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 investigate the role of peptidyl prolyl cis-trans isomerase 1 (Pin1) in mediating stemness of tumor cells and the molecular mechanism of inducing epithelial-mesenchymal transition (EMT) in cervical cancer cells. Methods The Siha and Hele cells of Pin1 low-expression stable transfection uterine cervical neoplasm cell lines were constructed using lentivirus transfection technology and were divided into control group (shPin1-NON), knockdown group 1 (shPin1-1) and knockdown group 2 (shPin1-2). Western blotting and quantitative real-time polymerase chain reaction (qRT-PCR) were used to detect the expressions of Sex-determining region Y transcription factor 2 (SOX2), Aldehyde dehydrogenase 1A1 (ALDH1A1), and Cell adhesion molecule 44 (CD44). The serum-free spheroidization method was used to induce cervical cancer spheroids, with the adherent culture of cervical cancer cells as a control. Subsequently, Western blotting and qRT-PCR were employed to detect the expression of SOX2, ALDH1A1 and CD44 in both spheroid cells and adherent cells. Spheroid formation assay was used to detect the spheroid formation of cervical cancer cells after Pin1 knockdown. Transwell assay was used to detect the migration and invasion abilities of cervical cancer cells following down-regulation of Pin1. Western blotting and qRT-PCR were used to detect the expression of E-cadherin and N-cadherin attribute proteins in cervical cancer cells after transfection with pin1 low expression lentivirus. Western blotting and qRT-PCR were also used to assess the effects of Pin1 low expression on the expression levels of key proteins (c-Jun and c-Fos) of the transcriptional complex of Activator protein 1 (AP-1). Immunofluorescence combined with co-immunoprecipitation assays were conducted to detect the interaction and colocalization of Pin1 with c-Jun. Results In Siha and Hele cells, the mRNA and protein expression levels of Pin1, SOX2, ALDH1A1 and CD44 in shPin1-NON group were significantly higher than those in shPin1-1 group and shPin1-2 group (P<0.05). The expression levels of SOX2, ALDH1A1 and CD44 mRNA and protein in cervical cancer spheroid group were significantly higher than those in adherent cervical cancer cells (P<0.05). Compared with shPin1-NON group, the spheroidism and migration invasion abilities of shPin1-1 group and shPin1-2 group were significantly reduced (P<0.05). Compared with shPin1-NON group, the mRNA and protein expressions of E-cadherin in shPin1-1 and shPin1-2 groups were significantly increased (P<0.05), while the mRNA and protein expression levels of N-cadherin were significantly decreased (P<0.05). The mRNA and protein expression levels of c-Jun and c-Fos in shPin1-NON group were significantly higher than those in shPin1-1 group and shPin1-2 group (P<0.05). Conclusions Down-regulation of Pin1 can inhibit the stemness and migration invasion of cervical cancer cells, and Pin1 may mediate AP-1 to regulate the occurrence of stemness-induced epithelial-mesenchymal transition in cervical cancer cells.

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.

Objective To assess the effectiveness of the evaluation of military physical function (EMPF) system in predicting the occurrence of military training injuries among new recruits to provide scientific guidance and methodological choice for military training. Methods A total of 527 new recruits from 5 grassroots units from July 2016 to February 2018 were selected for the study. The recruits underwent EMPF testing, and their military training injuries were monitored over a 2-year follow-up period. Those who sustained injuries during training were divided into injury group (n=163), while the remaining recruits were placed in healthy group (n=364). The predictive ability of the total EMPF score for training injuries was assessed using the receiver operating characteristic curve (ROC), and the correlation between the total EMPF score, individual test scores, and military training injuries were analyzed using binary logistic regression. Results The total EMPF score of new recruits in injury group (19.52±1.97) was significantly lower than that of healthy group (24.31±1.54) (P<0.001), which also demonstrated a high diagnostic value in predicting the risk of military training injuries, with an area under the curve (AUC) of ROC of 0.971 (P<0.001). A cut-off value of 22 scores was found to have the highest accuracy in predicting future training injuries, with an odds ratio (OR) of 25.63, sensitivity of 0.939, specificity of 0.879, positive likelihood ratio of 7.76, and a post-test probability of 0.67. Binary logistic regression analysis revealed that 6 EMPF tests, including holding the ball over and leaning back, bending forward and touching the ground with the ball, lunge squat and twist, swallow balance with holding the ball afterward, vertical jump, and respiratory pattern assessment, were negatively associated with the risk of military training injuries (P<0.0001). Conclusion The EMPF system can effectively predict the risk of military training injuries, with military personnel whose total EMPF score is less than 22 being at higher risk of sustaining such injuries.

Objective To investigate the effect of miR-185-5p-mediated targeted negative regulation of transmembrane 9 superfamily member 1 (TM9SF1) on proliferation, migration and autophagy in lung adenocarcinoma cells. Methods The expression of miR-185-5p in lung adenocarcinoma tissues was analyzed using dataset GSE51853 downloaded from the Gene Expression Omnibus (GEO) database. Potential target proteins of miR-185-5p were predicted using online databases (miRTargetLink, miRTarbase, and DIANA-microT-CD), and autophagy-related proteins were obtained from HADb. The intersected results from these four databases was identified, and survival curves of vascular endothelial growth factor A (VEGFA) and TM9SF1 within the overlapping candidates were analyzed using the StarBase database. TM9SF1 3'UTR wild-type (WT) or TM9SF1 3'UTR mutant (MUT) reporter plasmids were separately co-transfected with miR-185-5p control plasmid (CON) or miR-185-5p overexpression plasmid (over-miR-185-5p) into HEK-293T cells. A dual-luciferase reporter gene assay was employed to assess the binding interaction between miR-185-5p and TM9SF1 and quantify the subsequent luciferase activity. Western blotting was used to assess TM9SF1 protein expression levels in A549 cells transfected with over-miR-185-5p. A549 cells were divided into three groups: (1) CON+NC group, co-transfected with miR-185-5p control plasmid and TM9SF1 control plasmid; (2) over-miR-185-5p+NC group, co-transfected with over-miR-185-5p and TM9SF1 control plasmid; (3) over-miR-185-5p+over-TM9SF1 group, co-transfected with both miR-185-5p and TM9SF1 overexpression plasmids. EdU cell proliferation assay, wound healing assay, and Transwell migration assay were performed to validate the effects of miR-185-5p targeted binding to TM9SF1 on proliferation and migration capacities in lung adenocarcinoma. Changes in autophagic flux and mitochondrial membrane potential (MMP) of lung adenocarcinoma cells were detected using stubRFP-sensGFP-LC3 lentivirus and JC-1 assays, respectively. Results In the GSE51853 dataset, miR-185-5p expression level was significantly lower in lung adenocarcinoma tissues compared with normal lung tissues (P<0.01). qRT-PCR analysis revealed that miR-185-5p expression was downregulated in lung adenocarcinoma cell lines NCI-H1299 and A549 compared with normal lung epithelial cells BEAS-2B (P<0.01). Bioinformatics predictions using miRTargetLink, miRTarbase, DIANA-microT-CD, and HADb databases indicated that miR-185-5p could target and regulate the autophagy-related protein TM9SF1. Dual-luciferase reporter assays and Western blotting demonstrated that miR-185-5p directly bound to the 3'UTR region of TM9SF1 mRNA, and overexpression of miR-185-5p significantly reduced the expression of target protein TM9SF1 (P<0.05). EdU cell proliferation, wound healing, and Transwell migration assays demonstrated that miR-185-5p overexpression inhibited proliferation and migration capacities of lung adenocarcinoma cells, whereas TM9SF1 overexpression could attenuate this inhibition effect (P<0.05). Results of stubRFP-sensGFP-LC3 for autophagic flux analysis demonstrated that overexpression of miR-185-5p enhanced autophagic flux in A549 cells, whereas co-overexpression of miR-185-5p and TM9SF1 suppressed autophagic flux. JC-1 assays showed a decreased MMP level in A549 cells after miR-185-5p overexpression, with higher MMP level observed when miR-185-5p and TM9SF1 were co-overexpressed. Conclusion miR-185-5p may suppress proliferation, migration, and autophagy capacities in lung adenocarcinoma cells by targeting TM9SF1 through negative regulation.

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.

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.

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.