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Oleuropein (OLE), as the main effective active component in olive leaves, is a natural cyclic ether terpene polyphenolic compound found in plants of the genus Olea. It has antioxidant, anti-inflammatory and anti-apoptotic properties, and can reduce damage caused by reactive oxygen species. These characteristics indicate that it can enhance the maturation rate of oocytes and the developmental capacity of embryos—two key indicators in animal breeding. This study evaluated the effects of OLE on the in vitro maturation and early embryonic development of sheep oocytes. 20 μM OLE has the best promoting effect on the maturation rate of oocytes, and 30 μM OLE has the best increasing effect on the blastocyst rate. Compared with the control group, glutathione (GSH) level and mitochondrial membrane potential (MMP) level were significantly increased, ROS level was significantly decreased, the expression of antioxidant genes SOD1 and GPX3 was significantly elevated, and the expression of anti-apoptotic gene BCL2 was significantly elevated in the experimental group. In addition, during the in vitro development stage of early embryos, the expression level of the embryo development-related gene OCT4 significantly increased. The study has shown that OLE can effectively alleviate oxidative stress during in vitro culture, increase oocyte maturation rate and promote embryo development.

Natural pigment lycopene (LYC), a carotenoid, possesses antioxidant, anti-apoptotic, anticancer, and immunoenhancing properties. During in vitro culture, this substance protects oocytes and early embryos from damage caused by reactive oxygen species (ROS), thereby enhancing the in vitro maturation (IVM) rate of oocytes and the developmental competence of early embryos. This study aimed to investigate the effects of supplementing different concentrations of LYC (0, 5, 10, and 15 μM) during in vitro culture of sheep oocytes and early embryos on their developmental competence. In contrast to the control group, the 5 μM LYC treatment group displayed a marked increase in the first polar body extrusion rate and the extent of cumulus cell expansion, as well as a significantly higher proportion of normal spindle assembly in sheep oocytes, but 15 μM LYC appeared to negatively affect oocyte maturation. Relative to all other experimental groups, the 5 μM LYC treatment group displayed significantly elevated rates of cleavage and blastocyst rate during early in vitro embryonic development. The levels of ROS in mature oocytes and early embryos were significantly decreased, whereas the GSH level was significantly elevated. Furthermore, LYC treatment significantly enhanced mitochondrial activity and markedly elevated the mitochondrial membrane potential (MMP) in mature oocytes and early embryos. Moreover, the total cell number of blastocysts was significantly increased. Moreover, in early embryos, the transcript levels of genes associated with both oxidative stress and apoptosis were favorably regulated. In conclusion, LYC supplementation boosted the rates of oocyte maturation and blastocyst formation in sheep, while elevating the developmental capacity of early embryos.

Traditional treatments against advanced non-small cell lung cancer (NSCLC) with high morbidity and mortality continue to be dissatisfactory. Given this situation, there is an urgent requirement for alternative modalities that provide lower invasiveness, superior clinical effectiveness, and minimal adverse effects. The combination of photodynamic therapy (PDT) and immunotherapy gradually become a promising approach for high-grade malignant NSCLC. Nevertheless, owing to the absence of precise drug delivery techniques as well as the hypoxic and immunosuppressive characteristics of the tumor microenvironment (TME), the efficacy of this combination therapy approach is less than ideal. In this study, we construct a novel nanoplatform that indocyanine green (ICG), a photosensitizer, loads into hollow manganese dioxide (MnO2) nanospheres (NPs) (ICG@MnO2), and then encapsulated in PD-L1 monoclonal antibodies (anti-PD-L1) reprogrammed exosomes (named ICG@MnO2@Exo-anti-PD-L1), to effectively modulate the TME to oppose NSCLC by the synergy of PDT and immunotherapy modalities. The ICG@MnO2@Exo-anti-PD-L1 NPs are precisely delivered to the tumor sites by targeting specially PD-L1 highly expressed cancer cells to controllably release anti-PD-L1 in the acidic TME, thereby activating T cell response. Subsequently, upon endocytic uptake by cancer cells, MnO2 catalyzes the conversion of H2O2 to O2, thereby alleviating tumor hypoxia. Meanwhile, ICG further utilizes O2 to produce singlet oxygen (1O2) to kill tumor cells under 808 nm near-infrared (NIR) irradiation. Furthermore, a high level of intratumoral H2O2 reduces MnO2 to Mn2+, which remodels the immune microenvironment by polarizing macrophages from M2 to M1, further driving T cells. Taken together, the current study suggests that the ICG@MnO2@Exo-anti-PD-L1 NPs could act as a novel drug delivery platform for achieving multimodal therapy in treating NSCLC. Herein, we have constructed hollow MnO2 NPs loaded with ICG (ICG@MnO2), and then are encapsulated in DCs-derived exosomes treated with azide choline (AECho) via click chemistry reaction to obtain ICG@MnO2@Exo. The exosomes are reprogrammed using PD-L1 monoclonal antibodies (anti-PD-L1), generating ICG@MnO2@Exo-anti-PD-L1 to effectively modulate the TME and combat NSCLC through the synergistic effects of PDT and immunotherapy. In detail, an LLC (lewis lung carcinoma cells) allograft model in C57BL/6 mice was constructed and ICG@MnO2@Exo-anti-PD-L was injected through the tail vein. By specifically targeting cancer cells with high PD-L1 expression, the ICG@MnO2@Exo-anti-PD-L1 nanospheres (NPs) are precisely delivered to the tumor site and release anti-PD-L1 in the acidic TME, thereby activating T cell responses. Upon internalization by cancer cells, MnO2 catalyzes the conversion of hydrogen peroxide (H2O2) to oxygen, alleviating tumor hypoxia. In addition, ICG utilizes oxygen to generate singlet oxygen (1O2) under near-infrared (NIR) irradiation at 808 nm, leading to the destruction of tumor cells. Furthermore, the high levels of intratum oral H2O2 and H+ reduces MnO2 to Mn2+, which remodels the immune microenvironment by polarizing macrophages from M2 to M1, thereby further stimulating T cell responses. Collectively, the findings of this study suggest that ICG@MnO2@Exo-anti-PD-L1 NPs can serve as a novel drug delivery platform for achieving multimodal therapy for NSCLC by combining PDT with immunotherapy. [Display omitted] •In this study, we successfully developed an innovative nanodelivery system termed ICG@MnO2@Exo-anti-PD-L1 NPs for combining photodynamic therapy (PDT) effect with immunotherapy of non-small cell lung cancer (NSCLC).•The hollow MnO2 nanoplatform enables a more substantial photosensitizer loading to heighten PDT, and mitigates tumor hypoxia by catalyzing the conversion of H2O2 into O2 through MnO2.•The generation of Mn2+ through redox reactions due to the high level of intratumoral H2O2 and H+ induces polarization of M2 macrophages to M1. This, in conjunction with anti-PD-L1, activates T cells, enhancing the effectiveness of immunotherapy.

The significance of tertiary lymphoid structures (TLS) in hepatocellular carcinoma (HCC) with portal vein tumor thrombus (PVTT) remains ambiguous. This study evaluates the prognostic impact of intra-tumoral TLS (iTLS) and peri-tumoral TLS (pTLS) and explores the interplay between TLS and cancer-associated fibroblasts (CAF) in patients undergoing curative hepatic resection. A retrospective analysis of 83 HCC patients with PVTT assessed the prognostic value of TLS. Transcriptomic data were mined to identify TLS- and CAF-related genes, and a seven-gene prognostic model was constructed using LASSO and Cox regression analyses. Immune microenvironment, mutation characteristics, and response to immunotherapy were analyzed between risk groups. iTLS + and high pTLS density were independently associated with improved overall survival (OS), but not recurrence-free survival (RFS) or early recurrence. A novel risk model comprising KLF2, HBEGF, KLRB1, PGF, JAM2, CHORDC1, and YTHDF2 stratified patients into high- and low-risk groups, with the high-risk group demonstrating poorer OS and diminished immunotherapy responsiveness. Low-risk patients exhibited higher immune infiltration (e.g., B cells, T cells) and stronger antitumor activity, whereas high-risk tumors showed active proliferation and immune evasion. iTLS and pTLS are independent predictors of favorable OS in HCC patients with PVTT. The TLS/CAF-based risk model offers robust prognostic utility and highlights distinct biological and immune features between patient subgroups. These findings provide a foundation for personalized prognostic assessment and therapeutic decision-making in advanced HCC.

Physical injuries and neurodegenerative diseases often lead to irreversible damage to the organizational structure of the central nervous system (CNS) and peripheral nervous system (PNS), culminating in physiological malfunctions. Investigating these complex and diverse biological processes at the macro and micro levels will help to identify the cellular and molecular mechanisms associated with nerve degeneration and regeneration, thereby providing new options for the development of new therapeutic strategies for the functional recovery of the nervous system. Due to their distinct advantages, modern microfluidic platforms have significant potential for high-throughput cell and organoid cultures in vitro, the synthesis of a variety of tissue engineering scaffolds and drug carriers, and observing the delivery of drugs at the desired speed to the desired location in real time. In this review, we first introduce the types of nerve damage and the repair mechanisms of the CNS and PNS; then, we summarize the development of microfluidic platforms and their application in drug carriers. We also describe a variety of damage models, tissue engineering scaffolds, and drug carriers for nerve injury repair based on the application of microfluidic platforms. Finally, we discuss remaining challenges and future perspectives with regard to the promotion of nerve injury repair based on engineered microfluidic platform technology.

The tumor margin of hepatocellular carcinoma (HCC) is a critical zone where cancer cells invade the surrounding stroma, exhibiting unique and more invasive metabolic and migratory features compared to the tumor center, driving tumor expansion beyond the primary lesion. Studies have shown that at this critical interface, HCC cells primarily rely on fatty acid oxidation to meet their energy demands, although the underlying mechanisms remain unclear. This study demonstrates that activated hepatic stellate cells (HSCs) at the tumor margin play a pivotal role in sustaining the metabolic needs of HCC cells. Specifically, it is discovered that mitochondrial fission regulator 2 (MTFR2) in HSCs interacts with dynamin‐related protein 1 (DRP1, a known mitochondrial fission machinery), preventing its lysosomal degradation, which in turn promotes mitochondrial fission. This MTFR2‐driven mitochondrial fission enhances the transfer of both fatty acids and mitochondria to HCC cells, supplying essential metabolic substrates and reinforcing the mitochondrial machinery critical for tumor growth. The findings suggest that targeting MTFR2‐driven mitochondrial fission may offer a novel therapeutic avenue for interfering with the metabolic crosstalk between tumor cells and the stromal niche. In the tumor margin of hepatocellular carcinoma (HCC), activated hepatic stellate cells upregulate MTFR2, initiating inhibiting DRP1 degradation and mitochondrial fission. This enhances mitochondrial availability and facilitates FAs synthesis via ACC1. Additionally, fission promotes RAC1‐mediated cytoskeletal remodeling and Miro1‐mediated mitochondrial transport, enabling HCC cells to utilize transferred resources for increased fatty acid oxidation and ATP production.

Background: Breast cancer (BC) ranks as the most prevalent malignancy affecting women globally, with apoptosis playing a pivotal role in its pathological progression. Despite the crucial role of apoptosis in BC development, there is limited research exploring the relationship between BC prognosis and apoptosis-related genes (ARGs). Therefore, this study aimed to establish a BC-specific risk model centered on apoptosis-related factors, presenting a novel approach for predicting prognosis and immune responses in BC patients. Methods: Utilizing data from The Cancer Gene Atlas (TCGA), Cox regression analysis was employed to identify differentially prognostic ARGs and construct prognostic models. The accuracy and clinical relevance of the model, along with its efficacy in predicting immunotherapy outcomes, were evaluated using independent datasets, Receiver Operator Characteristic (ROC) curves, and nomogram. Additionally, Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene Ontology (GO) analyses were used to predict potential mechanical pathways. The CellMiner database is used to assess drug sensitivity of model genes. Results: A survival risk model comprising eight prognostically relevant apoptotic genes (PMAIP1, TP53AIP1, TUBA3D, TUBA1C, BCL2A1, EMP1, GSN, F2) was established based on BC patient samples from TCGA. Calibration curves validated the ROC curve and nomogram, demonstrating excellent accuracy and clinical utility. In samples from the Gene Expression Omnibus (GEO) datasets and immunotherapy groups, the low-risk group (LRG) demonstrated enhanced immune cell infiltration and improved immunotherapy responses. Model genes also displayed positive associations with sensitivity to multiple drugs, including vemurafenib, dabrafenib, PD-98059, and palbociclib. Conclusions: This study successfully developed and validated a prognostic model based on ARGs, offering new insights into prognosis and immune response prediction in BC patients. These findings hold promise as valuable references for future research endeavors in this field.

Industrial design (ID) refers to industrial product design based on engineering, aesthetics, and economy. Traditional industrial design refers to the creative activities of designing and designing products produced by industrial means to make the best match with the environment and the people who use them. This paper aims to study how to analyze and study the application of aesthetic art, that is, the concept of industrial design, based on functional nanomaterials, and this paper describes the electrospinning technology. This paper puts forward the problem of the industrial design concept, which is based on design aesthetics. Therefore, this paper focuses on the development of industrial design and related elements. The application of functional nanomaterials in industrial design is designed and analyzed. The experimental results show that when the acid soaking time is 4∼12 days, the mechanical strength of the nanofiber membrane is 7∼9 MPa. Compared with the untreated nanofiber membrane, it increased by 25.4%∼48.8%, and the ductility decreased from 81.5% to 44.1%.

Lactating oocytes consume a lot of energy during maturation, a large part of which comes from lipid metabolism. PPARγ is a key regulator of lipid metabolism. In this study, rosiglitazone (RSG), an activator of PPARγ, was added to a mature medium to investigate its effects on the levels of spindle and the chromosome arrangement, lipid deposition, reactive oxygen species (ROS), and glutathione (GSH) levels, oocyte secretion factors, apoptosis and lipid metabolism-related gene expression, and subsequent embryonic development during the maturation of sheep oocytes. The oocyte secretion factor affects gene expression related to apoptosis and lipid metabolism and subsequent embryonic development. The results showed that the proportion of spindle and normal chromosome arrangements increased in the 5 μM RSG treatment group, the lipid content increased after cell maturation, the ROS level decreased, and the GSH level increased. The expressions of oocyte secretion factor (GDF9 and BMP15), anti-apoptosis gene (BCL2), and lipid metabolism-related genes (ACAA1, CPT1A, PLIN2) were increased in the 5 μM treatment group. Finally, the development of blastocysts was examined. After the oocytes were treated with 5 μM RSG, the blastocyst rate and the gene expression of the totipotency gene (OCT4) were increased. It was concluded that increasing PPARγ activity during ovine oocyte maturation could promote lipid metabolism, reduce oxidative stress, and improve the ovine oocyte maturation rate and subsequent embryo development.

Necroptosis, pro-inflammatory programmed necrosis, has been reported to exert momentous roles in pancreatic cancer (PC). Herein, the objective of this study is to construct a necroptosis-related prognostic model for detecting pancreatic cancer. In this study, the intersection between necroptosis-related genes and differentially expressed genes (DEGs) of pancreatic ductal adenocarcinoma (PDAC) was obtained based on GeneCards database, GEO database (GSE28735 and GSE15471), and verified using The Cancer Genome Atlas (TCGA). Next, a prognostic model with Cox and LASSO regression analysis, and divided the patients into high-risk and low-risk groups. Subsequently, the Kaplan–Meier (KM) survival curve and the receiver operating characteristic (ROC) curves were generated to assess the predictive ability of overall survival (OS) of PC patients. Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) analyses were performed to predict the potential biofunction and possible mechanical pathways. The EMTome database and an immune analysis were applied to further explore underlying mechanism. Finally, clinical samples of PDAC patients were utilized to verify the expression of model genes via immunohistochemistry (IHC), and the normal human pancreatic ductal cell line, hTERT-HPNE as well as human pancreatic ductal carcinoma cell lines, PANC-1 and PL45, were used to identify the levels of model genes by Western blot (WB) and immunofluorescence (IF) in vitro. The results showed that 13 necroptosis-related DEGs (NRDEGs) were screened based on GEO database, and finally four of five prognostic genes, including KRT7, KRT19, IGF2BP3, CXCL5, were further identified by TCGA to successfully construct a prognostic model. Univariate and multivariate Cox analysis ultimately confirmed that this prognostic model has independent prognostic significance, KM curve suggested that the OS of low-risk group was longer than high-risk group, and the area under receiver (AUC) of ROC for 1, 3, 5 years was 0.733, 0.749 and 0.667, respectively. A GO analysis illustrated that model genes may participate in cell–cell junction, cadherin binding, cell adhesion molecule binding, and neutrophil migration and chemotaxis, while KEGG showed involvement in PI3K-Akt signaling pathway, ECMreceptor interaction, IL-17 signaling pathway, TNF signaling pathway, etc. Moreover, our results showed KRT7 and KRT19 were closely related to EMT markers, and EMTome database manifested that KRT7 and KRT19 are highly expressed in both primary and metastatic pancreatic cancer, declaring that model genes promoted invasion and metastasis potential through EMT. In addition, four model genes were positively correlated with Th2, which has been reported to take part in promoting immune escape, while model genes except CXCL5 were negatively correlated with TFH cells, indicating that model genes may participate in immunity. Additionally, IHC results showed that model genes were higher expressed in PC tissues than that in adjacent tumor tissues, and WB and IF also suggested that model genes were more highly expressed in PANC-1 and PL45 than in hTERT-HPNE. Tracing of a necroptosis-related prognostic model for pancreatic carcinoma reveals its invasion and metastasis potential through EMT and immunity. The construction of this model and the possible mechanism of necroptosis in PDAC was preliminarily explored to provide reliable new biomarkers for the early diagnosis, treatment, and prognosis for pancreatic cancer patients.