α­Fetoprotein­positive hepatoid adenocarcinoma of the stomach and a new classification: A case report.

α-Fetoprotein (AFP)-producing gastric carcinoma (AFPGC) is a rare subtype of gastric cancer (GC) with controversial classification methods. Hepatoid adenocarcinoma of the stomach (HAS) is another rare subtype of GC. Its definition intersects with that of AFPGC, but it is much rarer. The present report describes the case of an elderly patient with GC and AFPGC and HAS features in a serum test and pathology, respectively, and proposes a new classification of GC subtypes based on histological and AFP-producing features. A 75-year-old woman presented with a history of polydipsia and polyuria for over a decade and dizziness for 1 day. Serum AFP levels gradually elevated from 183.70 to 397.70 ng/ml in 1 month after the patient's first clinic visit. Subsequent pathological findings from endoscopic biopsy samples confirmed a hepatoid focus with positive immunohistochemical staining for AFP. The patient underwent a laparoscopic-assisted radical total gastrectomy and esophagojejunal Roux-en-Y anastomosis, and the serum AFP levels decreased to the normal range after the surgery. The present case indicates the diagnostic value of both the serum AFP level and pathological examinations in the diagnosis of AFPGC and HAS, and also highlights the contemporary circumstances of the vague classification based on different criteria for these two subtypes. Furthermore, the present report proposes a new classification considering both histological and AFP-producing features (using both serum biomarkers and immunohistochemistry tests) to cover all cases encompassed by AFPGC and HAS under all definition methods. This new method would give more precise diagnoses and add value to the subsequent treatment decision-making.

The impact of mind-body exercise on the quality of life in older adults: the chain mediation effect of perceived social support and psychological resilience.

Background: With the intensification of the global aging trend, there is a contradiction between the extended lifespan and the decline of physiological functions among the older adult. It has become a global consensus to focus on and improve the quality of life for the older adult. Mind-body exercises (Tai Chi, Ba Duan Jin, Yi Jin Jing) play a crucial role in promoting the quality of life for older adults, but the mechanisms and mediating effects are not yet clear. Objective: This study examines the impact of mind-body exercises (Tai Chi, Ba Duan Jin, Yi Jin Jing) on the quality of life in older adults, with a particular focus on exploring the chain mediating effects of perceived social support and psychological resilience. Methods: This study is a cross-sectional study that surveyed 1,087 older adults participating in mind-body exercises (Tai Chi, Ba Duan Jin, Yi Jin Jing) in 13 districts of Beijing, China, from March 25 to May 3, 2024. The Physical Activity Rating Scale (PARS-3), the World Health Organization Quality of Life Scale (WHOQOL-BREF), the Perceived Social Support Scale (PSSS), and the Connor-Davidson Resilience Scale (CD-RISC) were used to measure mind-body exercise, perceived social support, psychological resilience, and quality of life, respectively. Data were statistically analyzed using SPSS 26.0, and mediation effects were tested and effect analysis was conducted through structural equation modeling (AMOS) and the Bootstrap method. Results: The study results show that mind-body exercises (Tai Chi, Ba Duan Jin, Yi Jin Jing) are significantly and positively correlated with the quality of life in older adults (r = 0.549, p < 0.01). The path coefficients for the relationships mind-body exercise → perceived social support (ß = 0.46, p < 0.001) → psychological resilience (ß = 0.20, p < 0.001) → quality of life in older adults (ß = 0.39, p < 0.001) are significant, indicating that perceived social support and psychological resilience have a chain mediating effect between mind-body exercise and the quality of life in older adults. Conclusion: Mind-body exercises not only improve the quality of life for older adults but also indirectly enhance it by strengthening perceived social support and psychological resilience. This study provides significant reference for developing health intervention strategies targeted at older adults, suggesting that promoting mind-body exercises can improve their sense of perceived social support and psychological resilience, thereby increasing their quality of life.

Joint Beamforming Design and User Clustering Algorithm in NOMA-Assisted ISAC Systems.

To enhance the performance of non-orthogonal multiple access (NOMA)-assisted integrated sensing and communication (ISAC) systems in multi-user distributed scenarios, an improved Gaussian Mixture Model (GMM)-based user clustering algorithm is proposed. This algorithm is tailored for ISAC systems, significantly improving bandwidth reuse gains and reducing serial interference. First, using the Sum of Squared Errors (SSE), the algorithm reduces sensitivity to the initial cluster center locations, improving clustering accuracy. Then, direction weight factors are introduced based on the base station position and a penalty function involving users' Euclidean distances and sensing power. Modifications to the EM algorithm in calculating posterior probabilities and updating the covariance matrix help align user clusters with the characteristics of NOMAISAC systems. This improves users' interference resistance, lowers decoding difficulty, and optimizes the system's sensing capabilities. Finally, a fractional programming (FP) approach addresses the non-convex joint beamforming design problem, enhancing power and channel gains and achieving co-optimizing sensing and communication signals. The simulation results show that, under the improved GMM user clustering algorithm and FP optimization, the NOMA-ISAC system improves user spectral efficiency by 4.3% and base station beam intensity by 5.4% compared to traditional ISAC systems.

Intracellular C5aR1 inhibits ferroptosis in glioblastoma through METTL3-dependent m6A methylation of GPX4.

Glioblastoma (GBM) is the most common primary intracranial malignant tumor. Recent literature suggests that induction of programmed death has become a mainstream cancer treatment strategy, with ferroptosis being the most widely studied mode. Complement C5a receptor 1 (C5aR1) is associated with both tumorigenesis and tumor-related immunity. However, knowledge regarding the role of C5aR1 in GBM progression is limited. In the present study, we observed significant upregulation of C5aR1 in glioma tissue. In addition, C5aR1 expression was found to be closely associated with patient prognosis and survival. Subsequent experimental verification demonstrated that C5aR1 promoted the progression of GBM mainly by suppressing ferroptosis induction, inhibiting the accumulation of lipid peroxides, and stabilizing the expression of the core antiferroptotic factor glutathione peroxidase 4 (GPX4). Aberrant N6-methyladenosine (m6A) modification of GPX4 mRNA contributes significantly to epigenetic tumorigenesis, and here, we report that selective methyltransferase-like 3 (METTL3)-dependent m6A methylation of GPX4 plays a key role in C5AR1 knockdown-induced ferroptosis induction. Mechanistically, ERK1/2 signaling pathway activation increases the METTL3 protein abundance in GBM cells. This activation then increases the stability of METTL3-mediated m6A modifications on GPX4, enabling it to fulfill its transcriptional function. More importantly, in an intracranial xenograft mouse model, PMX205, a C5aR1 inhibitor, promoted alterations in ferroptosis in GBM cells and inhibited GBM progression. In conclusion, our findings suggest that C5aR1 inhibits ferroptosis in GBM cells and promotes MettL3-dependent GPX4 expression through ERK1/2, thereby promoting glioma progression. Our study reveals a novel mechanism by which the intracellular complement receptor C5aR1 suppresses ferroptosis induction and promotes GBM progression. These findings may facilitate the identification of a potential therapeutic target for glioma.

Single Molecular Dispersion of Crown Ether-Decorated Cobalt Phthalocyanineon Carbon Nanotubes for Robust CO2 Reduction through Host-Guest Interactions.

Immobilizing molecular catalysts on electro-conductive supports (for example, multi-walled carbon nanotubes, CNTs) represent a promising way to well-defined catalyst/support interfaces, which has shown appreciable performance for catalytic transformation. However, their full potential is far from achieved due to insufficient utilization of the intrinsic activity for each immobilized molecular catalyst, especially at loadings that should allow decent current densities. In the present work, we discover host-guest interaction between tetra-crown ether substituted cobalt phthalocyanine and metal ions, for example K+ ions, not only eliminate catalyst aggregation at immobilization procedures but also reinforce catalyst/support interactions by additional electrostatic attractions under operational conditions. Through simple dip-coating procedures, a successful single-molecular dispersion is achieved. Such a catalyst/electrode interface is stable and can selectively catalyze CO2-to-CO conversion (＞96%) with almost unchanged turnover frequency (TOF) at all loading conditions, which implies a full utilization of the intrinsic activity of supported molecular catalysts. Therefore, a simultaneous achievement of high TOF and high current density (TOF of 111 s-1 at 38 mA/cm2) is achieved, in an aqueous H-type electrolyzer at an overpotential of 570 mV.

Longikaurin A induces ferroptosis and inhibits glioblastoma progression through DNA methylation - Mediated GPX4 suppression.

Glioblastoma (GBM) is the most common primary intracranial tumor highly resistant to conventional clinical chemotherapy. Recently, the induction of ferroptosis is emerging as a putative strategy to treat various tumors. However, the identification of the effective and applicable tumor ferroptosis-inducing agents remains challenging. In this study, we showed that longikaurin A (LK-A), a natural diterpenoid isolated from the medicinal plant Isodon ternifolius with strong anti-GBM capacities, induced remarkable GBM cell ferroptosis along with suppressing the key anti-ferroptosis factor glutathione peroxidase 4 (GPX4). GPX4 promoter contains conserved CpG islands. The LK-A-induced GPX4 suppression coincided with the inhibition of ten-eleven translocation 2 (TET2), a key DNA demethylation enzyme and an increase in the hypermethylation of the GPX4 promoter. Further, LK-A promoted the GBM ferroptotic alterations and inhibited GBM progression in both subcutaneous and orthotopic xenograft mouse models, whereas GPX4 overexpression largely abrogated its anti-GBM effects both in vitro and in vivo, suggesting that LK-A inductions of the DNA methylation-incurred GPX4 suppression and ferroptosis are crucial for its anti-GBM functions. Together, our study has elaborated an important epigenetic pathway of GBM ferroptosis and uncovered a critical pharmacological property of LK-A for treating GBM patients.

Visual Endoscopic Retrograde Appendicitis Therapy versus Antibiotic Therapy for Treatment of Uncomplicated Acute Appendicitis.

BACKGROUND: Visual endoscopic retrograde appendicitis therapy (V-ERAT) involves a Single-use Video Scope, allowing real-time visualization of the appendiceal lumen during the procedure to treat uncomplicated acute appendicitis (AA). This study aims to compare V-ERAT to antibiotic therapy in treating uncomplicated AA. METHODS: This multicenter, retrospective cohort study was conducted at nine hospitals in China from August 2021 to July 2023. Propensity score matching was performed to minimize selection bias. A total of 692 uncomplicated AA patients were included, with 188 undergoing V-ERAT and 504 receiving antibiotic therapy. The primary outcome was treatment success rate. The secondary outcomes included recurrent appendicitis rate, the appendectomy rate during the initial hospitalization, length of initial hospitalization, time to disease recurrence, and overall adverse events. RESULTS: The treatment success rate did not differ between the V-ERAT and antibiotic groups (93.6%; 95% confidence interval [CI] 89.1% to 96.7% vs. 90.5%; 95% CI, 87.6% to 92.9%) ( P = 0.225). However, V-ERAT demonstrated a significantly lower risk of appendicitis recurrence compared to antibiotic therapy during the follow-up (log-rank P < 0.001), with a hazard ratio of 0.14 (95% CI 0.07-0.29, P < 0.001). V-ERAT was associated with a lower appendectomy rate during the initial hospitalization (4.3%; 95% CI, 1.9% to 8.2% vs. 9.5%; 95% CI, 7.1 to 12.4%) (P = 0.027), a shorter length of initial hospitalization (3 [IQR, 3-4] vs. 4 [IQR, 4-6] days, P < 0.001), and a longer time to recurrence (269 [IQR, 210-318] vs. 70 [IQR, 21-103] days, P < 0.001). The overall adverse event rates did not differ between the two groups (log-rank P = 0.064). CONCLUSION: V-ERAT appears to be a safe and effective alternative to antibiotic therapy in treating uncomplicated AA, significantly reducing the risk of appendicitis recurrence.

CTC-neutrophil interaction: A key driver and therapeutic target of cancer metastasis.

Circulating tumor cells (CTCs) are cancer cells that detach from the primary tumor and enter the bloodstream, where they can seed new metastatic lesions in distant organs. CTCs are often associated with white blood cells (WBCs), especially neutrophils, the most abundant and versatile immune cells in the blood. Neutrophils can interact with CTCs through various mechanisms, such as cell-cell adhesion, cytokine secretion, protease release, and neutrophil extracellular traps (NETs) formation. These interactions can promote the survival, proliferation, invasion, and extravasation of CTCs, as well as modulate the pre-metastatic niche and the tumor microenvironment. Therefore, inhibiting CTC-neutrophils interaction could be a potential strategy to reduce tumor metastasis and improve the prognosis of cancer patients. In this review, we summarize the current literature on CTC-neutrophils interaction' role in tumor metastasis and discuss the possible therapeutic approaches to target this interaction.

RACK1 and NEK7 mediate GSDMD-dependent macrophage pyroptosis upon Streptococcus suis infection.

Streptococcus suis serotype 2 (SS2) is an important zoonotic pathogen that induces an NLRP3-dependent cytokine storm. NLRP3 inflammasome activation triggers not only an inflammatory response but also pyroptosis. However, the exact mechanism underlying S. suis-induced macrophage pyroptosis is not clear. Our results showed that SS2 induced the expression of pyroptosis-associated factors, including lactate dehydrogenase (LDH) release, propidium iodide (PI) uptake and GSDMD-N expression, as well as NLRP3 inflammasome activation and IL-1ß secretion. However, GSDMD deficiency and NLRP3 inhibition using MCC950 attenuated the SS2-induced expression of pyroptosis-associated factors, suggesting that SS2 induces NLRP3-GSDMD-dependent pyroptosis. Furthermore, RACK1 knockdown also reduced the expression of pyroptosis-associated factors. In addition, RACK1 knockdown downregulated the expression of NLRP3 and Pro-IL-1ß as well as the phosphorylation of P65. Surprisingly, the interaction between RACK1 and P65 was detected by co-immunoprecipitation, indicating that RACK1 induces macrophage pyroptosis by mediating the phosphorylation of P65 to promote the transcription of NLRP3 and pro-IL-1ß. Similarly, NEK7 knockdown decreased the expression of pyroptosis-associated factors and ASC oligomerization. Moreover, the results of co-immunoprecipitation revealed the interaction of NEK7-RACK1-NLRP3 during SS2 infection, demonstrating that NEK7 mediates SS2-induced pyroptosis via the regulation of NLRP3 inflammasome assembly and activation. These results demonstrate the important role of RACK1 and NEK7 in SS2-induced pyroptosis. Our study provides new insight into SS2-induced cell death.

Association of statin use with risk of depression and anxiety: A prospective large cohort study.

OBJECTIVES: To examine associations between regular statin use and the incidence of depression and anxiety. METHODS: This cohort was based on UK Biobank participants without depression/anxiety recruited between 2006 and 2010. The self-reported regular statin use was collected at baseline. Depression and anxiety outcomes were assessed by diagnostic interviews (international classification of diseases codes) and nondiagnostic scales (mental well-being questionnaires). Cox proportional hazards models adjusted for a wide range of confounders were used to estimate associations of statins with incident depression/anxiety. RESULTS: Among 363,551 eligible participants, 55,838 reported regular statin use. During a 13-year follow-up, 14,765 cases of depression and 15,494 cases of anxiety were identified. Compared with non-statin users, statin use was associated with reduced risk of depression (hazard ratio [HR]: 0.87; 95% confidence interval [CI]: 0.81, 0.94) and anxiety (HR: 0.90, 95% CI: 0.84, 0.97). Effects of statins on depression were consistent in sensitivity analyses and may be less influenced by unmeasured confounders. However, results of online survey data showed that statin use might not be associated with incident anxiety (HR: 0.96, 95% CI: 0.85, 1.09). CONCLUSION: Regular statin use was associated with a lower risk of depression. No clear associations between statin use and anxiety were found.

Genome-wide identification of R2R3-MYB transcription factor subfamily genes involved in salt stress in rice (Oryza sativa L.).

BACKGROUND: R2R3-MYB transcription factors belong to one of the largest gene subfamilies in plants, and they are involved in diverse biological processes. However, the role of R2R3-MYB transcription factor subfamily genes in the response of rice (Oryza sativa L.) to salt stress has been rarely reported. RESULTS: In this study, we performed a genome-wide characterization and expression identification of rice R2R3-MYB transcription factor subfamily genes. We identified a total of 117 R2R3-MYB genes in rice and characterized their gene structure, chromosomal location, and cis-regulatory elements. According to the phylogenetic relationships and amino acid sequence homologies, the R2R3-MYB genes were divided into four groups. qRT-PCR of the R2R3-MYB genes showed that the expression levels of 10 genes significantly increased after 3 days of 0.8% NaCl treatment. We selected a high expression gene OsMYB2-115 for further analysis. OsMYB2-115 was highly expressed in the roots, stem, leaf, and leaf sheath. OsMYB2-115 was found to be localized in the nucleus, and the yeast hybrid assay showed that OsMYB2-115 has transcriptional activation activity. CONCLUSION: This result provides important information for the functional analyses of rice R2R3-MYB transcription factor subfamily genes related to the salt stress response and reveals that OsMYB2-115 may be an important gene associated with salt tolerance in rice.

Mechanisms of Abnormal Lipid Metabolism in the Pathogenesis of Disease.

Lipid metabolism is a critical component in preserving homeostasis and health, and lipids are significant chemicals involved in energy metabolism in living things. With the growing interest in lipid metabolism in recent years, an increasing number of studies have demonstrated the close relationship between abnormalities in lipid metabolism and the development of numerous human diseases, including cancer, cardiovascular, neurological, and endocrine system diseases. Thus, understanding how aberrant lipid metabolism contributes to the development of related diseases and how it works offers a theoretical foundation for treating and preventing related human diseases as well as new avenues for the targeted treatment of related diseases. Therefore, we discuss the processes of aberrant lipid metabolism in various human diseases in this review, including diseases of the cardiovascular system, neurodegenerative diseases, endocrine system diseases (such as obesity and type 2 diabetes mellitus), and other diseases including cancer.

Retraction: involvement of DNA methyltransferase 1 (DNMT1) and multidrug resistance-associated proteins in 2-methoxyestradiol-induced cytotoxicity in EC109/Taxol cells.

[This retracts the article DOI: 10.21037/tcr-20-2678.].

Red nucleus mGluR2 but not mGluR3 mediates inhibitory effect in the development of SNI-induced neuropathological pain by suppressing the expressions of TNF-α and IL-1ß.

Our previous study has verified that activation of group Ⅰ metabotropic glutamate receptors (mGluRⅠ) in the red nucleus (RN) facilitate the development of neuropathological pain. Here, we further discussed the functions and possible molecular mechanisms of red nucleus mGluR Ⅱ (mGluR2 and mGluR3) in the development of neuropathological pain induced by spared nerve injury (SNI). Our results showed that mGluR2 and mGluR3 both were constitutively expressed in the RN of normal rats. At 2 weeks post-SNI, the protein expression of mGluR2 rather than mGluR3 was significantly reduced in the RN contralateral to the nerve lesion. Injection of mGluR2/3 agonist LY379268 into the RN contralateral to the nerve injury at 2 weeks post-SNI significantly attenuated SNI-induced neuropathological pain, this effect was reversed by mGluR2/3 antagonist EGLU instead of selective mGluR3 antagonist ß-NAAG. Intrarubral injection of LY379268 did not alter the PWT of contralateral hindpaw in normal rats, while intrarubral injection of EGLU rather than ß-NAAG provoked a significant mechanical allodynia. Further studies indicated that the expressions of nociceptive factors TNF-α and IL-1ß in the RN were enhanced at 2 weeks post-SNI. Intrarubral injection of LY379268 at 2 weeks post-SNI significantly suppressed the overexpressions of TNF-α and IL-1ß, these effects were reversed by EGLU instead of ß-NAAG. Intrarubral injection of LY379268 did not influence the protein expressions of TNF-α and IL-1ß in normal rats, while intrarubral injection of EGLU rather than ß-NAAG significantly boosted the expressions of TNF-α and IL-1ß. These findings suggest that red nucleus mGluR2 but not mGluR3 mediates inhibitory effect in the development of SNI-induced neuropathological pain by suppressing the expressions of TNF-α and IL-1ß. mGluR Ⅱ may be potential targets for drug development and clinical treatment of neuropathological pain.

NLRP12 c.1382dup promotes the development of Crohn's disease through the ERK/NLRP3/ IL-1ß pathway.

Whole-genome sequencing was used to identify a dominant inherited NLRP12 c.1382dup mutation in refractory familial Crohn's disease (CD) patients. Additionally, we observed a T insertion at position 1382 in the third exon of NLRP12, leading to a frameshift mutation. Isolation of peripheral blood from mutation carriers and subsequent experiments demonstrated increased interleukin (IL)-1ß in CD patients with the NLRP12 c.1382dup mutation. However, the mechanisms by which the NLRP12 c.1382dup mutation mediates IL-1ß remain unclear. Our research findings reveal a close correlation between elevated p-ERK levels and increased expression of NLRP3 and IL-1ß in the presence of the NLRP12 c.1382dup mutation. Further experiments demonstrate that inhibiting p-ERK with PD98059 effectively reduces the production of NLRP3 and IL-1ß. This discovery provides new insights into the pathogenesis of CD, highlighting the significant role of the ERK/NLRP3/IL-1ß pathway in the progression of CD. Not only does this offer novel therapeutic targets for treating CD, but it also lays the groundwork for the development of treatment strategies targeting this pathway.

[Evaluation of nutritional value of common cooked food in Hubei Province by nutrient profiling].

OBJECTIVE: To understand the nutritional components of common cooked foods in Hubei Province. METHODS: Forty-nine common cooked foods consumed by residents in Hubei Province were collected, and their edible parts were homogenized and tested for various nutrient contents according to the national standard method. The nutrient-rich foods index(NRF)model was used to calculate the NRF index(NRF 9.3) of various cooked foods, and the nutritional value of common cooked foods in Hubei Province was evaluated. RESULTS: The result of the nutrient-rich food index model showed that the NRF 9.3 index of all cooked dishes ranged from-176.9 to 224.4, the NRF 9.3 index ranking of all types of cooked food was mainly related to cooking method. The NRF 9.3 index of cold mixed vegetable dishes was generally higher than the 75th percentile value(66.9) of the monitoring result, indicating higher nutritional value. The mean NRF 9.3 index of fish and shrimp cooked foods(72.4)monitored in this study was higher than that of meat cooked foods(21.5). The sodium content of pickled vegetables and some pre-packaged cooked foods was relatively high, RESULTS: ing in negative NRF 9.3 index and lower nutritional value. The NRF 9.3 index of Xiangyang beef noodles(33.1)and tofu noodles(37.1)was higher than that of beef offal noodles(5.1). CONCLUSION: Vegetables and fish and shrimp are better sources of nutrition, and "cold and dressed with sauce" are a better way to cook. Pickled vegetables contain too many restricted nutrients, and their consumption frequency and amount should be reduced.

Cerebral Endothelial CXCR2 Promotes Neutrophil Transmigration into Central Nervous System in LPS-Induced Septic Encephalopathy.

Septic encephalopathy (SE) represents a severe inflammatory syndrome linked to elevated septic mortality rates, lacking specific therapeutic interventions, and often resulting in enduring neurological sequelae. The present investigation endeavors to elucidate the involvement of C-X-C Motif Chemokine Receptor 2 (CXCR2) in the pathogenesis of SE and to explore the potential of CXCR2 modulation as a therapeutic avenue for SE. Employing a murine SE model induced by lipopolysaccharide (LPS) administration, CXCR2 knockout mice and the CXCR2 inhibitor SB225002 were utilized to assess neutrophil recruitment, endothelial integrity, and transendothelial migration. Our findings substantiate that either CXCR2 deficiency or its inhibition curtails neutrophil recruitment without impacting their adhesion to cerebral endothelial cells. This phenomenon is contingent upon endothelial CXCR2 expression rather than CXCR2's presence on neutrophils. Furthermore, the CXCR2 blockade preserves the integrity of tight junction protein ZO-1 and mitigates F-actin stress fiber formation in cerebral endothelial cells following septic challenge. Mechanistically, CXCL1-mediated CXCR2 activation triggers cerebral endothelial actin contraction via Rho signaling, thereby facilitating neutrophil transmigration in SE. These observations advocate for the potential therapeutic efficacy of CXCR2 inhibition in managing SE.

Network Security Prediction of Industrial Control Based on Projection Equalization Optimization Algorithm.

This paper predicts the network security posture of an ICS, focusing on the reliability of Industrial Control Systems (ICSs). Evidence reasoning (ER) and belief rule base (BRB) techniques are employed to establish an ICS network security posture prediction model, ensuring the secure operation and prediction of the ICS. This model first integrates various information from the ICS to determine its network security posture value. Subsequently, through ER iteration, information fusion occurs and serves as an input for the BRB prediction model, which necessitates initial parameter setting by relevant experts. External factors may influence the experts' predictions; therefore, this paper proposes the Projection Equalization Optimization (P-EO) algorithm. This optimization algorithm updates the initial parameters to enhance the prediction of the ICS network security posture through the model. Finally, industrial datasets are used as experimental data to improve the credibility of the prediction experiments and validate the model's predictive performance in the ICS. Compared with other methods, this paper's prediction model demonstrates a superior prediction accuracy. By further comparing with other algorithms, this paper has a certain advantage when using less historical data to make predictions.