Magnesium Depletion Score as a Novel Predictor of Cognitive Impairment: A Population-Based Cross-Sectional Study From NHANES.

Objective: Magnesium (Mg) deficiency may accelerate neurodegenerative disease progression, but current cognitive impairment biomarkers have significant limitations. This study aimed to investigate the association between Mg depletion score (MDS) and cognitive impairment.

Design: This study is a cross-sectional analysis using data from the 2011-2014 National Health and Nutrition Examination Survey (NHANES) to examine the relationship between MDS and cognitive performance.

Case Report: Posterior reversible encephalopathy syndrome after lenvatinib treatment for hepatocellular carcinoma.

Background: Posterior reversible encephalopathy syndrome (PRES) is characterized by headaches, vision loss, confusion, encephalopathy, seizures, and reversible focal edema on neuroimaging. Early recognition and treatment of PRES are essential to prevent severe complications. Lenvatinib is a multi-targeted kinase inhibitor that is used as a first-line treatment for patients with hepatocellular carcinoma (HCC).

Pyridostigmine attenuated high-fat-diet induced liver injury by the reduction of mitochondrial damage and oxidative stress via α7nAChR and M3AChR.

Obesity is a major cause of nonalcohol fatty liver disease (NAFLD), which is characterized by hepatic fibrosis, lipotoxicity, inflammation, and apoptosis. Previous studies have shown that an imbalance in the autonomic nervous system is closely related to the pathogenesis of NAFLD. In this study, we investigated the effects of pyridostigmine (PYR), a cholinesterase (AChE) inhibitor, on HFD-induced liver injury and explored the potential mechanisms involving mitochondrial damage and oxidative stress.

Baicalein ameliorated obesity-induced cardiac dysfunction by regulating the mitochondrial unfolded protein response through NRF2 signaling.

Background: The mitochondrial unfolded protein response (UPR) is the first line of defense against mitochondrial dysfunction in several diseases. Baicalein, which is an extract of Scutellaria baicalensis Georgi roots, exerts mitoprotective effects on metabolic disorders and cardiovascular diseases. However, it remains unclear whether baicalein alleviates obesity-induced cardiac damage through the UPR.

Impact of the Expert Consensus on Carbapenem Consumption Trends and Patterns in Public Healthcare Institutes: An Interrupted Time Series Analysis, 2017-2020.

Carbapenems are considered the last line of defence against bacterial infections, but their high consumption and the resulting antibacterial resistance are an increasing global concern. In this context, the Chinese health authority issued an expert consensus on the clinical applications of carbapenems. However, the long- and short-term effects of the expert consensus on carbapenem use are not clear.

Acetylcholine reduces palmitate-induced cardiomyocyte apoptosis by promoting lipid droplet lipolysis and perilipin 5-mediated lipid droplet-mitochondria interaction.

Lipid droplets (LDs), which are neutral lipid storage organelles, are important for lipid metabolism and energy homeostasis. LD lipolysis and interactions with mitochondria are tightly coupled to cellular metabolism and may be potential targets to buffer the effects of excessive toxic lipid species levels. Acetylcholine (ACh), the major neurotransmitter of the vagus nerve, exhibits cardioprotective effects.

[Recent progress on obesity-induced myocardial remodeling and its possible mechanism of mitochondrial dyshomeostasis].

Obesity is an important risk factor for cardiovascular diseases, which can lead to a variety of cardiovascular diseases including myocardial remodeling. Obesity may induce myocardial dysfunction by affecting hemodynamics, inducing autonomic imbalance, adipose tissue dysfunction, and mitochondrial dyshomeostasis. The key necessary biochemical functions for metabolic homeostasis are performed in mitochondria, and mitochondrial homeostasis is considered as one of the key determinants for cell viability.

Cholinergic drugs ameliorate endothelial dysfunction by decreasing O-GlcNAcylation via M3 AChR-AMPK-ER stress signaling.

Aims: Obesity is associated with increased cardiovascular morbidity and mortality. It is accompanied by augmented O-linked β-N-acetylglucosamine (O-GlcNAc) modification of proteins via increasing hexosamine biosynthetic pathway (HBP) flux. However, the changes and regulation of the O-GlcNAc levels induced by obesity are unclear.

Choline ameliorates cardiac hypertrophy by regulating metabolic remodelling and UPRmt through SIRT3-AMPK pathway.

Aims: Cardiac hypertrophy is characterized by a shift in metabolic substrate utilization, but the molecular events underlying the metabolic remodelling remain poorly understood. We explored metabolic remodelling and mitochondrial dysfunction in cardiac hypertrophy and investigated the cardioprotective effects of choline.

Methods And Results: The experiments were conducted using a model of ventricular hypertrophy by partially banding the abdominal aorta of Sprague Dawley rats.

Choline ameliorates cardiovascular damage by improving vagal activity and inhibiting the inflammatory response in spontaneously hypertensive rats.

Autonomic dysfunction and abnormal immunity lead to systemic inflammatory responses, which result in cardiovascular damage in hypertension. The aim of this report was to investigate the effects of choline on cardiovascular damage in hypertension. Eight-week-old male spontaneously hypertensive rats (SHRs) and Wistar-Kyoto rats were intraperitoneally injected with choline or vehicle (8 mg/kg/day).

Acetylcholine Attenuates Hypoxia/Reoxygenation Injury by Inducing Mitophagy Through PINK1/Parkin Signal Pathway in H9c2 Cells.

Acetylcholine (ACh) protected against cardiac injury via promoting autophagy and mitochondrial biogenesis, however, the involvement of mitophagy in ACh-elicited cardioprotection remains unknown. In the present study, H9c2 cardiomyocytes were subjected to hypoxia/reoxygenation (H/R) and ACh treatment during reoxygenation. Mitophagy markers PTEN-induced kinase 1 (PINK1) and Parkin translocation were examined using western blot and confocal fluorescence microscopy.