Catechin Protects against Lipopolysaccharide-induced Depressive-like Behaviour in Mice by Regulating Neuronal and Inflammatory Genes.

Background: Many studies have suggested that tea has antidepressant effects; however, the underlying mechanism is not fully studied. As the main anti-inflammatory polyphenol in tea, catechin may contribute to the protective role of tea against depression.

Objective: The objective of this study is to prove that catechin can protect against lipopolysaccharide (LPS)-induced depressive-like behaviours in mice, and then explore the underlying molecular mechanisms.

Effect of eIF2α in Neuronal Injury Induced by High Glucose and the Protective Mechanism of Resveratrol.

Diabetes mellitus (DM) is a type of metabolic disease characterized by chronic hyperglycemia, which can lead to different degrees of cognitive decline. Therefore, it is crucial to explore the molecular biological mechanisms of neuronal injury. In this study, we investigated the effect of high glucose on eIF2α expression and the mechanism of neuronal injury, and on this basis, the protective mechanism of resveratrol is explored.

A Novel PLLA/MgF Coating on Mg Alloy by Ultrasonic Atomization Spraying for Controlling Degradation and Improving Biocompatibility.

Problems of rapid degradation and poor biocompatibility (endothelialization and hemocompatibility) limit magnesium (Mg) alloy's further applications in vascular stents. To solve these problems, a novel composite coating was designed on Mg alloy via a two-step method. First, a Mg alloy sample was immersed in hydrofluoric acid.

Effects and mechanisms of probucol on aging-related hippocampus-dependent cognitive impairment.

Background: In the present study, we aimed to investigate the effects of probucol on aging-related hippocampus-dependent cognitive impairment and explore the potential mechanisms.

Methods: D-galactose (100 mg/kg, once daily for 6 weeks) was subcutaneously injected to induce aging in mice. Then the mice were administered with probucol or vehicle once a day for 2 weeks.

Overexpression of miR-99a in hippocampus leads to impairment of reversal learning in mice.

As one of the most common human genetic disorders, Down syndrome (DS) is characterized by a mild-to-moderate cognitive disability, which mainly results from genes overexpression on chromosome 21. The expression of miR-99a, a gene harboring on chromosome 21, is increased by 50 folds in DS brain samples. This study aims to investigate the effect of miR-99a overexpression in the hippocampus on mouse behaviors and explore the underlying mechanisms.

Cell cycle deregulation in neurodegenerative diseases.

: Cell cycle is critical for a wide range of cellular processes such as proliferation, differentiation and apoptosis in dividing cells. Neurons are postmitotic cells which have withdrawn from the cell division cycle. Recent data show us that inappropriate activation of cell cycle regulators including cyclins, cyclin dependent kinases (CDKs) and endogenous cyclin dependent kinase inhibitors (CDKIs) may take part in the aetiology of neurodegenerative diseases.

Influence and analysis of ambulance on the containment of COVID-19 in China.

New coronavirus (COVID-19) is a newly emerging and highly infectious form of typical pneumonia with a high rate of transmission. The COVID-19 pneumonia has spread to 147 countries and areas as of Mar.16th 2020, which has tremendous impact on the global public health.

Inhibition of lysine-specific demethylase 1A suppresses neointimal hyperplasia by targeting bone morphogenetic protein 2 and mediating vascular smooth muscle cell phenotype.

Objectives: Vascular disorders are associated with phenotypical switching of vascular smooth muscle cells (VSMCs). We investigated the effect of bone morphogenetic protein (BMP)-2 in controlling VSMC phenotype and vascular disorder progression. Lysine (K)-specific demethylase 1A (KDM1A) has been identified to target BMP-2 and is employed as a therapeutic means of regulating BMP-2 expression in VSMCs.

Metformin Protects Neurons against Oxygen-Glucose Deprivation/Reoxygenation -Induced Injury by Down-Regulating MAD2B.

Background/aims: Metformin, the common medication for type II diabetes, has protective effects on cerebral ischemia. However, the molecular mechanisms are far from clear. Mitotic arrest deficient 2-like protein 2 (MAD2B), an inhibitor of the anaphase-promoting complex (APC), is widely expressed in hippocampal and cortical neurons and plays an important role in mediating high glucose-induced neurotoxicity.

Metoprolol Inhibits Cardiac Apoptosis and Fibrosis in a Canine Model of Chronic Obstructive Sleep Apnea.

Aims: Emerging evidence suggested that obstructive sleep apnea (OSA) was independently associated with the development of heart failure. In this study, we explored the influence of chronic OSA on left ventricular structural remodeling in canines, and the potential therapeutical role of metoprolol.

Methods: Chronic OSA model was established by stopping the ventilator and closing the airway for 4 h/day apnea-ventilation cycles every other day for 12 weeks while metoprolol (5 mg· kg(-1)· day(-1)) were administered continuously.