White matter hyperintensities (WMH) are abnormal high-signal manifestations in white matter areas on magnetic resonance T₂-weighted or fluid-attenuated inversion recovery (FLAIR) sequences, with vasogenic WMH being the most common. Its pathological mechanism is related to cerebrovascular lesions and can lead to multi-dimensional brain functional impairments in cognition, movement, and emotions. Due to their unique working conditions, aircrews are more prone to vasogenic WMH than the general population. Moreover, with the widespread use of magnetic resonance imaging in cranial disease screening for aircrews, the detection rate of vasogenic WMH in aircrews has significantly increased. However, to date, no national or academic organization has issued standardized aviation medical assessment criteria for vasogenic WMH in aircrews. Therefore, led by Xijing Hospital of Air Force Medical University and the Chinese PLA General Hospital, a multi-disciplinary expert panel involved in aviation medicine, neurology, radiology, psychology, and related fields was assembled to formulate this consensus. The document integrates evidence from a systematic review of PubMed, CNKI, Wanfang Data, and VIP databases, incorporates existing WMH guidelines, and synthesizes clinical expertise from Chinese specialists. The consensus outlines three key domains: target population, neuroimaging protocols for vasogenic WMH screening, and clinical assessment and aeromedical identification for aircrews with vasogenic WMH. The aim is to provide evidence-based support and expert recommendations for standardizing and improving the accuracy of aviation medical evaluations of vasogenic WMH in aircrews.

Objective To compare the disease burden and evolving trends of major malignant tumors in China and globally from 1990 to 2021, and conduct predictive analysis, so as to provide a reference for formulating prevention and treatment policies for malignant tumor in China. Methods Based on the Global Burden of Disease Database 2021 (GBD 2021), descriptive research methods were used to analyze the incidence and mortality of major malignant tumors in China and globally, as well as the changes in their rankings. The Joinpoint log-linear model was applied to analyze trends in age-standardized incidence rates (ASIR) and age-standardized mortality rates (ASMR) of malignant tumors in China and globally from 1990-2021. A Bayesian age-period-cohort (BAPC) model was constructed using R 4.4.0 to predict the incidence trends of malignant tumor in China and globally from 2022 to 2035. Results In 2021, there were 17.2294 million new cases of malignant tumors (excluding non-melanoma skin cancer) and 9.7763 million deaths globally, with an ASIR of 201.06/100,000 and ASMR of 115.11/100,000. In China, 4.5375 million new cases and 2.7964 million deaths were reported, with ASIR and ASMR of 221.30/100,000 and 136.36/100,000, respectively. Lung cancer ranked first in both incidence and mortality of malignant tumors in China and globally. Female breast cancer had the second-highest ASIR in China. The number of incident cases and deaths from digestive system malignancies included in this study accounted for 42.0% of the total incident cases and 46.8% of the total deaths from all cancers in China, respectively. From 1990 to 2021, the average annual percentage change (AAPC) for overall ASIR of malignant tumors in China was 0.30, while ASMR declined (AAPC: -0.97). Globally, ASIR decreased slightly (AAPC: -0.10), and ASMR declined (AAPC: -0.78). The BAPC model predicted that by 2035, China's ASIR of malignant tumors may rise to 252.44/100,000, whereas the global ASIR is expected to decrease to 183.05/100,000. Conclusions China has achieved some success in cancer prevention and treatment, but still faces a heavy disease burden, with ASIR and ASMR exceeding global averages and ASIR persistently increasing. Cancer prevention and control work such as health education should be strengthened. Precise prevention and control measures should be taken for key cancer types, and preventive interventions should be focused on the elderly population.

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.

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.

Objective To systematically review and quantitatively analyze the safety of biologic agents for the clinical treatment of psoriasis during pregnancy and lactation. Methods The literature from start of database to June 27, 2023, was searched in MEDLINE (PubMed), Embase, Cochrane Library, and Web of Science by two researcher. Quality of included studies was assessed by the quality evaluation tool of case series from Australian JBI Evidence Based Healthcare Centre. According to Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA), a systematic review and was conducted to assess pregnancy or breastfeeding outcomes in psoriasis patients exposed to biologics within 3 months prior to pregnancy, during pregnancy or breastfeeding. Data on pregnancy and exposure characteristics were pooled, and the prevalence of adverse pregnancy outcome was summarized using a random effects model. Results A total of 54 studies involving 1206 pregnancies in 1177 female patients with psoriasis exposed to biologic agents were included in the analysis. Systematic review results demonstrated that the majority of the exposures were limited to early pregnancy, with pooled spontaneous abortion rates, elective abortion rates, overall mortality, preterm birth rates, incidence of low birth weights, and congenital anomalies similar to those of general population (P>0.05). Furthermore, no serious adverse reactions were reported during lactation. Conclusions The use of biologic agents in pregnant and breastfeeding women with psoriasis does not significantly increase the risk of adverse pregnancy outcomes and does not affect neonatal health or growth. However, the limited available safety data underscores the necessity of further studies to establish the relationship between psoriasis, biologic agents, and pregnancy/lactation outcomes, thereby providing comprehensive guidance for clinical practice.

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.

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.

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.

Objective To analyze the relationship between the visceral adiposity index (VAI) and nocturia in the US adult population. Methods A cross-sectional study was performed. Data from subjects aged ≥20 years in the National Health and Nutrition Examination Survey (NHANES) database from 2007 to 2020 were collected, including waist circumference, triglyceride, body mass index (BMI), high-density lipoprotein, age, gender, race, poverty income ratio, education level, marital status, smoking, alcohol consumption, sleep disorders, depression, occupation, hypertension, diabetes, congestive heart failure, cancer, and nocturnal urination frequency. Weighted analysis, multivariate logistic regression, generalized additive model (GAM), and curve fitting were employed to evaluate the association between VAI and nocturia, adjusting for age, gender, race, poverty income ratio, education level, marital status, smoking, alcohol consumption, sleep disorders, depression, occupation, hypertension, diabetes, congestive heart failure, and cancer. Subgroup analyses were conducted based on age, gender, race, hypertension and diabetes to further evaluate the relationship between VAI and the risk of nocturia. Results A total of 29,196 American adults were included. All subjects were divided into 4 groups based on VAI quartiles: Q₁ group (0.32≤VAI<1.01), Q₂ group (1.01≤VAI<1.70), Q₃ group (1.70≤VAI<2.95), and Q₄ group (2.95≤VAI<13.59), with nocturia prevalence rates of 28.5%, 31.4%, 33.3%, and 34.9%, respectively. In subgroup analyses, the risk of nocturia significantly increased with higher VAI in the 20-40 age group, females and other Hispanics (OR=1.04, 95%CI 1.01-1.08, P=0.006; OR=1.02, 95% CI 1.00-1.04, P=0.035; OR=1.05, 95%CI 1.01-1.09, P=0.026). GAM analysis results showed a nonlinear relationship between VAI and nocturia. Conclusion VAI is positively associated with the risk of nocturia, and may be an effective indicator for predicting the risk of nocturia occurrence.