Background Prolonged vibration exposure can lead to vascular endothelial cell dysfunction and cellular injury. However, research on the association between vibration and ferroptosis in vascular endothelial cells remains insufficient. Objective To explore whether occupational vibration exposure is associated with alterations in serum markers related to ferroptosis in patients with hand-arm vibration disease (HAVD), and to further investigate, through in vitro cell experiments, whether vibration exposure may induce ferroptosis in vascular endothelial cells. Methods ①A judgmental sampling method was employed to select 50 workers with HAVD (the HAVD group), 50 vibration-exposed workers without HAVD (the vibration exposure group), and 50 non–hand-transmitted vibration-exposed workers (the control group). Serum iron levels, malondialdehyde (MDA) content, and superoxide dismutase (SOD) levels were measured using serum iron assay kits, MDA detection kits, and SOD detection kits, respectively. One-way analysis of variance and binary logistic regression analysis were performed to examine the relationships between these indicators and HAVD. ②Human umbilical vein endothelial cells (HUVEC) were divided into a vibration group and a control group. The vibration group was subjected to vibration at 120 Hz with an acceleration of 6.5 m·s⁻² and further subdivided into four subgroups: 1 d 2 h, 1 d 4 h, 2 d 2 h, and 2 d 4 h. The control group was treated identically except for vibration exposure. Cellular iron (Fe²⁺) content and reduced glutathione (GSH) levels in HUVEC were measured using ferrous iron colorimetric assay kits and GSH colorimetric assay kits, respectively, to assess the effects of different vibration exposure schedules. Real-time quantitative polymerase chain reaction (RT-qPCR) was performed to detect the mRNA expression levels of ferroptosis-related genes, including acyl-CoA synthetase long-chain family member 4 (ACSL4), tumor suppressor protein P53 (P53), ferritin heavy chain 1 (FTH1), and glutathione peroxidase 4 (GPX4). Western blot analysis was conducted to determine the protein expression levels of ferroptosis-related markers in HUVEC. Results ①Compared with the control group, the patients in the HAVD group showed increased serum iron and MDA levels, along with decreased SOD levels (P<0.05). The logistic regression analysis indicated that elevated serum iron levels were significantly associated with an increased risk of HAVD (OR=4.034; 95%CI: 2.063, 7.887), and elevated MDA levels were also associated with an increased risk of HAVD (OR=1.523; 95%CI: 1.026, 1.936). ②Compared with the control group, increased intracellular Fe²⁺ content and decreased GSH content were observed in HUVECs in the 1 d 4 h and 2 d 4 h vibration subgroups (P<0.05). The RT-qPCR results showed that, compared with the control group, vibration exposures of 1 d 4 h and 2 d 4 h significantly upregulated the expression of ACSL4 and P53 (P<0.05), whereas the mRNA expression levels of GPX4 and FTH1 were downregulated in all vibration-exposed endothelial cells (P<0.05). The Western blot results revealed that, compared with the control group, the vibration exposure schedules of 1 d 2 h and 1 d 4 h significantly upregulated the protein expression levels of ACSL4 and P53 (P<0.05), while the vibration exposure schedules of 1 d 4 h, 2 d 2 h, and 2 d 4 h significantly downregulated the protein expression levels of FTH1 and GPX4 (P<0.05). Conclusion Occupational vibration exposure is associated with alterations in iron metabolism and oxidative stress status in workers with HAVD. The in vitro experiments further demonstrates that vibration stimulation induces intracellular iron accumulation and reduces antioxidant capacity in vascular endothelial cells, accompanied by dysregulated expression of ferroptosis-related molecules. These findings suggest that ferroptosis may play a role in vibration-induced vascular injury and the pathogenesis of HAVD.

Cancer remains a leading cause of global mortality, necessitating the development of advanced therapeutic strategies with enhanced efficacy and reduced systemic toxicity. Among promising bioactive agents, lactoferrin (LF)—a multifunctional iron-binding glycoprotein abundantly found in mammalian milk and exocrine secretions—has garnered significant interest for its potent and multifaceted anti-cancer properties. This review provides a comprehensive analysis of the current understanding of LF’s role in oncology, encompassing its structural biology, diverse mechanisms of action, and groundbreaking advancements in its application through nano-engineering. LF exerts anti-tumor effects through multiple pathways, including extracellular action, intracellular action, and immune regulation. It demonstrates a remarkable affinity for cancer cell membranes, binding to overexpressed anionic components such as glycosaminoglycans and sialic acids, as well as to specific receptors including the low-density lipoprotein receptor-related protein-1 (LRP-1). This selective binding facilitates targeted uptake. Upon internalization, LF orchestrates a direct assault by inducing cell-cycle arrest in phases such as G0/G1 or S phase through the modulation of key regulators including cyclins, CDKs, and p53. Furthermore, it promotes programmed cell death via apoptotic pathways, involving caspase activation and downregulation of anti-apoptotic proteins such as survivin. A more recently elucidated mechanism is the induction of ferroptosis, an iron-dependent form of cell death characterized by overwhelming lipid peroxidation. Beyond direct cytotoxicity, LF acts as a potent immunomodulator. It enhances natural killer (NK) cell activity, modulates T-lymphocyte populations, and crucially reprograms tumor-associated macrophages (TAMs) from a pro-tumor M2 state to an anti-tumor M1 state, thereby reversing the immunosuppressive tumor microenvironment (TME). The translation of LF’s potential has been significantly accelerated by nanotechnology. The inherent biocompatibility and natural tumor-targeting capabilities of LF make it an ideal platform for sophisticated drug-delivery systems. This review details various fabrication strategies for LF-based nanoparticles (NPs), including self-assembly, sol-in-oil emulsion, and electrostatic nanocomplexes, among others. Research demonstrates that nano-formulations not only protect LF from degradation but also enhance its bioactivity and anti-cancer potency. More importantly, LF NPs serve as versatile carriers for a wide array of therapeutic agents, including conventional chemotherapeutics, natural compounds, and imaging agents. These engineered systems enable synergistic therapy and facilitate site-specific delivery. Notably, the ability of LF to bind to receptors on the blood-brain barrier (BBB) has been leveraged to develop nano-systems for glioblastoma treatment. Other innovative designs utilize LF to modulate the TME—for instance, by alleviating tumor hypoxia to sensitize cells to radiotherapy and chemotherapy. Despite compelling pre-clinical evidence, the clinical translation of LF and its nano-formulations remains nascent. While early-phase trials have established a favorable safety profile for recombinant human LF, larger Phase III studies have yielded mixed results, underscoring the complexity of its action in humans. Key challenges include enhancing drug targeting, optimizing loading efficiency, ensuring batch-to-batch reproducibility, and achieving deep tumor penetration. Future research must focus on the rational design of next-generation LF-NPs. This entails developing standardized manufacturing protocols, engineering “smart” stimuli-responsive systems for targeted drug release in the TME, and constructing multi-targeting platforms. A concerted interdisciplinary effort is paramount to bridge the gap between bench and bedside. In conclusion, LF, particularly in its nano-engineered forms, represents a highly promising and versatile agent in the oncological arsenal, holding immense potential for precise and effective cancer therapy.

Cancer remains a leading cause of global mortality, necessitating the development of advanced therapeutic strategies with enhanced efficacy and reduced systemic toxicity. Among promising bioactive agents, lactoferrin (LF)—a multifunctional iron-binding glycoprotein abundantly found in mammalian milk and exocrine secretions—has garnered significant interest for its potent and multifaceted anti-cancer properties. This review provides a comprehensive analysis of the current understanding of LF’s role in oncology, encompassing its structural biology, diverse mechanisms of action, and groundbreaking advancements in its application through nano-engineering. LF exerts anti-tumor effects through multiple pathways, including extracellular action, intracellular action, and immune regulation. It demonstrates a remarkable affinity for cancer cell membranes, binding to overexpressed anionic components such as glycosaminoglycans and sialic acids, as well as to specific receptors including the low-density lipoprotein receptor-related protein-1 (LRP-1). This selective binding facilitates targeted uptake. Upon internalization, LF orchestrates a direct assault by inducing cell-cycle arrest in phases such as G0/G1 or S phase through the modulation of key regulators including cyclins, CDKs, and p53. Furthermore, it promotes programmed cell death via apoptotic pathways, involving caspase activation and downregulation of anti-apoptotic proteins such as survivin. A more recently elucidated mechanism is the induction of ferroptosis, an iron-dependent form of cell death characterized by overwhelming lipid peroxidation. Beyond direct cytotoxicity, LF acts as a potent immunomodulator. It enhances natural killer (NK) cell activity, modulates T-lymphocyte populations, and crucially reprograms tumor-associated macrophages (TAMs) from a pro-tumor M2 state to an anti-tumor M1 state, thereby reversing the immunosuppressive tumor microenvironment (TME). The translation of LF’s potential has been significantly accelerated by nanotechnology. The inherent biocompatibility and natural tumor-targeting capabilities of LF make it an ideal platform for sophisticated drug-delivery systems. This review details various fabrication strategies for LF-based nanoparticles (NPs), including self-assembly, sol-in-oil emulsion, and electrostatic nanocomplexes, among others. Research demonstrates that nano-formulations not only protect LF from degradation but also enhance its bioactivity and anti-cancer potency. More importantly, LF NPs serve as versatile carriers for a wide array of therapeutic agents, including conventional chemotherapeutics, natural compounds, and imaging agents. These engineered systems enable synergistic therapy and facilitate site-specific delivery. Notably, the ability of LF to bind to receptors on the blood-brain barrier (BBB) has been leveraged to develop nano-systems for glioblastoma treatment. Other innovative designs utilize LF to modulate the TME—for instance, by alleviating tumor hypoxia to sensitize cells to radiotherapy and chemotherapy. Despite compelling pre-clinical evidence, the clinical translation of LF and its nano-formulations remains nascent. While early-phase trials have established a favorable safety profile for recombinant human LF, larger Phase III studies have yielded mixed results, underscoring the complexity of its action in humans. Key challenges include enhancing drug targeting, optimizing loading efficiency, ensuring batch-to-batch reproducibility, and achieving deep tumor penetration. Future research must focus on the rational design of next-generation LF-NPs. This entails developing standardized manufacturing protocols, engineering “smart” stimuli-responsive systems for targeted drug release in the TME, and constructing multi-targeting platforms. A concerted interdisciplinary effort is paramount to bridge the gap between bench and bedside. In conclusion, LF, particularly in its nano-engineered forms, represents a highly promising and versatile agent in the oncological arsenal, holding immense potential for precise and effective cancer therapy.

ObjectiveTo verify the association between the Ddit3-Trib3-Akt signaling pathway and rat spermatogenesis by constructing an in vitro co-culture system of testis. MethodsTesticular tissue blocks from 20-25-day-old male rats were placed in an in vitro culture system， and the culture medium was replaced every 2 to 3 days. PCR was used to verify the expression of marker genes of various spermatogenic cells. RNA interference technology was employed to verify the correlation between the Ddit3-Trib3-Akt signaling pathway and rat spermatogenesis. ResultsThe co-culture system could be continuously cultured for more than 2.5 months in vitro. RT-PCR showed that specific marker genes of spermatogonia， spermatocyte and spermoblast were expressed. The RNA and protein expression of Trib3 and Akt changed after the knocking down of Ddit3 and Trib3， respectively. It demonstrated the existence of Ddit3-Trib3-Akt signaling pathway in rat spermatogenesis. ConclusionThe culture time of more than 2.5 months indicates that the culture system can temporarily maintain the proliferation and differentiation of stem cells， and simultaneously maintain and stabilize spermatogenesis in a simple system. The successful validation of the Ddit3-Trib3-Akt signaling pathway also confirms that this culture system can be used to study possible molecular mechanisms of spermatogenesis in vitro.

Objective: To explore the relationship of screen time and sleep duration with screening myopia among junior and senior high school students, so as to provide evidence for the prevention and control of myopia among students. Methods: From March to October 2024, 429 junior and senior high school students from a district of Guangzhou were selected using stratified cluster random sampling method. Standardized logarithmic visual acuity chart was used for vision assessment, while Questionnaire for the Physical Health Monitoring System of Students in Guangzhou was employed to collect students screen time and sleep duration. The Chi square test was used to compare differences across different groups, and binary Logistic regression analysis was employed to analyze the association of screen time and sleep duration with screening myopia. Results: The overall prevalence of screening myopia was 79.5%, with significant differences across educational stage, sex, screen time and sleep duration groups( χ 2=41.64, 9.75, 23.89 , 8.17, all P <0.05).Binary Logistic regression analysis revealed that, compared to the high screen time & insufficient sleep group, the low screen & sufficient sleep group ( OR=0.25, 95%CI =0.09-0.68), the low screen & insufficient sleep group ( OR= 0.27 , 95%CI =0.13-0.56), and the high screen & sufficient sleep group ( OR=0.26, 95%CI =0.10-0.70) exhibited significantly lower screening myopia risks (all P <0.05). After adjusting for sex and educational stage, low screen time & insufficient sleep was significantly associated with screening myopia ( OR=0.48, 95%CI =0.23-0.98); the multiplicative interaction term was statistically significant ( OR=0.99,95%CI =0.98-1.00)(both P <0.05). Conclusion The interaction effect between screen time and sleep duration in relation to screening myopia suggests a need to focus on daily routines and screen use habits among junior and senior high school students for ensuring sufficient sleep and limiting screen exposure.

ObjectiveTo investigate the mechanisms by which the combination of berberine （BBR） and baicalin （BAI） ameliorates type 2 diabetes mellitus （T2DM） due to internal accumulation of dampness-heat from the perspectives of gut microbiota and metabolomics. MethodsAntibiotics were used to induce pseudo-sterile mice. Thirty pseudo-sterile mice were randomized into a normal fecal microbiota transplantation group （n=10） and a T2DM （syndrome of internal accumulation of dampness-heat） fecal microbiota transplantation group （n=20）. The mice were then administrated with suspensions of fecal microbiota from healthy volunteers and a patient with T2DM due to internal accumulation of dampness-heat by gavage， respectively. Each mouse received 200 µL suspension every other day for a total of 15 times to reshape the gut microbiota. The T2DM model mice were then assigned into a model group （n=8） and a BBR-BAI group （n=11）. BBR was administrated at a dose of 200 mg·kg^-1， and BAI was administrated in a ratio of BBR-BAI 10∶1 based on preliminary research findings. The administration lasted for 8 consecutive weeks. Fasting blood glucose （FBG）， glycated hemoglobin （HbA1c）， insulin （INS）， triglycerides （TG）， total cholesterol （CHOL）， low-density lipoprotein cholesterol （LDL-C）， high-density lipoprotein cholesterol （HDL-C）， aspartate aminotransferase （AST）， and alanine aminotransferase （ALT） levels were measured to evaluate the effects of the BBR-BAI combination on glucose and lipid metabolism and liver function in T2DM mice. Hematoxylin-eosin staining was employed to observe pathological changes in the colon tissue. The expression of claudin-1， zonula occludens-1 （ZO-1）， and occludin in the colon tissue was determined by Western blot. Real-time quantitative polymerase chain reaction（Real-time PCR） was employed to assess the levels of tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6） in the colon tissue. The fecal microbiota composition and differential metabolites were analyzed by 16S rRNA sequencing and ultra-high performance liquid chromatography-quadrupole-time of flight tandem mass spectrometry （UPLC-Q-TOF-MS）， respectively. ResultsThe BBR-BAI combination lowered the FBG， HbA1c， and INS levels （P<0.05， P<0.01） and alleviated insulin resistance （P<0.01） in T2DM mice. Additionally， BBR-BAI elevated the levels of ZO-1， occludin， and claudin-1 （P<0.05， P<0.01） and down-regulated the expression levels of TNF-α， IL-1β， and IL-6 in the colon （P<0.05， P<0.01）. The results of 16S rRNA sequencing showed that BBR-BAI increased the relative abundance of Ligilactobacillus， Phascolarctobacterium， and Akkermansia （P<0.05）， while significantly decreasing the relative abundance of Alistipes， Odoribacter， and Colidextribacter （P<0.05）. UPLC-Q-TOF-MS identified 28 differential metabolites， which were primarily involved in arachidonic acid metabolism and α-linolenic acid metabolism. ConclusionBBR-BAI can ameliorate T2DM due to internal accumulation of dampness-heat by modulating the relative abundance of various bacterial genera in the gut microbiota and the expression of fecal metabolites.

Artificial intelligence(AI)technology has been demonstrated that have unique advantages in medical diagnosis based on massive clinical data.Its potential prospects has been found in the diagnosis and treatment of cardiovascular disease(CVD).AI technology has extent its priority in electrocardiogram reading,differential analysis and disease classification.Interventional therapy is an important part of the diagnosis and treatment of CVD.This paper aim to review the latest developments to summarize the AI-assisted CVD interventional diagnosis and treatment technology.

Objective:To investigate the correlation between interleukin-10, albumin levels and short-term prognosis in patients with acute lung injury.Methods:A retrospective study was conducted to collect data on 150 patients with acute lung injury admitted to the Fourth People′s Hospital of Longgang District, Shenzhen from January 2021 to December 2023. The short-term prognosis was evaluated based on the mortality rate within 28 d of admission, and the patients were divided into a mortality group 53 cases and a survival group 97 cases. General information, levels of interleukin-10 and albumin within 24 h of admission, and other laboratory indicators were compared between the two groups, with a focus on analyzing the correlation between interleukin-10, albumin levels and the short-term prognosis of patients.Results:Murray lung injury score, acute physiology and chronic health evaluation Ⅱ (APACHE Ⅱ) score and levels of C-reactive protein, interleukin-10 in the mortality group were higher than those in the survival group: (2.27 ± 0.36) scores vs. (1.98 ± 0.28) scores, (22.72 ± 3.27) scores vs. (19.85 ± 3.12) scores, (106.27 ± 14.22) mg/L vs. (93.22 ± 15.27) mg/L, (51.75 ± 8.12) ng/L vs. (46.27 ± 9.47) ng/L, the levels of platelet and albumin were lower than those in the survival group: (186.67 ± 23.11) ×10 9/L vs. (203.25 ± 25.36) ×10 9/L, (27.86 ± 4.75) g/L vs. (32.21 ± 5.61) g/L, with statistical significant differences ( P<0.05). Cox regression analysis showed that the mortality risk of patients with acute lung injury was related to Murray lung injury score, APACHEⅡ score, platelet, C-reactive protein, interleukin-10 and albumin levels at admission ( P<0.05). Restricted cubic spline (RCS) analysis and interaction testing found that the mortality risk of patients with acute lung injury showed a non-linear dose-response relationship with serum interleukin-10 and albumin levels ( P<0.05), and the two had a negative interaction with the mortality risk of patients. The interleukin-10, albumin-assisted Murray lung injury score, APACHE Ⅱ score, platelet and C-reactive protein were used to construct a nomogram prediction model, and the decision curve and nomogram measurement model were drawn. The model has certain predictive value for the short-term risk of death in patients with acute lung injury. Conclusions:The short-term mortality risk in patients with acute lung injury may be related to abnormal levels of interleukin-10 and albumin, which can assist in the early screening of high-risk mortality patients and serve as clinical intervention targets.

BACKGROUND:Implant restoration has become an important means to treat anterior tooth loss,and it is particularly important to select appropriate implant restoration materials.However,at present,there are some deficiencies in clinical implant materials,and researchers have been exploring suitable implant materials.OBJECTIVE:To compare the biomechanical characteristics of implants made of different materials in restoring single missing maxillary anterior teeth.METHODS:The cone beam CT data of a patient with single maxillary central incisor loss were imported into 3-matic software to establish a three-dimensional finite element analysis model of single maxillary anterior tooth loss.The model was then imported into Marc Mentat.Eight sets of implant restoration models were designed according to different implant materials(polyetheretherketone,titanium-zirconium alloy,titanium alloy,and zirconia,with the elastic modulus of the four materials increasing in sequence)and cancellous bone density(high density,low density)to simulate the stress conditions of the maxillary anterior teeth in centric occlusion.The total displacements and von Mises stresses of implants,cortical bone stresses and cancellous bone strains were compared and analyzed.RESULTS AND CONCLUSION:(1)The maximum displacement of the implant gradually decreased with the increase of the modulus of elasticity of the material,and the value of the maximum displacement of the implant in the polyetheretherketone group exceeded 10 μm;the implant stress was concentrated in the labial neck in the models.The maximum stress gradually increased with the increase of the modulus of elasticity of the implant material,among which,the zirconia-low density bone model had the highest stress,which was 21.31 MPa;the cortical bone stress was concentrated in the cortical bone at the junction of the implant with the labial side,and the polyetheretherketone-low density bone group had the highest value,which was 29.90 MPa.(2)From the biomechanical point of view,titanium-zirconium alloy,titanium alloy,and zirconia can be used as implant materials for restoration of a single missing anterior tooth,and implant displacement is one of the common problems during implant restorations,but pure polyetheretherketone material may cause excessive implant displacement in implant restorations of anterior areas,causing implant failure.

Aim To evaluate the continuous flow exposure sys-tem at the air-liquid interface(ALI)in vitro to provide reference data for in vitro studies on inhalation toxicology,and to conduct a preliminary evaluation of the inhalation toxicity of the com-pound limonene by using the system in conjunction with an ALI culture model of Calu-3 cells.Methods Fluorescein sodium(Na-flu)dosimetry supplemented with quartz microbalance(QCM)was used to evaluate the deposition volume and pore-to-pore homogeneity of the ALI continuous flow exposure system;limonene aerosol was exposed to an ALI-cultured model of Calu-3 cells for 3 h using the ALI continuous flow exposure system at exposure doses of high(0.213 μg·cm-2),medium(0.104μg·cm-2),low(0.064 5 μg·cm-2),clean air exposure was used as a negative control group,and the activity,lactate dehydrogenase(LDH)release,trans-epithelial electrical resist-ance(TEER),mucin MUC5AC and inflammatory factor gene expression of the exposed cells were detected after 24 h to evalu-ate the inhalation toxicity of limonene.Results The deposition of sodium fluorescein in the ALI continuous flow exposure system was 0.085±0.007 μg/30 min/well,and inter-well homogeneity was optimized from the initial 26％to less than 10％after sever-al debugging sessions;compared with the control group,there was no significant change in cellular activity and IL-8 gene ex-pression,but cellular IL-6 gene expression increased after limo-nene aerosol exposure;the mid-exposure dose of limonene pro-moted cellular release of LDH and inflammatory factor gene ex-pression.The medium exposure dose of limonene induced the cells to release LDH＞10％and decreased the expression of cel-lular tumor necrosis factor TNF-α gene;the high exposure dose of limonene decreased the cellular TEER value,impaired the cellular barrier function,and increased the expression of cellular mucin MUC5AC gene.Conclusions The ALI continuous flow exposure system can be used for inhalation toxicity in vitro stud-ies after commissioning;high and medium exposure doses of limonene are inhalation toxic.