Ecoflex is a commercial designation for elastomers developed based on the principles of environmental sustainability and flexibility. Various manufacturers offer different types of Ecoflex products with distinct compositions and functions. Among these, the platinum-catalyzed silicone rubber Ecoflex series has demonstrated considerable applicability in various fields of oral medicine due to its excellent flexibility, biocompatibility, stability across a wide temperature range, and tunable mechanical properties. In tissue engineering, it can simulate the mechanical behavior of oral mucosa, and is used in cleft lip surgical training models and preoperative evaluation for temporal bone defect reconstruction. In the field of wearable devices, leveraging its encapsulation protection and flexible characteristics, highly sensitive sensors constructed from Ecoflex can monitor signals such as oral bite force and masticatory muscle activity, thereby aiding in the diagnosis of temporomandibular joint disorders and postoperative evaluation of cleft lip and palate. Moreover, when combined with bio-waste materials, it promotes the functionalization and sustainability of oral wearable devices.In drug delivery systems, its conformability and controlled-release capability address challenges in localized oral drug administration. Designs such as flexible microneedles and temperature-responsive composite systems provide precise solutions for treating periodontitis and oral ulcers. In minimally invasive surgical instruments, its softness enables the development of soft robots and magnetically controlled microfluidic valves, enhancing surgical safety and precision. In the field of oral rehabilitation, Ecoflex soft liner materials, inspired by the suction cup structure of octopus tentacles, improve denture retention. Their low modulus reduces mucosal irritation, ensuring both comfort and durability. Although Ecoflex shows great potential in biomedical applications, it still faces certain challenges, particularly regarding long-term stability after implantation, mechanical fatigue resistance, and microbial colonization, which require further investigation. In the future, with advancements in 3D printing technology, Ecoflex is expected to achieve more precise clinical translation across multiple fields and drive innovation in intelligent biomaterials.

Objective To investigate the impact of Qizhi Jiangtang Capsule (QZJT) on renal damage in diabetic nephropathy (DN) mice via NOD like receptors family pyrin domain containing 3/caspase-1/ Gasdermin D (NLRP3/caspase-1/GSDMD) signaling pathway. Methods Mice were randomly allocated into six experimental groups: a normal control group (NC), a diabetic nephropathy model group (DN), a low-dose QZJT treatment group (L-QZJT), a high-dose QZJT treatment group (H-QZJT), a positive control group administered Shenqi Jiangtang Granules (SQJT), and an ML385 group (treated with an inhibitor of nuclear factor erythroid 2-related factor 2, Nrf2). Upon successful model induction, therapeutic interventions were commenced. Renal function impairment in the mice was evaluated through quantification of fasting blood glucose (FBG), 24-hour urinary albumin (UAlb), serum creatinine (SCr), blood urea nitrogen (BUN), and the kidney-to-body mass ratio (K/B). Renal tissue pathology was evaluated using HE and PAS staining. Serum levels of inflammatory cytokines IL-1β and IL-18 were quantified by ELISA. Levels of podocyte markers and proteins involved in relevant pathways were assessed using Western blot analysis. Results Compared with the NC group, FBG, 24 h UAlb, SCr, and BUN were increased in the DN group, and the K/B mass ratio was also increased. In contrast, compared with the DN group, FBG, 24 h UAlb, SCr, and BUN in both the low-dose (L-QZJT) and high-dose Quanzhou Jintang (H-QZJT) groups were decreased, and the K/B mass ratio was decreased as well. The therapeutic efficacy of H-QZJT was comparable to that of Shenqi Jiangtang Granules. QZJT ameliorated renal histopathological injury in DN mouse, increased the protein levels of Nephrin (a podocyte marker), and decreased the protein levels of NLRP3, apoptosis-associated speck-like protein containing CARD (ASC), pro-caspase-1, and GSDMD-N. After ML385 treatment, renal cells exhibited swelling and morphological changes, the inflammatory infiltrate area was enlarged, the protein levels of NLRP3, ASC, pro-caspase-1, and GSDMD-N were up-regulated, and the levels of IL-1β and IL-18 were increased. Conclusion QZJT may inhibit podocyte pyroptosis by acting on the Nrf2 to regulate the NLRP3/caspase-1/GSDMD pathway, thus improving renal damage in DN mouse.
Animals ; Diabetic Nephropathies/pathology* ; Podocytes/pathology* ; NLR Family, Pyrin Domain-Containing 3 Protein/genetics* ; Pyroptosis/drug effects* ; Drugs, Chinese Herbal/administration & dosage* ; Caspase 1/genetics* ; Signal Transduction/drug effects* ; Mice ; Phosphate-Binding Proteins/genetics* ; Male ; Intracellular Signaling Peptides and Proteins/metabolism* ; Mice, Inbred C57BL ; Kidney/pathology* ; Gasdermins

Triple-negative breast cancer (TNBC) represents an aggressive breast cancer subtype with poor prognosis and limited targeted treatment options. This investigation examined the anti-cancer potential of Caerulomycin A (Cae A), a natural compound derived from marine actinomycetes, against TNBC. Cae A demonstrated selective inhibition of viability and proliferation in TNBC cell lines, including 4T1, MDA-MB-231, and MDA-MB-468, through apoptosis induction. Mechanistic analyses revealed that the compound induced sustained endoplasmic reticulum (ER) stress and subsequent upregulation of C/EBP homologous protein (CHOP) expression, resulting in mitochondrial damage-mediated apoptosis. Inhibition of ER stress or CHOP expression knockdown reversed mitochondrial damage and apoptosis, highlighting the essential role of ER stress and CHOP in Cae A's anti-tumor mechanism. Both oxygen consumption rate (OCR) and extracellular acidification rate (ECAR) decreased in TNBC cells following Cae A treatment, indicating reduced mitochondrial respiratory and glycolytic capacities. This diminished energy metabolism potentially triggers ER stress and subsequent apoptosis. Furthermore, Cae A exhibited significant anti-tumor effects in the 4T1 tumor model in vivo without apparent toxicity. The compound also effectively inhibited human TNBC organoid growth. These results indicate that Cae A may serve as a potential therapeutic agent for TNBC, with its efficacy likely mediated through the disruption of glucose metabolism and the induction of ER stress-associated apoptosis.
Humans ; Endoplasmic Reticulum Stress/drug effects* ; Triple Negative Breast Neoplasms/genetics* ; Apoptosis/drug effects* ; Cell Line, Tumor ; Female ; Animals ; Glucose/metabolism* ; Mice ; Cell Proliferation/drug effects* ; Transcription Factor CHOP/genetics* ; Antineoplastic Agents/pharmacology* ; Mitochondria/metabolism* ; Mice, Inbred BALB C

Cancer multidrug resistance (MDR) impairs the therapeutic efficacy of various chemotherapeutics. Novel approaches, particularly the development of MDR reversal agents, are critically needed to address this challenge. This study demonstrates that tenacissoside I (TI), a compound isolated from Marsdenia tenacissima (Roxb.) Wight et Arn, traditionally used in clinical practice as an ethnic medicine for cancer treatment, exhibits significant MDR reversal effects in ABCB1-mediated MDR cancer cells. TI reversed the resistance of SW620/AD300 and KBV200 cells to doxorubicin (DOX) and paclitaxel (PAC) by downregulating ABCB1 expression and reducing ABCB1 drug transport function. Mechanistically, protein arginine methyltransferase 1 (PRMT1), whose expression correlates with poor prognosis and shows positive association with both ABCB1 and EGFR expressions in tumor tissues, was differentially expressed in TI-treated SW620/AD300 cells. SW620/AD300 and KBV200 cells exhibited elevated levels of EGFR asymmetric dimethylarginine (aDMA) and enhanced PRMT1-EGFR interaction compared to their parental cells. Moreover, TI-induced PRMT1 downregulation impaired PRMT1-mediated aDMA of EGFR, PRMT1-EGFR interaction, and EGFR downstream signaling in SW620/AD300 and KBV200 cells. These effects were significantly reversed by PRMT1 overexpression. Additionally, TI demonstrated resistance reversal to PAC in xenograft models without detectable toxicities. This study establishes TI's MDR reversal effect in ABCB1-mediated MDR human cancer cells through inhibition of PRMT1-mediated aDMA of EGFR, suggesting TI's potential as an MDR modulator for improving chemotherapy outcomes.
Humans ; Protein-Arginine N-Methyltransferases/antagonists & inhibitors* ; Drug Resistance, Neoplasm/drug effects* ; ErbB Receptors/genetics* ; Animals ; Cell Line, Tumor ; Drug Resistance, Multiple/drug effects* ; Methylation/drug effects* ; Saponins/administration & dosage* ; Mice ; Mice, Nude ; Mice, Inbred BALB C ; ATP Binding Cassette Transporter, Subfamily B/genetics* ; Doxorubicin/pharmacology* ; Paclitaxel/pharmacology* ; Female ; Repressor Proteins

Objective: To explore the association between mediterranean diet (MD) patterns and dental caries among children and adolescents with neurodevelopmental disorders (NDD), so as to provide a basis for developing scientific anti caries strategies related to diet. Methods: From December 2021 to June 2024, a questionnaire survey, a three day 24 hour dietary review survey, oral health examination, physical development measurement and Childhood Autism Rating Scale (CARS) evaluation were conducted involving 147 children and adolescents aged 2-22 years with NDD from nine special education schools and rehabilitation institutions in Tianjin. Group comparisons were carried out using the Mann-Whitney U test, Chi-square test, or Fisher s exact probability method. The correlation between dietary quality and dental caries was analyzed by adopting multiple linear regression analysis and restricted cubic spline. Results: There were 46 children and adolescents (31.3%) in the non dental caries group and 101 children and adolescents (68.7%) in the dental caries group. The number of decayed missing and filled teeth (dmft) was 2.0 (4.0), and the MD score was 4.0 (2.0) points. There were 62 children and adolescents (42.2%) in the low MD scores group and 85 children and adolescents (57.8%) in the high MD scores group. There was no significant difference in MD scores between NDD children in the non dental caries group and those in the dental caries group [nondental caries group:4.0(2.0), dental caries group:4.0(2.0), Z= -0.14, P >0.05]. The MD scores and dmft exhibited increasing and then decreasing trend ( P total =0.02, P non lineary = 0.04 ). Children and adolescents with NDD in the MD high scores group had a lower number of dmft than those in the MD low scores group ( β= -2.00 , 95%CI =-3.39 to -0.62, P <0.05). However, in children and adolescents with NDD and CARS scores ≥30, the above association was insignificant ( β=-0.63, 95%CI=-0.29-0.15, P >0.05). Conclusion Children and adolescents with NDD who have dietary patterns similar to the Mediterranean diet, are found to have fewer dental caries, and this is observed among those with no or mild symptoms of autism spectrum disorder.

Objective To investigate the knowledge of tuberculin skin test(TST)among healthcare workers and provide evidence for improving the standardization of TST screening in primary healthcare staff.Methods A questionnaire survey was conducted among 248 licensed physicians or nurses who were qualified as licensed physicians or nurses and responsible for TST work from 27 districts/counties of Chongqing in 2023.The awareness of TST-related knowledge and its influencing factors were statistically analyzed.Results The average TST knowledge score of 248 healthcare workers was(78.3±10.6)points.The overall awareness rate was 78.9%(8 213/10 416),with specific rates as follows:65.4%(1 135/1 736)for tubercu-losis knowledge,87.3%(3 248/3 720)for TST general knowledge,53.4%(795/1 488)for TST principles,88.0%(1 964/2 232)for TST procedures,and 86.4%(1 071/1 240)for TST result interpretation.Nurses showed higher awareness rates than physicians and other staff(P＞0.05).Healthcare workers from medium-epidemic areas demonstrated significantly higher awareness rates than those from high-and low-epidemic are-as(P＜0.001).No statistically significant differences were observed in gender,age,occupation type,institu-tion type,or regional epidemic level between the qualified group and non-qualified group about TST-related knowl-edge(P＞0.05).Conclusion Healthcare workers exhibit incomplete mastery of TST-related knowledge.Strengthening TST-related knowledge training for standardizing TST implementation.

Objective:To investigate ferroptosis-related genes in pterygium tissue by using bioinformatic analysis.Methods:The pterygium gene expression profile dataset GSE2513 was downloaded from the Gene Expression Omnibus Database to identify differentially expressed genes (DEGs) related to ferroptosis.Functional annotation and enrichment analysis of the DEGs were performed using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG).Hub genes were identified from the DEGs using LASSO logistic regression analysis and a support vector machine recursive feature elimination (SVM-REF).Single-gene GSEA analysis was performed on hub genes and a competitive endogenous RNA interaction network was constructed to determine the RNA regulatory relationships of the hub genes.Pterygium tissue samples from 9 patients (9 eyes) undergoing pterygium surgery and conjunctival tissue samples from 9 patients (9 eyes) undergoing strabismus surgery who visited the First Affiliated Hospital of Zhengzhou University were collected from 2022 to 2023 during surgery, and the expression of hub genes and ferroptosis-related marker genes was detected by fluorescence quantitative PCR.This study followed the Declaration of Helsinki, and the study protocol was reviewed and approved by the Ethics Committee of the First Affiliated Hospital of Zhengzhou University (No.2022-KY-0006-001).Results:In the dataset, there were 37 ferroptosis-related genes with significant expression differences, including 16 upregulated genes and 21 downregulated genes.GO analysis revealed significant enrichment in responses to external stimuli, responses to nutritional levels, responses to extracellular stimuli, responses to oxidative stress and starvation, transcription regulatory complexes, and RNA polymerase Ⅱ transcription regulatory complexes, RNA polymerase Ⅱ-specific transcription, and DNA-binding transcription.KEGG analysis showed that the DEGs were primarily enriched in ferroptosis and NOD-like receptor signaling pathways.LASSO regression analysis identified DUOX2, ATF3, NDRG1, EGR1, and ALDH3A2 as hub genes, and SVM-REF analysis identified NDRG1, NF2, IDH2, DUOX2, CHP1, ATF3, and SREBF1 as hub genes. DUOX2, ATF3, and NDRG1 were identified as the intersection hub genes.Single-gene GSEA analysis revealed that DUOX2 was enriched in the cell adhesion molecule CAMs pathway, the heparan sulfate glycosaminoglycan biosynthesis pathway, and the glycosaminoglycan biosynthesis ganglioside series pathway. ATF3 and NDRG1 were enriched in the PPAR signaling pathway and other pathways.Compared with normal conjunctival tissue, the relative expression levels of the ferroptosis markers PTGS2 and TFRC mRNA were increased in pterygium tissue, while the relative expression levels of FTH1, GPX4, SLC40A1, HSPB1, and NFE2L2 mRNA were decreased, with statistically significant differences ( t=12.220, 16.580, 5.664, 6.455, 8.691, 9.883, 17.590; all P<0.01). Conclusions:Ferroptosis may play an important role in the pathogenesis of pterygium. DUOX2, ATF3, and NDRG1 may be the hub genes affecting this complicated process.

Objective:To analyze effects of T11TS in the treatment of Cryptococcus neoformans fungal infection and the regula-tion of T-cell calcineurin(CaN)-activated T lymphoid nuclear factor(NFAT)pathway.Methods:SD rats infected with Cryptococcus neoformans were treated with immunoenhancer T11TS.Flow cytometry,Western blot and nuclear translocation were used to detect the changes of T cell function and related signal pathway.Results:The number of Cryptococcus neoformans in lung and spleen of CT3 group was significantly less than Cryptococcus neoformans infection group,CT1 group and CT2 group(P<0.05).The results of flow cy-tometry showed that the expression levels of LCK,FYN,LAT,PLCγ1,CaN,NFAT and IL-2 in Cryptococcus neoformans infection group were significantly lower than control group(P<0.05).The expression levels of LCK,FYN,LAT,PLCγ1,CaN,NFAT and IL-2 of CT1,CT2 and CT3 groups were significantly higher than Cryptococcus neoformans infection group(P<0.05).The results of Western blot were similar to those of flow cytometry.Conclusion:T11TS in the treatment of Cryptococcus neoformans infection can enhance the immunity of the body by up-regulating the expression of related signal factors in the CaN-NFAT pathway of T lymphocytes,increasing the expression of NFAT and IL-2,stimulating the activation and proliferation of T lymphocytes.

Objective To investigate the effects of acteoside in a rat model on of diabetic nephropathy(DN)and high-glucose-induced glomerular mesangial cells(GMCs),focusing on the role of acteoside in the silent information regulator 1(SIRT1)/nuclear factor eryth-roid 2-related factor 2(Nrf2)signaling pathway.Methods GMCs were cultured under normal glucose conditions or stimulated with high glucose.Fibrosis,oxidative stress,SIRT1 and Nrf2 protein expression,and mitochondrial structure were assessed in four groups:normal glucose,high glucose,high glucose+acteoside,and high glucose+acteoside+SIRT1 inhibitor(hsa62).DN was induced in rats via intraperitoneal streptozotocin injection,and animals were divided into control,model,and acteoside-treated groups.Pathological kidney changes,blood glucose changes,renal function indices,and protein expression of SIRT1 and Nrf2 were evaluated.Results Compared with controls,DN model rats showed significantly elevated fasting blood glucose,serum creatinine,blood urea nitrogen,and 24-h urinary protein levels of rats in the model group were significantly increased(P＜0.01).GMCs exhibited increased fibrosis,oxidative stress,and mitochondrial damage.Acteoside treatment significantly improved all measured parameters(P＜0.01);and mitigated mitochondrial injury.In vitro,acteoside reduced high-glucose-induced fibrosis and oxidative stress in GMCs,effects that were reversed by SIRT1 inhibition.Western blotting confirmed upregulation of SIRT1 and Nrf2 expression in both treated rat kidney tissues and GMCs(P＜0.01).Conclusion Acteoside alleviates glomerular fibrosis and oxidative stress in DN by activating the SIRT1/Nrf2 signaling pathway,suggesting its potential therapeutic agent for DN.