Ultrasensitive detection of SCCA employing a graphene oxide integrated microfiber ring laser biosensor.

Squamous cell carcinoma antigen (SCCA) is one of the most commonly detected cancer biomarkers for a variety of cancers. In this paper, a microfiber ring laser biosensor with a graphene oxide linking layer for SCCA detection was proposed and experimentally demonstrated. SCCA antibody immobilized on graphene oxide surface binds specifically to SCCA, and induces refractive index variation over the surface of the microfiber biosensor, which leads to a wavelength shift of the microfiber ring laser biosensor. The experimental results show that the proposed laser biosensor can detect SCCA with concentrations from 0.01 to 50 ng/mL, and the calculated detection limit can be as low as 1.3 pg/mL. Additionally, the label-free quantitative detection of SCCA using the proposed microfiber biosensor was verified experimentally according to the corresponding regression equation, and the results agree well with clinical examination detection. This constructed microfiber biosensor may have promising practical applications in analytical detection, medical diagnostics, etc.

Minimally invasive thoracoscopic resection of a micronodular thymoma with lymphoid stroma via a subxiphoid single-incision approach: A case report.

RATIONALE: This study aims to present a novel surgical approach for the resection of anterior mediastinal tumors, specifically focusing on micronodular thymoma with lymphoid stroma (MNT), a rare and distinct variant of thymoma. The single subxiphoid incision technique, although reported in limited cases, offers a minimally invasive option with potential benefits. We report the case of a 76-year-old male who underwent this innovative procedure and was diagnosed with MNT, providing insight into the management and outcomes of this rare pathology. PATIENT CONCERNS: The patient presented for the excision of an anterior mediastinal tumor, with the surgery facilitated by sternal hooks to improve visualization. The rarity of MNT and its unclear prognosis underscore the need for enhanced diagnostic accuracy and tailored treatment strategies. DIAGNOSES: Initially diagnosed preoperatively with a thymic cyst, the patient's final diagnosis was revised to MNT following surgery, highlighting the diagnostic challenges associated with this rare tumor. INTERVENTIONS: The tumor was successfully removed using minimally invasive thoracoscopic surgery through a subxiphoid single-incision, demonstrating the feasibility and potential advantages of this approach. OUTCOMES: The patient had a favorable postoperative course, with a swift recovery and no complications, and remained in good health without signs of relapse at the 9-month follow-up. LESSONS: This case underscores the importance of recognizing the unique pathological features of MNT and the need for a cautious diagnostic approach to differentiate it from other cystic lesions. Additionally, the successful use of single-port thoracoscopy under the xiphoid process for the removal of thymic tumors suggests its potential as an effective surgical method for these challenging cases.

Autophagy-enabled protein degradation: Key to platelet activation and ANGII production in patients with type 2 diabetes mellitus.

Background: Type 2 diabetes mellitus (T2DM) presents a thrombotic environment, contributing to diabetic macroangiopathy and microangiopathy. In this study, the regulation of microthrombosis in T2DM was assessed. Methods: Platelets from T2DM patients and healthy controls were analyzed using 4D label-free proteomics and bioinformatics. The role of autophagy in T2DM platelet activation and conversion of platelet-derived angiotensinogen (AGT) was investigated. Results: The results showed that complement and coagulation cascades, platelet activation, metabolic pathways, endocytosis, autophagy, and other protein digestion-related pathways were enriched. The levels of the key protein AGT were increased in T2DM platelets. Chloroquine (CQ) inhibited ADP- or arachidonic acid (AA)-stimulated platelet aggregation and granule release in a dose-dependent manner, while the effects were less pronounced or even reversed for the proteasome inhibitor PYR-41 and the endocytosis inhibitor Pitstop 2. This indicated the dependence of platelet activation and the accompanying protein digestion on the autophagy-lysosome pathway. Mitophagy occurred in fresh T2DM platelets and ADP- or storage-stimulated platelets; mitophagy was inhibited by CQ. However, the mitophagy inhibitor Mdivi-1 failed to show effects similar to those of CQ. AGT, which could be transformed into ANGII in vitro by ADP-stimulated platelets, was upregulated in T2DM platelets and in MEG-01 cell-derived platelets cultured in a high-glucose medium. Finally, microthrombosis was alleviated as indicated by a reduction in the levels of red blood cells in the liver, spleen, heart, and kidney tissues of db/db mice treated with CQ or valsartan. Conclusion: In platelets, macroautophagy promotes protein digestion, subsequently facilitating platelet activation, ANGII-mediated vasoconstriction, and microthrombosis. Our results suggested that lysosome is a promising therapeutic target for antithrombotic treatment in T2DM.

Exploring the molecular and immune landscape of cellular senescence in lung adenocarcinoma.

Introduction: The connection between aging and cancer is complex. Previous research has highlighted the association between the aging process of lung adenocarcinoma (LUAD) cells and the immune response, yet there remains a gap in confirming this through single-cell data validation. Here, we aim to develop a novel aging-related prognostic model for LUAD, and verify the alterations in the genome and immune microenvironment linked to cellular senescence. Methods: We integrated a comprehensive collection of senescence genes from the GenAge and CellAge databases and employed the least absolute shrinkage and selection operator (LASSO) Cox analysis to construct and validate a novel prognostic model for LUAD. This model was then utilized to examine the relationship between aging, tumor somatic mutations, and immune cell infiltration. Additionally, we explored the heterogeneity of senescence and intercellular communication within the LUAD tumor microenvironment (TME) through single-cell transcriptomic data analysis. Results: By exploring the expression profiles of 586 cellular senescence-related genes in 428 LUAD patients, we constructed an aging-related genes (ARGs) risk model included 10 ARGs and validated it as an independent prognostic predictor for LUAD patients. Notably, patients with low aging scores (LAS group) exhibited better survival, lower tumor mutation burden (TMB), lower somatic mutation frequency, lower tumor proliferation rate, and an immune activated phenotype compared to patients with high aging scores (HAS group). While the HAS group was enriched in tumor cells and showed a lower infiltration of CD8-CCR7, CD8- CXCL13, CD8-GNLY, FCGR3A NK cells, XCL1 NK cells, plasma cell (PC) and other immune subsets. Furthermore, the SPP1 and TENASCIN pathways, associated with tumor immune escape and tumor progression, were also enriched in the HAS group. Additionally, our study also indicated that senescence levels were heterogeneous in the LUAD tumor microenvironment (TME), especially with tumor cells in the LAS group showing higher age scores compared to those in the HAS group. Conclusions: Collectively, our findings underscore that ARRS through ARGs serves as a robust biomarker for the prognosis in LUAD.

Soluble inorganic quantum dots as an electrolyte additive to boost lithium-sulfur battery performance.

Herein, MoS2 quantum dots (QDs) are constructed to serve as electrolyte additives for lithium-sulfur batteries, which can 'solidify' soluble polysulfides by chemisorption and promote sulfur conversion chemistry by electrocatalysis. The Li-S cell with MoS2 QDs shows high retained capacity and high-rate capability, much better than the counterpart without MoS2 QDs.

Exploiting Dual-Wavelength Depolarization of Skin-tissues for Camera-based Perfusion Monitoring.

Perfusion index (PI), the ratio between variable pulsatile (AC) and non-pulsatile (DC) components in a photoplethysmographic (PPG) signal, is an indirect and non-invasive measure of peripheral perfusion. PI has been widely used in assessing sympathetic block success, and monitoring hemodynamics in anesthesia and intensive care. Based on the principle of dual-wavelength depolarization (DWD) of skin tissues, we propose to investigate its opportunity in quantifying the skin perfusion contactlessly. The proposed method exploits the characteristic changes in chromaticity caused by skin depolarization and chromophore absorption. The experimental results of DWD, obtained with the post occlusive reactive hyperemia test and the local cooling and heating test, were compared to the PI values obtained from the patient monitor and photoplethysmography imaging (PPGI). The comparison demonstrated the feasibility of using DWD for PI measurement. Clinical trials conducted in the anesthesia recovery room and operating theatre further showed that DWD is potentially a new metric for camera-based non-contact skin perfusion monitoring during clinical operations, such as the guidance in anesthetic surgery.

Simultaneous determination of Obeticholic acid and its two major metabolites in human plasma after administration of Obeticholic acid tablets using ultra-high performance liquid chromatography tandem mass spectrometry.

Obeticholic acid (OCA), a semisynthetic bile acid derivative, was approved for its therapeutic use in primary biliary cirrhosis. OCA has a enterohepatic circulation and host-gut microbiota metabolic interaction, which produce various metabolites. Such metabolites, especially structural isomers of OCA, together with the need to achieve idea lower limit of quantitation (LLOQ) with minimum matrix interference, bring about significant difficulties to the bioanalysis of OCA. Herein, by applying a combination of solid-phase extraction (SPE) and ultra-high performance liquid chromatography tandem mass spectrometry (UPLC-MS/MS), we introduced an approach for the bioanalysis of OCA along with its two major metabolites-glyco-OCA (GOA) and tauro-OCA (TOA) in human plasma, the full validation results of which showed excellent performance. The quantitative range is 0.2506 âˆ¼ 100.2 ng/mL for OCA, 0.2500 âˆ¼ 100.0 ng/mL for GOA, as well as 0.1250 âˆ¼ 50.00 ng/mL for TOA, respectively. This method was successfully applied to the pharmacokinetic studies in healthy subjects following administration of OCA tablets.

Metformin enhances endogenous neural stem cells proliferation, neuronal differentiation, and inhibits ferroptosis through activating AMPK pathway after spinal cord injury.

BACKGROUND: Inadequate nerve regeneration and an inhibitory local microenvironment are major obstacles to the repair of spinal cord injury (SCI). The activation and differentiation fate regulation of endogenous neural stem cells (NSCs) represent one of the most promising repair approaches. Metformin has been extensively studied for its antioxidative, anti-inflammatory, anti-aging, and autophagy-regulating properties in central nervous system diseases. However, the effects of metformin on endogenous NSCs remains to be elucidated. METHODS: The proliferation and differentiation abilities of NSCs were evaluated using CCK-8 assay, EdU/Ki67 staining and immunofluorescence staining. Changes in the expression of key proteins related to ferroptosis in NSCs were detected using Western Blot and immunofluorescence staining. The levels of reactive oxygen species, glutathione and tissue iron were measured using corresponding assay kits. Changes in mitochondrial morphology and membrane potential were observed using transmission electron microscopy and JC-1 fluorescence probe. Locomotor function recovery after SCI in rats was assessed through BBB score, LSS score, CatWalk gait analysis, and electrophysiological testing. The expression of the AMPK pathway was examined using Western Blot. RESULTS: Metformin promoted the proliferation and neuronal differentiation of NSCs both in vitro and in vivo. Furthermore, a ferroptosis model of NSCs using erastin treatment was established in vitro, and metformin treatment could reverse the changes in the expression of key ferroptosis-related proteins, increase glutathione synthesis, reduce reactive oxygen species production and improve mitochondrial membrane potential and morphology. Moreover, metformin administration improved locomotor function recovery and histological outcomes following SCI in rats. Notably, all the above beneficial effects of metformin were completely abolished upon addition of compound C, a specific inhibitor of AMP-activated protein kinase (AMPK). CONCLUSION: Metformin, driven by canonical AMPK-dependent regulation, promotes proliferation and neuronal differentiation of endogenous NSCs while inhibiting ferroptosis, thereby facilitating recovery of locomotor function following SCI. Our study further elucidates the protective mechanism of metformin in SCI, providing new mechanistic insights for its candidacy as a therapeutic agent for SCI.

Design, Synthesis, and Biological Evaluation of Potent EZH2/LSD1 Dual Inhibitors for Prostate Cancer.

As histone modification enzymes, EZH2 mediates H3K27 trimethylation (H3K27me3), whereas LSD1 removes methyl groups from H3K4me1/2 and H3K9me1/2. Synergistic anticancer effects of combining inhibitors of these two enzymes are observed in leukemia and prostate cancer. Thus, a series of EZH2/LSD1 dual inhibitors are designed and synthesized to evaluate their anticancer activity. After the structure-activity study, one of the best compounds, ML234, displayed excellent antiproliferative capacity against prostate cancer cell lines LNCAP, PC3, and 22RV1. Enzymatic assays ascertained that the anticancer potency of ML234 was mediated through coinhibition of EZH2 and LSD1. Moreover, the accumulation of H3K4me2 and H3K9me2 and the decrease of H3K27me3 induced by ML234 were verified by Western blot analysis. More importantly, the compound remarkably suppressed the tumor growth and enhanced the therapeutic efficacy of clinical drug enzalutamide in the 22RV1 xenograft mouse model, indicating that it may have potential as an anticancer agent in prostate cancer.

Controlling bacterial growth and inactivation using thin film-based surface acoustic waves.

Formation of bacterial films on structural surfaces often leads to severe contamination of medical devices, hospital equipment, implant materials, etc., and antimicrobial resistance of microorganisms has indeed become a global health issue. Therefore, effective therapies for controlling infectious and pathogenic bacteria are urgently needed. Being a promising active method for this purpose, surface acoustic waves (SAWs) have merits such as nanoscale earthquake-like vibration/agitation/radiation, acoustic streaming induced circulations, and localised acoustic heating effect in liquids. However, only a few studies have explored controlling bacterial growth and inactivation behaviour using SAWs. In this study, we proposed utilising piezoelectric thin film-based SAW devices on a silicon substrate for controlling bacterial growth and inactivation with and without using ZnO micro/nanostructures. Effects of SAW powers on bacterial growth for two types of bacteria, i.e., E. coli and S. aureus, were evaluated. Varied concentrations of ZnO tetrapods were also added into the bacterial culture to study their effects and the combined antimicrobial effects along with SAW agitation. Our results showed that when the SAW power was below a threshold (e.g., about 2.55 W in this study), the bacterial growth was apparently enhanced, whereas the further increase of SAW power to a high power caused inactivation of bacteria. Combination of thin film SAWs with ZnO tetrapods led to significantly decreased growth or inactivation for both E. coli and S. aureus, revealing their effectiveness for antimicrobial treatment. Mechanisms and effects of SAW interactions with bacterial solutions and ZnO tetrapods have been systematically discussed.

ERK5 promotes autocrine expression to sustain mitogenic balance for cell fate specification in human pluripotent stem cells.

The homeostasis of human pluripotent stem cells (hPSCs) requires the signaling balance of extracellular factors. Exogenous regulators from cell culture medium have been widely reported, but little attention has been paid to the autocrine factor from hPSCs themselves. In this report, we demonstrate that extracellular signal-related kinase 5 (ERK5) regulates endogenous autocrine factors essential for pluripotency and differentiation. ERK5 inhibition leads to erroneous cell fate specification in all lineages even under lineage-specific induction. hPSCs can self-renew under ERK5 inhibition in the presence of fibroblast growth factor 2 (FGF2) and transforming growth factor ß (TGF-ß), although NANOG expression is partially suppressed. Further analysis demonstrates that ERK5 promotes the expression of autocrine factors such as NODAL, FGF8, and WNT3. The addition of NODAL protein rescues NANOG expression and differentiation phenotypes under ERK5 inhibition. We demonstrate that constitutively active ERK5 pathway allows self-renewal even without essential growth factors FGF2 and TGF-ß. This study highlights the essential contribution of autocrine pathways to proper maintenance and differentiation.

Genetic architecture of telomere length in 462,666 UK Biobank whole-genome sequences.

Telomeres protect chromosome ends from damage and their length is linked with human disease and aging. We developed a joint telomere length metric, combining quantitative PCR and whole-genome sequencing measurements from 462,666 UK Biobank participants. This metric increased SNP heritability, suggesting that it better captures genetic regulation of telomere length. Exome-wide rare-variant and gene-level collapsing association studies identified 64 variants and 30 genes significantly associated with telomere length, including allelic series in ACD and RTEL1. Notably, 16% of these genes are known drivers of clonal hematopoiesis-an age-related somatic mosaicism associated with myeloid cancers and several nonmalignant diseases. Somatic variant analyses revealed gene-specific associations with telomere length, including lengthened telomeres in individuals with large SRSF2-mutant clones, compared with shortened telomeres in individuals with clonal expansions driven by other genes. Collectively, our findings demonstrate the impact of rare variants on telomere length, with larger effects observed among genes also associated with clonal hematopoiesis.

A LASSO Cox Regression Predictive Model for Patients Undergoing Surgery for Pancreatic Body and Tail Adenocarcinoma Patients: Comparative Long-Term Survival Analysis of Radical Antegrade Modular Pancreatosplenectomy (RAMPS) and Standard Retrograde Pancreatosplenectomy (SPRS).

PURPOSE: This study was designed to assess the advantages of radical antegrade modular pancreatosplenectomy (RAMPS) over standard retrograde pancreatosplenectomy (SPRS) in terms of disease-free survival (DFS) by comparing clinical outcomes. METHODS: Clinical data from 154 patients who underwent distal pancreatectomy at Tianjin Medical University Cancer Institute and Hospital between January 2015 and August 2018 were collected. We compared the preoperative conditions, postoperative complications, and survival outcomes of patients who underwent two different surgical procedures. By creating a LASSO-Cox model, we determined the parameters affecting DFS and the risk ratios of the two surgical procedures on DFS. RESULTS: The R0 resection rate (85.23% vs. 68.18%, P = 0.003), negative posterior margin rate (96.59% vs. 75.76%, P < 0.001), and tumor bed recurrence rate (15.29% vs. 40.00%, P = 0.001) significantly differed between the RAMPS and SPRS groups. The 1-, 3-, and 5-year survival and DFS rates of the RAMPS group were significantly better than those of the SPRS group (P < 0.05). Disease-free survival analysis based on Kaplan-Meier curves revealed that RAMPS was superior to SPRS (P < 0.001). CONCLUSIONS: We recommend RAMPS as the preferred procedure for treating ductal adenocarcinoma of the pancreatic body and tail due to its enhanced lymph node repair capacity and visualization of posterior pancreatic sections, which can increase DFS in patients.

Flexible surface acoustic wave technology for enhancing transdermal drug delivery.

Transdermal drug delivery provides therapeutic benefits over enteric or injection delivery because its transdermal routes provide more consistent concentrations of drug and avoid issues of drugs affecting kidneys and liver functions. Many technologies have been evaluated to enhance drug delivery through the relatively impervious epidermal layer of the skin. However, precise delivery of large hydrophilic molecules is still a great challenge even though microneedles or other energized (such as electrical, thermal, or ultrasonic) patches have been used, which are often difficult to be integrated into small wearable devices. This study developed a flexible surface acoustic wave (SAW) patch platform to facilitate transdermal delivery of macromolecules with fluorescein isothiocyanates up to 2000 kDa. Two surrogates of human skin were used to evaluate SAW based energized devices, i.e., delivering dextran through agarose gels and across stratum corneum of pig skin into the epidermis. Results showed that the 2000 kDa fluorescent molecules have been delivered up to 1.1 mm in agarose gel, and the fluorescent molecules from 4 to 2000 kDa have been delivered up to 100 µm and 25 µm in porcine skin tissue, respectively. Mechanical agitation, localised streaming, and acousto-thermal effect generated on the skin surface were identified as the main mechanisms for promoting drug transdermal transportation, although micro/nanoscale acoustic cavitation induced by SAWs could also have its contribution. SAW enhanced transdermal drug delivery is dependent on the combined effects of wave frequency and intensity, duration of applied acoustic waves, temperature, and drug molecules molecular weights.

Regulating Surface Metal Abundance via Lattice-Matched Coordination for Versatile and Environmentally-Viable Sn-Pb Alloying Perovskite Solar Cells.

Narrow-bandgap Sn-Pb alloying perovskites showcased great potential in constructing multiple-junction perovskite solar cells (PSCs) with efficiencies approaching or exceeding the Shockley-Queisser limit. However, the uncontrollable surface metal abundance (Sn2+ and Pb2+ ions) hinders their efficiency and versatility in different device structures. Additionally, the undesired Pb distribution mainly at the buried interface accelerates the Pb leakage when devices are damaged. In this work, a novel strategy is presented to modulate crystallization kinetics and surface metal abundance of Sn-Pb perovskites using a cobweb-like quadrangular macrocyclic porphyrin material, which features a molecular size compatible with the perovskite lattice and robustly coordinates with Pb2+ ions, thus immobilizing them and increasing surface Pb abundance by 61%. This modulation reduces toxic Pb leakage rates by 24-fold, with only ∼23 ppb Pb in water after severely damaged PSCs are immersed in water for 150 h.This strategy can also enhance chemical homogeneity, reduce trap density, release tensile strain and optimize carrier dynamics of Sn-Pb perovskites and relevant devices. Encouragingly, the power conversion efficiency (PCEs) of 23.28% for single-junction, full-stack devices and 21.34% for hole transport layer-free Sn-Pb PSCs are achieved.Notably, the related monolithic all-perovskite tandem solar cell also achieves a PCE of 27.03% with outstanding photostability.

NRBP1 promotes malignant phenotypes of glioblastoma by regulating PI3K/Akt activation.

OBJECTIVES: Glioblastoma (GBM) is the most aggressive of intracranial gliomas. Despite the maximal treatment intervention, the median survival rate is still about 14-16 months. Nuclear receptor-binding protein 1 (NRBP1) has a potential growth-promoting role on biology function of cells. In this study, we investigated whether NRBP1 promotes GBM malignant phenotypes and the potential mechanisms. METHODS: The correlation between NRBP1 and glioma grade, prognosis in TCGA/CGGA databases and our clinical data were analyzed. Next, we conducted knockout and overexpression of NRBP1 on GBM cells to verify that NRBP1 promoted cell proliferation, invasion, and migration in vitro and in vivo. Finally, we detected the impact of NRBP1 on PI3K/Akt signaling pathway and EMT. RESULTS: There was a correlation between elevated NRBP1 expression and advanced stage glioma, as well as decreased overall and disease-free survival. The suppression of proliferation, invasion, and migration of tumor cells was observed upon NRBP1 knockout, and in vitro studies also demonstrated the induction of apoptotic cell death. Whereas, its overexpression is associated with high multiplication rate, migration, invasion, and apoptotic escape. GO enrichment and KEGG analysis revealed that NRBP1 regulated differentially expressed gene clusters are involved in PI3K/Akt signaling pathway, as well as EMT mediated by this pathway. Moreover, the effects of NRBP1 knockdown and overexpression on GBM were mitigated by MK-2206 and SC79, both of which respectively function as an inhibitor and an activator of the PI3K/Akt signaling pathway. Similarly, the suppression of NRBP1 led to a decrease in tumor growth, whereas its overexpression promoted tumor growth in a mouse model. CONCLUSIONS: This study shows that NRBP1 promotes malignant phenotypes in GBM by activating PI3K/Akt pathway. Hence, it can function as both a predictive indicator and a new target for therapies in GBM treatment.

Unveiling the Presence of Short- and Medium-Chain Chlorinated Paraffins in the Hadal Trenches of the Western Pacific Ocean.

This study delves into the unexplored distribution and accumulation of chlorinated paraffins (CPs), pervasive industrial contaminants used as flame retardants and plasticizers, within the hadal trenches, some of Earth's most isolated marine ecosystems. Analysis of sediments from the Mussau (MS) and Mariana trench (MT) reveals notably high total CP concentrations (∑SCCPs + ∑MCCPs) of 10,963 and 14,554 ng g-1 dw, respectively, surpassing those in a reference site in the western Pacific abyssal plain (8533 ng g-1 dw). In contrast, the New Britain Trench (NBT) exhibits the lowest concentrations (2213-5880 ng g-1 dw), where CP distribution correlates with clay content, δ13C and δ15N values, but little with total organic carbon and depth. Additionally, amphipods from these trenches display varying CP levels, with MS amphipods reaching concerning concentrations (8681-16,138 ng g-1 lw), while amphipods in the MT-1 site show the lowest (4414-5010 ng g-1 lw). These bioaccumulation trends appear to be primarily influenced by feeding behaviors (δ13C) and trophic levels (δ15N). Utilizing biota-sediment accumulation factor values and principal component analysis, we discern that CPs in sediment may come from surface-derived particulate organic matters, while those in amphipods may come from the above carrion. Our findings elucidate the profound impacts of the emerging pollutants on the Earth's least explored marine ecosystems.

EMS: A Large-Scale Eye Movement Dataset, Benchmark, and New Model for Schizophrenia Recognition.

Schizophrenia (SZ) is a common and disabling mental illness, and most patients encounter cognitive deficits. The eye-tracking technology has been increasingly used to characterize cognitive deficits for its reasonable time and economic costs. However, there is no large-scale and publicly available eye movement dataset and benchmark for SZ recognition. To address these issues, we release a large-scale Eye Movement dataset for SZ recognition (EMS), which consists of eye movement data from 104 schizophrenics and 104 healthy controls (HCs) based on the free-viewing paradigm with 100 stimuli. We also conduct the first comprehensive benchmark, which has been absent for a long time in this field, to compare the related 13 psychosis recognition methods using six metrics. Besides, we propose a novel mean-shift-based network (MSNet) for eye movement-based SZ recognition, which elaborately combines the mean shift algorithm with convolution to extract the cluster center as the subject feature. In MSNet, first, a stimulus feature branch (SFB) is adopted to enhance each stimulus feature with similar information from all stimulus features, and then, the cluster center branch (CCB) is utilized to generate the cluster center as subject feature and update it by the mean shift vector. The performance of our MSNet is superior to prior contenders, thus, it can act as a powerful baseline to advance subsequent study. To pave the road in this research field, the EMS dataset, the benchmark results, and the code of MSNet are publicly available at https://github.com/YingjieSong1/EMS.