Objective: To explore the effects of microwave radiation on cognitive function and neuroinflammation in mice with experimental periodontitis, providing experimental evidence for understanding how environmental exposure may be linked to the risk of neurodegenerative diseases by modulating chronic inflammation as a shared pathological mechanism Methods: This study was approved by the Animal Ethics Committee of the Academy of Military Medical Sciences. C57BL/6J mice were randomly divided into a control group (C group, untreated), a microwave radiation group (R group, exposed to microwave radiation only), a periodontitis group (P group, ligation-induced periodontitis only), and a periodontitis + microwave radiation group (PR group, ligation-induced periodontitis plus microwave radiation exposure). A periodontitis model was established using the silk ligation method. Eight weeks after modeling, the R and PR groups were subjected to whole-body microwave radiation at 2 800 MHz and 10 mW/cm2 for 10 h/day for 7 consecutive days. Behavioral tests were conducted: the open field test and elevated plus maze test were used to assess anxiety-like behavior, the Y-maze test to evaluate spatial memory, and the novel object recognition test to assess learning and memory abilities. Micro-CT, hematoxylin & eosin staining (HE), and quantitative real-time polymerase chain reaction (qPCR) were used to analyze periodontal tissue pathology and local inflammation. Serum and brain levels of lipopolysaccharide (LPS), interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α) were measured using enzyme-linked immunosorbent assay (ELISA). The composition of the oral microbiota was analyzed based on 16S rRNA sequencing. Results: Behavioral tests showed that anxiety-like behavior was significantly exacerbated in the R and PR groups, and spatial and recognition memory impairments in the PR and P groups were more severe compared with the R and C groups, respectively (P < 0.05). Histological and molecular biological analyses revealed that periodontal inflammation infiltration, alveolar bone resorption, and local expression of pro-inflammatory cytokines (TNF-α, IL-1β, IL-6) were further exacerbated in the PR and P groups compared with the R and C groups, respectively (P < 0.05). ELISA results showed that in serum, LPS levels in group P and group PR were increased compared with group C and group R, respectively. The levels of TNF-α, IL-1β, and IL-6 in group PR were significantly higher than those in group P and group R, with a synergistic increase in TNF-α level (P < 0.05). In brain tissue, LPS and TNF-α, IL-1β, IL-6 levels in group P were significantly higher than those in group C; all the above indicators in group PR were significantly higher than those in group P and group R, and LPS and IL-6 levels showed a synergistic increase (P < 0.05). Oral microbiota analysis found that microwave radiation further reduced microbial diversity on the basis of periodontitis, leading to increased relative abundances of Lactobacillus and Enterococcus, and decreased relative abundances of Staphylococcus. Correlation analysis confirmed that these differential bacterial genera were positively correlated with brain inflammation levels and negatively correlated with cognitive function indicators. Conclusion Microwave radiation exposure can exacerbate cognitive impairment in mice with experimental periodontitis, and its mechanism may be related to aggravated local periodontal damage, disruption of oral microbiota homeostasis, and subsequent induction of systemic and central neuroinflammatory cascades.

Objective To explore the prevalence of depressive symptoms in postoperative patients with ovarian cancer and to analyze its influencing factors from multiple dimensions, including clinical characteristics, psychological factors, and laboratory indicators. Methods A cross-sectional study was conducted, which enrolled 235 postoperative patients with ovarian cancer. Depressive status was assessed using the patient health questionnaire, and the demographic, pathological, and medical record data of the patients were collected using the generalized anxiety disorder scale, Pittsburgh sleep quality index, European organization for research and treatment of cancer quality of life questionnaire core 30, and ECOG performance status score. Peripheral blood tumor marker (CA125), routine blood test, lymphocyte subsets, and serum cytokine levels were measured. Univariate and multivariate binary logistic regression analysis were used for statistical analysis. Results The prevalence of depression in postoperative patients with ovarian cancer was 39.15% (92/235). Univariate analysis showed that ECOG score ≥ 2 points, pain, anxiety, poor sleep quality, low quality of life, low life satisfaction, tumor recurrence, six or more cycles of chemotherapy, as well as higher levels of CA125, NLR, and NAR, and lower hemoglobin levels were significantly associated with depression (all P<0.05). Multivariate binary Logistic regression analysis showed that anxiety (OR=1.975, 95%CI: 1.231-3.170), sleep efficiency (OR=4.181, 95%CI: 1.211-14.43), sleep latency (OR=34.806, 95%CI: 4.258-284.542), ECOG performance status score, cognitive function (OR=0.918, 95%CI: 0.868-0.97), and life satisfaction were independent risk factors for depression (all P<0.05). Laboratory indicators were not independent influencing factors in the multivariate Logistic regression model. Conclusion Depression in postoperative patients with ovarian cancer is influenced by physiological, psychological, and social factors. Clinical management should focus on patients with anxiety, sleep disorders, poor physical condition, and low life satisfaction, and a comprehensive prevention and treatment strategy centered on psychological intervention and taking into account symptom management and social support should be implemented.

Objective To investigate the impact of two different algorithms, AAA and AXB, on the dose distribution of postoperative radiotherapy for left-sided breast cancer after breast-conserving surgery. Methods A total of 96 target volumes from patients who underwent breast-conserving surgery for left-sided breast cancer were selected for dose verification using a two-dimensional matrix system. The planned dose distributions were simulated using both AAA and AXB algorithms. Dosimetric differences in organs at risk and the target volumes were then compared to identify the algorithm that could reduce the radiation dose to organs at risk without compromising the dose distribution to the target volume. Dose verification was performed on the plans generated by both algorithms, and the pass rates of plans for each target volume using both algorithms were compared to provide a quantitative basis for the precise selection of subsequent radiotherapy plans. Results Both AAA and AXB plans met the radiotherapy requirements. The AXB algorithm demonstrated significant advantages in the D₉₈, D₂, homogeneity index, and conformity index for the planning target volume, as well as in the V₅ and V₂₀ for the left lung. The AXB algorithm showed advantages in the V₃₀ for the heart and the maximum and mean doses for the skin. With the 2 mm/2% criterion in dose verification, the gamma pass rate was higher for the AXB algorithm. Conclusion Through a comparative analysis of the two algorithms, this study revealed that the AXB algorithm offers certain advantages in the dose distribution of radiotherapy after breast-conserving surgery for left-sided breast cancer. These findings provide an important reference for the rational selection of algorithms in clinical practice and are expected to improve radiotherapy efficacy and patient prognosis.

Objective Mendelian randomization was used to analyze the causal association between 20 serum metabolites and the risk of ovarian cancer.Methods The gene variations of 20 serum metabolites were obtained from the MRC IEU database as tool variables reflecting exposure levels,while gene variations of ovarian cancer patients were used as instrumental variables reflecting outcome levels.The ovarian cancer dataset ieu-a-1120 included 66,450 European women samples(of which 25,509 were ovarian cancer),and the dataset ieu-a-1228 included 54,990 European women samples(of which 14,049 were ovarian cancer).Two-sample two-way Mendelian randomization analysis was performed on both datasets.This study used inverse variance-weighted(IVW),weigh-ted median method,MR-Egger regression,and combined various analysis methods such as simple mode,and weighted mode.The caus-al effects of 20 metabolites and the risk of ovarian cancer were analyzed.Cochran's Q test was used to perform sensitivity analysis and to verify the reliability of the results.MR Egger intercept test was used to assess the horizontal pleiotropy of tool variables,and use the leave-one-out method to assess whether there were single nucleotide polymorphisms(SNPs)in the results that might have a potential impact on the incidence of ovarian cancer.Finally,the effects of uridine on ovarian cancer cells were verified through cell proliferation and apoptosis experiments.Results The results showed a negative correlation between uridine and the occurrence of ovarian cancer,with statistically significance(ieu-a-1228:P=0.025;ieu-a-1120:P=0.017).MR-Egger regression analysis confirmed the sensitiv-ity and robustness of the analysis results.The CCK8 assay confirmed that uridine inhibited the proliferation of ovarian cancer cells in a concentration-dependent manner,and uridine at a concentration of 10 mM significantly promoted apoptosis in SKOV3 cells(P<0.001)and A2780 cells(P<0.001).Flow cytometry analysis showed that after treatment for 24 hours,uridine at a concentration of 10 mM had the strongest pro-apoptotic effect on ovarian cancer cells,which was significant in SKOV3 and A2780 cells(P<0.05 and P<0.001,respectively).Conclusion Uridine is negatively correlated with the risk of ovarian cancer,which lays a theoretical founda-tion for further understanding the pathogenesis of ovarian cancer and optimizing clinical treatment strategies.

Immunotherapy for cancer,as an emerging treatment modality,has made significant strides in recent years and has become a crucial therapeutic approach following surgery,radiotherapy,chemotherapy,and targeted therapy.In particular,the clinical utilization of immune checkpoint inhibitors(ICIs)has not only enhanced the survival rates of patients with refractory or recurrent tumors but has also significantly optimized the overall strategy for cancer treatment.However,as the population undergoing cancer immunotherapy continues to grow,this expansion not only yields clinical benefits but also precipitates a range of specific adverse reactions known as immune-related adverse events(irAEs).Pleural effusion is a common and severe complication in cancer patients,significantly affecting both their quality of life and treatment outcomes.Typically,tumor-related pleural effusion is often due to pleural metastasis,with malignant pleural effusion(MPE)characterized by rapid growth,being difficult to control,and tendency for recurrence.With the approval of new drugs and the expansion of indications for existing medications,the number of cancer patients receiving ICIs treatment is increasing,bringing ICIs-related pleural effusion into focus.While ICIs treatment-related pleural effusion is relatively rare in clinical practice,it is closely linked to treatment choices of patients and prognosis.Unlike MPE,the pathogenesis of ICIs treatment-related pleural effusion is more complex,not only involving non-specific immune activation leading to autoimmune inflammatory reactions but also potentially related to nodular pleural granulomatous reactions,eosinophilic chronic pleurisy,and tumor-infiltrating lymphocytes.In terms of diagnosis,ICIs treatment-related pleural effusion is typically diagnosed through exclusion,requiring the exclusion of other causes such as tumor progression,radiotherapy,and chemotherapy-induced pleural effusion,adding complexity and difficulty to the diagnostic process.Treatment for ICIs treatment-related pleural effusion often involves glucocorticoids,tocilizumab,or infliximab,aiming to alleviate symptoms and improve prognosis by suppressing excessive immune reactions.Preventing the occurrence of ICIs treatment-related pleural effusion is equally crucial,necessitating comprehensive patient assessment before ICIs administration and continuous monitoring during treatment to promptly detect and manage potential adverse reactions.Through this comprehensive management approach,the impact of ICIs treatment-related pleural effusion on patient quality of life and treatment outcomes can be minimized,optimizing overall treatment results.This review aimed to explore the pathogenesis,histological features,clinical manifestations,diagnostic methods and treatment strategies of ICIs treatment-related pleural effusion,and delve into the characteristics of ICIs treatment-related pleural effusion,in order to enhance understanding of this complication and provide a reference for clinical practice.

Objective Mendelian randomization was used to analyze the causal association between 20 serum metabolites and the risk of ovarian cancer.Methods The gene variations of 20 serum metabolites were obtained from the MRC IEU database as tool variables reflecting exposure levels,while gene variations of ovarian cancer patients were used as instrumental variables reflecting outcome levels.The ovarian cancer dataset ieu-a-1120 included 66,450 European women samples(of which 25,509 were ovarian cancer),and the dataset ieu-a-1228 included 54,990 European women samples(of which 14,049 were ovarian cancer).Two-sample two-way Mendelian randomization analysis was performed on both datasets.This study used inverse variance-weighted(IVW),weigh-ted median method,MR-Egger regression,and combined various analysis methods such as simple mode,and weighted mode.The caus-al effects of 20 metabolites and the risk of ovarian cancer were analyzed.Cochran's Q test was used to perform sensitivity analysis and to verify the reliability of the results.MR Egger intercept test was used to assess the horizontal pleiotropy of tool variables,and use the leave-one-out method to assess whether there were single nucleotide polymorphisms(SNPs)in the results that might have a potential impact on the incidence of ovarian cancer.Finally,the effects of uridine on ovarian cancer cells were verified through cell proliferation and apoptosis experiments.Results The results showed a negative correlation between uridine and the occurrence of ovarian cancer,with statistically significance(ieu-a-1228:P=0.025;ieu-a-1120:P=0.017).MR-Egger regression analysis confirmed the sensitiv-ity and robustness of the analysis results.The CCK8 assay confirmed that uridine inhibited the proliferation of ovarian cancer cells in a concentration-dependent manner,and uridine at a concentration of 10 mM significantly promoted apoptosis in SKOV3 cells(P<0.001)and A2780 cells(P<0.001).Flow cytometry analysis showed that after treatment for 24 hours,uridine at a concentration of 10 mM had the strongest pro-apoptotic effect on ovarian cancer cells,which was significant in SKOV3 and A2780 cells(P<0.05 and P<0.001,respectively).Conclusion Uridine is negatively correlated with the risk of ovarian cancer,which lays a theoretical founda-tion for further understanding the pathogenesis of ovarian cancer and optimizing clinical treatment strategies.

This study investigated the effects and underlying mechanisms of the luteolin-naringenin combination(LN)on liver injury induced by acetaminophen(APAP).Forty-eight Kunming mice were randomly allocated into six groups:a normal control group,an APAP-induced liver injury model group,a positive drug treatment group,and three LN treatment groups with low,medium,and high doses.After the final drug administration,the mice were fasted for 12 hours prior to eu-thanasia for sample collection.Serum transaminase activity,oxidative stress indices,and hematoxy-lin-eosin(HE)staining were assessed to evaluate the effects of LN on APAP-induced hepatic inju-ry.Additionally,Western blot analysis was conducted to examine the expression levels of sphingo-sine kinase 1(SPHK1)and endoplasmic reticulum stress(ERS)-related proteins,thereby elucida-ting the potential mechanisms by which LN mitigates APAP-induced liver injury.The results dem-onstrated that varying concentrations of LN effectively ameliorated serum aminotransferase activi-ty and oxidative stress levels induced by APAP in a dose-dependent manner.Histopathological ex-amination via HE staining revealed significant improvement in APAP-induced liver tissue injury following treatment with different concentrations of LN.Furthermore,Western blot analysis indi-cated that the protein expressions of SPHK1,CHOP,p-IRE1α,ATF6,p-PERK,p-eIF2α,and ATF4 were markedly reduced after administration of various concentrations of LN.The results demonstrate that LN exhibits a significant protective effect against APAP-induced liver injury by inhibiting the SPHK1-mediated aberrant expression of ERS-related molecules.This study high-lights the importance of targeting SPHK1 in the treatment of APAP liver injury and provides a no-vel therapeutic approach through the multi-target and multi-pathway combination of monomers.

Objective To explore the applicative value of blue Laser imaging combined with magnifying endoscope(BLI+ME)system for the lesion of esophagogastric junction(EGJ).Methods Retrospective study endoscopic and pathological reported during February 2022 to February 2024.6 803 patients who met the inclusion and exclusion criteria were enrolled.They were divided into BLI+ME group(2 931 cases)and white light imaging group(WLI group,3 872 cases)according to the different gastroscopy types used in the examination.Finally,the EGJ biopsy rate,positive biopsy rate,detection rate of various lesions and early diagnosis rate between the two groups were compared.Results The biopsy rate of the BLI+ME group was 27.60%,the positive biopsy rate was 68.73%,and the detection rate of all the lesions was 20.74%,the detection rate of non-cancerous lesions was 20.30%,the detection rate of early cancer was 0.10%,the detection rate of non-cancerous lesions above the dentate line was 5.53%,the detection rate of non-cancerous lesions below the dentate line was 14.77%,the detection rate of cancerous lesions below the dentate line was 0.27%,significantly higher than those of the WLI group,which the biopsy rate was 17.74%,the positive biopsy rate was 60.26%,and the detection rate of all the lesions was 11.90%,the detection rate of non-cancerous lesions was 11.67%,the detection rate of early cancer was 0.00%,the detection rate of non-cancerous lesions above the dentate line was 3.49%,the detection rate of non-cancerous lesions below the dentate line was 8.19%,the detection rate of cancerous lesions below the dentate line was 0.05%,the differences were statistically significant(P＜0.05).Conclusion The BLI+ME system can enhance the biopsy rate,positive biopsy rate,the detection rate of all the lesions,early cancer detection rate,non-cancerous lesions detection rate above and below the dentate line,and cancerous lesions detection rate below the dentate line at the EGJ.It is helpful to improve the early diagnosis rate and early treatment rate of EGJ.It is worthy of clinical application.

Objective To explore the mechanism of modified maimendong decoction (MMD) in inhibiting lung cancer metastasis from the perspective of immune regulation. Methods CTC-TJH-01 and LLC cells were intervened with different concentrations of modified maimendong decoction. The cell proliferation was detected with a CCK-8 kit, apoptosis was detected with an Annexin V-FITC/PI kit, and cell migration was detected through Transwell assays. A lung metastasis model was established through the tail vein injection of LLC cells into C57BL/6 mice, and body weight change and lung tumor metastasis in the mice were evaluated after continuous gavage intervention with MMD. HE staining, immunohistochemistry, and immunofluorescence were employed to observe the histomorphology, Ki-67 protein level, and NK and T cell levels of metastatic lesions. The levels of NK and T cells in the peripheral blood of mice were detected throughflow cytometry. Results MMD had no significant inhibitory effect on the proliferation, apoptosis, and migration of CTC-TJH-01 and LLC cells in vitro. In mice, MMD could significantly inhibit the lung metastasis of LLC cells, increase the proportion of NK and CD8⁺ T cells in peripheral blood and tumor microenvironment (P<0.05), and reduce the expression of Ki-67 protein in metastatic tumor tissues (P<0.05). Conclusion MMD may inhibit the growth of metastatic tumors by upregulating the expression levels of NK and CD8⁺ T cells in peripheral blood to promote the elimination of circulating tumor cells, and regulating the infiltration of NK and CD8⁺ T cells in the immune microenvironment of metastatic tumors, then play an antimetastatic role in lung cancer.

Objective To analyze the risk factors associated with the occurrence of rectal neuroendocrine tumors (RNETs) and construct a risk prediction model. Methods Clinical data of patients who underwent electronic colonoscopy were collected. The clinical information on patients with and without RNETs were compared, and potential risk factors for RNETs were identified. Binary logistic regression was performed to analyze the relevant risk factors and construct a risk prediction model. Results Among 164 patients, 66 were diagnosed with RNETs, and 98 who did not have such a condition were randomly selected. Univariate logistic regression analysis revealed that age, fatty liver, anxiety and depression, total cholesterol, triglyceride levels, and carcinoembryonic antigen (CEA) were significant factors influencing the occurrence of RNETs (P<0.05). Multivariate logistic regression analysis identified age (P=0.015), anxiety and depression (P=0.031), cholesterol level (P=0.009), fatty liver (P=0.001), and CEA (P<0.001) as independent risk factors for RNETs. The participants were randomly divided into training and test sets at a 7:3 ratio. The training set was used to construct a nomogram-based risk prediction model, and the testing set was used for internal validation. The area under the curve values for the training and testing sets were 0.843 and 0.772, respectively (P>0.05). These findings indicate a good discriminative performance. The calibration curves for the training and testing sets were in good agreement with the 45° standard line, which suggests that the predicted probabilities were consistent with the actual outcomes. Decision curve analysis showed that the model provided a high net benefit within a threshold range of 0.2 to 0.7 for clinical decision making. Conclusion Young age, fatty liver, high CEA levels, high cholesterol levels, and anxiety and depression are independent risk factors for RNETs. The nomogram model constructed based on these risk factors exhibits a strong capability to predict the occurrence of RNETs, and clinical intervention can be considered based on the predicted probability values.