Browse Articles

Climate change threatens water resources over the Qinghai-Tibetan plateau

Elite leader dwarf mongoose optimization algorithm

Two stage malware detection model in internet of vehicles (IoV) using deep learning-based explainable artificial intelligence with optimization algorithms

Transcranial direct current stimulation over motor cortex improves pain in end stage renal disease a randomized controlled trial

Abstract Improving pain management and physical function remains a significant challenge for patients affected by end-stage renal disease (ESRD) undergoing hemodialysis. Non-pharmacological interventions, such as transcranial direct current stimulation (tDCS), have gained attention for their potential to alleviate pain and improve functional outcomes. This study explored the effects of tDCS on pain, fatigue, and functional performance in patients affected by ESRD undergoing hemodialysis and experiencing chronic pain. Thirty-four participants were randomized to receive either active or sham tDCS, with 15 sessions administered over five weeks. Anodal tDCS over C3 with an intensity of 2 mA was administered in 15 sessions, 3 times per week. Visual Analogue Scale for pain (VAS), fatigue, functional performance (sit-to-stand test, stationary walk, timed up and go test (TUG), elbow flexion test, and manual dynamometry) were assessed. We found a significant difference in VAS (p < 0.001) between groups and across time (fifteenth session p < 0.001; at the first, p < 0.001; and second follow-up, p < 0.001). TUG showed significant differences between-group analysis (p = 0.009). No significant differences between groups were observed for fatigue (p = 0.21) and all others functional tests. These findings suggest that tDCS may be a promising, non-invasive intervention for managing pain and improving mobility in patients affected by ESRD undergoing hemodialysis. Future studies with larger samples and extended follow-ups are warranted to further validate these findings and explore the long-term benefits of tDCS. Trial registration: The study is registered on the Brazilian Clinical Trials Registry (ID: RBR-7kym6v8).

A follow-up study on the novel use of contrast-enhanced susceptibility-weighted imaging for extremity desmoid fibromatosis response assessment

Independent component analysis of oddball EEG recordings to detect Parkinson’s disease

MeshHSTGT: hierarchical spatio-temporal fusion for mesh network traffic forecasting

Effect of regular soccer training on morphological and motor characteristics of deaf girls aged 14–18 years: a comparative analysis

In vivo pulse-chase in Caenorhabditis elegans reveals intestinal histone turnover changes upon starvation

RBPMS2 can inhibit the NLRP3 / caspase-1 / GSDMD signaling pathway to resist pyroptosis in gastric cancer cells

Design of a plasmonic optical biosensor based on a metal-insulator-metal ring resonator for the detection of various bacterial pathogens

Prediction of rock burst risk in underground openings based on intuitionistic fuzzy set

Functional brain abnormalities in post COVID-19 condition and their relationship with cognition

A novel UHPLC-HRMS method for simultaneous determination of 20 amino metabolites and proteins in lymphoma patients’ cells and serum

An enzyme-free electrochemical biosensor for sensitive and specific detection of microRNA-21 based on target recycling amplification and non-linear hybridization chain reaction

Evaluation the low cost of vibration and acoustics techniques based on novel cavitation detecting in axial pumps by varying load conditions and statistical method

Comparative transcriptomics of salinomycin molecular toxicity in chicken and turkey

Abstract Salinomycin (Sal) is an antiparasitic agent used in veterinary medicine and is characterized by low therapeutic index and high toxicity. Among poultry, chickens are resistant to Sal toxicity, but turkeys are considered susceptible. However, underlying mechanisms of Sal toxicity are poorly understood. This comparative transcriptomic study aimed to determine molecular toxicity mechanisms of Sal in both species. We conducted two experiments on chickens and turkeys exposed to Sal (0.9 mg/kg b.w/day) vs. unexposed. Heart and liver (n = 6) were collected post-mortem (chicken 5th; turkey 13th week). RNA was isolated and examined by RNA-seq to identify differentially expressed (DE) genes and pathways. Number of significant DE genes in chicken was 673 (heart) and 3049 (liver), and in turkey, 485 (heart) and 2337 (liver). Enrichment analysis revealed that Sal exposure activated platelet signaling in chicken heart, while it induced cell cycle arrest in turkey heart. In liver, impaired Sal biotransformation was determined as a shared response. In turkey liver, we determined that extracellular matrix pathway was upregulated, which could indicate liver fibrosis. Our findings demonstrate that molecular toxicity of Sal differs between species and turkey confirmed being more susceptible to Sal toxicity also at molecular level via induced cell cycle arrest and fibrosis.

Spatiotemporal patterns of wet–dry encounters between water source and receiving areas in the South-to-North water transfer project

Secreted EMC10 inhibits muscle GLUT4 activity and glucose uptake in mice

Inetetamab triggers cardiotoxicity through its interaction with apoptosis, oxidative stress and autophagy pathways

Abstract Inetetamab, a trastuzumab biosimilar, has obtained approval for the treatment of HER2-positive advanced metastatic breast cancer. Despite studies indicating its cardiotoxic properties, the intricate mechanisms underlying its toxicity remain elusive. In the present study, we demonstrated in vitro that exogenous administration of Inetetamab triggered injury in H9c2 myocardial cells, characterized by a significant decrease in cell viability and noticeable morphological changes. Furthermore, exogenous exposure to Inetetamab elicited a series of toxic effects within H9c2 cells, notably promoting apoptosis and autophagy, diminishing the mitochondrial membrane potential (DCm), and elevating intracellular ROS production. Concurrently, there was a notable decrease in intracellular MDA generation, accompanied by disruption of the GSH/GSSG balance. In vivo mouse model, Inetetamab administration prominently induced cardiomyocyte injury, characterized by the pathological change in the myocardial tissue and a marked elevation in serum levels of creatine kinase isoenzyme (CK-MB), brain natriuretic peptide (BNP) and cardiac troponin I (cTnI). Similarly, Inetetamab administration also initiated cardiomyocyte apoptosis and oxidative stress injury in vivo. Furthermore, Inetetamab administration significantly modulated the expression of apoptosis- and autophagy-related proteins both in vivo and in vitro. Our study highlights Inetetamab induces cardiotoxicity by affecting apoptosis, oxidative stress and autophagy.