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Accumulation of advanced oxidative protein products exacerbate satellite glial cells activation and neuropathic pain.

Mol Med

January 2025

Division of Spine Surgery, Department of Orthopedics, Nanfang Hospital, Southern Medical University, 1838 North Guangzhou Ave, Guangzhou, 510515, People's Republic of China.

Background: Neuropathic pain (NP) is a debilitating condition caused by lesion or dysfunction in the somatosensory nervous system. Accumulation of advanced oxidation protein products (AOPPs) is implicated in mechanical hyperalgesia. However, the effects of AOPPs on NP remain unclear.

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Functional properties of aged hypothalamic cells.

Vitam Horm

January 2025

Department Normal Physiology, Yaroslavl State Medical University, Yaroslavl, Russia. Electronic address:

The hypothalamus, in addition to controlling the main body's vital functions, is also involved in aging regulation. The aging process in the hypothalamus is accompanied by disturbed intracellular pathways, including Ca signaling and neuronal excitability in the brain. Intrinsic electrophysiological properties of individual neurons and synaptic transmission between cells is disrupted in the central nervous system of old animals.

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AhASRK1, a peanut dual-specificity kinase that activates the Ca-ROS-MAPK signalling cascade to mediate programmed cell death induced by aluminium toxicity via ABA.

Plant Physiol Biochem

January 2025

Guangxi Key Laboratory for Agro-Environment and Agro-Product Safety, College of Agriculture, GuangXi University, Nanning, 530004, China; National Demonstration Center for Experimental Plant Science Education/College of Agriculture, Nanning, 530004, China; Guangxi University Key Laboratory of Crop Cultivation and Tillage, Nanning, 530004, China. Electronic address:

Aluminium (Al)-induced programmed cell death (PCD) is thought to be a main cause of Al phytotoxicity. However, the underlying mechanism by which Al induces PCD in plants is unclear. In this study, we characterized the function of AhASRK1 (Aluminum Sensitive Receptor-like protein Kinase1), an Al-induced LRR-type receptor-like kinase gene.

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Mechanisms of epigallocatechin-3-gallate-loaded metal-organic framework in preventing oxidative degradation of shrimp (Litopenaeus vannamei) surimi gel.

Food Chem

January 2025

Shenzhen Key Laboratory of Food Nutrition and Health, Guangdong Engineering Technology Research Center of Aquatic Food Processing and Safety Control, College of Chemistry and Environmental Engineering, Shenzhen University, Shenzhen 518060, China; State Key Laboratory of Marine Food Processing & Safety Control, National Engineering Research Center of Seafood, Collaborative Innovation Center of Seafood Deep Processing, School of Food Science and Technology, Dalian Polytechnic University, Dalian 116034, China. Electronic address:

This work aimed to elucidate the deterioration mechanisms of shrimp surimi gels during refrigerated storage, and the regulatory mechanisms of epigallocatechin-3-gallate loaded cyclodextrin-based metal-organic framework (EGCG@CD-MOF) as a model antioxidant. Labele-free proteomics provided a quantitative analysis of the differential proteomic signatures of degraded proteins. Structural proteins, like myosin, paramyosin, titin, laminin, and α-actinin, along with calcium regulatory proteins, like calcineurin and sarcoplasmic calcium-binding protein were found to be highly susceptible to oxidative degradation during refrigeration.

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In 2017, Kidney Disease: Improving Global Outcomes (KDIGO) published a Clinical Practice Guideline Update for the Diagnosis, Evaluation, Prevention, and Treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD). Since then, new lines of evidence have been published related to evaluating disordered mineral metabolism and bone quality and turnover, identifying and inhibiting vascular calcification, targeting vitamin D levels, and regulating parathyroid hormone. For an in-depth consideration of the new insights, in October 2023, KDIGO held a Controversies Conference on CKD-MBD: Progress and Knowledge Gaps Toward Personalizing Care.

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