Xinxiang Medical University has a vast campus with about 7000 undergraduates.The Foreign Students Programme of Xinxiang Medical University under the International Education Institute of XXMU, has been running successfully at the university since 2001.More than 1000 foreign students from Nepal and India have already graduated from the university since 2001.There are more than 120 foreign students pursuing Western Medicine studies at this college..
This research was developed a neuron specific enolase (NSE) biosensor on titanium oxide (TiO2) modified interdigitated microelectrodes (IDME). Biotin-streptavidin strategy was utilized to immobilize the aptamer on IDME. It was identified that higher number of streptavidin and aptamer complex captured on IDME when the surface modified with TiO2 compared with a direct immobilization. The sandwich pattern with aptamer and antibody was performed on TiO2-modified surfaces. The detection limit of NSE was identified as 0.1 ng/mL with an R2 value of 0.9826 [y = 9.6984x—13.089]. To enhance the detection performance, the antibody was conjugated with goldurchin and it increases the current flow, detecting NSE-spiked serum as low as 0.1 ng/mL. Besides, control experiments with Interleukin-6, Carcinoembryonic antigen, and complementary aptamer sequence (a non-binding aptamer) fail to enhance the current responses. This NSE biosensor quantifies the lower level of target and helps to diagnose lung cancer and severity.
Fruit preservation and shelf life extension rely heavily on effective materials, but current methods often fail to combine key functions like antibacterial protection and freshness retention. This study aims to develop a multifunctional hydrogel to address the existing challenges in grape preservation. The hydrogel, termed as CS-se-HAgel, was fabricated via Schiff base reactions between dialdehyde chitosan (DACS) and 2,2’-diselanediyldiethanamine (DD)-conjugated hyaluronic acid (DDHA) polymers. Studies found that CS-se-HAgel possessed an outstanding swelling ratio, low cytotoxicity, good water retention, and excellent mechanical properties. Besides, it also showed potent antibacterial activity, which prevented the treated grapes from rotting and wrinkling. Significantly, CS-se-HAgel also decreased water loss from grapes and maintained their total soluble solid (TSS) and pH stability, prolonging the shelf life of harvested grapes at ambient temperature. Therefore, it could be speculated that CS-se-HAgel has potential applications for fruit preservation in the food industry.
Frataxin (FXN) is a mitochondrial protein involved in various cellular processes. To date, the role of FXN in the initiation and progression of colon adenocarcinoma (COAD) remains unclear. This study aimed to investigate FXN expression in COAD and its involvement in COAD initiation and progression. FXN expression in COAD was assessed via bioinformatics and immunohistochemistry (IHC) validation. The association between FXN expression and prognosis was evaluated using Kaplan‑Meier analysis and Cox regression analysis. Gene Ontology-Biological Process (GO-BP) enrichment analysis was performed to explore the potential biological functions of FXN in COAD. Functional assays (CCK-8, colony formation, Transwell) were used to confirm the critical role of FXN in COAD cell proliferation, migration, and invasion. R language, single‑sample gene-based enrichment analysis (ssGSEA), and correlation analysis were applied to identify associations between FXN expression and immune infiltration, immunotherapy response, and drug sensitivity. Compared with normal colon tissue, FXN expression was upregulated in COAD tissue (p < 0.05), and high FXN expression predicted poor prognosis in COAD patients (p < 0.05). GO-BP enrichment analysis revealed that FXN correlated with cell proliferation and microtubule dynamics (p < 0.05). Downregulating FXN inhibited proliferation, migration, and invasion of COAD cells (p < 0.05). FXN expression showed a correlation with several immune cells and immune cell markers, but no significant correlation with immunophenoscore (IPS). Drug sensitivity analysis indicated that FXN was associated with COAD samples’ sensitivity to several anticancer drugs (p < 0.001). FXN may promote the malignant phenotype of COAD and correlate with immune infiltration, serving as a prognostic biomarker and a potential reference for chemotherapy but not for immune checkpoint blockade.
Keloid formation originates from the abnormal activation of fibroblasts, which differentiate into myofibroblasts and excessively secrete collagen, leading to dysregulated deposition of extracellular matrix (ECM) and tissue fibrosis. We aim to explore the role and the mechanism of USP53 in keloid-derived fibroblasts (KFs) proliferation, invasion, and telomerase activity. Bioinformatics analysis was performed to obtain the genes differentially expressed between keloid tissue and normal tissue, as well as the enriched pathways. The KFs were isolated and transfected with USP53 silencing and overexpression plasmids. KFs proliferation, apoptosis, EMT and telomerase properties were explored. The protein expression of CDK1, Collagen I, E-cadherin, Snail, Slug, Cleaved-Caspase 3, and Caspase 3 was examined by western blotting. The interaction between USP53 and TJP2 was explored by Co-IP, and the rescue experiment was also performed. Finally, the in vivo experiments of keloid in nude mice was conducted. USP53 was downregulated in keloid tissues. Knockdown of USP53 promoted the proliferation, epithelial–mesenchymal transition (EMT), and telomerase activity, while inhibiting cell apoptosis in KFs. In contrast, USP53 overexpression exerted opposite effects. USP53 could interact with TJP2. Overexpression of USP53 led to slower TJP 2 degradation, and USP53 enhanced the stability of TJP 2. Moreover, USP53 activated the AMPK pathway. USP53 inhibited cell proliferation in vivo. USP53 regulates the AMPK pathway by deubiquitinating of TJP2 and inhibits the KFs proliferation, invasion, and telomerase activity.
Diabetic kidney disease (DKD) constitutes a major microvascular sequela of diabetes mellitus. Ferroptosis, a distinct cell death modality contingent upon ferrous ion dysregulation, is involved in the pathogenesis of DKD. Celastrol is an active compound isolated from Tripterygium wilfordii, which has anti-inflammatory and antioxidant properties and is related to the improvement of DKD, but its exact molecular basis has not been fully determined. This study aimed to determine whether celastrol attenuates renal tubular ferroptosis in early DKD through modulation of NADPH oxidase 2 (NOX2) expression. Renal tissue samples from patients with early DKD and controls were analyzed for ferroptosis-related pathological changes using Perls staining, immunohistochemistry, and transmission electron microscopy. In addition, we established an early DKD rat model in which the animals were treated with celastrol to investigate its molecular mechanisms of action. The results showed that renal tissue from patients with early DKD and model rats had increased iron deposition, reduced glutathione peroxidase 4 (GPX4) expression, lipid peroxide accumulation, and mitochondrial structural damage. Celastrol reversed these pathological changes while significantly reducing urinary protein levels. Additionally, NOX2 expression was significantly elevated in early DKD renal tissue but was effectively suppressed by celastrol. The NOX2 agonist PMA co-treatment partially abrogated the renoprotective effects of celastrol. Collectively, these findings demonstrate that celastrol ameliorates ferroptosis-mediated renal tubular injury in early DKD, and this protective mechanism is associated with the downregulation of NOX2 expression. This study furnishes preliminary evidence for investigating celastrol's mechanistic role against early DKD.
