工程技术最新文献

Objective: To explore the synergistic effect of nano-pearl powder (NPP) and adipose-derived stem cell exosomes (ADSC-Exos) on the osteogenic potential of MC3T3-E1 cells.

Methods: The water-soluble matrix of NPP (NPP-WSM) was extracted via freeze-drying, and ADSC-Exos were isolated by ultracentrifugation. NPP-WSM was incorporated into ADSC-Exos through co-incubation to generate NPP-WSM-Exos. MC3T3-E1 cells were treated with NPP-WSM or NPP-WSM-Exos. Cell proliferation and migration were evaluated using CCK-8 and wound-healing assays, respectively. Osteogenic differentiation was assessed by Alizarin Red S staining and alkaline phosphatase (ALP) activity. The expression of osteogenesis-related genes (COL1A1, RUNX2, OCN, and OPN) was measured by qPCR and Western blotting. Transcriptome sequencing (RNA-seq) was conducted to identify signaling pathways activated by NPP-WSM-Exos.

Results: NPP-WSM-Exos displayed distinct exosome morphology and biomarkers, confirming their successful preparation. Significantly, NPP-WSM-Exos enhanced the viability of MC3T3-E1 cells compared to NPP-WSM alone and upregulated the expression of osteogenic genes, including COL1A1, RUNX2, OCN, and OPN, at both the transcriptional and translational levels. Additionally, NPP-WSM-Exos strongly promoted mineralization, as evidenced by the increased calcification observed through Alizarin Red S staining, and elevated alkaline phosphatase (ALP) activity, indicating excellent potential for osteogenic differentiation. Transcriptome sequencing showed that NPP-WSM-Exos significantly enhanced the PI3K/AKT pathway in MC3T3-E1 cells, while protein level detection indicated that NPP-WSM-Exos could increase AKT phosphorylation levels and inhibit GSK3β activity to improve osteogenic efficiency.

Conclusion: The use of adipose-derived stem cell exosomes to encapsulate NPP-WSM can increase the utilization of WSM, promote the proliferation of MC3T3-E1, and enhance the osteogenic differentiation ability.

Environmental risk assessment (ERA) of genetically modified (GM) crops is essential for evaluating their potential impact on non-target organisms under field conditions. In this study, a long-term field assessment was conducted to evaluate the ecological effects of glufosinate-tolerant GM zoysiagrass (Zoysia japonica Steud.; events JG21 and JG21-MS1) on non-target arthropod communities at two geographically distinct living modified organism isolation sites in South Korea (Jeonju and Seogwipo). A total of 528,796 arthropods were collected and classified into three functional groups: pests (45.73%), natural enemies (14.51%), and other arthropods (39.76%). Arthropod community composition exhibited clear regional and temporal variations. Linear mixed-effects model (LMM) analyses indicated that arthropod abundance and diversity indices were primarily influenced by the year and region, whereas treatment effects, defined as differences between GM events and non-GM controls, were not significant. Although occasional statistical differences were detected, post hoc comparisons confirmed that arthropod communities associated with GM treatments were ecologically comparable to those of non-GM controls within each region and year (p > .05). Non-metric multidimensional scaling (NMDS) ordination revealed clear clustering by region and year, with substantial overlap among treatments. Permutational multivariate analysis of variance showed that year explained the largest proportion of the variation (R² = 0.640), whereas treatment effects were negligible (R² = 0.006). Overall, these results provide robust field-based evidence that glufosinate-tolerant and male-sterile GM zoysiagrass does not adversely affect non-target arthropod communities, supporting its environmental safety in perennial agroecosystems.

Spina bifida (SB) is associated with progressive spinal cord injury and limited therapeutic options for neural protection. Amniotic fluid stem cells (AFSCs) have shown regenerative potential, but their effects on SB-related neuronal injury and the underlying mechanisms remain unclear. In this study, we investigated whether AFSCs alleviate neuronal injury-related changes in SB rats through the modulation of autophagy via the FOXO1/STAT3 pathway. SB-like lesions were induced in neonatal rats, followed by the intramedullary injection of AFSCs or vehicle on postnatal day 1. Behavioral assessment was performed using Basso, Beattie, and Bresnahan locomotor scoring on days 2, 7, and 14 after injection, and lesion-centered lumbosacral spinal cord tissues were collected on day 15. AFSC treatment partially improved hindlimb locomotor scores and reduced neuronal injury-related alterations in SB rats. AFSCs also increased autophagy-associated markers, including LC3II/I and Beclin1, and reduced p62 mRNA expression in vivo and in neural stem cells isolated from SB rats. Mechanistically, AFSC treatment was associated with reduced FOXO1 and enhanced STAT3 signaling. FOXO1 overexpression or STAT3 inhibition attenuated AFSC-mediated effects, whereas siRNA-mediated FOXO1 knockdown enhanced these effects; combined STAT3 knockdown partially reversed the effects of FOXO1 silencing. These findings suggest that AFSCs alleviate SB-related neuronal injury-associated changes by regulating autophagy through the FOXO1/STAT3 axis. This study provides preclinical evidence for an experimental neuroprotective mechanism of AFSCs, although further validation is required before translational applicability can be considered.

Initial risk assessments of genetically modified (GM) crops began in the early 1990 s, focusing on herbicide tolerance and insect resistance, with approvals by the mid-1990s. These assessments compare GM crops to non-GM equivalents, a framework unchanged for over 30 years. Since the first assessment in 1994, over 4,400 evaluations have been conducted across more than 70 countries for both cultivation and food/feed use. To date, none have identified increased risk relative to conventional varieties. This article analyzes three decades of GM crop approvals, highlighting the consistency of scientific assessment processes. Fourteen crops underwent 692 cultivation and 1,891 food-release assessments for herbicide tolerance, while insect resistance accounted for 523 cultivation and 1,396 food-release assessments, largely involving Bacillus thuringiensis (Bt). The findings underscore that GM crops are equivalent in risk to conventional varieties, supporting reliance on established international scientific expertise, particularly in resource-constrained regions.

Background: While secreted phosphoprotein 1 (SPP1) drives macrophage M2 polarization and cancer progression in multiple malignancies, its role in thyroid cancer remains poorly understand. This study investigated the roles and mechanisms of thyroid cancer-derived exosomal SPP1 in regulating macrophage M2 polarization and malignant progression in thyroid cancer.

Methods: SPP1 protein expression in thyroid cancer tissues and cell lines was assessed. Exosomes from TPC1 cells were isolated and characterized for SPP1 expression. THP-1 cell-differentiated M0 macrophages were treated with unmodified or SPP1-knockdown exosomes, followed by detection of M2 phenotype markers and analysis of cytokine secretion profiling in response to LPS stimulation. The conditioned macrophages were then co-cultured with thyroid cancer cells, and cell proliferation, migration and invasion were examined. Mechanistic studies focused on CD44/JAK2/STAT3 signaling using an anti-CD44 monoclonal antibody. Additionally, tumor growth and macrophage infiltration were assessed in a xenograft tumor mouse model following exosomal SPP1 knockdown.

Results: SPP1 was upregulated in thyroid cancer and enriched in TPC1-derived exosomes. These exosomes induced macrophage M2 polarization, thereby promoting cancer cell proliferation, migration and invasion. However, SPP1 knockdown in exosomes abolished these effects. Exosomal SPP1 directly interacted with CD44 receptors and activated the JAK2/STAT3 signaling pathway to drive M2 polarization. CD44 blockade reversed M2 polarization and pro-tumorigenic effects. SPP1-deficient exosomes reversed tumor growth and attenuated M2 macrophage infiltration in xenograft model.

Conclusions: Thyroid cancer-derived exosomal SPP1 promotes tumor progression by driving macrophage M2 polarization via the CD44/JAK2/STAT3 signaling pathway. The exosomal SPP1-CD44 axis represents a promising therapeutic target for thyroid cancer.

Decellularized blood vessels with low immunogenicity and excellent biocompatibility are promising for tissue engineering and clinical applications. However, current decellularization methods face limitations in cell removal efficiency, matrix preservation, and biosafety. This study optimized the Triton X-100/SDS (TX-100/SDS) decellularization method using ultrasound technology by systematically evaluating the effects of ultrasound power, temperature, and processing time on decellularization efficiency. The optimized method achieved a 72% reduction in nucleic acid residues at 100 W power while preserving matrix integrity and significantly reducing chemical reagent residues. Structural and biosafety evaluations confirmed that the optimized scaffolds met biological safety standards and demonstrated excellent stability, providing a strong foundation for developing high-performance decellularized vascular materials for clinical applications.

Animal experimental studies involving the Igaki-Tamai stent (ITS), a bioresorbable poly-l-lactic acid scaffold, in peripheral arteries are limited, and existing studies evaluated only short-term (3-month) outcomes. This study compared arterial responses associated with the ITS and bare metal stent (BMS) over 6 months using intravascular ultrasound (IVUS) analysis and evaluated feasibility in porcine iliac arteries. Four miniature pigs underwent stent implantation with the ITS in the right iliac artery and the BMS in the left iliac artery. Follow-up evaluations at 6, 12, and 24 weeks included angiographic and IVUS analyses to assess neointimal hyperplasia, percent area stenosis (%AS), and percent in-stent volume obstruction (%VO). Histological analysis was performed to evaluate tissue injury and inflammation scores. At 6 weeks, the neointimal area did not differ significantly between the ITS and BMS groups (8.49 ± 2.10 mm² vs 13.47 ± 6.67 mm², P = .205). However, the ITS group exhibited a significantly smaller neointimal area at 12 weeks (6.87 ± 1.15 mm² vs 20.65 ± 10.99 mm², P = .050) and 24 weeks (5.20 ± 0.85 mm² vs 22.32 ± 12.03 mm², P = .042). %AS and %VO were significantly lower in the ITS group at all follow-ups. The ITS group showed reduced tissue damage (injury score: 0.80 ± 0.430 vs 1.74 ± 0.908, P < .001) and inflammation (inflammation score: 1.25 ± 0.516 vs 1.67 ± 0.832, P < .001) compared with the BMS group. The ITS was associated with reduced vessel injury, lower inflammatory response, and favorable luminal remodeling over 6 months in healthy porcine iliac arteries.

Background: Periodontitis is a chronic inflammatory condition characterized by destruction of periodontal support tissues and dysregulated immune responses, particularly involving cytokines like tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β). Identifying molecules that regulate both inflammation and tissue regeneration is essential for targeted therapies. Following preliminary transcriptomic evidence on periodontal tissues, this study aimed to define the specific immunomodulatory and osteogenic regulatory effects of TRAB domain-containing protein 2A (TRABD2A).

Methods: RNA sequencing was performed on periodontal tissues from patients with periodontitis and periodontally healthy individuals to identify differentially expressed genes and conduct functional enrichment analysis. TRABD2A expression and its effects on cell proliferation, inflammation, osteogenic markers expression, and mineralization were assessed in human periodontal ligament stem cells (hPDLSCs) treated with recombinant TRABD2A, Porphyromonas gingivalis lipopolysaccharide (LPS), or a TRABD2A inhibitor (o-Phenanthroline).

Results: RNA sequencing revealed significant TRABD2A upregulation in periodontitis tissues, along with elevated bone-related genes runt-related transcription factor 2 (Runx2) and receptor activator of nuclear factor-κB Ligand (RANKL) expression. In vitro experiments demonstrated that TRABD2A reduced the secretion of tumor necrosis factor-alpha (TNF-α) and interleukin-1 beta (IL-1β) and promoted the proliferation of hPDLSCs. Furthermore, TRABD2A upregulated Runx2 expression and suppressed RANKL expression, while Alizarin Red staining results further confirmed its role in promoting osteogenic differentiation. The underlying mechanism may be associated with the enhancement of β-catenin expression.

Conclusion: TRABD2A exerts dual functions by promoting osteogenic differentiation and modulating inflammatory responses, highlighting its potential as an immunoregulatory and pro-regenerative target for periodontitis treatment.

Background: This study aimed to determine the potential mechanism by which pancreatic stem cell-derived beta cells (PSCs-β) assist in the body's glucose-lowering capacity in type 1 diabetes (T1D) rats.

Methods: We screened the transcriptomic changes in the pancreatic islets of T1D mice to extract key genes from the GSE169275 dataset. Cell proliferation, cell cycle distribution, apoptosis, PSC-β differentiation ability, and insulin production levels were analyzed after MLPH overexpression/knockdown in PSCs. PSC-β-overexpressing MLPH were transplanted into T1D rats, and the changes in fasting blood glucose level, glucose tolerance and insulin, glucagon and C-peptide contents were examined. After the target genes of MLPH were analysed using the database, immunoprecipitation was introduced for validation. Whether RAB3A is involved in the regulatory effects of MLPH on the proliferation and differentiation of PSCs was further verified.

Results: MLPH overexpression further enhanced the proliferation of PSCs, inhibited apoptosis and accelerated the differentiation of PSCs to PSC-β cells and insulin secretion. After the transplantation of MLPH-overexpressing PSC-β cells, the pancreatic islet tissue damage was restored, the insulin expression was substantially elevated and the glucagon content decreased. RAB3A knockdown counteracted the effects of MLPH on the proliferation, differentiation and insulin secretion of PSCs.

Conclusion: MLPH overexpression is favourable for the differentiation of PSCs to insulin β-cells. Transplantation of MLPH-overexpressing PSC-β cells restored the ability of T1D rats to manage a glycemic load by promoting RAB3A expression.

Endovascular aneurysm repair (EVAR) is a widely accepted treatment for aortic pathologies owing to its minimally invasive nature. However, long-term complications, such as stent graft migration and infection, remain unresolved, primarily due to the persistent presence of synthetic materials and limited tissue integration. This pilot study evaluated the feasibility of a novel tissue-engineered stent graft (TESG) combining a bioresorbable poly-L-lactic acid (PLLA) stent with decellularized porcine veins. The veins were processed using a sodium dodecyl sulfate and the Triton X-100 decellularization protocol. Histological and ultrastructural analyses confirmed effective cell removal while preserving extracellular matrix components. Quantitative deoxyribonucleic acid (DNA) analysis showed a > 97% reduction in DNA content. The TESGs were assembled by suturing the decellularized veins into bioresorbable PLLA stents and implanted into porcine iliac arteries (n = 3). Commercially available prosthetic grafts were used as control implants to evaluate differences in tissue responses. Graft patency and morphology were assessed at implantation and on postoperative day 14 using angiography and intravascular ultrasonography. All TESGs remained patent, with no evidence of thrombosis or aneurysmal changes. Histological analysis revealed early endothelialization and smooth muscle cell infiltration within the TESG wall, in contrast to the prosthetic graft controls, which lacked comparable cellular integration. This study demonstrated the short-term feasibility and biological compatibility of a fully bioresorbable TESG. Although long-term outcomes remain to be established, these results support further development of TESG to reduce late complications through improved tissue integration and avoidance of permanent synthetic materials.