Publications by authors named "Y C Kan"

Recently study has found a new form of copper-dependent death called cuproptosis, which differs from apoptosis, ferroptosis, and necrosis. The main process of cuproptosis is copper directly combined with lipid-acetylated proteins in the TCA cycle of mitochondrial response, leading to the aggregation of lipid-acetylated proteins and the loss of Fe-S cluster proteins, resulting in mitochondrial dysfunction, and eventually causing cell death. Previous studies demonstrated that an imbalance in copper homeostasis exacerbates the pathological progression of Alzheimer's disease (AD) through the induction of oxidative stress, inflammatory response, and the accumulation of Aβ deposition and tau protein hyperphosphorylation.

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Background: Fomesafen is a selective herbicide widely used to control post-emergent broad-leaf weeds in soybean and peanut fields. Because of its persistent nature in soil, it can suppress subsequent crops, including wheat. There is limited information focusing on methods of protecting wheat from fomesafen injury by soil residue.

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Background: Despite the increasing number of publications on glioma radiomics, challenges persist in clinical translation.

Aim: To assess the development and reporting quality of radiomics in brain gliomas since 2019.

Methods: A bibliometric analysis was conducted to reveal trends in brain glioma radiomics research.

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Fomesafen is a herbicide with long persistence in soil, causing damage to succeeding crops. Dichlormid is a widely used safener protecting maize from chloroacetanilide and thiocarbamate injury. We found that dichlormid treatment could restore the growth of wheat seedlings exposed to fomesafen stress.

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Neurovascular coupling (NVC) refers to the process of local changes in cerebral blood flow (CBF) after neuronal activity, which ensures the timely and adequate supply of oxygen, glucose, and substrates to the active regions of the brain. Recent clinical imaging and experimental technology advancements have deepened our understanding of the cellular mechanisms underlying NVC. Pathological conditions such as stroke, subarachnoid hemorrhage, cerebral small vascular disease, and vascular cognitive impairment can disrupt NVC even before clinical symptoms appear.

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