Objective: To develop a dual-branch deep learning framework for accurate multi-label classification of fundus diseases, addressing the key limitations of insufficient complementary feature extraction and inadequate cross-modal feature fusion in existing automated diagnostic methods. Methods: The fundus multi-label classification dataset with 12 disease categories (FMLC-12) dataset was constructed by integrating complementary samples from Ocular Disease Intelligent Recognition (ODIR) and Retinal Fundus Multi-Disease Image Dataset (RFMiD), yielding 6 936 fundus images across 12 retinal pathology categories, and the framework was validated on both FMLC-12 and ODIR. Inspired by the holistic multi-regional assessment principle of the Five Wheels theory in traditional Chinese medicine (TCM) ophthalmology, the dual-branch multi-label network (DBMNet) was developed as a novel framework integrating complementary visual feature extraction with pathological correlation modeling. The architecture employed a TransNeXt backbone within a dual-branch design: one branch processed red-green-blue (RGB) images to capture color-dependent features, such as vascular patterns and lesion morphology, while the other processed grayscale-converted images to enhance subtle textural details and contrast variations. A feature interaction module (FIM) effectively integrated the multi-scale features from both branches. Comprehensive ablation studies were conducted to evaluate the contributions of the dual-branch architecture and the FIM. The performance of DBMNet was compared against four state-of-the-art methods, including EfficientNet Ensemble, transfer learning-based convolutional neural network (CNN), BFENet, and EyeDeep-Net, using mean average precision (mAP), F1-score, and Cohen's kappa coefficient. Results: The dual-branch architecture improved mAP by 15.44 percentage points over the single-branch TransNeXt baseline, increasing from 34.41% to 44.24%, and the addition of FIM further boosted mAP to 49.85%. On FMLC-12, DBMNet achieved an mAP of 49.85%, a Cohen’s kappa coefficient of 62.14%, and an F1-score of 70.21%. Compared with BFENet (mAP: 45.42%, kappa: 46.64%, F1-score: 71.34%), DBMNet outperformed it by 4.43 percentage points in mAP and 15.50 percentage points in kappa, while BFENet achieved a marginally higher F1-score. On ODIR, DBMNet achieved an F1-score of 85.50%, comparable to state-of-the-art methods. Conclusion DBMNet effectively integrates RGB and grayscale visual modalities through a dual-branch architecture, significantly improving multi-label fundus disease classification. The framework not only addresses the issue of insufficient feature fusion in existing methods but also demonstrates outstanding performance in balancing detection across both common and rare diseases, providing a promising and clinically applicable pathway for standardized, intelligent fundus disease classification.

ObjectiveTo evaluate the detection specificity for clinical samples and the detection capability for standard substances of five commercially available multiplex polymerase chain reaction (PCR) nucleic acid detection kits (hereinafter referred to as the kits) for respiratory pathogens, and to provide a reference for selecting appropriate detection kits for multi-pathogen nucleic acid testing of respiratory infections. MethodsA total of 60 respiratory pathogen-positive clinical samples with known redults were selected and tested using the five kits (labeled as A, B, C, D, and E). The detection rates and Kappa coefficients were calculated to evaluate the consistency between the results from these kits and those from single-pathogen PCR kits. According to the limit of detection (LOD) provided by the kits, standard substances of respiratory pathogens (including 12 types such as influenza virus, Mycoplasma pneumoniae, and Bordetella pertussis) were diluted to four concentrations (250, 500, 1 000, and 2 000 copies·mL⁻¹). All five kits were used for detection to evaluate their respective detection capabilities. ResultsCompared with the results from single-pathogen PCR kits, the five tested kits demonstrated good consistency (all Kappa >0.80). Among them, Kit A had the highest detection rate (100.00%), followed by Kits C and E (98.33%), and then Kits B and D (95.00%). All five kits showed a relatively low false negative rate (FNR) for samples with a cycle threshold (Ct) value ≤35 (≤2.38%). However, for samples with Ct values>35, the FNR increased accordingly(average FNR=6.67%, P=0.029). Kit C exhibited the highest detection sensitivity for the tested standard substances (average LOD: 458.33 copies·mL⁻¹), followed by Kit D, then Kits A/E, and finally Kit B. ConclusionThe five multiplex PCR kits showed good consistency with single-pathogen detection results, but each had its own performance emphasis. Kit A, with the highest detection rate and high throughput, is suitable for targeted viral screening. Kit B, covering the broadest pathogen spectrum (including fungi/bacteria), is suitable for comprehensive respiratory pathogen screening. Kits C, D and E, are applicable for rapid detection. It is important to note that the detection efficacy of all kits decreases for low viral load samples with Ct values >35. In practical application, selection should be based on specific screening objectives, throughput requirements, and sample types.

ObjectiveTo investigate the effect and mechanism of long intergenic non-coding RNA02086 （LINC02086） overexpression mediated macrophage polarization on the proliferation， migration and invasion of gastric cancer cells. MethodsThe expression levels of LINC02086 in the human gastric epithelial cell line GES-1 and human gastric cancer cell lines HCG-27， NCI-N87， and AGS were determined by qRT-PCR. Human acute monocytic leukemia cells （THP-1） were induced to differentiate into M0 macrophages using phorbol 12-myristate 13-acetate （PMA）. HGC-27 cells were infected with either LINC02086 overexpression lentivirus （OE-LINC02086） or its negative control lentivirus （Vector）， and the culture supernatants were collected as conditioned medium （CM1）. M0 macrophages were co-cultured with the infected HGC-27 cells， and the resulting supernatants were designated as conditioned medium 2 （CM2）. M0 macrophages were treated with CM1 alone or in combination with Wnt/β-catenin pathway inhibitor IWR-1， forming the Vector+CM1， OE-LINC02086+CM1， and OE-LINC02086+CM1+IWR-1 groups， respectively. Flow cytometry was used to detect mannose receptor C-type 1 （CD206） expression， and qRT-PCR was employed to measure mRNA levels of interleukin-10 （IL⁃10）， transforming growth factor-β （TGF⁃β）， vascular endothelial growth factor （VEGF）， and chemokine ligand 22 （CCL22）. Western blot was performed to evaluate protein expression of CD206， VEGF， and key components of the Wnt/β-catenin pathway—Wnt family member 3a （Wnt3a）， glycogen synthase kinase-3β （GSK-3β）， and β-catenin. HGC-27 cells were treated with CM2 alone or combined with IWR-1， establishing the Vector+CM2， OE-LINC02086+CM2， and OE-LINC02086+CM2+IWR-1 groups. CCK-8 assay was used to evaluate cell proliferation， and Transwell assays were conducted to assess migration and invasion capabilities. ResultsCompared with GES-1 cells， the expression levels of LINC02086 were upregulated in HCG-27， NCI-N87， and AGS cells （P < 0.05）， with the smallest increase observed in HCG-27 cells. Compared with Vector+CM1 group， the level of CD206 and the expression levels of IL⁃10， TGF⁃β， VEGF and CCL22 mRNA in macrophages stimulated by OE-LINC02086+CM1 increased （P<0.05）. Meanwhile， the expression levels of Wnt3a and β-catenin proteins in cells increased （P<0.05）， and the expression level of GSK-3β protein decreased （P<0.05）. However， co-treatment with IWR-1 markedly reversed the promoting effects of LINC02086 overexpression on the expression of M2 polarization markers， including CD206， IL⁃10， and TGF⁃β mRNA， in macrophages （P<0.05）， as well as its activation of the Wnt/β-catenin signaling pathway （P<0.05）. Compared with Vector+CM2 group， HGC-27 cells infected with OE-LINC02086+CM2 had increased proliferation activity and increased number of migration and invasion cells （P<0.05）. However， the combined intervention of IWR-1 significantly reversed the promotion of LINC02086 overexpression on the proliferation， migration and invasion of HGC-27 cells （P<0.05）. ConclusionLINC02086 overexpression promotes the proliferation， migration and invasion of gastric cancer cells by activating Wnt/β-catenin pathway to mediate M2 polarization of macrophages.

ObjectiveZheng’s San Qi San (ZSQS) power, a classic traditional Chinese medicine (TCM) formula, is used for treating soft tissue injuries involving muscles, tendons, and ligaments. However, its underlying therapeutic mechanisms remain unclear. This study aimed to screen and identify pharmaceutically active ingredients and their candidate biomolecule targets, and further elucidate the molecular mechanism of ZSQS in the treatment of skeletal muscle injury. MethodsNetwork pharmacology was employed to construct “ZSQS-component-target”, “protein-protein interaction (PPI)” and “active ingredient-core protein-pathway” networks to predict the key active ingredients and potential core targets of ZSQS for skeletal muscle injury. The predicted results were then validated via microarray data from the GEO database. Molecular docking was then performed to assess the binding ability between the screened active ingredients of ZSQS and the candidate core targets. Moreover, liquid chromatography-mass spectrometry (LC-MS) was used for qualitative and quantitative analysis to verify the active components of the drug and ZSQS serum. Finally, an animal model of eccentric exercise-induced skeletal muscle injury and a myotube cell model of oxidative stress-induced injury were established to validate the effects of ZSQS and its interventional effects on the biological functions of critical targets, thereby demonstrating the potential therapeutic mechanism of ZSQS. ResultsAmong the 111 active components identified in ZSQS and their corresponding 204 targets related to the skeletal muscle injury repair process, 14 core targets (including AKT1) and 4 core active components (quercetin, luteolin, kaempferol, and β‑sitosterol) were screened out, while the corresponding metabolites of quercetin, luteolin and kaempferol were detected in the ZSQS serum. Among these targets, 5 candidate genes (IL-6, CASP3, HIF1A, STAT3, and JUN) overlapped with the differential expression screening results with GEO data, and IL-6 was confirmed to be enriched in the PI3K/AKT pathway. Combined with the prediction results of the AKT expression levels, these findings suggest that the phosphorylation level of AKT1 plays a core role in the therapeutic mechanism of ZSQS. Molecular docking analysis further revealed that the PH domain of AKT1 had high binding energy with all 4 core active components, as verified by LC-MS. Finally, animal model studies have shown the promoting effect of ZSQS administration on skeletal muscle injury repair and its possible antioxidant damage mechanism. Cell model studies further demonstrated that ZSQS-containing serum, core active ingredient combination therapy, and quercetin monomer could increase the phosphorylation level of AKT, promote the nuclear translocation of Nrf2, upregulate the expression of downstream antioxidant enzymes (SOD, GPx, and GR), and inhibit the expression of inflammatory factors (IL-6 and TNF-α), thereby alleviating oxidative stress and the inflammatory response. ConclusionZSQS alleviates skeletal muscle injury mainly by activating the AKT/Nrf2 signaling pathway, enhancing cellular antioxidant and anti-inflammatory capabilities. The results of this study provide a scientific basis for the clinical application and modernized development of ZSQS.

Osteoarthritis (OA), a highly prevalent degenerative joint disease worldwide, is defined by articular cartilage degradation, abnormal bone remodeling, and persistent chronic inflammation. It severely compromises patients’ quality of life, and currently, there is no radical cure. Abnormal mechanical stress is widely regarded as a core driver of OA pathogenesis, and the exploration of mechanical signal perception and transduction mechanisms has become crucial for deciphering OA’s pathophysiological processes. Piezo1, a key mechanosensitive cation channel belonging to the Piezo protein family, has recently gained significant attention due to its pivotal role in mediating cellular responses to mechanical stimuli in joint tissues. This review systematically examines Piezo1’s expression patterns, regulatory mechanisms, and pathological functions in OA, with a particular focus on its dual roles in modulating chondrocyte homeostasis and bone metabolism disorders, while also delving into the underlying molecular signaling pathways and potential therapeutic implications. Piezo1, consisting of approximately 2 500 amino acids and forming a unique trimeric propeller-like structure, is widely expressed in chondrocytes, osteocytes, mesenchymal stem cells, and synovial cells. It exhibits permeability to cations such as Ca²⁺, K⁺, and Na⁺, and directly responds to membrane tension changes induced by mechanical stimuli like fluid shear stress and mechanical overload. In OA patients and animal models, Piezo1 expression is significantly upregulated, especially in cartilage regions subjected to abnormal mechanical stress (e.g., human temporomandibular joint cartilage). This overexpression is closely associated with aggravated cartilage degeneration, increased chondrocyte apoptosis, accelerated cellular senescence, and intensified inflammatory responses. Mechanical overload and pro-inflammatory cytokines (e.g., IL-1β) are key inducers of Piezo1 upregulation: IL-1β activates the PI3K/AKT/mTOR signaling pathway to enhance Piezo1 expression, forming a pathogenic positive feedback loop that inhibits chondrocyte autophagy, promotes apoptosis, and further accelerates joint degeneration. Mechanistically, Piezo1 mediates OA progression through multiple interconnected pathways. When activated by mechanical stress, Piezo1 triggers excessive Ca²⁺ influx, leading to endoplasmic reticulum stress (ERS) and mitochondrial dysfunction, which directly induce chondrocyte apoptosis. This process involves the activation of downstream signaling cascades such as cGAS-STING and YAP-MMP13/ADAMTS5. YAP, a transcriptional regulator, upregulates the expression of matrix metalloproteinase 13 (MMP13) and aggrecanase (ADAMTS5), thereby accelerating cartilage matrix degradation. Additionally, Piezo1-driven Ca²⁺ overload promotes the accumulation of reactive oxygen species (ROS) and upregulates senescence markers (p16 and p21), accelerating chondrocyte senescence via the p38MAPK and NF-κB pathways. Senescent chondrocytes secrete senescence-associated secretory phenotype (SASP) factors (e.g., IL-6, IL-1β), further amplifying joint inflammation. In terms of bone metabolism, Piezo1 maintains joint homeostasis by promoting the differentiation of fibrocartilage stem cells into chondrocytes and balancing bone formation and resorption through regulating the FoxC1/YAP axis and RANKL/OPG ratio. Therapeutically, targeting Piezo1 shows promising potential. Preclinical studies have demonstrated that Piezo1 inhibitors (e.g., GsMTx4) can reduce joint damage and alleviate pain in OA mice. Simultaneously, siRNA-mediated co-silencing of Piezo1 and TRPV4 (another mechanosensitive channel) decreases intracellular Ca²⁺ concentration, inhibits chondrocyte apoptosis, and promotes cartilage repair. Conditional knockout of Piezo1 using Gdf5-Cre transgenic mice alleviates cartilage degeneration in post-traumatic OA models by downregulating MMP13 and ADAMTS5 expression. Despite existing challenges, such as off-target effects of inhibitors, inefficient local drug delivery, and interindividual genetic variability, strategies like developing selective Piezo1 antagonists, optimizing targeted nanocarriers, and combining Piezo1-targeted therapy with physical therapy provide viable avenues for clinical translation. The authors propose that Piezo1 serves as a critical therapeutic target for OA, and future research should focus on deciphering its context-dependent regulatory networks, developing tissue-specific intervention strategies, and validating their efficacy and safety in clinical trials to address the unmet medical needs of OA patients.

ObjectiveTo investigate the mechanisms of Runmu Dihuang decoction （RMDHD） in treating perimenopausal dry eye with liver-kidney Yin deficiency syndrome based on the silent information regulator 3 （SIRT3）/hypoxia-inducible factor-1α （HIF-1α）/nuclear factor-κB （NF-κB） signaling pathway. MethodsSixty female Sprague-Dawley rats were randomly divided into six groups （n=10 per group）： Sham operation group， model group， sodium hyaluronate eye drop group， and low-， medium-， and high-dose RMDHD groups （5.625， 11.25， 22.50 g·kg^-1）. Except for the sham operation group， all rats underwent bilateral ovariectomy and were administered 0.1% benzalkonium chloride eye drops combined with long-term chronic irritation to establish a perimenopausal dry eye model with liver-kidney Yin deficiency syndrome. Drug administration began in the 11th week after modeling and continued for 21 days. General conditions， screen-grip test scores， tear secretion volume， tear film breakup time （TFBUT）， and corneal fluorescein staining were recorded. Serum levels of reactive oxygen species （ROS）， follicle-stimulating hormone （FSH）， estradiol （E₂）， and progesterone （PROG） were measured by enzyme-linked immunosorbent assay （ELISA）. Pathological changes in the lacrimal glands， corneas， and uteri were observed using hematoxylin-eosin （HE） staining. Protein expression levels of SIRT3， HIF-1α， phosphorylated NF-κB p65 （p-NF-κB p65）， and total NF-κB p65 in the lacrimal glands were detected by Western blot. The expression of inflammatory cytokines interleukin-1β （IL-1β） and tumor necrosis factor-α （TNF-α） in the lacrimal glands was assessed by immunohistochemistry （IHC）. ResultsAfter model establishment， no significant differences were observed among the groups except the sham operation group. Compared with the sham operation group， the other groups exhibited slowed movement， dull responses， increased irritability， reduced body weight， elevated rectal temperature， decreased screen-grip test scores， reduced tear secretion， and significantly shortened TFBUT （P<0.05）. After treatment， compared with the model group， the sodium hyaluronate eye drop group and all RMDHD groups showed improved general conditions， significantly increased tear secretion （P<0.05）， prolonged TFBUT （P<0.05）， and elevated screen-grip test scores （P<0.05）. Serum ROS and FSH levels were significantly decreased， while E₂ and PROG levels were significantly increased （P<0.05）. Pathological damage to the cornea， lacrimal glands， and uterus was ameliorated. In addition， protein expression levels of SIRT3 and HIF-1α in the lacrimal glands were significantly upregulated （P<0.05）， whereas the expression of p-NF-κB p65， IL-1β， and TNF-α was significantly downregulated （P<0.05）. ConclusionRMDHD increases tear secretion and TFBUT， improves lacrimal gland and corneal injury， and alleviates dry eye symptoms in a perimenopausal dry eye rat model with liver-kidney Yin deficiency syndrome. The underlying mechanism may be related to regulation of the SIRT3/HIF-1α/NF-κB signaling pathway， inhibition of oxidative stress and inflammatory responses， and reduction of ocular surface tissue damage.

Objective To understand the individual radiation dose levels and changes of occupational external exposure among radiation workers in a steel group from 2020 to 2023, and to provide a basis for strengthening radiation protection in the group. Methods According to the Specifications for individual monitoring of occupational external exposure (GBZ 128-2019), individual monitoring was conducted using a thermoluminescent dosimeter, with each monitoring cycle lasting 90 days, totaling four cycles per year. Individual monitoring data of occupational external exposure among radiation workers in the steel group from 2020 to 2023 were collected for statistical analysis. Results A total of 5889 monitoring records were collected from radiation workers across 37 affiliated units of the steel group during the period of 2020-2023. The average annual effective dose was 0.150 mSv, the maximum annual effective dose was 3.84 mSv, and 0.3% monitored workers showed annual effective doses exceeding 1 mSv. The average annual effective dose in 2023 was 0.146 mSv, which was lower than in 2020 but higher than in 2021 and 2022 (Z = −6.657 to 14.129, P < 0.001). The number of monitored workers in industrial and medical sectors accounted for 86.9% and 13.1%, respectively. Their average annual effective doses were 0.152 mSv and 0.140 mSv, respectively, and the difference was statistically significant (Z = −7.969, P < 0.001). In the industrial sector, the average annual effective dose for the monitored workers in industrial radiography was significantly higher than other occupations (Z = −8.094, P < 0.001). There was a significant difference in average annual effective dose among workers of different occupational categories in the medical sector (H = 67.040, P < 0.001). The average annual effective doses were relatively high for diagnostic radiology and nuclear medicine. Additionally, the average annual effective doses for male and female radiation workers were 0.150 mSv and 0.152 mSv, respectively (P > 0.05). Conclusion The average annual effective dose of radiation workers in the steel group was at low levels for four consecutive years, which meet the requirements of the national standard. However, to maintain the individual radiation dose levels of radiation workers as low as reasonably achievable, it remains necessary to strengthen radiation protection management in the steel group.

ObjectiveBased on functional near-infrared spectroscopy (fNIRS), we investigated the brain activity characteristics of gross motor tasks in children with autism spectrum disorder (ASD) and motor dysfunctions (MDs) to provide a theoretical basis for further understanding the mechanism of MDs in children with ASD and designing targeted intervention programs from a central perspective. MethodsAccording to the inclusion and exclusion criteria, 48 children with ASD accompanied by MDs were recruited into the ASD group and 40 children with typically developing (TD) into the TD group. The fNIRS device was used to collect the information of blood oxygen changes in the cortical motor-related brain regions during single-handed bag throwing and tiptoe walking, and the differences in brain activation and functional connectivity between the two groups of children were analyzed from the perspective of brain activation and functional connectivity. ResultsCompared to the TD group, in the object manipulative motor task (one-handed bag throwing), the ASD group showed significantly reduced activation in both left sensorimotor cortex (SMC) and right secondary visual cortex (V2) (P<0.05), whereas the right pre-motor and supplementary motor cortex (PMC&SMA) had significantly higher activation (P<0.01) and showed bilateral brain region activity; in terms of brain functional integration, there was a significant decrease in the strength of brain functional connectivity (P<0.05) and was mainly associated with dorsolateral prefrontal cortex (DLPFC) and V2. In the body stability motor task (tiptoe walking), the ASD group had significantly higher activation in motor-related brain regions such as the DLPFC, SMC, and PMC&SMA (P<0.05) and showed bilateral brain region activity; in terms of brain functional integration, the ASD group had lower strength of brain functional connectivity (P<0.05) and was mainly associated with PMC&SMA and V2. ConclusionChildren with ASD exhibit abnormal brain functional activity characteristics specific to different gross motor tasks in object manipulative and body stability, reflecting insufficient or excessive compensatory activation of local brain regions and impaired cross-regions integration, which may be a potential reason for the poorer gross motor performance of children with ASD, and meanwhile provides data support for further unraveling the mechanisms underlying the occurrence of MDs in the context of ASD and designing targeted intervention programs from a central perspective.

OBJECTIVE To evaluate the efficacy and safety of immune checkpoint inhibitors combined with neoadjuvant chemotherapy and adjuvant chemotherapy in the treatment of early-stage triple-negative breast cancer （TNBC）. METHODS A systematic search was conducted in PubMed， Embase， Cochrane Library， CNKI， and Wanfang Data to collect randomized controlled trials （RCT） on the use of immune checkpoint inhibitors combined with neoadjuvant chemotherapy and adjuvant chemotherapy （experimental group） versus neoadjuvant chemotherapy and adjuvant chemotherapy （control group） in the treatment of TNBC. After literature screening， data extraction and literature quality evaluation， meta-analysis was performed using Stata 17.0. RESULTS A total of 5 RCT involving 1 498 patients were included. The meta-analysis results showed that the pathological complete response rate （pCR） [RR＝1.34， 95%CI （1.09， 1.63）， P＝0.03]， pCR in patients with positive programmed death-1 （PD-1） and its ligand （PD-L1） [RR＝1.33， 95%CI （1.16， 1.51）， P＝0.01]， pCR in patients with positive lymph nodes [RR＝ 1.56， 95%CI （1.27， 1.93）， P＝0.01]， the incidence of grade 3-4 adverse events （AEs） [RR＝1.07， 95%CI （1.01， 1.14）， P＝ 0.04]， the incidence of serious AEs [RR＝1.57， 95%CI （1.31， 1.87）， P＝0.03]， and the incidence of treatment discontinuation due to AEs [RR＝1.45， 95%CI （1.19， 1.76）， P＝0.01] were significantly higher in the experimental group than control group. There were no statistically significant difference in pCR in patients with negative PD-1/PD-L1[RR＝ E-mail：biejun23@126.com 1.26， 95%CI （0.98， 1.62）， P＝0.08] and pCR in patients with negative lymph nodes [RR＝1.14， 95%CI （0.97， 1.33）， P＝0.17] between the two groups. CONCLUSIONS Immune checkpoint inhibitors combined with neoadjuvant chemotherapy and adjuvant chemotherapy demonstrates significant efficacy in early-stage TNBC patients， with more pronounced benefits observed in those who are PD-1/PD-L1 positive and lymph node- positive. However， the incidence of AEs is relatively high.

Cell Biology is one of the most rapidly developing branches of modern life sciences, characterized by distinct interdisciplinary integration. It provides theoretical foundations, experimental skills, and cutting-edge perspectives for undergraduate and graduate students in bioscience and related majors. Against the backdrop of higher education reform in the new era, the Cell Biology teaching team at the University of Chinese Academy of Sciences (UCAS) has restructured the curriculum. The course focuses on the fundamental structures and life processes of cells while incorporating ideological and political elements to foster students’ scientific mindset, patriotic sentiment, and social responsibility. By optimizing teaching design, enhancing practical components, and innovating assessment methods, the course integrates knowledge transfer, skill development, and value education. This paper summarizes preliminary experiences from the teaching development and educational practice of the undergraduate Cell Biology course at UCAS, serving as a reference for collaborative research- and teaching-oriented courses in science and engineering.