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Transition metal sulfides have been explored as electrode materials for non-enzymatic detection. In this work, we investigated the effects of phosphorus doping on the electrochemical performances of NiCoS electrodes (P-NiCoS) towards glucose oxidation. The fabricated non-enzymatic biosensor displayed better sensing performances than pristine NiCoS, with a good sensitivity of 250 µA mM cm, a low detection limit (LOD) of 0.46 µM (S/N = 3), a wide linear range of 0.001 to 5.2 mM, and high selectivity. Moreover, P-NiCoS demonstrated its feasibility for glucose determination for practical sample testing. This is due to the fact that the synergetic effects between Ni and Co species, and the partial substitution of S vacancies with P can help to increase electronic conductivity, enrich binary electroactive sites, and facilitate surface electroactivity. Thus, it is found that the incorporation of dopants into NiCoS is an effective strategy to improve the electrochemical activity of host materials.
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http://dx.doi.org/10.3390/bios12100823 | DOI Listing |
Int J Vitam Nutr Res
August 2025
Department of Pharmaceutical Technology, Faculty of Pharmacy, University of Dhaka, 1000 Dhaka, Bangladesh.
Diabetes mellitus (DM) is a chronic metabolic disorder characterized by persistent hyperglycemia and associated with severe complications, including cardiovascular diseases, neuropathy, nephropathy, and retinopathy. Although synthetic antidiabetic drugs are available, the side effects and limited long-term effectiveness of these medications highlight the urgent need for safer, more potent alternative therapies. L.
View Article and Find Full Text PDFInt J Vitam Nutr Res
August 2025
Department of Endocrinology, Affiliated Hospital of Integrated Chinese and Western Medicine, Nanjing University of Chinese Medicine, 210028 Nanjing, Jiangsu, China.
Background: Dietary interventions have exhibited promise in restoring microbial balance in chronic kidney disease. A low-protein calorie-restricted diet can reduce kidney injury in diabetic rodents. However, whether the renoprotective effects of this dietary intervention in murine diabetic kidney disease models are linked to gut microbiota modulation remains to be determined.
View Article and Find Full Text PDFFront Mol Neurosci
August 2025
Department of Cardiovascular Sciences, Lewis Katz School of Medicine, Lemole Center for Integrated Lymphatics and Vascular Research, Temple University, Philadelphia, PA, United States.
Introduction: Endothelial-to-mesenchymal transition (EndoMT), cell death, and fibrosis are increasingly recognized as contributing factors to Alzheimer's disease (AD) pathology, but the underlying transcriptomic mechanisms remain poorly defined. This study aims to elucidate transcriptomic changes associated with EndoMT, diverse cell death pathways, and fibrosis in AD using the 3xTg-AD mouse model.
Methods: Using RNA-seq data and knowledge-based transcriptomic analysis on brain tissues from the 3xTg-AD mouse model of AD.
Int J Nanomedicine
September 2025
School of Pharmaceutical Sciences, Key Laboratory of Targeting Therapy and Diagnosis for Critical Diseases, Zhengzhou University, Zhengzhou, 450001, People's Republic of China.
Purpose: This study aimed to develop a composite nanozyme system (Au/PB-Ce6-HA) based on gold nanoparticles (AuNPs) and Prussian blue nanoparticles (PBNPs) to combat tumor hypoxia and insufficient endogenous hydrogen peroxide (HO) deficiency, thus enhancing the efficacy of sonodynamic therapy (SDT) and starvation therapy for liver cancer.
Methods: The Au/PB-Ce6-HA system was constructed by in situ embedding AuNPs on PBNPs, loading the sonosensitizer Chlorin e6 (Ce6), and surface-coating with thiolated hyaluronic acid (HA-SH). The system was evaluated both in vitro and in vivo to assess its ability to catalyze glucose to generate HO, decompose HO to produce oxygen, and generate highly toxic reactive oxygen species (ROS) under ultrasound irradiation.
Front Pharmacol
August 2025
Department of Neurology, Fujian Medical University Union Hospital, Fuzhou, Fujian, China.
Introduction: Ischemic stroke is a leading cause of mortality and disability worldwide, with limited therapeutic options and high rates of recurrence. Mitochondrial dysfunction plays a critical role in neuronal injury during ischemia-reperfusion, making mitochondrial autophagy a potential therapeutic target. Gypenoside XLIX, a major active metabolite of Gynostemma pentaphyllum, exhibits antioxidant and organ-protective properties, but its effects on neuronal mitochondrial damage in stroke remain unclear.
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