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The purpose of Fuzzy Comprehensive CS-SVR Model (FCCS-SVR) is to evaluate and monitor the health status of a radar equipment and then keep its safe operation. Due to reasons such as few samples, slow changes and the nonlinear structure of data of fault monitoring signal, the health status evaluation of a radar system is quite difficult. By establishing the evaluation index system of a radar, the combination of AHP method and Entropy weight method is studied in this paper. In order to evaluate the value of health status, several optimization algorithms including PSO, GA, BA and CS are used for optimizing the parameters of SVR model. Meanwhile, in order to avoid the problem that the system is at the edge of the state, a radar health assessment method based on the combination of Fuzzy Comprehensive Evaluation and Cuckoo Search-Support Vector Regression (CS-SVR), which is named as Fuzzy Comprehensive CS-SVR (FCCS-SVR), is further proposed. The result of case analysis reflects that the state evaluation of the radar system is realized. The system performance analysis shows that the use of FCCS-SVR evaluation method provides a high recognition rate and can accurately assess the health status of the radar system.

For the construction of a subway station, temporary vertical shafts were commonly used to facilitate machine operation. In densely urban areas, the requirement of settlement control and environmental impact called for a novel construction method of vertical shafts. In this paper, a novel swift-assembled support (SAS) structure and construction method for vertical shafts of a metro station was proposed, using prefabricated steel components. A comprehensive scheme of full-time monitoring was conducted to evaluate the performance of this novel support structure and ground response. Field monitoring results indicated that the SAS method was able to control the settlement of ground and adjacent buildings. Based on the field measurements, the calculation theory for design parameters were discussed. The active earth pressure yield from the method considering wall movement was closer to the field measurements. All of the local buckling values were both overestimated based on the technical standards’ methods. The calculation methods were thereby adopted carefully to determine the designed loading share ratio of structure components. The advantage of the SAS method, including rapid construction, safety, and lower environmental impacts, were obviously clear.

Stroke incidence is the most severe complication associated with atrial fibrillation (AF), and the most common site of thrombus formation in AF patients is the left atrial appendage (LAA). This study was developed to use two-dimensional speckle tracking imaging (2D-STI) to explore associations between LAA strain/strain rate and stroke incidence and to evaluate the value of utilizing LAA strain and strain rate values to support the stratification of nonvalvular AF (NVAF) patients based on stroke risk. A total of 486 AF patients who had undergone transesophageal echocardiography to exclude potential intracardiac thrombosis between March 2021 and November 2022 were consecutively enrolled. Patients meeting the inclusion criteria were separated into two groups according to their history of stroke/transient ischemic attack (TIA). LAA strain and strain rate values in these patients were measured via 2D-STI. Multivariable logistic regression analysis was employed to determine independent risk factors for the construction of a combined predictive model. Of the 333 analyzed patients (134 females, aged 65 (56,72) years), 39 (11.71%, 39/333) had a history of stroke at the time of evaluation. Multivariate logistic regression analysis demonstrated that nonparoxysmal AF, CHA2DS2VASc score, LAA thrombus/spontaneous echo contrast (SEC), LAA strain, and strain rate were all predictors of stroke incidence among NVAF patients. The combined predictive model demonstrated excellent discriminative ability, with an AUC of 0.91 (95%CI 0.87–0.95, P < 0.001), and a sensitivity and specificity of 79.49% and 89.46%, respectively. The Hosmer-Lemeshow test confirmed good calibration, yielding a value of 0.98. Comparative decision curve analysis showed that the model provided superior net benefits compared to the CHA2DS2VASc score. Furthermore, the model exhibited improved predictive performance and reclassification for stroke when compared to the CHA2DS2VASc score (AUC 0.91 vs. 0.88, Z = 2.32, P = 0.02), accompanied by a significant increase in the net reclassification index (+ 5.44%, P < 0.001) and integrated discrimination improvement (8.21%, P < 0.001). These data demonstrate that LAA strain and strain rate, as measured via 2D-STI, can offer value when assessing LAA function in AF patients, potentially providing further predictive value to extant clinical risk scoring strategies.

TGF‐β1 is the strongest cytokine known to promote liver fibrosis. It has been previously demonstrated that the activation of TGF‐β1 initiates a temporary collagen accumulation program, which is important for wound repair in several organs. Furthermore, temporary extracellular matrix enhancement often leads to progressive fibrosis, which is accountable for cases of severe morbidity and mortality worldwide. However, its action mechanism has not been fully explored. It was previously reported that UCA1 could promote its occurrence and development in various tumors. Importantly, it was reported that TGF‐β1 could activate the expression of UCA1 in liver cancer, gastric cancer, and breast cancer. However, the role of UCA1 in organ fibrosis, including liver fibrosis, remains unreported. The present study reported for the first time that TGF‐β1/Smad3 could promote liver fibrosis by upregulating UCA1, which further affected DKK1 and collagen, such as COL1A1, COL1A2, and COL3A1. Meanwhile, UCA1 could competitively bind with miR18a to stabilize Smad3 to constitute a positive feedback pathway, which played a significant role in the promotion of liver fibrosis. Altogether, the present study provides a theoretical basis for devising promising treatment strategies for liver fibrosis.Key messagesUCA1 was found to promote the progression of liver fibrosis in vitro.UCA1 is regulated by TGF-β1 and promotes liver fibrosis through the canonical Smad pathway.UCA1 can competitively bind with miR18a, promote liver fibrosis by stabilizing Smad3, and form a UCA1-miR18a/Smad3 positive feedback.UCA1 binds EZH2 to inhibit the DKK1 expression and promote liver fibrosis.

Although liver cancer is a malignant tumor with the highest mortality across the world, its pathogenesis and therapeutic targets remain unclear. Apoptosis, a natural cell death mechanism, is an important target of anticancer therapy. The discovery of effective apoptotic regulators can lead to the identification of novel therapeutic targets for treating cancer. Neurotrophin 3 (NTF3) is a member of the nerve growth factor (NGF) family that is involved in the progression of various cancers, including medulloblastoma, primitive neuroectodermal brain tumors, and breast cancer. NTF3 is under-expressed in human hepatocellular carcinoma (HCC), albeit its specific effects and the action mechanism have not been elucidated. Here, we confirmed that NTF3 expression was significantly low in HCC with reference to the GSEA database. By collecting patient data from our center and performing qRT-PCR analysis, we found that expression was significantly downregulated in 74 patients with HCC. Low NTF3 expression was associated with a shorter overall survival (OS), recurrence-free survival (RFS), progression-free survival (PFS), and disease-specific survival (DSS). Both and experiments revealed that NTF3 considerably inhibited the progression of HCC cells. We found that the ligand NTF3 is regulated by c-Jun and binds to the p75 neurotrophin receptor (p75NTR) and then activates the JNK and P38 MAPK pathways to induce apoptosis. Entinostat (the target of HDAC1/HDAC3) can activate the NTF3/p75NTR pathway. These results indicate that NTF3 is a tumor suppressor, and that its low expression can help in predict poor clinical outcomes in HCC. Therefore, NTF3 can be used as a potential treatment molecule for HCC.

Thermal desalination evaporation of high-salt wastewater has been widely used in industry because of the proposed concept of ‘zero liquid discharge’. However, due to the high content of Ca2+ and Mg2+ in high-salt wastewater, the heat exchanger, as the main treatment equipment, suffers from serious scaling problems. This review presents descaling and scale inhibition technologies of high-salt wastewater. The advantages and disadvantages of various technologies are summarized and analyzed to provide theoretical support for the research of descaling and anti-scaling of heat exchangers with high-salt wastewater. In future industrial development, the synergistic application of electromagnetic water treatment technology and scale inhibitors can significantly improve the anti-scaling effect, which can reach over 95% stably. Furthermore, the addition of a physical field can also expand the application range of scale inhibitors.

Rosa laevigata Michx., an endemic perennial herbaceous plant in China, possesses significant medicinal value in traditional herbal practices. However, the absence of a reference genome has hindered its development and utilization. In this study, we present a chromosome-level de novo genome assembly of two haplotypes (Hap1 and Hap2) of R. laevigata by integration of Hifi long reads, BGI short reads, and Hi-C reads. The assembled Hap1 genome spans 493 Mb, Hap2 genome spans 479 Mb, and both of them were assigned to 7 chromosomes each. The mapping rate of BGI short reads to the two haplotypes genome is approximately 99.26% and 99.23%, and BUSCO assessment reveals that 98.6% and 98.7% of the genes are complete. Furthermore, we predicted 43,480 and 41,251 protein-coding genes in two haplotype genomes, respectively. The chromosome-level genome of R. laevigata enhances the genetic resources available for Rosa species and lays the groundwork for subsequent medicinal development.

BackgroundEsophageal squamous cell carcinoma (ESCC) remains one of the most aggressive and lethal cancers, with high incidence and mortality rates in East Asia. Neoadjuvant chemotherapy (NC) has traditionally been the standard approach for improving resectability in ESCC, but its limited efficacy in achieving complete pathological responses and enhancing survival has driven interest in combining it with immune checkpoint inhibitors (ICIs), resulting in neoadjuvant chemoimmunotherapy (NIC). Based on randomized controlled trials (RCTs), this meta-analysis compares the risks and clinical benefits of NIC versus NC in resectable ESCC patients.MethodsThis meta-analysis systematically reviewed data from randomized controlled trials (RCTs) comparing NIC and NC in the treatment of resectable ESCC. Primary outcomes included pathological complete response (pCR) and major pathological response (MPR), while secondary outcomes focused on overall survival (OS), event-free survival(EFS), surgery rate, microscopically margin-negative resection(R0 resection), Intraoperative and hospitalization indicators, T Staging, Response evaluation criteria in solid tumors(RECIST), and adverse events (AEs).ResultsSix high-quality RCTs (1070 patients) were included. NIC significantly improved major pathological response(MPR) (42.8% vs. 22.2%, Odds Ratio(OR) = 2.40, p = 0.0007) and pathological complete response(pCR) (22.2% vs. 8.0%, OR = 3.53, p < 0.00001). NIC was also associated with borderline statistically significant improvements in overall survival (OS) (HR = 0.57, p = 0.05) and R0 resection rate (OR = 2.56, p = 0.05). In addition, NIC enhanced surgical rate (OR = 1.57, p = 0.02), lymph node resection (Mean Difference (MD) = 1.76, P = 0.008), and NIC with a longer interval to surgery (MD = 4.73, p = 0.003, I2 = 95%), although this pooled estimate is less reliable because of considerable heterogeneity. However, immune-related adverse events (iRAEs) were higher in NIC (23.21% vs. 1.16%, p < 0.00001), though severe AEs were similar.ConclusionsNIC significantly improves pathological response and other perioperative benefits (e.g., surgical rate and lymph node resection) in resectable ESCC compared with NC, with a trend toward improved survival, despite a higher incidence of irAEs. Further studies are needed to optimize treatment protocols and clarify the long-term impact of immune-related toxicities.

Genomic instability is a core characteristic of cancer, often stemming from defects in DNA damage response (DDR) or increased replication stress. DDR defects can lead to significant genetic alterations, including changes in gene copy numbers, gene rearrangements, and mutations, which accumulate over time and drive the clonal evolution of cancer cells. However, these vulnerabilities also present opportunities for targeted therapies that exploit DDR deficiencies, potentially improving treatment efficacy and patient outcomes. The development of PARP inhibitors like Olaparib has significantly improved the treatment of cancers with DDR defects (e.g., BRCA1 or BRCA2 mutations) based on synthetic lethality. This achievement has spurred further research into identifying additional therapeutic targets within the DDR pathway. Recent progress includes the development of inhibitors targeting other key DDR components such as DNA-PK, ATM, ATR, Chk1, Chk2, and Wee1 kinases. Current research is focused on optimizing these therapies by developing predictive biomarkers for treatment response, analyzing mechanisms of resistance (both intrinsic and acquired), and exploring the potential for combining DDR-targeted therapies with chemotherapy, radiotherapy, and immunotherapy. This article provides an overview of the latest advancements in targeted anti-tumor therapies based on DDR and their implications for future cancer treatment strategies.

Esophageal squamous cell carcinoma (ESCC) carries a high risk of recurrence after neoadjuvant immunochemotherapy and surgery. Both host inflammatory-nutritional status and circulating tumor markers may jointly influence clinical outcomes. We evaluated the prognostic value of the Advanced Lung Cancer Inflammation Index (ALI) and a composite Tumor Load Index (TL) to refine risk stratification in this setting. We retrospectively analyzed 460 consecutive ESCC patients who received 2-3 cycles of PD-1 inhibitor plus platinum/taxane-based chemotherapy followed by esophagectomy. ALI was calculated as BMI × albumin/NLR. TL was derived via LASSO Cox regression from pre-treatment SCC-Ag, CEA, and CA19-9. Optimal cutoffs were identified using maximally selected rank statistics (ALI: 31.22; TL: 0.224). Patients were categorized as low-risk (high ALI/low TL), intermediate-risk (high ALI/high TL or low ALI/low TL), and high-risk (low ALI/high TL). Endpoints included overall survival (OS), disease-free survival (DFS), pathologic complete response (pCR), and major pathologic response (MPR). With a median follow-up of 42 months, 3-year OS rates were 84.7%, 66.0%, and 34.6% for the low-, intermediate-, and high-risk groups, respectively (log-rank P < 0.001). Corresponding 3-year DFS rates were 75.4%, 61.6%, and 29.0%. In multivariable Cox models, intermediate- and high-risk groups had progressively worse OS (adjusted HR = 2.11 and 3.43) and DFS (adjusted HR = 1.64 and 2.62) compared with the low-risk reference (all P < 0.01). High-risk status independently predicted lower odds of achieving MPR (adjusted OR = 0.34, P = 0.002) and pCR (OR = 0.07, P = 0.011). A prognostic nomogram integrating risk group, ASA score, MPR, and ypN status showed strong discrimination (C-index = 0.742) and favorable calibration for 2-, 3-, and 4-year OS, with time-dependent AUCs of 0.759, 0.789, and 0.712. Pre-treatment ALI and TL jointly provide robust and complementary prognostic information in ESCC patients receiving neoadjuvant immunochemotherapy. Low ALI combined with high TL identifies a biologically aggressive subset with poor pathologic response and inferior survival. Integration of ALI and TL may facilitate risk-adapted perioperative strategies and personalized treatment optimization.