ObjectivePost-ischemic acute inflammation and the subsequent persistent dysregulation of the immune microenvironment represent major pathological drivers that aggravate neuronal injury and severely restrict functional recovery following ischemic stroke. Although current reperfusion therapies partially restore blood flow, they fail to effectively modulate the secondary inflammatory cascade and oxidative stress, which remain critical barriers to neurological restoration. To address this challenge, this study aimed to engineer and systematically evaluate a biomimetic nanosystem composed of transforming growth factor-β1 (TGF-β1)-loaded platelet membrane-camouflaged lipid nanoparticles (PLP). This nanosystem was designed to achieve dual lesion-targeted delivery and immune microenvironment remodeling. By verifying its spatiotemporal accumulation, anti-inflammatory activity, and neuroprotective efficacy, we sought to establish an integrated therapeutic strategy that simultaneously enables lesion targeting, immune regulation, and functional recovery after ischemic injury. MethodsThe physicochemical properties of PLP, including hydrodynamic particle size, zeta potential, structural stability, and morphology, were characterized using dynamic light scattering, zeta potential analysis, and transmission electron microscopy. The preservation of platelet membrane-derived adhesion and immunoregulatory proteins was confirmed by SDS-PAGE through comparative analysis of protein band profiles between PLP and native platelet membranes. The in vitro biological activities of PLP were evaluated using two complementary cellular models. LPS-induced M1-polarized RAW264.7 macrophages were employed to assess inflammatory modulation, while oxygen glucose deprivation/reperfusion (OGD/R)-induced BV2 microglial cells and SH-SY5Y neuronal cells were utilized to investigate neuroinflammatory regulation and neuronal protection. For in vivo validation, a transient middle cerebral artery occlusion (tMCAO) mouse model was established to mimic ischemia-reperfusion injury. The spatiotemporal biodistribution and lesion-targeting capability of the PLP were monitored through live fluorescence imaging. Therapeutic efficacy was comprehensively evaluated by triphenyltetrazolium chloride (TTC) staining, glial fibrillary acidic protein (GFAP) immunofluorescence analysis, body weight monitoring, and neurological severity score (NSS) assessment. ResultsPLP nanoparticles displayed a uniform spherical morphology, nanoscale particle size distribution, and stable negative surface charge, indicating favorable colloidal stability and circulation potential. SDS-PAGE results confirmed the effective retention of key platelet membrane proteins associated with endothelial adhesion, immune evasion, and inflammatory regulation, demonstrating the successful biomimetic construction. Optimal therapeutic concentrations were determined in OGD/R-induced BV2 cells, where PLP exhibited excellent cytocompatibility and anti-inflammatory activity.In vitro experiments demonstrated that PLP significantly inhibited the polarization of RAW264.7 macrophages toward the pro-inflammatory M1 phenotype and markedly reduced neuronal apoptosis under ischemia-reperfusion conditions. In vivo fluorescence imaging revealed that PLP rapidly accumulated in the ischemic brain hemisphere and maintained prolonged retention for up to 7 d, suggesting enhanced lesion-specific targeting and sustained drug release. Compared with control group, PLP treatment significantly reduced cerebral infarct volume, attenuated reactive astrogliosis, improved weight recovery, and accelerated neurological functional restoration, as reflected by significantly improved NSS scores. ConclusionThis study establishes a multifunctional biomimetic nanoplatform that integrates platelet membrane-mediated active targeting with the anti-inflammatory, antioxidative, and neuroprotective properties of TGF-β1. The PLP system enables rapid lesion homing and long-term retention while synergistically regulating the post-stroke inflammatory microenvironment by suppressing pro-inflammatory immune activation, reducing neuronal apoptosis, and limiting excessive astrocyte reactivity. Importantly, this study proposes a conceptually therapeutic paradigm that combines targeted delivery with immune microenvironment remodeling to achieve comprehensive neurovascular protection. These findings provide strong experimental evidence supporting the translational potential of biomimetic nanotherapeutics as next-generation precision interventions for ischemic stroke.

Objective: To explore the feasibility, precision, and clinical value of a personalized primary repair approach centered on digital design, integrating 3D printing technology with multiple materials such as titanium mesh, polyetheretherketone (PEEK), and titanium plates, for complex craniofacial bone defects involving the skull, mandible, orbit, and zygoma resulting from traffic accidents, providing a reference for primary repair of clinically complex craniofacial bone defects. Methods: One patient who was admitted in September 2021 with multiple comminuted fractures of the right craniomaxillofacial region and large-area bone defects caused by a traffic accident was selected. Digital design was integrated throughout the entire repair process. First, preoperative computed tomography (CT) data were used for 3D reconstruction of the craniomaxillofacial region; then, based on the model, the anatomical contour of the healthy left side was reproduced via mirroring technology for the defects on the right side. A targeted repair plan was designed: 3D-printed PEEK material was used to reconstruct the right orbital floor and zygomaticomaxillary complex, a 0.6-mm-thick titanium mesh was adopted to repair the right skull defect, and a 2.0-mm-thick titanium plate was applied for rigid internal fixation of the mandibular fracture. A one-stage repair surgery was completed simultaneously. In addition, a literature review was conducted on studies related to the repair of complex combined craniomaxillofacial defects. Results: CT examination at 1 week postoperatively showed that the average fitting gap of the implants was 0.3 mm, and the symmetry difference of the facial contour was less than 5 mm. At 3 months postoperatively, the patient’s maximum mouth opening reached 38 mm, the occlusal relationship returned to normal, and the diplopia symptom completely disappeared. During the 6-month postoperative follow-up, no complications such as implant loosening, infection, or displacement occurred; the FACE-Q scale score was 91, indicating a high level of subjective patient satisfaction. The literature review indicated that digital design combined with 3D printing technology can significantly improve the accuracy of complex craniomaxillofacial bone defect reconstruction. PEEK material is suitable for the reconstruction of the orbital floor and zygomaticomaxillary complex. Titanium mesh and plates can ensure the stability of the reconstruction. Multi-materials combined reconstruction represents an important therapeutic strategy for such defects. Conclusion The individualized one-stage repair scheme, centered on digital design and combined with 3D printing technology and multi-materials (titanium mesh, PEEK, and titanium plates), can achieve precise anatomical reduction and simultaneous functional recovery for complex combined craniomaxillofacial bone defects caused by traffic accidents.

Methods: Fifty patients who underwent UBE-TLIF and 50 patients who underwent W-TLIF, each with >2 years of follow-up, were retrospectively analyzed. Outcomes included operative parameters, time to postoperative mobilization, paravertebral muscle atrophy and fat infiltration rates, clinical scores (Visual Analog Scale [VAS], Oswestry Disability Index [ODI], Japanese Orthopaedic Association [JOA]), modified Macnab criteria, fusion rates, and complications. Results: Compared with W-TLIF, the UBE-TLIF group had significantly less intraoperative blood loss, shorter operative times, and lower postoperative drainage volumes (p <0.05). The UBE-TLIF group showed faster postoperative recovery and shorter hospital stays. At 6 months, 1 year, and 2 years, W-TLIF patients had higher multifidus and erector spinae atrophy, and greater paravertebral muscle fat infiltration (p <0.05). The UBE-TLIF group also had lower VAS and ODI scores at 1 year and 2 years (p <0.05) and fewer surgical complications (6% vs. 10%). Fusion rates (94% vs. 92%) and modified Macnab outcomes (88% vs. 86%) were comparable (p >0.05). Conclusions UBE-TLIF is associated with reduced intraoperative trauma, quicker recovery, and fewer complications. In the long-term, it better preserves paravertebral muscle integrity and provides superior pain and functional outcomes.

Objectives: . This study aimed to explore the role of the Pcdh15 gene in hearing maintenance and to examine the effects of its deficiency on cochlear structure, cochlear function, and hearing loss in mice. Methods: . CRISPR/Cas9 technology was used to generate Pcdh15 knockout (KO) mice. Auditory function was evaluated using hearing tests, while histological approaches were employed to assess morphological changes in cochlear hair cells and spiral ganglion neurons (SGNs). RNA sequencing (RNA-seq) was performed on cochlear tissue from postnatal day 18 (P18) wild-type (WT) and Pcdh15 KO mice to identify differentially expressed genes (DEGs). These DEGs were subjected to functional annotation and pathway analysis, with particular emphasis on oxidative phosphorylation (OXPHOS). Reactive oxygen species (ROS) levels were quantified using flow cytometry and DCFH-DA assays. Results: . Pcdh15 KO mice exhibited progressive sensorineural hearing loss, which worsened to profound deafness by P18. Notably, cochlear hair cells and SGNs showed substantial loss and pronounced morphological abnormalities, particularly within the basal high-frequency region. RNA-seq analysis identified 1,359 DEGs, including 1,024 downregulated and 335 upregulated genes. Pathway analysis indicated that Pcdh15 deficiency was associated with inhibition of the OXPHOS pathway, potentially disrupting mitochondrial respiratory chain complexes I, III, IV, and V and thereby impairing energy production and ATP metabolism. In addition, early-stage cochleae from KO mice demonstrated elevated ROS levels and increased oxidative stress, suggesting that redox imbalance may contribute to hearing damage. Conclusion . Pcdh15 plays a critical role in hearing maintenance. Its deficiency is associated with severe hearing loss and marked cochlear abnormalities, which are linked to inhibition of OXPHOS, disruption of energy metabolism, and exacerbation of oxidative stress. Together, these findings provide new insights into the mechanisms underlying hearing loss and suggest potential targets for therapeutic intervention.

Farrerol is a dihydroflavone compound extracted from the dried leaves of Rhododendron dauricum belonging to the Ericaceae family. This article systematically reviews relevant research on farrerol both domestically and internationally， summarizes its pharmacological activities and mechanisms of action， and finds that it exerts cardiovascular and cerebrovascular protective effects by maintaining the homeostasis of vascular endothelial function and inhibiting vascular intimal hyperplasia； exerts renal protective effects by activating the nuclear factor erythroid 2-related factor 2 （Nrf2） signaling pathway to reduce renal damage； exerts liver protective effects by inhibiting the phosphatidylinositol 3-kinase/protein kinase B signaling pathway， activating the Nrf2 signaling pathway， improving insulin resistance， and reducing lipid deposition in the liver； exerts neuroprotective effects by activating the Nrf2/Keap1 signaling pathway， inhibiting the Toll-like receptor 4 and cyclic GMP-AMP synthase/stimulator of interferon genes signaling pathways to reduce neuroinflammatory damage； exerts bone protective effects by promoting tendon formation and inhibiting osteoclast differentiation； exerts antitumor effects by inducing tumor cell apoptosis and weakening tumor cell invasion and metastasis； and exerts antibacterial effects by downregulating α -toxin expression， interfering with β -lactamase/penicillin-binding protein 2a （PBP2a）， and inhibiting PBP2a oligomerization. Currently， research on the pharmacological effects of farrerol is still mainly focused on animal and cell experiments. Further mechanistic studies and clinical trials are needed to provide theoretical basis for its new drug development and clinical application.

Farrerol is a dihydroflavone compound extracted from the dried leaves of Rhododendron dauricum belonging to the Ericaceae family. This article systematically reviews relevant research on farrerol both domestically and internationally， summarizes its pharmacological activities and mechanisms of action， and finds that it exerts cardiovascular and cerebrovascular protective effects by maintaining the homeostasis of vascular endothelial function and inhibiting vascular intimal hyperplasia； exerts renal protective effects by activating the nuclear factor erythroid 2-related factor 2 （Nrf2） signaling pathway to reduce renal damage； exerts liver protective effects by inhibiting the phosphatidylinositol 3-kinase/protein kinase B signaling pathway， activating the Nrf2 signaling pathway， improving insulin resistance， and reducing lipid deposition in the liver； exerts neuroprotective effects by activating the Nrf2/Keap1 signaling pathway， inhibiting the Toll-like receptor 4 and cyclic GMP-AMP synthase/stimulator of interferon genes signaling pathways to reduce neuroinflammatory damage； exerts bone protective effects by promoting tendon formation and inhibiting osteoclast differentiation； exerts antitumor effects by inducing tumor cell apoptosis and weakening tumor cell invasion and metastasis； and exerts antibacterial effects by downregulating α -toxin expression， interfering with β -lactamase/penicillin-binding protein 2a （PBP2a）， and inhibiting PBP2a oligomerization. Currently， research on the pharmacological effects of farrerol is still mainly focused on animal and cell experiments. Further mechanistic studies and clinical trials are needed to provide theoretical basis for its new drug development and clinical application.

Objective: To explore the association between executive function and emotional and behavioral problems in first-grade elementary school students, so as to provide a reference for promoting children s mental health. Methods: From March to May 2024, 423 first-grade elementary school students from 6 primary schools aged 6-7 were selected by using stratified cluster random sampling in Shanxi, Shanghai, Shandong, Guangxi, Xinjiang, and Jiangxi. Data were collected by using the Executive Function Assessment Scale and the Strengths and Difficulties Questionnaire. An independent samples t-test was used to analyze differences in executive function of different genders and differences in emotional and behavioral problems among first-grade school students with varying executive function levels; a linear regression model was employed to analyze the association between children s executive function and emotional and behavioral problems. Results: A total of 42 first-grade elementary school students (9.9%) were identified as having executive function deficits. Students in the executive function deficit group scored higher on internalizing behavior (7.50±0.52), externalizing behavior (11.26±0.52), and total difficulties (18.52± 0.93 ) were significantly higher than those of children without deficits (4.37±0.14, 6.69±0.17, 10.64±0.27) ( t =5.79, 8.50, 9.23, all P <0.05). Results of linear regression analysis showed that, after controlling for relevant covariates such as gender, age, family economic status, being an only child, and body mass index, the factor scores, dimensional scores, and total scores of executive function were all positively correlated with scores for externalizing problems, internalizing problems, and total difficulties ( β =0.07-0.32, all P <0.05). Conclusions Children s executive function is closely associated with emotional and behavioral problems, and those with poorer executive function exhibit more pronounced emotional and behavioral problems. Improving children s executive function may help promote their mental health.

Objective: To examine the effects of combined aerobic and resistance exercise on health related physical fitness (HPF) and depressive symptoms among senior high school freshmen, and to examine whether HPF mediates the relationship between exercise intervention and depressive symptoms, so as to provide a scientific basis for the coordinated promotion of mental health and physical fitness in schools. Methods: In March 2022, 190 senior high school freshmen from a secondary school of Suzhou in Anhui Province were selected by the random cluster sampling method and randomly assigned to an intervention group ( n = 99) and a control group ( n =91). The control group maintained routine activities, while the intervention group underwent a 10 week combined aerobic and resistance exercise program, three sessions per week, 40 minutes per session. Height, weight, standing long jump, sit ups, 20 m shuttle run, and sit and reach were measured before and after the intervention. Depressive symptoms were assessed using the Center for Epidemiological Studies Depression Scale (CES-D). Analysis of covariance (ANCOVA), Mann-Whitney U test, and Wilcoxon test were employed to compare outcomes before and after the intervention, and mediation analysis was conducted. Results: After controlling for pre test scores, ANCOVA results showed that compared with the control group, the intervention group demonstrated the following post intervention changes: a lower body mass index of 0.1 kg/m 2 among girls; higher standing long jump (13.2 cm for boys, 7.4 cm for girls), higher sit ups (5.5 reps for boys, 3.7 reps for girls), higher 20 m shuttle run (7.4 times for boys, 5.1 times for girls), and higher sit and reach (3.2 cm for boys, 0.4 cm for girls) ( F =17.88-84.44); and lower CES-D scores (5.5 for boys, 4.0 for girls) ( Z =-2.51, -2.06) (all P <0.05). The indirect effect of HPF in the relationship between combined aerobic and resistance exercise and depressive symptoms was -2.11, supporting a partial mediation effect ( P < 0.01 ). Conclusions Combined aerobic and resistance exercise improves HPF and alleviates depressive symptoms to varying degrees among senior high school freshmen. HPF served as a partial mediator through which exercise intervention reduces depressive symptoms.

Alzheimer’s disease (AD) is a prevalent neurodegenerative condition characterized by progressive cognitive decline and memory loss. As the incidence of AD continues to rise annually, researchers have shown keen interest in the active components found in natural plants and their neuroprotective effects against AD. Quercetin, a flavonol widely present in fruits and vegetables, has multiple biological effects including anticancer, anti-inflammatory, and antioxidant. Oxidative stress plays a central role in the pathogenesis of AD, and the antioxidant properties of quercetin are essential for its neuroprotective function. Quercetin can modulate multiple signaling pathways related to AD, such as Nrf2-ARE, JNK, p38 MAPK, PON2, PI3K/Akt, and PKC, all of which are closely related to oxidative stress. Furthermore, quercetin is capable of inhibiting the aggregation of β‑amyloid protein (Aβ) and the phosphorylation of tau protein, as well as the activity of β‑secretase 1 and acetylcholinesterase, thus slowing down the progression of the disease.The review also provides insights into the pharmacokinetic properties of quercetin, including its absorption, metabolism, and excretion, as well as its bioavailability challenges and clinical applications. To improve the bioavailability and enhance the targeting of quercetin, the potential of quercetin nanomedicine delivery systems in the treatment of AD is also discussed. In summary, the multifaceted mechanisms of quercetin against AD provide a new perspective for drug development. However, translating these findings into clinical practice requires overcoming current limitations and ongoing research. In this way, its therapeutic potential in the treatment of AD can be fully utilized.

Alzheimer’s disease (AD) is a chronic neurodegenerative disorder that severely affects the health of the elderly, marked by its incurability, high prevalence, and extended latency period. The current approach to AD prevention and treatment emphasizes early detection and intervention, particularly during the pre-AD stage of mild cognitive impairment (MCI), which provides an optimal “window of opportunity” for intervention. Clinical detection methods for MCI, such as cerebrospinal fluid monitoring, genetic testing, and imaging diagnostics, are invasive and costly, limiting their broad clinical application. Speech, as a vital cognitive output, offers a new perspective and tool for computer-assisted analysis and screening of cognitive decline. This is because elderly individuals with cognitive decline exhibit distinct characteristics in semantic and audio information, such as reduced lexical richness, decreased speech coherence and conciseness, and declines in speech rate, voice rhythm, and hesitation rates. The objective presence of these semantic and audio characteristics lays the groundwork for computer-based screening of cognitive decline. Speech information is primarily sourced from databases or collected through tasks involving spontaneous speech, semantic fluency, and reading, followed by analysis using computer models. Spontaneous language tasks include dialogues/interviews, event descriptions, narrative recall, and picture descriptions. Semantic fluency tasks assess controlled retrieval of vocabulary items, requiring participants to extract information at the word level during lexical search. Reading tasks involve participants reading a passage aloud. Summarizing past research, the speech characteristics of the elderly can be divided into two major categories: semantic information and audio information. Semantic information focuses on the meaning of speech across different tasks, highlighting differences in vocabulary and text content in cognitive impairment. Overall, discourse pragmatic disorders in AD can be studied along three dimensions: cohesion, coherence, and conciseness. Cohesion mainly examines the use of vocabulary by participants, with a reduction in the use of nouns, pronouns, verbs, and adjectives in AD patients. Coherence assesses the ability of participants to maintain topics, with a decrease in the number of subordinate clauses in AD patients. Conciseness evaluates the information density of participants, with AD patients producing shorter texts with less information compared to normal elderly individuals. Audio information focuses on acoustic features that are difficult for the human ear to detect. There is a significant degradation in temporal parameters in the later stages of cognitive impairment; AD patients require more time to read the same paragraph, have longer vocalization times, and produce more pauses or silent parts in their spontaneous speech signals compared to normal individuals. Researchers have extracted audio and speech features, developing independent systems for each set of features, achieving an accuracy rate of 82% for both, which increases to 86% when both types of features are combined, demonstrating the advantage of integrating audio and speech information. Currently, deep learning and machine learning are the main methods used for information analysis. The overall diagnostic accuracy rate for AD exceeds 80%, and the diagnostic accuracy rate for MCI also exceeds 80%, indicating significant potential. Deep learning techniques require substantial data support, necessitating future expansion of database scale and continuous algorithm upgrades to transition from laboratory research to practical product implementation.