory status in CKD, focusing on the research progress of targeted microbiota intervention, aiming to discuss the effectiveness and scientific basis of these strategies, providing a foundation for the treatment of CKD and the expansion of targeted microbiota research, as well as offering references for the clinical application of probiotics, prebiotics, and synbiotics.

Alzheimer's disease (AD), a major cause of dementia, is a common neurodegenerative disease, beginning with memory loss and difficulties with thinking, language and problem-solving skills. Intensification of population aging and the increasing incidence of AD have imposed a heavy burden on healthcare systems. Currently, the main pathological explanation remains the excessive accumulation of β‑amyloid plaques, formation of neurofibrillary tangles and neuronal loss, but the true etiology and pathogenesis of AD remain unknown. The advances of research in AD, with respect to genetics, pathophysiological mechanism, imaging diagnosis and laboratory diagnosis, are reviewed in this article, aiming to provide references for relevant research and potential clinical applications.

In recent years, the incidence and mortality of heatstroke have been increasing annually alongside global warming, with a marked rise in cases exhibiting atypical symptoms. To address the increasingly complex challenges in heatstroke prevention and treatment, Heatstroke Prevention and Treatment Research Center of Chinese PLA, Expert Group of Heatstroke Prevention and Treatment of Chinese PLA, and Chinese PLA Professional Committee of Critical Care Medicine have jointly developed this guideline (2025 edition). Utilizing the Grading of Recommendations Assessment, Development and Evaluation (GRADE) system, Appraisal of Guidelines for Research and Evaluation (AGREE) criteria, and Reporting Items for Practice Guidelines in Healthcare (RIGHT) standards, and based on the 2015 draft "Expert Consensus on the Standardized Diagnosis and Treatment of Heatstroke" and the 2019 "Chinese Expert Consensus on the Diagnosis and Treatment of Heatstroke", this guideline has been crafted. This guideline provides 25 evidence-based recommendations to guide the prevention, treatment and research of heatstroke, which thoroughly covers 8 critical domains: clinical classification, pathophysiological mechanisms, clinical manifestations, diagnostic criteria, differential diagnosis, treatment protocols, rehabilitation and return to work, and prevention.

Non-functioning pituitary adenomas (NFPAs) are relatively common. Apart from hyperprolactinemia caused by pituitary compression, they typically lack overt hormonal hypersecretion and usually present with clinical symptoms due to mass effects. Previously considered a uniform entity, NFPAs are actually a highly heterogeneous group of tumors, including aggressive subtypes like silent corticotroph adenomas (SCA) and null cell adenomas. The 2022 WHO new classification of pituitary tumors employs transcription factors [e.‍g., pituitary-specific transcription factor 1 (PIT-1), T-box transcription factor 19 (TBX19, also known as TPIT), steroidogenic factor 1 (SF-1)] for detailed categorization, allowing precise subclassification of NFPAs into multiple subtypes derived from distinct cell lineages, including silent gonadotroph adenomas, SCA, and plurihormonal PIT-1-positive adenomas. This helps identify highly invasive subtypes with high recurrence risk, guiding clinical diagnosis and treatment, prognostic assessment, and individualized management. The new classification also provides a theoretical basis for targeted therapies of NFPAs (e.g., somatostatin analogs and temozolomide). This review comprehensively discusses the latest pathological classification of NFPAs and its clinical implications, aiming to enhance understanding of this disease and offer valuable insights for precise diagnosis, treatment, and prognostic assessment.

Objective To investigate the risk factors associated with recurrence of high-grade non-functioning pituitary neuroendocrine tumors (NF-PitNETs) following total resection. Methods A retrospective study was conducted on the clinical data of 252 patients with high-grade NF-PitNETs who underwent surgical treatment at the Department of Neurosurgery, Beijing Tiantan Hospital from January 2012 to December 2023, and met the inclusion criteria. High-grade NF-PitNETs included Knosp 3A, 3B, and 4-grade subtypes. Kaplan-Meier curves and Log-rank tests were employed to compare the progression-free survival (PFS) of Knosp 3A, 3B, and 4-grade patients. Cox regression analysis was applied to identify the risk factors associated with the recurrence of high-grade NF-PitNETs. Receiver operating characteristic (ROC) curve was used to calculate the area under the curve (AUC) of each recurrence-related factor to evaluate the diagnostic efficiency. Results Survival analysis revealed that there were significant differences in PFS among Knosp 3A, 3B, and 4-grade patients (P<0.001). The PFS of Knosp 3A was significantly better than that of grade 3B and 4-grade (P<0.05), while there was no significant difference between Knosp 3B and 4-grade (P=0.118). After integrating the three groups into Knosp 3A group and 3B-4 group, there were significant differences in PFS and some clinical features between the two groups (P<0.05). Cox regression analysis indicated that age <55 years old (HR=2.883, 95%CI 1.253-6.634; P=0.013), T₂ heterogeneous signal (HR=1.842, 95%CI 1.061-3.197; P=0.030), Knosp 3B-4 (HR=2.190, 95%CI 1.069-4.488; P=0.032), and Ki-67 ≥3% (HR=2.266, 95%CI 1.265-4.061; P=0.006) were risk factors related to tumor recurrence. ROC curve analysis showed that the AUCs of the above-mentioned risk factors were 0.682, 0.706, 0.709 and 0.750, respectively, and the AUC of the multi-factor combined model (age+T₂ signal+Knosp grade+Ki-67) was 0.838, which was significantly larger than that of each single risk factor (P<0.05). Conclusion High-grade NF-PitNETs patients with age <55 years old, T₂ heterogeneous signal, Knosp 3B-4 and Ki-67≥3% have a higher recurrence risk. The combined application of multiple risk factors can improve the predictive value of recurrence.